Dermatology

For parents living in poverty, “diaper math” is a familiar and distressingly pressing daily calculation. Babies in the U.S. go through 6-10 disposable diapers a day, at an average cost of $70-$80 a month. Name-brand diapers with high-end absorption sell for as much as a half a dollar each, and can result in upwards of $120 a month in expenses.

One in every three American families cannot afford enough diapers to keep their infants and toddlers clean, dry, and healthy, according to the National Diaper Bank Network. For many parents, that leads to wrenching choices: diapers, food, or rent?

The COVID-19 pandemic has exacerbated the situation, both by expanding unemployment rolls and by causing supply chain disruptions that have triggered higher prices for a multitude of products, including diapers. Diaper banks – community-funded programs that offer free diapers to low-income families – distributed 86% more diapers on average in 2020 than in 2019, according to the National Diaper Bank Network. In some locations, distribution increased by as much as 800%.

Yet no federal program helps parents pay for this childhood essential. The government’s food assistance program does not cover diapers, nor do most state-level public aid programs.

California is the only state to directly fund diapers for families, but support is limited. CalWORKS, a financial assistance program for families with children, provides $30 per month to help families pay for diapers for children under age 3. Federal policy shifts also may be in the works: Democratic lawmakers are pushing to include $200 million for diaper distribution in the massive budget reconciliation package.

Without adequate resources, low-income parents are left scrambling for ways to get the most use out of each diaper. This stressful undertaking is the subject of a recent article in American Sociological Review by Jennifer Randles, PhD, professor of sociology at California State University–Fresno. In 2018, Randles conducted phone interviews with 70 mothers in California over nine months. She tried to recruit fathers as well, but only two men responded.

Dr. Randles spoke with KHN’s Jenny Gold about how the cost of diapers weighs on low-income moms, and the “inventive mothering” many low-income women adopt to shield their children from the harms of poverty. The conversation has been edited for length and clarity.

Q: How do diapers play into day-to-day anxieties for low-income mothers?

In my sample, half of the mothers told me that they worried more about diapers than they worried about food or housing.

I started to ask mothers, “Can you tell me how many diapers you have on hand right now?” Almost every one told me with exact specificity how many they had – 5 or 7 or 12. And they knew exactly how long that number of diapers would last, based on how often their children defecated and urinated, if their kid was sick, if they had a diaper rash at the time. So just all the emotional and cognitive labor that goes into keeping such careful track of diaper supplies.

They were worrying and figuring out, “OK, I’m down to almost my last diaper. What do I do now? Do I go find some cans [to sell]? Do I go sell some things in my house? Who in my social network might have some extra cash right now?” I talked to moms who sell blood plasma just to get their infants diapers.

Q: What coping strategies stood out to you?

Those of us who study diapers often call them diaper-stretching strategies. One was leaving on a diaper a little bit longer than someone might otherwise leave it on and letting it get completely full. Some mothers figured out if they bought a [more expensive] diaper that held more and leaked less, they could leave the diaper on longer.

They would also do things like letting the baby go diaperless, especially when they were at home and felt like they wouldn’t be judged for letting their baby go without a diaper. And they used every household good you can imagine to make makeshift diapers. Mothers are using cloth, sheets, and pillowcases. They’re using things that are disposable like paper towels with duct tape. They’re making diapers out their own period supplies or adult incontinence supplies when they can get a sample.

One of the questions I often get is, “Why don’t they just use cloth?” A lot of the mothers that I spoke with had tried cloth diapers and they found that they were very cost- and labor-prohibitive. If you pay for a full startup set of cloth diapers, you’re looking at anywhere from $500 to $1,000. And these moms never had that much money. Most of them didn’t have in-home washers and dryers. Some of them didn’t even have homes or consistent access to water, and it’s illegal in a lot of laundromats and public laundry facilities to wash your old diapers. So the same conditions that would prevent moms from being able to readily afford disposable diapers are the same conditions that keep them from being able to use cloth.

Q: You found that, for many women, the concept of being a good mother is wrapped up in diapering. Why is that?

Diapers and managing diapers was so fundamental to their identity as good moms. Most of the mothers in my sample went without their own food. They weren’t paying a cellphone bill or buying their own medicine or their own menstrual supplies, as a way of saving diaper money.

I talked to a lot of moms who said, when your baby is hungry, that’s horrible. Obviously, you do everything to prevent that. But there’s something about a diaper that covers this vulnerable part of a very young baby’s body, this very delicate skin. And being able to do something to meet this human need that we all have, and to maintain dignity and cleanliness.

A lot of the moms had been through the welfare system, and so they’re living in this constant fear [of losing their children]. This is especially true among mothers of color, who are much more likely to get wrapped up in the child welfare system. People can’t necessarily see when your baby’s hungry. But people can see a saggy diaper. That’s going to be one of the things that tags you as a bad mom.

Q: Was your work on diapers influenced by your experience as a parent?

When I was doing these interviews, my daughter was about 2 or 3. So still in diapers. When my daughter peed during a diaper change, I thought, “Oh, I can just toss that one. Here, let me get another clean one.” That’s a really easy choice. For me. That’s a crisis for the mothers I interviewed. Many of them told me they have an anxiety attack with every diaper change.

Q: Do you see a clear policy solution to diaper stress?

What’s kind of ironic is how much physical, emotional, and cognitive labor goes into managing something that society and lawmakers don’t even recognize. Diapers are still not really recognized as a basic need, as evidenced by the fact that they’re still taxed in 35 states.

I think what California is doing is an excellent start. And I think diaper banks are a fabulous type of community-based organization that are filling a huge need that is not being filled by safety net policies. So, public support for diaper banks.

The direct cash aid part of the social safety net has been all but dismantled in the last 25 years. California is pretty generous. But there are some states where just the cost of diapers alone would use almost half of the average state TANF [Temporary Assistance for Needy Families] benefit for a family of three. I think we really do have to address the fact that the value of cash aid buys so much less than it used to.

Q: Your body of work on marriage and families is fascinating and unusual. Is there a single animating question behind your research?

The common thread is: How do our safety net policies support low-income families’ parenting goals? And do they equalize the conditions of parenting? I think of it as a reproductive justice issue. The ability to have a child or to not have a child, and then to parent that child in conditions where the child’s basic needs are met.

We like to say that we’re child and family friendly. The diaper issue is just one of many, many issues where we don’t really put our money or our policies where our mouth is, in terms of supporting families and supporting children. I think my work is trying to get people to think more collectively about having a social responsibility to all families and to each other. No country, but especially the richest country on the planet, should have one in three very young children not having one of their basic needs met.

I interviewed one dad who was incarcerated because he wrote a bad check. And as he described it to me, he had a certain amount of money, and they needed both diapers and milk for the baby. And I’ll never forget, he said, “I didn’t make a good choice, but I made the right one.”

These are not fancy shoes. These are not name-brand clothes. This was a dad needing both milk and diapers. I don’t think it gets much more basic than that.
 

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

For parents living in poverty, “diaper math” is a familiar and distressingly pressing daily calculation. Babies in the U.S. go through 6-10 disposable diapers a day, at an average cost of $70-$80 a month. Name-brand diapers with high-end absorption sell for as much as a half a dollar each, and can result in upwards of $120 a month in expenses.

One in every three American families cannot afford enough diapers to keep their infants and toddlers clean, dry, and healthy, according to the National Diaper Bank Network. For many parents, that leads to wrenching choices: diapers, food, or rent?

The COVID-19 pandemic has exacerbated the situation, both by expanding unemployment rolls and by causing supply chain disruptions that have triggered higher prices for a multitude of products, including diapers. Diaper banks – community-funded programs that offer free diapers to low-income families – distributed 86% more diapers on average in 2020 than in 2019, according to the National Diaper Bank Network. In some locations, distribution increased by as much as 800%.

Yet no federal program helps parents pay for this childhood essential. The government’s food assistance program does not cover diapers, nor do most state-level public aid programs.

California is the only state to directly fund diapers for families, but support is limited. CalWORKS, a financial assistance program for families with children, provides $30 per month to help families pay for diapers for children under age 3. Federal policy shifts also may be in the works: Democratic lawmakers are pushing to include $200 million for diaper distribution in the massive budget reconciliation package.

Without adequate resources, low-income parents are left scrambling for ways to get the most use out of each diaper. This stressful undertaking is the subject of a recent article in American Sociological Review by Jennifer Randles, PhD, professor of sociology at California State University–Fresno. In 2018, Randles conducted phone interviews with 70 mothers in California over nine months. She tried to recruit fathers as well, but only two men responded.

Dr. Randles spoke with KHN’s Jenny Gold about how the cost of diapers weighs on low-income moms, and the “inventive mothering” many low-income women adopt to shield their children from the harms of poverty. The conversation has been edited for length and clarity.

Q: How do diapers play into day-to-day anxieties for low-income mothers?

In my sample, half of the mothers told me that they worried more about diapers than they worried about food or housing.

I started to ask mothers, “Can you tell me how many diapers you have on hand right now?” Almost every one told me with exact specificity how many they had – 5 or 7 or 12. And they knew exactly how long that number of diapers would last, based on how often their children defecated and urinated, if their kid was sick, if they had a diaper rash at the time. So just all the emotional and cognitive labor that goes into keeping such careful track of diaper supplies.

They were worrying and figuring out, “OK, I’m down to almost my last diaper. What do I do now? Do I go find some cans [to sell]? Do I go sell some things in my house? Who in my social network might have some extra cash right now?” I talked to moms who sell blood plasma just to get their infants diapers.

Q: What coping strategies stood out to you?

Those of us who study diapers often call them diaper-stretching strategies. One was leaving on a diaper a little bit longer than someone might otherwise leave it on and letting it get completely full. Some mothers figured out if they bought a [more expensive] diaper that held more and leaked less, they could leave the diaper on longer.

They would also do things like letting the baby go diaperless, especially when they were at home and felt like they wouldn’t be judged for letting their baby go without a diaper. And they used every household good you can imagine to make makeshift diapers. Mothers are using cloth, sheets, and pillowcases. They’re using things that are disposable like paper towels with duct tape. They’re making diapers out their own period supplies or adult incontinence supplies when they can get a sample.

One of the questions I often get is, “Why don’t they just use cloth?” A lot of the mothers that I spoke with had tried cloth diapers and they found that they were very cost- and labor-prohibitive. If you pay for a full startup set of cloth diapers, you’re looking at anywhere from $500 to $1,000. And these moms never had that much money. Most of them didn’t have in-home washers and dryers. Some of them didn’t even have homes or consistent access to water, and it’s illegal in a lot of laundromats and public laundry facilities to wash your old diapers. So the same conditions that would prevent moms from being able to readily afford disposable diapers are the same conditions that keep them from being able to use cloth.

Q: You found that, for many women, the concept of being a good mother is wrapped up in diapering. Why is that?

Diapers and managing diapers was so fundamental to their identity as good moms. Most of the mothers in my sample went without their own food. They weren’t paying a cellphone bill or buying their own medicine or their own menstrual supplies, as a way of saving diaper money.

I talked to a lot of moms who said, when your baby is hungry, that’s horrible. Obviously, you do everything to prevent that. But there’s something about a diaper that covers this vulnerable part of a very young baby’s body, this very delicate skin. And being able to do something to meet this human need that we all have, and to maintain dignity and cleanliness.

A lot of the moms had been through the welfare system, and so they’re living in this constant fear [of losing their children]. This is especially true among mothers of color, who are much more likely to get wrapped up in the child welfare system. People can’t necessarily see when your baby’s hungry. But people can see a saggy diaper. That’s going to be one of the things that tags you as a bad mom.

Q: Was your work on diapers influenced by your experience as a parent?

When I was doing these interviews, my daughter was about 2 or 3. So still in diapers. When my daughter peed during a diaper change, I thought, “Oh, I can just toss that one. Here, let me get another clean one.” That’s a really easy choice. For me. That’s a crisis for the mothers I interviewed. Many of them told me they have an anxiety attack with every diaper change.

Q: Do you see a clear policy solution to diaper stress?

What’s kind of ironic is how much physical, emotional, and cognitive labor goes into managing something that society and lawmakers don’t even recognize. Diapers are still not really recognized as a basic need, as evidenced by the fact that they’re still taxed in 35 states.

I think what California is doing is an excellent start. And I think diaper banks are a fabulous type of community-based organization that are filling a huge need that is not being filled by safety net policies. So, public support for diaper banks.

The direct cash aid part of the social safety net has been all but dismantled in the last 25 years. California is pretty generous. But there are some states where just the cost of diapers alone would use almost half of the average state TANF [Temporary Assistance for Needy Families] benefit for a family of three. I think we really do have to address the fact that the value of cash aid buys so much less than it used to.

Q: Your body of work on marriage and families is fascinating and unusual. Is there a single animating question behind your research?

The common thread is: How do our safety net policies support low-income families’ parenting goals? And do they equalize the conditions of parenting? I think of it as a reproductive justice issue. The ability to have a child or to not have a child, and then to parent that child in conditions where the child’s basic needs are met.

We like to say that we’re child and family friendly. The diaper issue is just one of many, many issues where we don’t really put our money or our policies where our mouth is, in terms of supporting families and supporting children. I think my work is trying to get people to think more collectively about having a social responsibility to all families and to each other. No country, but especially the richest country on the planet, should have one in three very young children not having one of their basic needs met.

I interviewed one dad who was incarcerated because he wrote a bad check. And as he described it to me, he had a certain amount of money, and they needed both diapers and milk for the baby. And I’ll never forget, he said, “I didn’t make a good choice, but I made the right one.”

These are not fancy shoes. These are not name-brand clothes. This was a dad needing both milk and diapers. I don’t think it gets much more basic than that.
 

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

For parents living in poverty, “diaper math” is a familiar and distressingly pressing daily calculation. Babies in the U.S. go through 6-10 disposable diapers a day, at an average cost of $70-$80 a month. Name-brand diapers with high-end absorption sell for as much as a half a dollar each, and can result in upwards of $120 a month in expenses.

One in every three American families cannot afford enough diapers to keep their infants and toddlers clean, dry, and healthy, according to the National Diaper Bank Network. For many parents, that leads to wrenching choices: diapers, food, or rent?

The COVID-19 pandemic has exacerbated the situation, both by expanding unemployment rolls and by causing supply chain disruptions that have triggered higher prices for a multitude of products, including diapers. Diaper banks – community-funded programs that offer free diapers to low-income families – distributed 86% more diapers on average in 2020 than in 2019, according to the National Diaper Bank Network. In some locations, distribution increased by as much as 800%.

Yet no federal program helps parents pay for this childhood essential. The government’s food assistance program does not cover diapers, nor do most state-level public aid programs.

California is the only state to directly fund diapers for families, but support is limited. CalWORKS, a financial assistance program for families with children, provides $30 per month to help families pay for diapers for children under age 3. Federal policy shifts also may be in the works: Democratic lawmakers are pushing to include $200 million for diaper distribution in the massive budget reconciliation package.

Without adequate resources, low-income parents are left scrambling for ways to get the most use out of each diaper. This stressful undertaking is the subject of a recent article in American Sociological Review by Jennifer Randles, PhD, professor of sociology at California State University–Fresno. In 2018, Randles conducted phone interviews with 70 mothers in California over nine months. She tried to recruit fathers as well, but only two men responded.

Dr. Randles spoke with KHN’s Jenny Gold about how the cost of diapers weighs on low-income moms, and the “inventive mothering” many low-income women adopt to shield their children from the harms of poverty. The conversation has been edited for length and clarity.

