Jan Dyer

In young children, hepatitis A is usually asymptomatic. So a childcare facility (CCF) in Ireland surprised by an outbreak of hepatitis A that infected 7 adults and 5 children, hospitalizing 6 of the adults. By the time the investigation and interventions were over, > 554 contacts had been followed up, and it had all cost > €45,000 ($53,000).

The outbreak was traced to a man with hepatitis A whose child had been unwell for 3 weeks with fever, fatigue, abdominal pain, diarrhea, pale stools, and possible jaundice. The child (and an infected cousin) attended a local CCF but because several other cases seemed to be limited to the family and their friends, no one immediately considered the CCF as a possible source of infection. However, approximately 10 days after the first 2 cases were reported, an outbreak was officially declared.

At the time, 93 children were attending the CCF. All 7 adults were household contacts of children in the CCF. None of the 23-member CCF staff developed symptoms of hepatitis A.

As many as 70% of infections are asymptomatic in children under age 6, the researchers note, but that group is often a source of transmission due to suboptimal hygiene. Transmission is usually fecal-oral and person-to-person. Although the initial source of outbreak was not identified, the subsequent transmission suggested person-to-person spread. The researchers say the distribution of cases suggests that the transmission probably happened in the school, with asymptomatic children infecting their families, highlighting the fact that symptomatic cases of hepatitis A only represent a portion of the cases in an outbreak.

A preschool inspection report that preceded the outbreak highlighted deficiencies in the staff’s handwashing practices. An infection control audit undertaken because of the outbreak found a number of deficits, including lack of foot-operated bins and the use of cloth covers on furnishings rather than waterproof material. Medical expenses, including hospitalization, serology, and vaccine, cost between €43,400 - €47, 400 ($51,000 - $56,000).

The researchers say the delayed notification to public health of the first case probably contributed to the extent of the outbreak. Medical professionals, they note, should be aware that although uncommon, hepatitis A still occurs. Prompt recognition and notification can mitigate the significant morbidity associated with the infection.

Source:
O'Connor L, McGovern E, O'Meara M, et al. Epidemiol Infect. 2018;146(6):705-711.

In young children, hepatitis A is usually asymptomatic. So a childcare facility (CCF) in Ireland surprised by an outbreak of hepatitis A that infected 7 adults and 5 children, hospitalizing 6 of the adults. By the time the investigation and interventions were over, > 554 contacts had been followed up, and it had all cost > €45,000 ($53,000).

The outbreak was traced to a man with hepatitis A whose child had been unwell for 3 weeks with fever, fatigue, abdominal pain, diarrhea, pale stools, and possible jaundice. The child (and an infected cousin) attended a local CCF but because several other cases seemed to be limited to the family and their friends, no one immediately considered the CCF as a possible source of infection. However, approximately 10 days after the first 2 cases were reported, an outbreak was officially declared.

At the time, 93 children were attending the CCF. All 7 adults were household contacts of children in the CCF. None of the 23-member CCF staff developed symptoms of hepatitis A.

As many as 70% of infections are asymptomatic in children under age 6, the researchers note, but that group is often a source of transmission due to suboptimal hygiene. Transmission is usually fecal-oral and person-to-person. Although the initial source of outbreak was not identified, the subsequent transmission suggested person-to-person spread. The researchers say the distribution of cases suggests that the transmission probably happened in the school, with asymptomatic children infecting their families, highlighting the fact that symptomatic cases of hepatitis A only represent a portion of the cases in an outbreak.

A preschool inspection report that preceded the outbreak highlighted deficiencies in the staff’s handwashing practices. An infection control audit undertaken because of the outbreak found a number of deficits, including lack of foot-operated bins and the use of cloth covers on furnishings rather than waterproof material. Medical expenses, including hospitalization, serology, and vaccine, cost between €43,400 - €47, 400 ($51,000 - $56,000).

The researchers say the delayed notification to public health of the first case probably contributed to the extent of the outbreak. Medical professionals, they note, should be aware that although uncommon, hepatitis A still occurs. Prompt recognition and notification can mitigate the significant morbidity associated with the infection.

Source:
O'Connor L, McGovern E, O'Meara M, et al. Epidemiol Infect. 2018;146(6):705-711.

In young children, hepatitis A is usually asymptomatic. So a childcare facility (CCF) in Ireland surprised by an outbreak of hepatitis A that infected 7 adults and 5 children, hospitalizing 6 of the adults. By the time the investigation and interventions were over, > 554 contacts had been followed up, and it had all cost > €45,000 ($53,000).