Q: How do diapers play into day-to-day anxieties for low-income mothers?

In my sample, half of the mothers told me that they worried more about diapers than they worried about food or housing.

I started to ask mothers, “Can you tell me how many diapers you have on hand right now?” Almost every one told me with exact specificity how many they had – 5 or 7 or 12. And they knew exactly how long that number of diapers would last, based on how often their children defecated and urinated, if their kid was sick, if they had a diaper rash at the time. So just all the emotional and cognitive labor that goes into keeping such careful track of diaper supplies.

They were worrying and figuring out, “OK, I’m down to almost my last diaper. What do I do now? Do I go find some cans [to sell]? Do I go sell some things in my house? Who in my social network might have some extra cash right now?” I talked to moms who sell blood plasma just to get their infants diapers.

Q: What coping strategies stood out to you?

Those of us who study diapers often call them diaper-stretching strategies. One was leaving on a diaper a little bit longer than someone might otherwise leave it on and letting it get completely full. Some mothers figured out if they bought a [more expensive] diaper that held more and leaked less, they could leave the diaper on longer.

They would also do things like letting the baby go diaperless, especially when they were at home and felt like they wouldn’t be judged for letting their baby go without a diaper. And they used every household good you can imagine to make makeshift diapers. Mothers are using cloth, sheets, and pillowcases. They’re using things that are disposable like paper towels with duct tape. They’re making diapers out their own period supplies or adult incontinence supplies when they can get a sample.

One of the questions I often get is, “Why don’t they just use cloth?” A lot of the mothers that I spoke with had tried cloth diapers and they found that they were very cost- and labor-prohibitive. If you pay for a full startup set of cloth diapers, you’re looking at anywhere from $500 to $1,000. And these moms never had that much money. Most of them didn’t have in-home washers and dryers. Some of them didn’t even have homes or consistent access to water, and it’s illegal in a lot of laundromats and public laundry facilities to wash your old diapers. So the same conditions that would prevent moms from being able to readily afford disposable diapers are the same conditions that keep them from being able to use cloth.

Q: You found that, for many women, the concept of being a good mother is wrapped up in diapering. Why is that?

Diapers and managing diapers was so fundamental to their identity as good moms. Most of the mothers in my sample went without their own food. They weren’t paying a cellphone bill or buying their own medicine or their own menstrual supplies, as a way of saving diaper money.

I talked to a lot of moms who said, when your baby is hungry, that’s horrible. Obviously, you do everything to prevent that. But there’s something about a diaper that covers this vulnerable part of a very young baby’s body, this very delicate skin. And being able to do something to meet this human need that we all have, and to maintain dignity and cleanliness.

A lot of the moms had been through the welfare system, and so they’re living in this constant fear [of losing their children]. This is especially true among mothers of color, who are much more likely to get wrapped up in the child welfare system. People can’t necessarily see when your baby’s hungry. But people can see a saggy diaper. That’s going to be one of the things that tags you as a bad mom.

Q: Was your work on diapers influenced by your experience as a parent?

When I was doing these interviews, my daughter was about 2 or 3. So still in diapers. When my daughter peed during a diaper change, I thought, “Oh, I can just toss that one. Here, let me get another clean one.” That’s a really easy choice. For me. That’s a crisis for the mothers I interviewed. Many of them told me they have an anxiety attack with every diaper change.

Q: Do you see a clear policy solution to diaper stress?

What’s kind of ironic is how much physical, emotional, and cognitive labor goes into managing something that society and lawmakers don’t even recognize. Diapers are still not really recognized as a basic need, as evidenced by the fact that they’re still taxed in 35 states.

I think what California is doing is an excellent start. And I think diaper banks are a fabulous type of community-based organization that are filling a huge need that is not being filled by safety net policies. So, public support for diaper banks.

The direct cash aid part of the social safety net has been all but dismantled in the last 25 years. California is pretty generous. But there are some states where just the cost of diapers alone would use almost half of the average state TANF [Temporary Assistance for Needy Families] benefit for a family of three. I think we really do have to address the fact that the value of cash aid buys so much less than it used to.

Q: Your body of work on marriage and families is fascinating and unusual. Is there a single animating question behind your research?

The common thread is: How do our safety net policies support low-income families’ parenting goals? And do they equalize the conditions of parenting? I think of it as a reproductive justice issue. The ability to have a child or to not have a child, and then to parent that child in conditions where the child’s basic needs are met.

We like to say that we’re child and family friendly. The diaper issue is just one of many, many issues where we don’t really put our money or our policies where our mouth is, in terms of supporting families and supporting children. I think my work is trying to get people to think more collectively about having a social responsibility to all families and to each other. No country, but especially the richest country on the planet, should have one in three very young children not having one of their basic needs met.

I interviewed one dad who was incarcerated because he wrote a bad check. And as he described it to me, he had a certain amount of money, and they needed both diapers and milk for the baby. And I’ll never forget, he said, “I didn’t make a good choice, but I made the right one.”

These are not fancy shoes. These are not name-brand clothes. This was a dad needing both milk and diapers. I don’t think it gets much more basic than that.
 

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

The patient’s history and presentation, as well as a positive varicella zoster virus (VZV) culture of vesicular fluid, led to a diagnosis of disseminated herpes zoster (DHZ). The patient’s laboratory studies were remarkable for mild lymphopenia, thrombocytopenia, and elevated liver function tests. Shave and punch biopsies of the lesion showed ballooning epithelial necrosis with multinucleated giant cells.

DHZ is characterized by more than 20 vesicles outside of a primary or adjacent dermatome and is caused by extensive reactivation of VZV. DHZ is most often encountered in immunocompromised patients.¹ Untreated DHZ can lead to encephalitis, myelitis, nerve palsies, pneumonitis, hepatitis, and ocular complications.

Diagnosis is usually made clinically and confirmed by a polymerase chain reaction test, direct fluorescent antibody testing, or viral culture.² In immunocompetent patients, uncomplicated DHZ is treated with oral acyclovir 800 mg 5 times daily, valacyclovir 1 g 3 times daily, or famciclovir 500 mg 3 times daily for 7 days. Hospital admission for intravenous acyclovir is recommended for immunocompromised patients, especially those with internal organ involvement, such as hepatitis or encephalitis.³

Early treatment is imperative to avoid life-threatening complications. Active herpes zoster lesions are infectious by contact with vesicular fluid until they dry and crust over. Patients should be instructed to avoid contact with susceptible people, including those who are immunocompromised, babies who have not received their varicella vaccine, and pregnant women. It is important to keep DHZ on the differential—especially in an immunosuppressed patient with a diffuse vesicular rash—as it can lead to significant morbidity and mortality.

Our patient was treated with oral valacyclovir 1 g tid for 10 days and he improved without developing systemic symptoms.

‌

Image courtesy of Christen B. Samaan, MD. Text courtesy of Christen B. Samaan, MD, and Matthew F. Helm, MD, Department of Dermatology, and Nanjiba Nawaz, BA, Penn State College of Medicine, Hershey.

The patient’s history and presentation, as well as a positive varicella zoster virus (VZV) culture of vesicular fluid, led to a diagnosis of disseminated herpes zoster (DHZ). The patient’s laboratory studies were remarkable for mild lymphopenia, thrombocytopenia, and elevated liver function tests. Shave and punch biopsies of the lesion showed ballooning epithelial necrosis with multinucleated giant cells.

DHZ is characterized by more than 20 vesicles outside of a primary or adjacent dermatome and is caused by extensive reactivation of VZV. DHZ is most often encountered in immunocompromised patients.¹ Untreated DHZ can lead to encephalitis, myelitis, nerve palsies, pneumonitis, hepatitis, and ocular complications.

Diagnosis is usually made clinically and confirmed by a polymerase chain reaction test, direct fluorescent antibody testing, or viral culture.² In immunocompetent patients, uncomplicated DHZ is treated with oral acyclovir 800 mg 5 times daily, valacyclovir 1 g 3 times daily, or famciclovir 500 mg 3 times daily for 7 days. Hospital admission for intravenous acyclovir is recommended for immunocompromised patients, especially those with internal organ involvement, such as hepatitis or encephalitis.³

Early treatment is imperative to avoid life-threatening complications. Active herpes zoster lesions are infectious by contact with vesicular fluid until they dry and crust over. Patients should be instructed to avoid contact with susceptible people, including those who are immunocompromised, babies who have not received their varicella vaccine, and pregnant women. It is important to keep DHZ on the differential—especially in an immunosuppressed patient with a diffuse vesicular rash—as it can lead to significant morbidity and mortality.

Our patient was treated with oral valacyclovir 1 g tid for 10 days and he improved without developing systemic symptoms.

‌

Image courtesy of Christen B. Samaan, MD. Text courtesy of Christen B. Samaan, MD, and Matthew F. Helm, MD, Department of Dermatology, and Nanjiba Nawaz, BA, Penn State College of Medicine, Hershey.

The patient’s history and presentation, as well as a positive varicella zoster virus (VZV) culture of vesicular fluid, led to a diagnosis of disseminated herpes zoster (DHZ). The patient’s laboratory studies were remarkable for mild lymphopenia, thrombocytopenia, and elevated liver function tests. Shave and punch biopsies of the lesion showed ballooning epithelial necrosis with multinucleated giant cells.

DHZ is characterized by more than 20 vesicles outside of a primary or adjacent dermatome and is caused by extensive reactivation of VZV. DHZ is most often encountered in immunocompromised patients.¹ Untreated DHZ can lead to encephalitis, myelitis, nerve palsies, pneumonitis, hepatitis, and ocular complications.

Diagnosis is usually made clinically and confirmed by a polymerase chain reaction test, direct fluorescent antibody testing, or viral culture.² In immunocompetent patients, uncomplicated DHZ is treated with oral acyclovir 800 mg 5 times daily, valacyclovir 1 g 3 times daily, or famciclovir 500 mg 3 times daily for 7 days. Hospital admission for intravenous acyclovir is recommended for immunocompromised patients, especially those with internal organ involvement, such as hepatitis or encephalitis.³

Early treatment is imperative to avoid life-threatening complications. Active herpes zoster lesions are infectious by contact with vesicular fluid until they dry and crust over. Patients should be instructed to avoid contact with susceptible people, including those who are immunocompromised, babies who have not received their varicella vaccine, and pregnant women. It is important to keep DHZ on the differential—especially in an immunosuppressed patient with a diffuse vesicular rash—as it can lead to significant morbidity and mortality.

Our patient was treated with oral valacyclovir 1 g tid for 10 days and he improved without developing systemic symptoms.

‌

Image courtesy of Christen B. Samaan, MD. Text courtesy of Christen B. Samaan, MD, and Matthew F. Helm, MD, Department of Dermatology, and Nanjiba Nawaz, BA, Penn State College of Medicine, Hershey.

Among patients with immune-mediated inflammatory diseases (IMIDs) who get COVID-19, the risk for hospitalization and death is lower if they are receiving tumor necrosis factor (TNF) inhibitor monotherapy, compared with receiving most other common drugs for these conditions, with or without TNF inhibitors, according to a study published in JAMA Network Open The only combination not associated with an increased risk for hospitalization or death was TNF inhibitor therapy with methotrexate.

“These findings support the continued use of TNF inhibitor monotherapy during the pandemic and warrant further research investigating the association of other biologic therapies with COVID-19 outcomes,” write Zara Izadi, MPharm, of the University of California, San Francisco, and her colleagues. “Treatment with TNF inhibitor combination therapy was associated with a more favorable safety profile when methotrexate rather than azathioprine/6-mercaptopurine was used, suggesting that clinicians would benefit from weighing the risks versus benefits of deescalating treatment or changing medications when a patient is receiving concomitant TNF inhibitors and azathioprine/6-mercaptopurine,” they write.
 

Findings mirror those seen in other settings

These findings are in line with what has been found in other settings, according to Joel M. Gelfand, MD, director of the psoriasis and phototherapy treatment center, vice chair of clinical research, and medical director of the dermatology clinical studies unit at the University of Pennsylvania, Philadelphia.

“In the beginning of the pandemic, there was concern about use of immune-modulating treatments, and many patients self-discontinued treatments like TNF inhibitors,” Dr. Gelfand, who was not involved in the study, told this news organization. “This has ultimately proved unnecessary and unfortunately resulted in harm to many patients due to flaring of their underlying disease.”

Dr. Gelfand emphasized the importance of vaccinating patients against COVID-19 as soon as possible and of getting a third dose for those who are already fully vaccinated with the Pfizer or Moderna shots, as recommended by the Centers for Disease Control and Prevention.

“I typically recommend this third dose be taken 6 months after the second dose,” Dr. Gelfand said. “The good news is that TNF inhibitors do not seem to meaningfully impact response to mRNA vaccines.”
 

Study details

The researchers analyzed data from three international registries of adults with rheumatic diseases, inflammatory bowel disease, and psoriasis who had COVID-19 between March 12, 2020, and Feb. 1, 2021. The registries included the Secure Epidemiology of Coronavirus Under Research Exclusion for Inflammatory Bowel Disease (SECURE-IBD) registry, the Psoriasis Patient Registry for Outcomes, Therapy and Epidemiology of COVID-19 Infection (PsoProtect), and the physician-reported registry from the Global Rheumatology Alliance (GRA).

The population included 6,077 patients from 74 countries. About half of the cohort (52.9%) were from Europe; more than half were women (58.6%). The average age was 48 years. A little over one-third of the patients (35.3%) had rheumatoid arthritis, 25.3% had Crohn’s disease, 12.5% had ulcerative colitis, 10.3% had spondyloarthritis, and 9.3% had psoriatic arthritis. Smaller percentages had psoriasis (4.9%), another type of arthritis or multiple types (1.7%), or another inflammatory bowel disease (0.6%).

One in five patients (21.3%) were hospitalized, and 3.1% died. The researchers compared outcomes for those who were receiving TNF inhibitor therapy alone to outcomes for those who were taking azathioprine/6-mercaptopurine therapy (alone or with a TNF inhibitor), methotrexate (alone or with a TNF inhibitor), and Janus kinase (JAK) inhibitors. They adjusted their analysis to account for active disease and common comorbidities, as well as geography and the period during the pandemic in which the person was admitted, because treatment regimens and hospitalization indications have varied over time.

All of the therapies except the combination of TNF inhibitors and methotrexate were associated with higher odds of hospitalization and death than TNF inhibitor monotherapy.

The researchers explored several possible explanations for the findings, including the possibility that high serum TNF concentrations may have been associated with more organ damage at the time of COVID-19 admission, owing to interaction with SARS-CoV-2–associated hyperinflammation.

“Therefore, blocking TNF could inhibit this detrimental immune response,” the authors write. “Multiple case series reporting favorable outcomes among patients receiving TNF inhibitor therapy support this assertion.”

Another possibility relates to the effects of taking non–TNF inhibitor medications for immunosuppression. The authors note that thiopurine medications are linked to a greater risk for opportunistic viral infections and that JAK inhibitors may reduce the body’s ability to clear the virus because of its suppression of innate immune response.

The authors also postulate that methotrexate may lower the likelihood of cytokine storm linked to COVID-19, even though methotrexate monotherapy was associated with poorer outcomes. “This association could mean that TNF inhibitor therapy is exerting a protective benefit or that methotrexate therapy is exerting a harmful consequence,” the authors write.

 

Caution needed in interpreting uncontrolled, registry-based data

The findings were not surprising to Stephen B. Hanauer, MD, medical director of the Digestive Health Center at Northwestern University, Chicago, who was not involved in the research.

Northwestern University

“We’ve been monitoring IBD [inflammatory bowel disease] patients through the Secure registry similar to the rheumatologic and dermatologic societies and have not identified a signal of harm from any international groups,” Dr. Hanauer told this news organization. He noted that these registries also have not shown an increased risk for COVID-19 complications among patients receiving TNF inhibitors, antiadhesion therapies, or anti–IL12/23 inhibitors, compared with the general population not taking these therapies.

The study’s size and the diversity of patients strengthen its findings. However, the registries’ use of convenience sampling increases the potential for reporting bias, although the results remained similar after a sensitivity analysis. The study also lacked a control group, and the registries did not collect data uniformly.

“These are databases that rely on reporting from investigators and are not comprehensive prospective studies,” Dr. Hanauer noted as another study limitation.

Dr. Gelfand similarly advised caution in interpreting these findings, inasmuch as the study is a “collection of spontaneous reports” that should be viewed as hypothesis-generating rather than testing.

“Fortunately, more rigorous studies have been conducted, typically in large medical record systems, and have confirmed the hypothesis that TNF inhibitors are associated with a lower risk of poor COVID-19 outcomes, compared to other treatments,” Dr. Gelfand said.

Previous smaller studies similarly found better outcomes among patients taking TNF inhibitors, compared with other therapies, but their participants were predominantly from North America and Europe, noted Licio A. Velloso, MD, PhD, of the University of Campinas, in São Paulo, in an accompanying commentary.

On the basis of the findings of this study, “which included a much larger sample comprising distinct diseases and patients with a multitude of genetic backgrounds, the evidence in favor of the continued use of TNF inhibitor monotherapy for patients with IMIDs during the COVID-19 pandemic has become more substantial,” Dr. Velloso writes. “The finding that maintenance of TNF inhibitor monotherapy is associated with reductions in the risk of severe COVID-19 among patients with IMIDs offers new perspective that may guide health care professionals in the difficult decisions regarding therapeutic approaches among this specific group of patients.”

The research was funded by the American College of Rheumatology, the European Alliance of Associations for Rheumatology, the United Kingdom’s National Institute for Health Research Biomedical Research Center, and the Psoriasis Association. Many authors reported receiving grants and/or personal fees from a variety of pharmaceutical companies. Dr. Velloso has disclosed no relevant financial relationships. Dr. Hanauer has served as a consultant to companies that market TNF inhibitors. Dr. Gelfand has consulted for and received research grants from companies that market TNF inhibitors.

A version of this article first appeared on Medscape.com.

Among patients with immune-mediated inflammatory diseases (IMIDs) who get COVID-19, the risk for hospitalization and death is lower if they are receiving tumor necrosis factor (TNF) inhibitor monotherapy, compared with receiving most other common drugs for these conditions, with or without TNF inhibitors, according to a study published in JAMA Network Open The only combination not associated with an increased risk for hospitalization or death was TNF inhibitor therapy with methotrexate.

“These findings support the continued use of TNF inhibitor monotherapy during the pandemic and warrant further research investigating the association of other biologic therapies with COVID-19 outcomes,” write Zara Izadi, MPharm, of the University of California, San Francisco, and her colleagues. “Treatment with TNF inhibitor combination therapy was associated with a more favorable safety profile when methotrexate rather than azathioprine/6-mercaptopurine was used, suggesting that clinicians would benefit from weighing the risks versus benefits of deescalating treatment or changing medications when a patient is receiving concomitant TNF inhibitors and azathioprine/6-mercaptopurine,” they write.
 

Findings mirror those seen in other settings

These findings are in line with what has been found in other settings, according to Joel M. Gelfand, MD, director of the psoriasis and phototherapy treatment center, vice chair of clinical research, and medical director of the dermatology clinical studies unit at the University of Pennsylvania, Philadelphia.

“In the beginning of the pandemic, there was concern about use of immune-modulating treatments, and many patients self-discontinued treatments like TNF inhibitors,” Dr. Gelfand, who was not involved in the study, told this news organization. “This has ultimately proved unnecessary and unfortunately resulted in harm to many patients due to flaring of their underlying disease.”

Dr. Gelfand emphasized the importance of vaccinating patients against COVID-19 as soon as possible and of getting a third dose for those who are already fully vaccinated with the Pfizer or Moderna shots, as recommended by the Centers for Disease Control and Prevention.

“I typically recommend this third dose be taken 6 months after the second dose,” Dr. Gelfand said. “The good news is that TNF inhibitors do not seem to meaningfully impact response to mRNA vaccines.”
 

Study details

The researchers analyzed data from three international registries of adults with rheumatic diseases, inflammatory bowel disease, and psoriasis who had COVID-19 between March 12, 2020, and Feb. 1, 2021. The registries included the Secure Epidemiology of Coronavirus Under Research Exclusion for Inflammatory Bowel Disease (SECURE-IBD) registry, the Psoriasis Patient Registry for Outcomes, Therapy and Epidemiology of COVID-19 Infection (PsoProtect), and the physician-reported registry from the Global Rheumatology Alliance (GRA).

The population included 6,077 patients from 74 countries. About half of the cohort (52.9%) were from Europe; more than half were women (58.6%). The average age was 48 years. A little over one-third of the patients (35.3%) had rheumatoid arthritis, 25.3% had Crohn’s disease, 12.5% had ulcerative colitis, 10.3% had spondyloarthritis, and 9.3% had psoriatic arthritis. Smaller percentages had psoriasis (4.9%), another type of arthritis or multiple types (1.7%), or another inflammatory bowel disease (0.6%).

One in five patients (21.3%) were hospitalized, and 3.1% died. The researchers compared outcomes for those who were receiving TNF inhibitor therapy alone to outcomes for those who were taking azathioprine/6-mercaptopurine therapy (alone or with a TNF inhibitor), methotrexate (alone or with a TNF inhibitor), and Janus kinase (JAK) inhibitors. They adjusted their analysis to account for active disease and common comorbidities, as well as geography and the period during the pandemic in which the person was admitted, because treatment regimens and hospitalization indications have varied over time.

All of the therapies except the combination of TNF inhibitors and methotrexate were associated with higher odds of hospitalization and death than TNF inhibitor monotherapy.

The researchers explored several possible explanations for the findings, including the possibility that high serum TNF concentrations may have been associated with more organ damage at the time of COVID-19 admission, owing to interaction with SARS-CoV-2–associated hyperinflammation.

“Therefore, blocking TNF could inhibit this detrimental immune response,” the authors write. “Multiple case series reporting favorable outcomes among patients receiving TNF inhibitor therapy support this assertion.”

Another possibility relates to the effects of taking non–TNF inhibitor medications for immunosuppression. The authors note that thiopurine medications are linked to a greater risk for opportunistic viral infections and that JAK inhibitors may reduce the body’s ability to clear the virus because of its suppression of innate immune response.

The authors also postulate that methotrexate may lower the likelihood of cytokine storm linked to COVID-19, even though methotrexate monotherapy was associated with poorer outcomes. “This association could mean that TNF inhibitor therapy is exerting a protective benefit or that methotrexate therapy is exerting a harmful consequence,” the authors write.

 

Caution needed in interpreting uncontrolled, registry-based data

The findings were not surprising to Stephen B. Hanauer, MD, medical director of the Digestive Health Center at Northwestern University, Chicago, who was not involved in the research.

Northwestern University

“We’ve been monitoring IBD [inflammatory bowel disease] patients through the Secure registry similar to the rheumatologic and dermatologic societies and have not identified a signal of harm from any international groups,” Dr. Hanauer told this news organization. He noted that these registries also have not shown an increased risk for COVID-19 complications among patients receiving TNF inhibitors, antiadhesion therapies, or anti–IL12/23 inhibitors, compared with the general population not taking these therapies.

The study’s size and the diversity of patients strengthen its findings. However, the registries’ use of convenience sampling increases the potential for reporting bias, although the results remained similar after a sensitivity analysis. The study also lacked a control group, and the registries did not collect data uniformly.

“These are databases that rely on reporting from investigators and are not comprehensive prospective studies,” Dr. Hanauer noted as another study limitation.

Dr. Gelfand similarly advised caution in interpreting these findings, inasmuch as the study is a “collection of spontaneous reports” that should be viewed as hypothesis-generating rather than testing.

“Fortunately, more rigorous studies have been conducted, typically in large medical record systems, and have confirmed the hypothesis that TNF inhibitors are associated with a lower risk of poor COVID-19 outcomes, compared to other treatments,” Dr. Gelfand said.

Previous smaller studies similarly found better outcomes among patients taking TNF inhibitors, compared with other therapies, but their participants were predominantly from North America and Europe, noted Licio A. Velloso, MD, PhD, of the University of Campinas, in São Paulo, in an accompanying commentary.

On the basis of the findings of this study, “which included a much larger sample comprising distinct diseases and patients with a multitude of genetic backgrounds, the evidence in favor of the continued use of TNF inhibitor monotherapy for patients with IMIDs during the COVID-19 pandemic has become more substantial,” Dr. Velloso writes. “The finding that maintenance of TNF inhibitor monotherapy is associated with reductions in the risk of severe COVID-19 among patients with IMIDs offers new perspective that may guide health care professionals in the difficult decisions regarding therapeutic approaches among this specific group of patients.”

The research was funded by the American College of Rheumatology, the European Alliance of Associations for Rheumatology, the United Kingdom’s National Institute for Health Research Biomedical Research Center, and the Psoriasis Association. Many authors reported receiving grants and/or personal fees from a variety of pharmaceutical companies. Dr. Velloso has disclosed no relevant financial relationships. Dr. Hanauer has served as a consultant to companies that market TNF inhibitors. Dr. Gelfand has consulted for and received research grants from companies that market TNF inhibitors.

A version of this article first appeared on Medscape.com.

Among patients with immune-mediated inflammatory diseases (IMIDs) who get COVID-19, the risk for hospitalization and death is lower if they are receiving tumor necrosis factor (TNF) inhibitor monotherapy, compared with receiving most other common drugs for these conditions, with or without TNF inhibitors, according to a study published in JAMA Network Open The only combination not associated with an increased risk for hospitalization or death was TNF inhibitor therapy with methotrexate.

“These findings support the continued use of TNF inhibitor monotherapy during the pandemic and warrant further research investigating the association of other biologic therapies with COVID-19 outcomes,” write Zara Izadi, MPharm, of the University of California, San Francisco, and her colleagues. “Treatment with TNF inhibitor combination therapy was associated with a more favorable safety profile when methotrexate rather than azathioprine/6-mercaptopurine was used, suggesting that clinicians would benefit from weighing the risks versus benefits of deescalating treatment or changing medications when a patient is receiving concomitant TNF inhibitors and azathioprine/6-mercaptopurine,” they write.
 

Findings mirror those seen in other settings

These findings are in line with what has been found in other settings, according to Joel M. Gelfand, MD, director of the psoriasis and phototherapy treatment center, vice chair of clinical research, and medical director of the dermatology clinical studies unit at the University of Pennsylvania, Philadelphia.

“In the beginning of the pandemic, there was concern about use of immune-modulating treatments, and many patients self-discontinued treatments like TNF inhibitors,” Dr. Gelfand, who was not involved in the study, told this news organization. “This has ultimately proved unnecessary and unfortunately resulted in harm to many patients due to flaring of their underlying disease.”

Dr. Gelfand emphasized the importance of vaccinating patients against COVID-19 as soon as possible and of getting a third dose for those who are already fully vaccinated with the Pfizer or Moderna shots, as recommended by the Centers for Disease Control and Prevention.

“I typically recommend this third dose be taken 6 months after the second dose,” Dr. Gelfand said. “The good news is that TNF inhibitors do not seem to meaningfully impact response to mRNA vaccines.”
 

Study details

The researchers analyzed data from three international registries of adults with rheumatic diseases, inflammatory bowel disease, and psoriasis who had COVID-19 between March 12, 2020, and Feb. 1, 2021. The registries included the Secure Epidemiology of Coronavirus Under Research Exclusion for Inflammatory Bowel Disease (SECURE-IBD) registry, the Psoriasis Patient Registry for Outcomes, Therapy and Epidemiology of COVID-19 Infection (PsoProtect), and the physician-reported registry from the Global Rheumatology Alliance (GRA).

The population included 6,077 patients from 74 countries. About half of the cohort (52.9%) were from Europe; more than half were women (58.6%). The average age was 48 years. A little over one-third of the patients (35.3%) had rheumatoid arthritis, 25.3% had Crohn’s disease, 12.5% had ulcerative colitis, 10.3% had spondyloarthritis, and 9.3% had psoriatic arthritis. Smaller percentages had psoriasis (4.9%), another type of arthritis or multiple types (1.7%), or another inflammatory bowel disease (0.6%).

One in five patients (21.3%) were hospitalized, and 3.1% died. The researchers compared outcomes for those who were receiving TNF inhibitor therapy alone to outcomes for those who were taking azathioprine/6-mercaptopurine therapy (alone or with a TNF inhibitor), methotrexate (alone or with a TNF inhibitor), and Janus kinase (JAK) inhibitors. They adjusted their analysis to account for active disease and common comorbidities, as well as geography and the period during the pandemic in which the person was admitted, because treatment regimens and hospitalization indications have varied over time.

All of the therapies except the combination of TNF inhibitors and methotrexate were associated with higher odds of hospitalization and death than TNF inhibitor monotherapy.

The researchers explored several possible explanations for the findings, including the possibility that high serum TNF concentrations may have been associated with more organ damage at the time of COVID-19 admission, owing to interaction with SARS-CoV-2–associated hyperinflammation.

“Therefore, blocking TNF could inhibit this detrimental immune response,” the authors write. “Multiple case series reporting favorable outcomes among patients receiving TNF inhibitor therapy support this assertion.”

Another possibility relates to the effects of taking non–TNF inhibitor medications for immunosuppression. The authors note that thiopurine medications are linked to a greater risk for opportunistic viral infections and that JAK inhibitors may reduce the body’s ability to clear the virus because of its suppression of innate immune response.

The authors also postulate that methotrexate may lower the likelihood of cytokine storm linked to COVID-19, even though methotrexate monotherapy was associated with poorer outcomes. “This association could mean that TNF inhibitor therapy is exerting a protective benefit or that methotrexate therapy is exerting a harmful consequence,” the authors write.

 

Caution needed in interpreting uncontrolled, registry-based data

The findings were not surprising to Stephen B. Hanauer, MD, medical director of the Digestive Health Center at Northwestern University, Chicago, who was not involved in the research.

Northwestern University

“We’ve been monitoring IBD [inflammatory bowel disease] patients through the Secure registry similar to the rheumatologic and dermatologic societies and have not identified a signal of harm from any international groups,” Dr. Hanauer told this news organization. He noted that these registries also have not shown an increased risk for COVID-19 complications among patients receiving TNF inhibitors, antiadhesion therapies, or anti–IL12/23 inhibitors, compared with the general population not taking these therapies.

The study’s size and the diversity of patients strengthen its findings. However, the registries’ use of convenience sampling increases the potential for reporting bias, although the results remained similar after a sensitivity analysis. The study also lacked a control group, and the registries did not collect data uniformly.

“These are databases that rely on reporting from investigators and are not comprehensive prospective studies,” Dr. Hanauer noted as another study limitation.

Dr. Gelfand similarly advised caution in interpreting these findings, inasmuch as the study is a “collection of spontaneous reports” that should be viewed as hypothesis-generating rather than testing.

“Fortunately, more rigorous studies have been conducted, typically in large medical record systems, and have confirmed the hypothesis that TNF inhibitors are associated with a lower risk of poor COVID-19 outcomes, compared to other treatments,” Dr. Gelfand said.

Previous smaller studies similarly found better outcomes among patients taking TNF inhibitors, compared with other therapies, but their participants were predominantly from North America and Europe, noted Licio A. Velloso, MD, PhD, of the University of Campinas, in São Paulo, in an accompanying commentary.

On the basis of the findings of this study, “which included a much larger sample comprising distinct diseases and patients with a multitude of genetic backgrounds, the evidence in favor of the continued use of TNF inhibitor monotherapy for patients with IMIDs during the COVID-19 pandemic has become more substantial,” Dr. Velloso writes. “The finding that maintenance of TNF inhibitor monotherapy is associated with reductions in the risk of severe COVID-19 among patients with IMIDs offers new perspective that may guide health care professionals in the difficult decisions regarding therapeutic approaches among this specific group of patients.”

The research was funded by the American College of Rheumatology, the European Alliance of Associations for Rheumatology, the United Kingdom’s National Institute for Health Research Biomedical Research Center, and the Psoriasis Association. Many authors reported receiving grants and/or personal fees from a variety of pharmaceutical companies. Dr. Velloso has disclosed no relevant financial relationships. Dr. Hanauer has served as a consultant to companies that market TNF inhibitors. Dr. Gelfand has consulted for and received research grants from companies that market TNF inhibitors.

A version of this article first appeared on Medscape.com.

Granuloma annulare (GA) is a benign cutaneous disorder with an unknown cause. All races and ages may be affected, although women are more often affected than men. GA most commonly appears in the first 3 decades of life. Although the etiology is not known, GA may represent a delayed hypersensitivity reaction. A link between GA and diabetes mellitus, autoimmune thyroiditis, dyslipidemia, and rarely, malignancy may exist.

GA is most commonly localized, presenting as an asymptomatic, erythematous, annular plaque with a firm border and central clearing localized to the wrists, ankles, and dorsal hands or feet. This form is the type most often seen in children. Generalized GA is far less common and presents later in life as multiple asymptomatic or pruritic papules and plaques on the trunk and extremities. Less common variants include subcutaneous GA, patch GA, atypical GA, and perforating GA. Perforating GA occurs on the dorsal hands and presents as (umbilicated) papules, and seems consistent with this patient’s clinical presentation. Histologically, transepidermal elimination of collagen is typically seen in perforating GA.¹

Histology in this patient’s biopsy revealed a granulomatous dermatitis consistent with granuloma annulare. A palisaded arrangement of histiocytic cells surrounding altered collagen with increased dermal mucin was seen. There was associated perivascular mononuclear inflammatory infiltrates. The overlying epidermis was unremarkable.

Granuloma annulare often spontaneously resolves without sequelae. In some cases, atrophy may result. Lesions may also recur. Localized GA is often treated with high-potency topical corticosteroids or intralesional corticosteroids. For generalized GA, topical or intralesional corticosteroids may be used for select lesions. Topical calcineurin inhibitors, light therapy, cryotherapy, imiquimod, hydroxychloroquine, isotretinoin, and dapsone have also been reported in the literature as possible treatments.

This case and photo were provided by Dr. Berke, of Three Rivers Dermatology, Pittsburgh, and Dr. Bilu Martin.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

References

1 Alves J, Barreiros H, Bartolo E. Healthcare (Basel). 2014 Sep 4;2(3):338-45.

2. Bolognia J et al. Dermatology (St. Louis: Mosby/Elsevier, 2008).

3. “Andrews’ Diseases of the Skin,” 13th ed. James W et al. Philadelphia: Saunders Elsevier, 2006.

Granuloma annulare (GA) is a benign cutaneous disorder with an unknown cause. All races and ages may be affected, although women are more often affected than men. GA most commonly appears in the first 3 decades of life. Although the etiology is not known, GA may represent a delayed hypersensitivity reaction. A link between GA and diabetes mellitus, autoimmune thyroiditis, dyslipidemia, and rarely, malignancy may exist.

GA is most commonly localized, presenting as an asymptomatic, erythematous, annular plaque with a firm border and central clearing localized to the wrists, ankles, and dorsal hands or feet. This form is the type most often seen in children. Generalized GA is far less common and presents later in life as multiple asymptomatic or pruritic papules and plaques on the trunk and extremities. Less common variants include subcutaneous GA, patch GA, atypical GA, and perforating GA. Perforating GA occurs on the dorsal hands and presents as (umbilicated) papules, and seems consistent with this patient’s clinical presentation. Histologically, transepidermal elimination of collagen is typically seen in perforating GA.¹

Histology in this patient’s biopsy revealed a granulomatous dermatitis consistent with granuloma annulare. A palisaded arrangement of histiocytic cells surrounding altered collagen with increased dermal mucin was seen. There was associated perivascular mononuclear inflammatory infiltrates. The overlying epidermis was unremarkable.

Granuloma annulare often spontaneously resolves without sequelae. In some cases, atrophy may result. Lesions may also recur. Localized GA is often treated with high-potency topical corticosteroids or intralesional corticosteroids. For generalized GA, topical or intralesional corticosteroids may be used for select lesions. Topical calcineurin inhibitors, light therapy, cryotherapy, imiquimod, hydroxychloroquine, isotretinoin, and dapsone have also been reported in the literature as possible treatments.

This case and photo were provided by Dr. Berke, of Three Rivers Dermatology, Pittsburgh, and Dr. Bilu Martin.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

References

1 Alves J, Barreiros H, Bartolo E. Healthcare (Basel). 2014 Sep 4;2(3):338-45.

2. Bolognia J et al. Dermatology (St. Louis: Mosby/Elsevier, 2008).

3. “Andrews’ Diseases of the Skin,” 13th ed. James W et al. Philadelphia: Saunders Elsevier, 2006.

Granuloma annulare (GA) is a benign cutaneous disorder with an unknown cause. All races and ages may be affected, although women are more often affected than men. GA most commonly appears in the first 3 decades of life. Although the etiology is not known, GA may represent a delayed hypersensitivity reaction. A link between GA and diabetes mellitus, autoimmune thyroiditis, dyslipidemia, and rarely, malignancy may exist.

GA is most commonly localized, presenting as an asymptomatic, erythematous, annular plaque with a firm border and central clearing localized to the wrists, ankles, and dorsal hands or feet. This form is the type most often seen in children. Generalized GA is far less common and presents later in life as multiple asymptomatic or pruritic papules and plaques on the trunk and extremities. Less common variants include subcutaneous GA, patch GA, atypical GA, and perforating GA. Perforating GA occurs on the dorsal hands and presents as (umbilicated) papules, and seems consistent with this patient’s clinical presentation. Histologically, transepidermal elimination of collagen is typically seen in perforating GA.¹

Histology in this patient’s biopsy revealed a granulomatous dermatitis consistent with granuloma annulare. A palisaded arrangement of histiocytic cells surrounding altered collagen with increased dermal mucin was seen. There was associated perivascular mononuclear inflammatory infiltrates. The overlying epidermis was unremarkable.

Granuloma annulare often spontaneously resolves without sequelae. In some cases, atrophy may result. Lesions may also recur. Localized GA is often treated with high-potency topical corticosteroids or intralesional corticosteroids. For generalized GA, topical or intralesional corticosteroids may be used for select lesions. Topical calcineurin inhibitors, light therapy, cryotherapy, imiquimod, hydroxychloroquine, isotretinoin, and dapsone have also been reported in the literature as possible treatments.

This case and photo were provided by Dr. Berke, of Three Rivers Dermatology, Pittsburgh, and Dr. Bilu Martin.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

References

1 Alves J, Barreiros H, Bartolo E. Healthcare (Basel). 2014 Sep 4;2(3):338-45.

2. Bolognia J et al. Dermatology (St. Louis: Mosby/Elsevier, 2008).

3. “Andrews’ Diseases of the Skin,” 13th ed. James W et al. Philadelphia: Saunders Elsevier, 2006.

This pruritic, eruption with yellowing atrophy and telangiectasias on the lower extremities is a classic presentation for necrobiosis lipoidica (NL).

NL is a chronic granulomatous disorder with a predilection for the lower extremities. Patients with NL present with progressive, yellow-brown atrophic plaques on the pretibial aspect of the legs. The plaques have underlying telangiectasias, revealed by the atrophy, and may ulcerate. While these lesions are primarily asymptomatic, associated symptoms may include pruritus, pain, or altered sensation on the affected skin. The classic pathology of NL is notable for altered collagen bundles layered with palisading granulomas extending deep into the dermis. Other notable findings may include mixed inflammatory cells, multinucleated giant cells, and plasma cells; mucin is notably absent.

There is an established relationship between NL and diabetes. When these 2 entities are present, the skin eruption may be referred to as “necrobiosis lipoidica diabeticorum” or “NLD.” Only a small percentage of patients with diabetes will develop NL. Furthermore, there is growing evidence to suggest that NL may be associated with other comorbidities, such as obesity, hypertension, dyslipidemia, and thyroid disease.¹ Additionally, squamous cell carcinoma has been reported as arising within skin affected by NL.²

The etiology of NL is not completely understood. Current theories suggest that blood vessel inflammation related to autoimmune factors may be at work.² The differential diagnosis of NL includes granuloma annulare, pretibial myxedema, stasis dermatitis, panniculitis, morphea, and lichen sclerosis.

NL can be refractory to therapy. Paramount to management is the avoidance of trauma to the affected skin. Topical therapies include corticosteroids, tretinoin, and tacrolimus. Systemic immunomodulation with infliximab, etanercept, thalidomide, and cyclosporine has also been trialed. There is evidence for the utility of pentoxifylline (400 mg po tid), a xanthine derivative often used for peripheral artery disease, to reverse ulceration that can arise in NL.

The patient in this case opted for topical therapy with clobetasol 0.05% ointment and tacrolimus 0.1% ointment. She was subsequently lost to follow-up.

‌

Image courtesy of Cyrelle Fermin, MD, Department of Dermatology, University of New Mexico School of Medicine, Albuquerque. Text courtesy of Cyrelle Fermin, MD, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

This pruritic, eruption with yellowing atrophy and telangiectasias on the lower extremities is a classic presentation for necrobiosis lipoidica (NL).

NL is a chronic granulomatous disorder with a predilection for the lower extremities. Patients with NL present with progressive, yellow-brown atrophic plaques on the pretibial aspect of the legs. The plaques have underlying telangiectasias, revealed by the atrophy, and may ulcerate. While these lesions are primarily asymptomatic, associated symptoms may include pruritus, pain, or altered sensation on the affected skin. The classic pathology of NL is notable for altered collagen bundles layered with palisading granulomas extending deep into the dermis. Other notable findings may include mixed inflammatory cells, multinucleated giant cells, and plasma cells; mucin is notably absent.

There is an established relationship between NL and diabetes. When these 2 entities are present, the skin eruption may be referred to as “necrobiosis lipoidica diabeticorum” or “NLD.” Only a small percentage of patients with diabetes will develop NL. Furthermore, there is growing evidence to suggest that NL may be associated with other comorbidities, such as obesity, hypertension, dyslipidemia, and thyroid disease.¹ Additionally, squamous cell carcinoma has been reported as arising within skin affected by NL.²

The etiology of NL is not completely understood. Current theories suggest that blood vessel inflammation related to autoimmune factors may be at work.² The differential diagnosis of NL includes granuloma annulare, pretibial myxedema, stasis dermatitis, panniculitis, morphea, and lichen sclerosis.

NL can be refractory to therapy. Paramount to management is the avoidance of trauma to the affected skin. Topical therapies include corticosteroids, tretinoin, and tacrolimus. Systemic immunomodulation with infliximab, etanercept, thalidomide, and cyclosporine has also been trialed. There is evidence for the utility of pentoxifylline (400 mg po tid), a xanthine derivative often used for peripheral artery disease, to reverse ulceration that can arise in NL.

The patient in this case opted for topical therapy with clobetasol 0.05% ointment and tacrolimus 0.1% ointment. She was subsequently lost to follow-up.

‌

Image courtesy of Cyrelle Fermin, MD, Department of Dermatology, University of New Mexico School of Medicine, Albuquerque. Text courtesy of Cyrelle Fermin, MD, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

This pruritic, eruption with yellowing atrophy and telangiectasias on the lower extremities is a classic presentation for necrobiosis lipoidica (NL).

NL is a chronic granulomatous disorder with a predilection for the lower extremities. Patients with NL present with progressive, yellow-brown atrophic plaques on the pretibial aspect of the legs. The plaques have underlying telangiectasias, revealed by the atrophy, and may ulcerate. While these lesions are primarily asymptomatic, associated symptoms may include pruritus, pain, or altered sensation on the affected skin. The classic pathology of NL is notable for altered collagen bundles layered with palisading granulomas extending deep into the dermis. Other notable findings may include mixed inflammatory cells, multinucleated giant cells, and plasma cells; mucin is notably absent.

There is an established relationship between NL and diabetes. When these 2 entities are present, the skin eruption may be referred to as “necrobiosis lipoidica diabeticorum” or “NLD.” Only a small percentage of patients with diabetes will develop NL. Furthermore, there is growing evidence to suggest that NL may be associated with other comorbidities, such as obesity, hypertension, dyslipidemia, and thyroid disease.¹ Additionally, squamous cell carcinoma has been reported as arising within skin affected by NL.²

The etiology of NL is not completely understood. Current theories suggest that blood vessel inflammation related to autoimmune factors may be at work.² The differential diagnosis of NL includes granuloma annulare, pretibial myxedema, stasis dermatitis, panniculitis, morphea, and lichen sclerosis.

NL can be refractory to therapy. Paramount to management is the avoidance of trauma to the affected skin. Topical therapies include corticosteroids, tretinoin, and tacrolimus. Systemic immunomodulation with infliximab, etanercept, thalidomide, and cyclosporine has also been trialed. There is evidence for the utility of pentoxifylline (400 mg po tid), a xanthine derivative often used for peripheral artery disease, to reverse ulceration that can arise in NL.

The patient in this case opted for topical therapy with clobetasol 0.05% ointment and tacrolimus 0.1% ointment. She was subsequently lost to follow-up.

‌

Image courtesy of Cyrelle Fermin, MD, Department of Dermatology, University of New Mexico School of Medicine, Albuquerque. Text courtesy of Cyrelle Fermin, MD, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

A biopsy of the lesion was performed which showed an increased number of eccrine glands and blood vessels within the dermis. Some areas showed an increase in adipocytes and smooth muscle bundles. The changes were consistent with eccrine angiomatous hamartoma (EAH).

The boy was referred to vascular laser therapy for treatment of the lesion.

EAH is a rare benign vascular growth characterized by an increased number of mature eccrine glands and blood vessels in the dermis and subcutis. The lesions are mostly present on the extremities, but cases of diffuse congenital lesions and lesions on the face and trunk have also been described. The lesions can be seen at birth or during the first years of life in about half of the cases, and the others tend to occur later in puberty and rarely in adulthood^.1

Clinically, EAH lesions present as red, yellow to brown papules and plaques. Different dermoscopic patterns have been described which include the popcorn pattern that presents as yellow, confluent nodules with popcornlike shapes over a background of erythema, and linear arborizing vessels. The spitzoid pattern are brown globules on a background of erythema and pseudoreticular pigmentation around the globules. The verrucous hemangiomalike pattern has a bluish-white hue, reddish-blue or bluish lacunae, as seen in our patient.^2-4

Most of the lesions are asymptomatic, but in some patients, they can be associated with pain, hyperhidrosis, and sometimes bleeding. Hyperhidrosis has been reported early in the presentation or during puberty or pregnancy. Our patient had started on amphetamines when hyperhidrosis occurred. Hyperhidrosis is a knowns side effect of this type of medication and may have had a role in the increased sweating noted on the hamartoma.

EAH can clinically look like verrucous hemangiomas, angiokeratomas, and vascular malformations, and histopathology may be needed to differentiate between them. Eccrine nevi and EAH can be similar. Hyperhidrosis is an early and predominant component of eccrine nevi, compared with one-third of EAH.

The exact etiology of this lesion is not known. It is thought to be caused by an abnormal differentiation of the epithelium, adnexal structure, and the mesenchyme during organogenesis.³ No other associated conditions have been described with EAH.

EAH are benign lesions that rarely require treatment. If the lesions are symptomatic or because of cosmetic reasons, they can be removed surgically. There are some reports of successful treatment with pulse dual-wavelength sequential 595- and 1064-nm lasers.⁵ Botulinum toxin has also been used in cases of symptomatic hyperhidrosis.
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She has no conflicts. Email her at pdnews@mdedge.com.

References

1. Smith SD et al. Pediatr Dermatol. 2019 Nov;36(6):909-12.

2. Patterson AT et al. Am J Dermatopathol. 2016;38:413-7.

3. Garcıa-Garcıa SC et al. JAAD Case Rep. 2018;4(2):165-7.

4. Awatef Kelati et al. JAAD Case Rep. 2018;4(8)835-6.

5. Felgueiras J et al. Dermatol Surg. 2015 Mar;41(3):428-30.

A biopsy of the lesion was performed which showed an increased number of eccrine glands and blood vessels within the dermis. Some areas showed an increase in adipocytes and smooth muscle bundles. The changes were consistent with eccrine angiomatous hamartoma (EAH).

The boy was referred to vascular laser therapy for treatment of the lesion.

EAH is a rare benign vascular growth characterized by an increased number of mature eccrine glands and blood vessels in the dermis and subcutis. The lesions are mostly present on the extremities, but cases of diffuse congenital lesions and lesions on the face and trunk have also been described. The lesions can be seen at birth or during the first years of life in about half of the cases, and the others tend to occur later in puberty and rarely in adulthood^.1

Clinically, EAH lesions present as red, yellow to brown papules and plaques. Different dermoscopic patterns have been described which include the popcorn pattern that presents as yellow, confluent nodules with popcornlike shapes over a background of erythema, and linear arborizing vessels. The spitzoid pattern are brown globules on a background of erythema and pseudoreticular pigmentation around the globules. The verrucous hemangiomalike pattern has a bluish-white hue, reddish-blue or bluish lacunae, as seen in our patient.^2-4

Most of the lesions are asymptomatic, but in some patients, they can be associated with pain, hyperhidrosis, and sometimes bleeding. Hyperhidrosis has been reported early in the presentation or during puberty or pregnancy. Our patient had started on amphetamines when hyperhidrosis occurred. Hyperhidrosis is a knowns side effect of this type of medication and may have had a role in the increased sweating noted on the hamartoma.

EAH can clinically look like verrucous hemangiomas, angiokeratomas, and vascular malformations, and histopathology may be needed to differentiate between them. Eccrine nevi and EAH can be similar. Hyperhidrosis is an early and predominant component of eccrine nevi, compared with one-third of EAH.

The exact etiology of this lesion is not known. It is thought to be caused by an abnormal differentiation of the epithelium, adnexal structure, and the mesenchyme during organogenesis.³ No other associated conditions have been described with EAH.

EAH are benign lesions that rarely require treatment. If the lesions are symptomatic or because of cosmetic reasons, they can be removed surgically. There are some reports of successful treatment with pulse dual-wavelength sequential 595- and 1064-nm lasers.⁵ Botulinum toxin has also been used in cases of symptomatic hyperhidrosis.
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She has no conflicts. Email her at pdnews@mdedge.com.

References

1. Smith SD et al. Pediatr Dermatol. 2019 Nov;36(6):909-12.

2. Patterson AT et al. Am J Dermatopathol. 2016;38:413-7.

3. Garcıa-Garcıa SC et al. JAAD Case Rep. 2018;4(2):165-7.

4. Awatef Kelati et al. JAAD Case Rep. 2018;4(8)835-6.

5. Felgueiras J et al. Dermatol Surg. 2015 Mar;41(3):428-30.

A biopsy of the lesion was performed which showed an increased number of eccrine glands and blood vessels within the dermis. Some areas showed an increase in adipocytes and smooth muscle bundles. The changes were consistent with eccrine angiomatous hamartoma (EAH).

The boy was referred to vascular laser therapy for treatment of the lesion.

EAH is a rare benign vascular growth characterized by an increased number of mature eccrine glands and blood vessels in the dermis and subcutis. The lesions are mostly present on the extremities, but cases of diffuse congenital lesions and lesions on the face and trunk have also been described. The lesions can be seen at birth or during the first years of life in about half of the cases, and the others tend to occur later in puberty and rarely in adulthood^.1

Clinically, EAH lesions present as red, yellow to brown papules and plaques. Different dermoscopic patterns have been described which include the popcorn pattern that presents as yellow, confluent nodules with popcornlike shapes over a background of erythema, and linear arborizing vessels. The spitzoid pattern are brown globules on a background of erythema and pseudoreticular pigmentation around the globules. The verrucous hemangiomalike pattern has a bluish-white hue, reddish-blue or bluish lacunae, as seen in our patient.^2-4

Most of the lesions are asymptomatic, but in some patients, they can be associated with pain, hyperhidrosis, and sometimes bleeding. Hyperhidrosis has been reported early in the presentation or during puberty or pregnancy. Our patient had started on amphetamines when hyperhidrosis occurred. Hyperhidrosis is a knowns side effect of this type of medication and may have had a role in the increased sweating noted on the hamartoma.

EAH can clinically look like verrucous hemangiomas, angiokeratomas, and vascular malformations, and histopathology may be needed to differentiate between them. Eccrine nevi and EAH can be similar. Hyperhidrosis is an early and predominant component of eccrine nevi, compared with one-third of EAH.

The exact etiology of this lesion is not known. It is thought to be caused by an abnormal differentiation of the epithelium, adnexal structure, and the mesenchyme during organogenesis.³ No other associated conditions have been described with EAH.

EAH are benign lesions that rarely require treatment. If the lesions are symptomatic or because of cosmetic reasons, they can be removed surgically. There are some reports of successful treatment with pulse dual-wavelength sequential 595- and 1064-nm lasers.⁵ Botulinum toxin has also been used in cases of symptomatic hyperhidrosis.
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She has no conflicts. Email her at pdnews@mdedge.com.

References

1. Smith SD et al. Pediatr Dermatol. 2019 Nov;36(6):909-12.

2. Patterson AT et al. Am J Dermatopathol. 2016;38:413-7.

3. Garcıa-Garcıa SC et al. JAAD Case Rep. 2018;4(2):165-7.

4. Awatef Kelati et al. JAAD Case Rep. 2018;4(8)835-6.

5. Felgueiras J et al. Dermatol Surg. 2015 Mar;41(3):428-30.

A 35-year-old woman presented to our clinic with a purple-red cyst on her right cheek that had been present for about 4 years but had worsened over the prior 2 weeks (FIGURE 1). She said she was experiencing excruciating pain and that the cyst had purulent drainage. She denied any history of diabetes, dental problems, recent trauma, or an inciting event.

On physical examination, there was no cervical lymphadenopathy, and her vital signs were normal. An incision and drainage procedure was performed. About 2 mL of purulent fluid was extracted and sent for aerobic and anaerobic cultures.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Cervicofacial actinomycosis

Direct Gram stain showed gram-positive cocci, so the patient was started on a 7-day course of cephalexin 500 mg tid. Five days later, the anaerobic culture grew Actinomyces neuii, revealing the diagnosis as cervicofacial actinomycosis; the patient stopped taking cephalexin. The patient was then switched to a 3-month course of amoxicillin 875 mg bid.

Actinomyces are natural inhabitants of the human oropharynx and gastrointestinal and genitourinary tracts.^1-4 They are filamentous, gram-positive rods with characteristic sulfur granules (although these are not always present).^1-4 It is believed that actinomycosis is endogenously acquired from deep tissue either through dental trauma, penetrating wounds, or compound fractures.^2,4

The most common presentations of actinomycosis include cervicofacial (sometimes referred to as “lumpy jaw syndrome”), followed by abdominopelvic and thoracic/pulmonary, manifestations.^2-4 Primary cutaneous actinomycosis is rare.^5-9 Actinomycosis infection often manifests with indolent constitutional symptoms such as fatigue and anorexia.¹ Most cases occur in men ages 20 to 60 years, although cases in women are increasingly being reported.^2-4

Risk factors include poor dental hygiene or dental procedures, alcoholism, intrauterine device use, immunosuppression, appendicitis, and diverticulitis.^2-4 The exact cause of this patient’s actinomycosis was unknown, as she did not have any known risk factors.

Furunculosis and sporotrichosis are part of the differential

Actinomycosis is often called a “great mimicker” due to its ability to masquerade as infection, malignancy, or fungus.¹ The differential diagnosis for this patient’s presentation included bacterial soft-tissue infection (eg, furunculosis), infected epidermoid cyst, cutaneous tuberculosis, sporotrichosis, deep fungal infection, and nocardiosis.

Continue to: Furunculosis was initially suspected

Furunculosis was initially suspected, but the original wound culture demonstrated actinomycoses instead of traditional gram-positive bacteria.

A clinical diagnosis

The diagnosis of actinomycosis is usually made clinically, but definitive confirmation requires culture, which can be challenging with a slow-growing facultative or strict anaerobe that may take up to 14 days to appear.^2-4 A Gram stain can aid in the diagnosis, but overall, there is a high false-negative rate in identifying actinomycosis.^1,3,4

Treatment time can be lengthy, but prognosis is favorable

Unfortunately, there are no randomized controlled studies for treatment of actinomycosis. The majority of evidence for treatment comes from in vitro and clinical case studies.^2-4,10 In general, prognosis of actinomycosis is favorable with low mortality, but chronic infection without complete resolution of symptoms can occur.^1-4,7,8,10

First-line therapy for actinomycosis is a beta-lactam antibiotic, typically penicillin G or amoxicillin.^2-4,10 High doses of prolonged intravenous (IV) and oral antibiotic therapy (2 to 12 months) based on location and complexity are standard.^3,11 However, if there is minimal bone involvement and the patient shows rapid improvement, treatment could be shortened to a 4 to 6–week oral regimen.^1,11 Surgical intervention can also shorten the required length of antibiotic duration.^1,10

Cutaneous actinomycosis Tx. Amoxicillin/clavulanic acid has been shown to be an effective treatment for cutaneous actinomycosis, especially if polymicrobial infection is suspected.^5,6 Individualized regimens for cutaneous actinomycosis—based on severity, location, and treatment response—are acceptable with close monitoring.^1,2,11

Continue to: A lengthy recovery for our patient

A lengthy recovery for our patient

Seven weeks after the initial visit, the patient reported that she had taken only 20 days’ worth of the recommended 3-month course of amoxicillin. Fortunately, the lesion appeared to be healing well with no apparent fluid collection (FIGURE 2).

Actinomycosis is often called a “great mimicker” due to its ability to masquerade as infection, malignancy, or fungus.

The patient was then prescribed, and completed, a 3-month course of amoxicillin/clavulanic acid 875 mg/125 mg bid.

Nineteen months after initial treatment, the lesion reappeared as a painless cyst in a similar location (FIGURE 3). Plastic Surgery incised and drained the lesion and Infectious Diseases continued her on 3 months of amoxicillin/clavulanic acid 875 mg/125 mg bid, which she did complete.

Due to the continued presence of the lesion, a computed tomography scan of the face was ordered 2 years after the initial visit and demonstrated a superficial skin lesion with no mandibular involvement (FIGURE 4). She was then treated with 3 more months of amoxicillin/clavulanic acid 875 mg/125 mg bid, with the possibility of deep debridement if not improved. However, debridement was unnecessary as the cyst did not recur.

We believe that the course of this patient’s treatment was protracted because she never took oral antibiotics for more than 3 months at a time, and thus, her infection never completely resolved. In retrospect, we would have treated her more aggressively from the outset.

A 35-year-old woman presented to our clinic with a purple-red cyst on her right cheek that had been present for about 4 years but had worsened over the prior 2 weeks (FIGURE 1). She said she was experiencing excruciating pain and that the cyst had purulent drainage. She denied any history of diabetes, dental problems, recent trauma, or an inciting event.

On physical examination, there was no cervical lymphadenopathy, and her vital signs were normal. An incision and drainage procedure was performed. About 2 mL of purulent fluid was extracted and sent for aerobic and anaerobic cultures.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Cervicofacial actinomycosis

Direct Gram stain showed gram-positive cocci, so the patient was started on a 7-day course of cephalexin 500 mg tid. Five days later, the anaerobic culture grew Actinomyces neuii, revealing the diagnosis as cervicofacial actinomycosis; the patient stopped taking cephalexin. The patient was then switched to a 3-month course of amoxicillin 875 mg bid.

Actinomyces are natural inhabitants of the human oropharynx and gastrointestinal and genitourinary tracts.^1-4 They are filamentous, gram-positive rods with characteristic sulfur granules (although these are not always present).^1-4 It is believed that actinomycosis is endogenously acquired from deep tissue either through dental trauma, penetrating wounds, or compound fractures.^2,4

The most common presentations of actinomycosis include cervicofacial (sometimes referred to as “lumpy jaw syndrome”), followed by abdominopelvic and thoracic/pulmonary, manifestations.^2-4 Primary cutaneous actinomycosis is rare.^5-9 Actinomycosis infection often manifests with indolent constitutional symptoms such as fatigue and anorexia.¹ Most cases occur in men ages 20 to 60 years, although cases in women are increasingly being reported.^2-4

Risk factors include poor dental hygiene or dental procedures, alcoholism, intrauterine device use, immunosuppression, appendicitis, and diverticulitis.^2-4 The exact cause of this patient’s actinomycosis was unknown, as she did not have any known risk factors.

Furunculosis and sporotrichosis are part of the differential

Actinomycosis is often called a “great mimicker” due to its ability to masquerade as infection, malignancy, or fungus.¹ The differential diagnosis for this patient’s presentation included bacterial soft-tissue infection (eg, furunculosis), infected epidermoid cyst, cutaneous tuberculosis, sporotrichosis, deep fungal infection, and nocardiosis.

Continue to: Furunculosis was initially suspected

Furunculosis was initially suspected, but the original wound culture demonstrated actinomycoses instead of traditional gram-positive bacteria.

A clinical diagnosis

The diagnosis of actinomycosis is usually made clinically, but definitive confirmation requires culture, which can be challenging with a slow-growing facultative or strict anaerobe that may take up to 14 days to appear.^2-4 A Gram stain can aid in the diagnosis, but overall, there is a high false-negative rate in identifying actinomycosis.^1,3,4

Treatment time can be lengthy, but prognosis is favorable

Unfortunately, there are no randomized controlled studies for treatment of actinomycosis. The majority of evidence for treatment comes from in vitro and clinical case studies.^2-4,10 In general, prognosis of actinomycosis is favorable with low mortality, but chronic infection without complete resolution of symptoms can occur.^1-4,7,8,10

First-line therapy for actinomycosis is a beta-lactam antibiotic, typically penicillin G or amoxicillin.^2-4,10 High doses of prolonged intravenous (IV) and oral antibiotic therapy (2 to 12 months) based on location and complexity are standard.^3,11 However, if there is minimal bone involvement and the patient shows rapid improvement, treatment could be shortened to a 4 to 6–week oral regimen.^1,11 Surgical intervention can also shorten the required length of antibiotic duration.^1,10

Cutaneous actinomycosis Tx. Amoxicillin/clavulanic acid has been shown to be an effective treatment for cutaneous actinomycosis, especially if polymicrobial infection is suspected.^5,6 Individualized regimens for cutaneous actinomycosis—based on severity, location, and treatment response—are acceptable with close monitoring.^1,2,11

Continue to: A lengthy recovery for our patient

A lengthy recovery for our patient

Seven weeks after the initial visit, the patient reported that she had taken only 20 days’ worth of the recommended 3-month course of amoxicillin. Fortunately, the lesion appeared to be healing well with no apparent fluid collection (FIGURE 2).

Actinomycosis is often called a “great mimicker” due to its ability to masquerade as infection, malignancy, or fungus.

The patient was then prescribed, and completed, a 3-month course of amoxicillin/clavulanic acid 875 mg/125 mg bid.

Nineteen months after initial treatment, the lesion reappeared as a painless cyst in a similar location (FIGURE 3). Plastic Surgery incised and drained the lesion and Infectious Diseases continued her on 3 months of amoxicillin/clavulanic acid 875 mg/125 mg bid, which she did complete.

Due to the continued presence of the lesion, a computed tomography scan of the face was ordered 2 years after the initial visit and demonstrated a superficial skin lesion with no mandibular involvement (FIGURE 4). She was then treated with 3 more months of amoxicillin/clavulanic acid 875 mg/125 mg bid, with the possibility of deep debridement if not improved. However, debridement was unnecessary as the cyst did not recur.

We believe that the course of this patient’s treatment was protracted because she never took oral antibiotics for more than 3 months at a time, and thus, her infection never completely resolved. In retrospect, we would have treated her more aggressively from the outset.

A 35-year-old woman presented to our clinic with a purple-red cyst on her right cheek that had been present for about 4 years but had worsened over the prior 2 weeks (FIGURE 1). She said she was experiencing excruciating pain and that the cyst had purulent drainage. She denied any history of diabetes, dental problems, recent trauma, or an inciting event.

On physical examination, there was no cervical lymphadenopathy, and her vital signs were normal. An incision and drainage procedure was performed. About 2 mL of purulent fluid was extracted and sent for aerobic and anaerobic cultures.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Cervicofacial actinomycosis

Direct Gram stain showed gram-positive cocci, so the patient was started on a 7-day course of cephalexin 500 mg tid. Five days later, the anaerobic culture grew Actinomyces neuii, revealing the diagnosis as cervicofacial actinomycosis; the patient stopped taking cephalexin. The patient was then switched to a 3-month course of amoxicillin 875 mg bid.

Actinomyces are natural inhabitants of the human oropharynx and gastrointestinal and genitourinary tracts.^1-4 They are filamentous, gram-positive rods with characteristic sulfur granules (although these are not always present).^1-4 It is believed that actinomycosis is endogenously acquired from deep tissue either through dental trauma, penetrating wounds, or compound fractures.^2,4

The most common presentations of actinomycosis include cervicofacial (sometimes referred to as “lumpy jaw syndrome”), followed by abdominopelvic and thoracic/pulmonary, manifestations.^2-4 Primary cutaneous actinomycosis is rare.^5-9 Actinomycosis infection often manifests with indolent constitutional symptoms such as fatigue and anorexia.¹ Most cases occur in men ages 20 to 60 years, although cases in women are increasingly being reported.^2-4

Risk factors include poor dental hygiene or dental procedures, alcoholism, intrauterine device use, immunosuppression, appendicitis, and diverticulitis.^2-4 The exact cause of this patient’s actinomycosis was unknown, as she did not have any known risk factors.

Furunculosis and sporotrichosis are part of the differential

Actinomycosis is often called a “great mimicker” due to its ability to masquerade as infection, malignancy, or fungus.¹ The differential diagnosis for this patient’s presentation included bacterial soft-tissue infection (eg, furunculosis), infected epidermoid cyst, cutaneous tuberculosis, sporotrichosis, deep fungal infection, and nocardiosis.

Continue to: Furunculosis was initially suspected

Furunculosis was initially suspected, but the original wound culture demonstrated actinomycoses instead of traditional gram-positive bacteria.

A clinical diagnosis

The diagnosis of actinomycosis is usually made clinically, but definitive confirmation requires culture, which can be challenging with a slow-growing facultative or strict anaerobe that may take up to 14 days to appear.^2-4 A Gram stain can aid in the diagnosis, but overall, there is a high false-negative rate in identifying actinomycosis.^1,3,4

Treatment time can be lengthy, but prognosis is favorable

Unfortunately, there are no randomized controlled studies for treatment of actinomycosis. The majority of evidence for treatment comes from in vitro and clinical case studies.^2-4,10 In general, prognosis of actinomycosis is favorable with low mortality, but chronic infection without complete resolution of symptoms can occur.^1-4,7,8,10

First-line therapy for actinomycosis is a beta-lactam antibiotic, typically penicillin G or amoxicillin.^2-4,10 High doses of prolonged intravenous (IV) and oral antibiotic therapy (2 to 12 months) based on location and complexity are standard.^3,11 However, if there is minimal bone involvement and the patient shows rapid improvement, treatment could be shortened to a 4 to 6–week oral regimen.^1,11 Surgical intervention can also shorten the required length of antibiotic duration.^1,10

Cutaneous actinomycosis Tx. Amoxicillin/clavulanic acid has been shown to be an effective treatment for cutaneous actinomycosis, especially if polymicrobial infection is suspected.^5,6 Individualized regimens for cutaneous actinomycosis—based on severity, location, and treatment response—are acceptable with close monitoring.^1,2,11

Continue to: A lengthy recovery for our patient

A lengthy recovery for our patient

Seven weeks after the initial visit, the patient reported that she had taken only 20 days’ worth of the recommended 3-month course of amoxicillin. Fortunately, the lesion appeared to be healing well with no apparent fluid collection (FIGURE 2).

Actinomycosis is often called a “great mimicker” due to its ability to masquerade as infection, malignancy, or fungus.

The patient was then prescribed, and completed, a 3-month course of amoxicillin/clavulanic acid 875 mg/125 mg bid.

Nineteen months after initial treatment, the lesion reappeared as a painless cyst in a similar location (FIGURE 3). Plastic Surgery incised and drained the lesion and Infectious Diseases continued her on 3 months of amoxicillin/clavulanic acid 875 mg/125 mg bid, which she did complete.

Due to the continued presence of the lesion, a computed tomography scan of the face was ordered 2 years after the initial visit and demonstrated a superficial skin lesion with no mandibular involvement (FIGURE 4). She was then treated with 3 more months of amoxicillin/clavulanic acid 875 mg/125 mg bid, with the possibility of deep debridement if not improved. However, debridement was unnecessary as the cyst did not recur.

We believe that the course of this patient’s treatment was protracted because she never took oral antibiotics for more than 3 months at a time, and thus, her infection never completely resolved. In retrospect, we would have treated her more aggressively from the outset.

A 30-year-old man presented to the clinic with a complaint of small painful lumps in his armpit. He stated that he initially experienced some itching and discomfort, but after a while he noticed some red, tender, swollen areas. He also mentioned an odorous yellow fluid that would sometimes drain from the lumps. Since first noticing them 2 years earlier, he reported that the nodules had disappeared and reappeared on their own several times.

On physical exam, several small red subcutaneous nodules were present in the axilla and tender to palpation (FIGURE 1A). The patient also had comedonal acne on his back (FIGURE 1B). The patient’s body mass index was 31, and he was a nonsmoker.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Hidradenitis suppurativa

The characteristic location and morphology of the lesions, along with the chronicity and odor, were critical in arriving at a diagnosis of hidradenitis suppurativa (HS).

HS is a chronic, inflammatory skin condition that normally manifests in areas of apocrine sweat glands, including the axilla, groin, and perianal, perineal, and inframammary locations.¹ It begins when an abnormal hair follicle gets occluded and ruptures, spilling keratin and bacteria into the dermis. An inflammatory response can ensue with surrounding neutrophils and lymphocytes, which leads to abscess formation and destruction of the pilosebaceous unit. Sinus tracts form between the lesions, and a cycle of scarring, fistulas, and contractures can occur.

In this case, the comedones from acne conglobata on the patient’s back indicated a more global follicular occlusion disorder. The characteristic triad is hidradenitis suppurativa, acne conglobata, and dissecting cellulitis of the scalp—of which the patient had 2.

Even when surgical excisions are performed, medical treatment is needed to prevent new lesions and recurrences.

Other potential causes of the pathology include abnormal secretion of apocrine glands, abnormal antimicrobial peptides, deficient numbers of sebaceous glands, and abnormal invaginations of the epidermis.² Increased levels of tumor necrosis factor alpha and other cytokines have been detected in HS lesions and are a potential target for therapy.

The prevalence of HS in the United States is approximately 0.1%.³ The condition typically begins between the ages of 18 and 39 years. The ratio of women to men affected by the condition is 3:1.² There is no evident racial or ethnic predilection. There is an association with diabetes and Crohn disease.³ Obesity and smoking are risk factors.¹

Continue to: The differential includes an array of common skin conditions

 

 

The differential includes an array of common skin conditions

The differential diagnosis in this case included carbuncles, cysts, acne, and abscesses.

A furuncle or carbuncle can result from an infection of hair follicles that can manifest as individual (furuncle) or clusters of (carbuncle) red, painful boils. They form on parts of the skin where hair grows, including the face, neck, armpits, shoulders, and buttocks. They respond well to treatment with antibiotics and incision and drainage. They can be recurrent but usually don’t cluster together in apocrine-rich areas, as seen with HS.

Epidermal inclusion cysts are keratin-filled inclusion cysts with epithelial-lined cyst walls. The cysts are subcutaneous and occasionally more superficial. They can occur almost anywhere but are most often found on the back, scalp, neck, face, and chest. They are usually solitary; however, when there are multiple cysts, they are not linked by sinus tracts as found in HS.

Inflammatory acne lesions tend to form on the face, neck, back, chest, and shoulders, while HS lesions appear most often in apocrine-rich intertriginous areas.

Skin abscesses are local deep infections of the skin caused by bacterial pathogens. The most common agent is Staphylococcus aureus (frequently methicillin resistant). Injection drug use and immunosuppression are risk factors. Although bacteria do not cause HS lesions, bacteria can exacerbate HS through colonization.

Continue to: No lab test needed to diagnosis hidradenitis suppurativa

No lab test needed to diagnose hidradenitis suppurativa

Diagnosis of HS is largely clinical and based on a patient’s history and physical exam findings.² No specific laboratory test is needed.

Although the patient in this case did have comedonal acne on his back, the lesions that prompted his visit were in an apocrine-rich area, were recurrent, and broke open on their own to release foul-smelling contents—all typical characteristics of HS.

Treatment depends on the severity of the condition

There are 3 stages of HS: Hurley stage I involves abscess formation without tracts or scars. Hurley stage II involves recurrent abscesses with sinus tracts and scarring. Hurley stage III has diffuse involvement with multiple interconnected sinus tracts and abscesses across an entire area.² Our patient fits into Hurley stage III.

Evidence-based treatment of mild disease (Hurley stage I) includes topical clindamycin 1% solution/gel bid or doxycycline 100 mg bid for widespread disease (Hurley stage II or resistant stage I).² Chlorhexidine and benzoyl peroxide washes are also often recommended.³ If a patient does not respond to this treatment or the condition is moderate to severe, then clindamycin 300 po bid (with or without rifampin 600/d po) for 10 weeks should be considered.^4,5 In a randomized placebo-controlled trial that compared the efficacy of oral clindamycin vs clindamycin plus rifampin in patients with HS, both therapeutic options were statistically equivalent.⁵ One small, randomized controlled study of patients with mild-to-moderate HS showed that tetracycline 500 mg bid for 3 months resulted in fewer abscesses and nodules but was not superior to topical clindamycin.³

If the patient doesn’t show improvement (Hurley stage III), then adalimumab is an option, as follows: 160 mg subcutaneously at Week 0, 80 mg at Week 2, and then 40 mg weekly, if needed.⁴ Adalimumab is currently the only FDA-approved treatment for HS. Infliximab by IV infusion can be effective in improving pain, disease severity, and quality of life in patients with moderate-to-severe HS.³ This patient was also a candidate for treatment with systemic retinoids (isotretinoin or acitretin), which could have helped both the HS and the acne conglobata.

Continue to: Intralesional steroid injectiosn with triamcinolone

Intralesional steroid injections with triamcinolone 10 mg/mL can reduce local pain and inflammation rapidly. Pain management is also critical, as HS is painful. First-line therapy includes nonsteroidal anti-inflammatory drugs, acetaminophen, atypical anticonvulsants, and serotonin and norepinephrine reuptake inhibitors.² Opiate analgesics may be needed for breakthrough pain in patients with severe disease. Avoiding tight clothing, harsh products, and adhesive dressings, as well as using clear petroleum jelly, can prevent skin trauma and help with healing. Weight loss and smoking cessation are also associated with better outcomes.^6,7

If medical management fails …

If there is no improvement with medical management, it may be time to consider local procedures such as unroofing/deroofing, punch debridement, skin-tissue-sparing excision with electrosurgical peeling, and laser excision. Incision and drainage may be necessary for acutely inflamed, painful abscesses but should not be routinely performed because lesions can recur.³

Referral to a plastic surgeon is necessary when patients are considering wide excisions of largely affected areas. Even when surgical excisions are performed, medical treatment is needed to prevent new lesions and recurrences.

Our patient was treated initially with oral doxycycline 100 mg bid and intralesional triamcinolone (10 mg/mL) in the most tender lesions. He was also provided with a prescription for ibuprofen 800 mg tid to be taken with meals. The family physician encouraged the patient to lose weight. The patient derived some benefit from treatment but continued to experience new painful lesions.

Hidradenitis suppurativa is painful, and thus, pain management is critical.

The physician prescribed oral clindamycin 300 mg bid at a follow-up visit to replace the oral doxycycline. When this failed, the patient was sent for labs to determine if he would be a candidate for adalimumab. When the screening labs were normal, a prescription for adalimumab was provided: 160 mg subcutaneously at Week 0, 80 mg at Week 2, and then 40 mg weekly.⁴

A 30-year-old man presented to the clinic with a complaint of small painful lumps in his armpit. He stated that he initially experienced some itching and discomfort, but after a while he noticed some red, tender, swollen areas. He also mentioned an odorous yellow fluid that would sometimes drain from the lumps. Since first noticing them 2 years earlier, he reported that the nodules had disappeared and reappeared on their own several times.

On physical exam, several small red subcutaneous nodules were present in the axilla and tender to palpation (FIGURE 1A). The patient also had comedonal acne on his back (FIGURE 1B). The patient’s body mass index was 31, and he was a nonsmoker.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Hidradenitis suppurativa

The characteristic location and morphology of the lesions, along with the chronicity and odor, were critical in arriving at a diagnosis of hidradenitis suppurativa (HS).

HS is a chronic, inflammatory skin condition that normally manifests in areas of apocrine sweat glands, including the axilla, groin, and perianal, perineal, and inframammary locations.¹ It begins when an abnormal hair follicle gets occluded and ruptures, spilling keratin and bacteria into the dermis. An inflammatory response can ensue with surrounding neutrophils and lymphocytes, which leads to abscess formation and destruction of the pilosebaceous unit. Sinus tracts form between the lesions, and a cycle of scarring, fistulas, and contractures can occur.

In this case, the comedones from acne conglobata on the patient’s back indicated a more global follicular occlusion disorder. The characteristic triad is hidradenitis suppurativa, acne conglobata, and dissecting cellulitis of the scalp—of which the patient had 2.

Even when surgical excisions are performed, medical treatment is needed to prevent new lesions and recurrences.

Other potential causes of the pathology include abnormal secretion of apocrine glands, abnormal antimicrobial peptides, deficient numbers of sebaceous glands, and abnormal invaginations of the epidermis.² Increased levels of tumor necrosis factor alpha and other cytokines have been detected in HS lesions and are a potential target for therapy.

The prevalence of HS in the United States is approximately 0.1%.³ The condition typically begins between the ages of 18 and 39 years. The ratio of women to men affected by the condition is 3:1.² There is no evident racial or ethnic predilection. There is an association with diabetes and Crohn disease.³ Obesity and smoking are risk factors.¹

Continue to: The differential includes an array of common skin conditions

 

 

The differential includes an array of common skin conditions

The differential diagnosis in this case included carbuncles, cysts, acne, and abscesses.

A furuncle or carbuncle can result from an infection of hair follicles that can manifest as individual (furuncle) or clusters of (carbuncle) red, painful boils. They form on parts of the skin where hair grows, including the face, neck, armpits, shoulders, and buttocks. They respond well to treatment with antibiotics and incision and drainage. They can be recurrent but usually don’t cluster together in apocrine-rich areas, as seen with HS.

Epidermal inclusion cysts are keratin-filled inclusion cysts with epithelial-lined cyst walls. The cysts are subcutaneous and occasionally more superficial. They can occur almost anywhere but are most often found on the back, scalp, neck, face, and chest. They are usually solitary; however, when there are multiple cysts, they are not linked by sinus tracts as found in HS.

Inflammatory acne lesions tend to form on the face, neck, back, chest, and shoulders, while HS lesions appear most often in apocrine-rich intertriginous areas.

Skin abscesses are local deep infections of the skin caused by bacterial pathogens. The most common agent is Staphylococcus aureus (frequently methicillin resistant). Injection drug use and immunosuppression are risk factors. Although bacteria do not cause HS lesions, bacteria can exacerbate HS through colonization.

Continue to: No lab test needed to diagnosis hidradenitis suppurativa

No lab test needed to diagnose hidradenitis suppurativa

Diagnosis of HS is largely clinical and based on a patient’s history and physical exam findings.² No specific laboratory test is needed.

Although the patient in this case did have comedonal acne on his back, the lesions that prompted his visit were in an apocrine-rich area, were recurrent, and broke open on their own to release foul-smelling contents—all typical characteristics of HS.

Treatment depends on the severity of the condition

There are 3 stages of HS: Hurley stage I involves abscess formation without tracts or scars. Hurley stage II involves recurrent abscesses with sinus tracts and scarring. Hurley stage III has diffuse involvement with multiple interconnected sinus tracts and abscesses across an entire area.² Our patient fits into Hurley stage III.

Evidence-based treatment of mild disease (Hurley stage I) includes topical clindamycin 1% solution/gel bid or doxycycline 100 mg bid for widespread disease (Hurley stage II or resistant stage I).² Chlorhexidine and benzoyl peroxide washes are also often recommended.³ If a patient does not respond to this treatment or the condition is moderate to severe, then clindamycin 300 po bid (with or without rifampin 600/d po) for 10 weeks should be considered.^4,5 In a randomized placebo-controlled trial that compared the efficacy of oral clindamycin vs clindamycin plus rifampin in patients with HS, both therapeutic options were statistically equivalent.⁵ One small, randomized controlled study of patients with mild-to-moderate HS showed that tetracycline 500 mg bid for 3 months resulted in fewer abscesses and nodules but was not superior to topical clindamycin.³

If the patient doesn’t show improvement (Hurley stage III), then adalimumab is an option, as follows: 160 mg subcutaneously at Week 0, 80 mg at Week 2, and then 40 mg weekly, if needed.⁴ Adalimumab is currently the only FDA-approved treatment for HS. Infliximab by IV infusion can be effective in improving pain, disease severity, and quality of life in patients with moderate-to-severe HS.³ This patient was also a candidate for treatment with systemic retinoids (isotretinoin or acitretin), which could have helped both the HS and the acne conglobata.

Continue to: Intralesional steroid injectiosn with triamcinolone

Intralesional steroid injections with triamcinolone 10 mg/mL can reduce local pain and inflammation rapidly. Pain management is also critical, as HS is painful. First-line therapy includes nonsteroidal anti-inflammatory drugs, acetaminophen, atypical anticonvulsants, and serotonin and norepinephrine reuptake inhibitors.² Opiate analgesics may be needed for breakthrough pain in patients with severe disease. Avoiding tight clothing, harsh products, and adhesive dressings, as well as using clear petroleum jelly, can prevent skin trauma and help with healing. Weight loss and smoking cessation are also associated with better outcomes.^6,7

If medical management fails …

If there is no improvement with medical management, it may be time to consider local procedures such as unroofing/deroofing, punch debridement, skin-tissue-sparing excision with electrosurgical peeling, and laser excision. Incision and drainage may be necessary for acutely inflamed, painful abscesses but should not be routinely performed because lesions can recur.³

Referral to a plastic surgeon is necessary when patients are considering wide excisions of largely affected areas. Even when surgical excisions are performed, medical treatment is needed to prevent new lesions and recurrences.

Our patient was treated initially with oral doxycycline 100 mg bid and intralesional triamcinolone (10 mg/mL) in the most tender lesions. He was also provided with a prescription for ibuprofen 800 mg tid to be taken with meals. The family physician encouraged the patient to lose weight. The patient derived some benefit from treatment but continued to experience new painful lesions.

Hidradenitis suppurativa is painful, and thus, pain management is critical.

The physician prescribed oral clindamycin 300 mg bid at a follow-up visit to replace the oral doxycycline. When this failed, the patient was sent for labs to determine if he would be a candidate for adalimumab. When the screening labs were normal, a prescription for adalimumab was provided: 160 mg subcutaneously at Week 0, 80 mg at Week 2, and then 40 mg weekly.⁴

A 30-year-old man presented to the clinic with a complaint of small painful lumps in his armpit. He stated that he initially experienced some itching and discomfort, but after a while he noticed some red, tender, swollen areas. He also mentioned an odorous yellow fluid that would sometimes drain from the lumps. Since first noticing them 2 years earlier, he reported that the nodules had disappeared and reappeared on their own several times.

On physical exam, several small red subcutaneous nodules were present in the axilla and tender to palpation (FIGURE 1A). The patient also had comedonal acne on his back (FIGURE 1B). The patient’s body mass index was 31, and he was a nonsmoker.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Hidradenitis suppurativa

The characteristic location and morphology of the lesions, along with the chronicity and odor, were critical in arriving at a diagnosis of hidradenitis suppurativa (HS).

HS is a chronic, inflammatory skin condition that normally manifests in areas of apocrine sweat glands, including the axilla, groin, and perianal, perineal, and inframammary locations.¹ It begins when an abnormal hair follicle gets occluded and ruptures, spilling keratin and bacteria into the dermis. An inflammatory response can ensue with surrounding neutrophils and lymphocytes, which leads to abscess formation and destruction of the pilosebaceous unit. Sinus tracts form between the lesions, and a cycle of scarring, fistulas, and contractures can occur.

In this case, the comedones from acne conglobata on the patient’s back indicated a more global follicular occlusion disorder. The characteristic triad is hidradenitis suppurativa, acne conglobata, and dissecting cellulitis of the scalp—of which the patient had 2.

Even when surgical excisions are performed, medical treatment is needed to prevent new lesions and recurrences.

Other potential causes of the pathology include abnormal secretion of apocrine glands, abnormal antimicrobial peptides, deficient numbers of sebaceous glands, and abnormal invaginations of the epidermis.² Increased levels of tumor necrosis factor alpha and other cytokines have been detected in HS lesions and are a potential target for therapy.

The prevalence of HS in the United States is approximately 0.1%.³ The condition typically begins between the ages of 18 and 39 years. The ratio of women to men affected by the condition is 3:1.² There is no evident racial or ethnic predilection. There is an association with diabetes and Crohn disease.³ Obesity and smoking are risk factors.¹

Continue to: The differential includes an array of common skin conditions

 

 

The differential includes an array of common skin conditions

The differential diagnosis in this case included carbuncles, cysts, acne, and abscesses.

A furuncle or carbuncle can result from an infection of hair follicles that can manifest as individual (furuncle) or clusters of (carbuncle) red, painful boils. They form on parts of the skin where hair grows, including the face, neck, armpits, shoulders, and buttocks. They respond well to treatment with antibiotics and incision and drainage. They can be recurrent but usually don’t cluster together in apocrine-rich areas, as seen with HS.

Epidermal inclusion cysts are keratin-filled inclusion cysts with epithelial-lined cyst walls. The cysts are subcutaneous and occasionally more superficial. They can occur almost anywhere but are most often found on the back, scalp, neck, face, and chest. They are usually solitary; however, when there are multiple cysts, they are not linked by sinus tracts as found in HS.

Inflammatory acne lesions tend to form on the face, neck, back, chest, and shoulders, while HS lesions appear most often in apocrine-rich intertriginous areas.

Skin abscesses are local deep infections of the skin caused by bacterial pathogens. The most common agent is Staphylococcus aureus (frequently methicillin resistant). Injection drug use and immunosuppression are risk factors. Although bacteria do not cause HS lesions, bacteria can exacerbate HS through colonization.

Continue to: No lab test needed to diagnosis hidradenitis suppurativa

No lab test needed to diagnose hidradenitis suppurativa

Diagnosis of HS is largely clinical and based on a patient’s history and physical exam findings.² No specific laboratory test is needed.

Although the patient in this case did have comedonal acne on his back, the lesions that prompted his visit were in an apocrine-rich area, were recurrent, and broke open on their own to release foul-smelling contents—all typical characteristics of HS.

Treatment depends on the severity of the condition

There are 3 stages of HS: Hurley stage I involves abscess formation without tracts or scars. Hurley stage II involves recurrent abscesses with sinus tracts and scarring. Hurley stage III has diffuse involvement with multiple interconnected sinus tracts and abscesses across an entire area.² Our patient fits into Hurley stage III.

Evidence-based treatment of mild disease (Hurley stage I) includes topical clindamycin 1% solution/gel bid or doxycycline 100 mg bid for widespread disease (Hurley stage II or resistant stage I).² Chlorhexidine and benzoyl peroxide washes are also often recommended.³ If a patient does not respond to this treatment or the condition is moderate to severe, then clindamycin 300 po bid (with or without rifampin 600/d po) for 10 weeks should be considered.^4,5 In a randomized placebo-controlled trial that compared the efficacy of oral clindamycin vs clindamycin plus rifampin in patients with HS, both therapeutic options were statistically equivalent.⁵ One small, randomized controlled study of patients with mild-to-moderate HS showed that tetracycline 500 mg bid for 3 months resulted in fewer abscesses and nodules but was not superior to topical clindamycin.³

If the patient doesn’t show improvement (Hurley stage III), then adalimumab is an option, as follows: 160 mg subcutaneously at Week 0, 80 mg at Week 2, and then 40 mg weekly, if needed.⁴ Adalimumab is currently the only FDA-approved treatment for HS. Infliximab by IV infusion can be effective in improving pain, disease severity, and quality of life in patients with moderate-to-severe HS.³ This patient was also a candidate for treatment with systemic retinoids (isotretinoin or acitretin), which could have helped both the HS and the acne conglobata.

Continue to: Intralesional steroid injectiosn with triamcinolone

Intralesional steroid injections with triamcinolone 10 mg/mL can reduce local pain and inflammation rapidly. Pain management is also critical, as HS is painful. First-line therapy includes nonsteroidal anti-inflammatory drugs, acetaminophen, atypical anticonvulsants, and serotonin and norepinephrine reuptake inhibitors.² Opiate analgesics may be needed for breakthrough pain in patients with severe disease. Avoiding tight clothing, harsh products, and adhesive dressings, as well as using clear petroleum jelly, can prevent skin trauma and help with healing. Weight loss and smoking cessation are also associated with better outcomes.^6,7

If medical management fails …

If there is no improvement with medical management, it may be time to consider local procedures such as unroofing/deroofing, punch debridement, skin-tissue-sparing excision with electrosurgical peeling, and laser excision. Incision and drainage may be necessary for acutely inflamed, painful abscesses but should not be routinely performed because lesions can recur.³

Referral to a plastic surgeon is necessary when patients are considering wide excisions of largely affected areas. Even when surgical excisions are performed, medical treatment is needed to prevent new lesions and recurrences.

Our patient was treated initially with oral doxycycline 100 mg bid and intralesional triamcinolone (10 mg/mL) in the most tender lesions. He was also provided with a prescription for ibuprofen 800 mg tid to be taken with meals. The family physician encouraged the patient to lose weight. The patient derived some benefit from treatment but continued to experience new painful lesions.

Hidradenitis suppurativa is painful, and thus, pain management is critical.

The physician prescribed oral clindamycin 300 mg bid at a follow-up visit to replace the oral doxycycline. When this failed, the patient was sent for labs to determine if he would be a candidate for adalimumab. When the screening labs were normal, a prescription for adalimumab was provided: 160 mg subcutaneously at Week 0, 80 mg at Week 2, and then 40 mg weekly.⁴

People with systemic lupus erythematosus (SLE) have a threefold greater likelihood of having up to five or more comorbidities in comparison with people in the general population, according to the results of two separate U.S. population-based studies.

The higher rate of comorbidities seen included many of those commonly reported before, such as cardiovascular and renal disease, but also some that may be less frequently associated with SLE, notably chronic obstructive pulmonary disease (COPD) and cardiac arrhythmias.

“In the past, the characterization of SLE comorbidities has relied on individual comorbidity assessment,” Alí Duarte García, MD, said at the 14th International Congress on Systemic Lupus Erythematosus, held together will the 6th International Congress on Controversies in Rheumatology and Autoimmunity.

“However, a patient-centric approach where a patient as a whole is seen and how many comorbidities they accrue has not been performed.” added Duarte García, who is a rheumatologist at the Mayo Clinic in Rochester, Minn.


 

Multiple conditions “overrepresented” in SLE patients

Dr. Duarte García reported the findings of one of the studies, both of which used data from the Rochester Epidemiology Project, a record-linkage system that collates clinical and hospital data from individuals who live in 19 counties in southeast Minnesota and eight counties in western Wisconsin; these patients have agreed to share their medical records for research.

The study population included 479 individuals diagnosed with SLE according to joint 2019 European Alliance of Associations for Rheumatology and American College of Rheumatology criteria. These were matched by age, sex, race, and county to 479 individuals without SLE.

The mean age of the study population was 53 years, 82% were women, and 86% were White.

“We defined multimorbidity as those patients who have two or more comorbidities and substantial multimorbidity as those patients who have five or more comorbidities,” Dr. Duarte García explained.

A previously published list of 44 categories of comorbidities was used to classify the multimorbidity seen, and 27 of these were “overrepresented” in patients with SLE.

Patients with SLE averaged 5.3 comorbidities, whereas control study subjects had 2.9. Comparing SLE with non-SLE individuals, the odds ratio for having two or more comorbid conditions was 2.96, and for five or more comorbidities it was 3.06.

The highest odds ratio comparing SLE with non-SLE individuals was seen for pulmonary disorders (39.0).

Dr. Duarte García highlighted four comorbidities that occurred in SLE patients that were perhaps more unusual: congestive heart failure (OR, 13.3), valvular heart disease (OR, 4.2), cardiac arrhythmias (OR, 2.85), and COPD (OR, 2.7).

“Given the association of multimorbidity with poor outcomes, care delivery strategies to manage multimorbidity are needed in SLE,” Dr. Duarte García concluded.
 

Similar findings seen in cutaneous lupus

There is also an excess of comorbid conditions in people with cutaneous lupus erythematosus (CLE), Mehmet Hocaoglu, MD, said in reporting the findings of the second study.

Dr. Hocaoglu, an internal medicine resident at the University of Maryland Medical Center in Baltimore, and part of the same team of researchers as Dr. Duarte García, noted that in skin-related lupus the risk of multimorbidity was about doubled.

For this separate analysis, a total of 303 patients with cutaneous lupus had been matched to 303 controls from the general population. Odds ratios for having two or more or five or more comorbidities were a respective 2.27 and 1.65.

Among the comorbidities seen that were higher in those with cutaneous lupus than in the general population subjects were fibromyalgia, liver disease, hypertension, anemia, hypothyroidism, and COPD.

“Further research is definitely needed to identify if the driver of this multimorbidity in CLE patients is the disease itself or the treatments CLE patients are receiving or a multifactorial cause that is driving the disease association,” Dr. Hocaoglu said.
 

Comment and perspective

“Comorbidities that are not appropriate to the general population, compared to SLE,” seem to have been included in the overall SLE and the cutaneous lupus analyses, Raquel Faria, MD, suggested.

Dr. Faria, an internal medicine consultant at Unidade de Imunologia Clínica – Centro Hospitalar Universitário Porto (Portugal), chaired the poster discussion session in which the two studies had been presented.

She wondered if the researchers had analyzed the data while accounting for “the comorbidities that you knew are due to activity in lupus, like anemia?”

The number of patients with SLE who had pulmonary circulation disorders – 7.5% vs. 0.2% of the general population – also caught Dr. Faria’s attention.

That’s “a really huge number,” Dr. Faria pointed out, “I think it is pretty overrepresented.”

Dr. Duarte García acknowledged that they “took a very broad approach” in using a “very large comorbidity index.”

“What we were observing initially is precisely what you’re mentioning,” he responded to Dr. Faria.

“We were pulling patients who were having disease manifestation rather than a comorbidity,” Dr. Duarte-García said.

These are initial and very exploratory data, he stressed. “We have now moved on to modify the index.” Some of the changes that they have made were to incorporate the SLICC Damage Index Score and tighten up the list of ICD codes used.

No outside funding was received for either of the studies. Dr. Duarte García and Dr. Hocaoglu individually stated that they had no actual or potential conflicts of interest in relation to their presentations.

A version of this article first appeared on Medscape.com.

People with systemic lupus erythematosus (SLE) have a threefold greater likelihood of having up to five or more comorbidities in comparison with people in the general population, according to the results of two separate U.S. population-based studies.

The higher rate of comorbidities seen included many of those commonly reported before, such as cardiovascular and renal disease, but also some that may be less frequently associated with SLE, notably chronic obstructive pulmonary disease (COPD) and cardiac arrhythmias.

“In the past, the characterization of SLE comorbidities has relied on individual comorbidity assessment,” Alí Duarte García, MD, said at the 14th International Congress on Systemic Lupus Erythematosus, held together will the 6th International Congress on Controversies in Rheumatology and Autoimmunity.

“However, a patient-centric approach where a patient as a whole is seen and how many comorbidities they accrue has not been performed.” added Duarte García, who is a rheumatologist at the Mayo Clinic in Rochester, Minn.


 

Multiple conditions “overrepresented” in SLE patients

Dr. Duarte García reported the findings of one of the studies, both of which used data from the Rochester Epidemiology Project, a record-linkage system that collates clinical and hospital data from individuals who live in 19 counties in southeast Minnesota and eight counties in western Wisconsin; these patients have agreed to share their medical records for research.

The study population included 479 individuals diagnosed with SLE according to joint 2019 European Alliance of Associations for Rheumatology and American College of Rheumatology criteria. These were matched by age, sex, race, and county to 479 individuals without SLE.

The mean age of the study population was 53 years, 82% were women, and 86% were White.

“We defined multimorbidity as those patients who have two or more comorbidities and substantial multimorbidity as those patients who have five or more comorbidities,” Dr. Duarte García explained.

A previously published list of 44 categories of comorbidities was used to classify the multimorbidity seen, and 27 of these were “overrepresented” in patients with SLE.

Patients with SLE averaged 5.3 comorbidities, whereas control study subjects had 2.9. Comparing SLE with non-SLE individuals, the odds ratio for having two or more comorbid conditions was 2.96, and for five or more comorbidities it was 3.06.

The highest odds ratio comparing SLE with non-SLE individuals was seen for pulmonary disorders (39.0).

Dr. Duarte García highlighted four comorbidities that occurred in SLE patients that were perhaps more unusual: congestive heart failure (OR, 13.3), valvular heart disease (OR, 4.2), cardiac arrhythmias (OR, 2.85), and COPD (OR, 2.7).

“Given the association of multimorbidity with poor outcomes, care delivery strategies to manage multimorbidity are needed in SLE,” Dr. Duarte García concluded.
 

Similar findings seen in cutaneous lupus

There is also an excess of comorbid conditions in people with cutaneous lupus erythematosus (CLE), Mehmet Hocaoglu, MD, said in reporting the findings of the second study.

Dr. Hocaoglu, an internal medicine resident at the University of Maryland Medical Center in Baltimore, and part of the same team of researchers as Dr. Duarte García, noted that in skin-related lupus the risk of multimorbidity was about doubled.

For this separate analysis, a total of 303 patients with cutaneous lupus had been matched to 303 controls from the general population. Odds ratios for having two or more or five or more comorbidities were a respective 2.27 and 1.65.

Among the comorbidities seen that were higher in those with cutaneous lupus than in the general population subjects were fibromyalgia, liver disease, hypertension, anemia, hypothyroidism, and COPD.

“Further research is definitely needed to identify if the driver of this multimorbidity in CLE patients is the disease itself or the treatments CLE patients are receiving or a multifactorial cause that is driving the disease association,” Dr. Hocaoglu said.
 

Comment and perspective

“Comorbidities that are not appropriate to the general population, compared to SLE,” seem to have been included in the overall SLE and the cutaneous lupus analyses, Raquel Faria, MD, suggested.

Dr. Faria, an internal medicine consultant at Unidade de Imunologia Clínica – Centro Hospitalar Universitário Porto (Portugal), chaired the poster discussion session in which the two studies had been presented.

She wondered if the researchers had analyzed the data while accounting for “the comorbidities that you knew are due to activity in lupus, like anemia?”

The number of patients with SLE who had pulmonary circulation disorders – 7.5% vs. 0.2% of the general population – also caught Dr. Faria’s attention.

That’s “a really huge number,” Dr. Faria pointed out, “I think it is pretty overrepresented.”

Dr. Duarte García acknowledged that they “took a very broad approach” in using a “very large comorbidity index.”

“What we were observing initially is precisely what you’re mentioning,” he responded to Dr. Faria.

“We were pulling patients who were having disease manifestation rather than a comorbidity,” Dr. Duarte-García said.

These are initial and very exploratory data, he stressed. “We have now moved on to modify the index.” Some of the changes that they have made were to incorporate the SLICC Damage Index Score and tighten up the list of ICD codes used.

No outside funding was received for either of the studies. Dr. Duarte García and Dr. Hocaoglu individually stated that they had no actual or potential conflicts of interest in relation to their presentations.

A version of this article first appeared on Medscape.com.

People with systemic lupus erythematosus (SLE) have a threefold greater likelihood of having up to five or more comorbidities in comparison with people in the general population, according to the results of two separate U.S. population-based studies.

The higher rate of comorbidities seen included many of those commonly reported before, such as cardiovascular and renal disease, but also some that may be less frequently associated with SLE, notably chronic obstructive pulmonary disease (COPD) and cardiac arrhythmias.

“In the past, the characterization of SLE comorbidities has relied on individual comorbidity assessment,” Alí Duarte García, MD, said at the 14th International Congress on Systemic Lupus Erythematosus, held together will the 6th International Congress on Controversies in Rheumatology and Autoimmunity.

“However, a patient-centric approach where a patient as a whole is seen and how many comorbidities they accrue has not been performed.” added Duarte García, who is a rheumatologist at the Mayo Clinic in Rochester, Minn.


 

Multiple conditions “overrepresented” in SLE patients

Dr. Duarte García reported the findings of one of the studies, both of which used data from the Rochester Epidemiology Project, a record-linkage system that collates clinical and hospital data from individuals who live in 19 counties in southeast Minnesota and eight counties in western Wisconsin; these patients have agreed to share their medical records for research.

The study population included 479 individuals diagnosed with SLE according to joint 2019 European Alliance of Associations for Rheumatology and American College of Rheumatology criteria. These were matched by age, sex, race, and county to 479 individuals without SLE.

The mean age of the study population was 53 years, 82% were women, and 86% were White.

“We defined multimorbidity as those patients who have two or more comorbidities and substantial multimorbidity as those patients who have five or more comorbidities,” Dr. Duarte García explained.

A previously published list of 44 categories of comorbidities was used to classify the multimorbidity seen, and 27 of these were “overrepresented” in patients with SLE.

Patients with SLE averaged 5.3 comorbidities, whereas control study subjects had 2.9. Comparing SLE with non-SLE individuals, the odds ratio for having two or more comorbid conditions was 2.96, and for five or more comorbidities it was 3.06.

The highest odds ratio comparing SLE with non-SLE individuals was seen for pulmonary disorders (39.0).

Dr. Duarte García highlighted four comorbidities that occurred in SLE patients that were perhaps more unusual: congestive heart failure (OR, 13.3), valvular heart disease (OR, 4.2), cardiac arrhythmias (OR, 2.85), and COPD (OR, 2.7).

“Given the association of multimorbidity with poor outcomes, care delivery strategies to manage multimorbidity are needed in SLE,” Dr. Duarte García concluded.
 

Similar findings seen in cutaneous lupus

There is also an excess of comorbid conditions in people with cutaneous lupus erythematosus (CLE), Mehmet Hocaoglu, MD, said in reporting the findings of the second study.

Dr. Hocaoglu, an internal medicine resident at the University of Maryland Medical Center in Baltimore, and part of the same team of researchers as Dr. Duarte García, noted that in skin-related lupus the risk of multimorbidity was about doubled.

For this separate analysis, a total of 303 patients with cutaneous lupus had been matched to 303 controls from the general population. Odds ratios for having two or more or five or more comorbidities were a respective 2.27 and 1.65.

Among the comorbidities seen that were higher in those with cutaneous lupus than in the general population subjects were fibromyalgia, liver disease, hypertension, anemia, hypothyroidism, and COPD.

“Further research is definitely needed to identify if the driver of this multimorbidity in CLE patients is the disease itself or the treatments CLE patients are receiving or a multifactorial cause that is driving the disease association,” Dr. Hocaoglu said.
 

Comment and perspective

“Comorbidities that are not appropriate to the general population, compared to SLE,” seem to have been included in the overall SLE and the cutaneous lupus analyses, Raquel Faria, MD, suggested.

Dr. Faria, an internal medicine consultant at Unidade de Imunologia Clínica – Centro Hospitalar Universitário Porto (Portugal), chaired the poster discussion session in which the two studies had been presented.

She wondered if the researchers had analyzed the data while accounting for “the comorbidities that you knew are due to activity in lupus, like anemia?”

The number of patients with SLE who had pulmonary circulation disorders – 7.5% vs. 0.2% of the general population – also caught Dr. Faria’s attention.

That’s “a really huge number,” Dr. Faria pointed out, “I think it is pretty overrepresented.”

Dr. Duarte García acknowledged that they “took a very broad approach” in using a “very large comorbidity index.”

“What we were observing initially is precisely what you’re mentioning,” he responded to Dr. Faria.

“We were pulling patients who were having disease manifestation rather than a comorbidity,” Dr. Duarte-García said.

These are initial and very exploratory data, he stressed. “We have now moved on to modify the index.” Some of the changes that they have made were to incorporate the SLICC Damage Index Score and tighten up the list of ICD codes used.

No outside funding was received for either of the studies. Dr. Duarte García and Dr. Hocaoglu individually stated that they had no actual or potential conflicts of interest in relation to their presentations.

A version of this article first appeared on Medscape.com.

ANSWER

All of these items were rightly considered to be in the differential for this lesion, so the answer is choice “f.”

DISCUSSION

Individuals with type IV skin are less likely than those with types II and III to develop skin cancer. So, although cancer was definitely in the differential, the other items were considered just as, if not more, likely in this case.

The only way to sort through these diagnostic possibilities was to perform a biopsy. In this case, the entire lesion was removed by saucerization technique, under local anesthesia. The specimen provided would be adequate to detect any cancer, which a smaller specimen could easily miss.

The pathology results showed pigmented basal cell carcinoma. Given the patient’s extensive history of sun exposure, and the steady growth of the lesion, this was hardly a surprise. But prior to the biopsy, one could just as easily imagine the lesion to be, for example, a wart.

The take-home message is obvious: Nothing can take the place of biopsy in establishing a precise diagnosis. With that information in hand, the patient was referred for consultation with a Mohs surgeon. Surgical removal and closure would likely set him back several thousand dollars and leave a considerable scar.

ANSWER

All of these items were rightly considered to be in the differential for this lesion, so the answer is choice “f.”

DISCUSSION

Individuals with type IV skin are less likely than those with types II and III to develop skin cancer. So, although cancer was definitely in the differential, the other items were considered just as, if not more, likely in this case.

The only way to sort through these diagnostic possibilities was to perform a biopsy. In this case, the entire lesion was removed by saucerization technique, under local anesthesia. The specimen provided would be adequate to detect any cancer, which a smaller specimen could easily miss.

The pathology results showed pigmented basal cell carcinoma. Given the patient’s extensive history of sun exposure, and the steady growth of the lesion, this was hardly a surprise. But prior to the biopsy, one could just as easily imagine the lesion to be, for example, a wart.

The take-home message is obvious: Nothing can take the place of biopsy in establishing a precise diagnosis. With that information in hand, the patient was referred for consultation with a Mohs surgeon. Surgical removal and closure would likely set him back several thousand dollars and leave a considerable scar.

ANSWER

All of these items were rightly considered to be in the differential for this lesion, so the answer is choice “f.”

DISCUSSION

Individuals with type IV skin are less likely than those with types II and III to develop skin cancer. So, although cancer was definitely in the differential, the other items were considered just as, if not more, likely in this case.

The only way to sort through these diagnostic possibilities was to perform a biopsy. In this case, the entire lesion was removed by saucerization technique, under local anesthesia. The specimen provided would be adequate to detect any cancer, which a smaller specimen could easily miss.

The pathology results showed pigmented basal cell carcinoma. Given the patient’s extensive history of sun exposure, and the steady growth of the lesion, this was hardly a surprise. But prior to the biopsy, one could just as easily imagine the lesion to be, for example, a wart.

The take-home message is obvious: Nothing can take the place of biopsy in establishing a precise diagnosis. With that information in hand, the patient was referred for consultation with a Mohs surgeon. Surgical removal and closure would likely set him back several thousand dollars and leave a considerable scar.