The outbreak was traced to a man with hepatitis A whose child had been unwell for 3 weeks with fever, fatigue, abdominal pain, diarrhea, pale stools, and possible jaundice. The child (and an infected cousin) attended a local CCF but because several other cases seemed to be limited to the family and their friends, no one immediately considered the CCF as a possible source of infection. However, approximately 10 days after the first 2 cases were reported, an outbreak was officially declared.

At the time, 93 children were attending the CCF. All 7 adults were household contacts of children in the CCF. None of the 23-member CCF staff developed symptoms of hepatitis A.

As many as 70% of infections are asymptomatic in children under age 6, the researchers note, but that group is often a source of transmission due to suboptimal hygiene. Transmission is usually fecal-oral and person-to-person. Although the initial source of outbreak was not identified, the subsequent transmission suggested person-to-person spread. The researchers say the distribution of cases suggests that the transmission probably happened in the school, with asymptomatic children infecting their families, highlighting the fact that symptomatic cases of hepatitis A only represent a portion of the cases in an outbreak.

A preschool inspection report that preceded the outbreak highlighted deficiencies in the staff’s handwashing practices. An infection control audit undertaken because of the outbreak found a number of deficits, including lack of foot-operated bins and the use of cloth covers on furnishings rather than waterproof material. Medical expenses, including hospitalization, serology, and vaccine, cost between €43,400 - €47, 400 ($51,000 - $56,000).

The researchers say the delayed notification to public health of the first case probably contributed to the extent of the outbreak. Medical professionals, they note, should be aware that although uncommon, hepatitis A still occurs. Prompt recognition and notification can mitigate the significant morbidity associated with the infection.

Source:
O'Connor L, McGovern E, O'Meara M, et al. Epidemiol Infect. 2018;146(6):705-711.

When young people successfully complete an Indian Health Service (IHS) Youth Regional Treatment Center (YRTC) program, they often leave the structured environment to return to a community and family that cannot provide them with the necessary aftercare. The IHS has launched the YRTC Aftercare Pilot Project to fill that gap.

The 12 federal and tribal YRTCs provide a range of clinical services “rooted in culturally relevant, holistic models of care” to American Indian and Alaska Native (AI/AN) adolescents who abuse alcohol or drugs. But without aftercare and case management, the young people are at risk for falling back into old ways.

The YRTC project will identify transitional services that can be culturally adapted to meet the needs of AI/AN youth to support resiliency and coping skills and provide support systems. The project developers aim to establish community-based approaches to reduce relapse and encourage reintegration.

The IHS has awarded $1.62 million for YRTC Aftercare Pilot Projects to Healing Lodge of the Seven Nations in Spokane Valley, Washington, and Desert Sage Youth Wellness Center in Hemet, California. The awards are for 3 years. Both sites will develop innovative, collaborative strategies to improve the health of Native youth as they transition back to their communities.

When young people successfully complete an Indian Health Service (IHS) Youth Regional Treatment Center (YRTC) program, they often leave the structured environment to return to a community and family that cannot provide them with the necessary aftercare. The IHS has launched the YRTC Aftercare Pilot Project to fill that gap.

The 12 federal and tribal YRTCs provide a range of clinical services “rooted in culturally relevant, holistic models of care” to American Indian and Alaska Native (AI/AN) adolescents who abuse alcohol or drugs. But without aftercare and case management, the young people are at risk for falling back into old ways.

The YRTC project will identify transitional services that can be culturally adapted to meet the needs of AI/AN youth to support resiliency and coping skills and provide support systems. The project developers aim to establish community-based approaches to reduce relapse and encourage reintegration.

The IHS has awarded $1.62 million for YRTC Aftercare Pilot Projects to Healing Lodge of the Seven Nations in Spokane Valley, Washington, and Desert Sage Youth Wellness Center in Hemet, California. The awards are for 3 years. Both sites will develop innovative, collaborative strategies to improve the health of Native youth as they transition back to their communities.

When young people successfully complete an Indian Health Service (IHS) Youth Regional Treatment Center (YRTC) program, they often leave the structured environment to return to a community and family that cannot provide them with the necessary aftercare. The IHS has launched the YRTC Aftercare Pilot Project to fill that gap.

The 12 federal and tribal YRTCs provide a range of clinical services “rooted in culturally relevant, holistic models of care” to American Indian and Alaska Native (AI/AN) adolescents who abuse alcohol or drugs. But without aftercare and case management, the young people are at risk for falling back into old ways.

The YRTC project will identify transitional services that can be culturally adapted to meet the needs of AI/AN youth to support resiliency and coping skills and provide support systems. The project developers aim to establish community-based approaches to reduce relapse and encourage reintegration.

The IHS has awarded $1.62 million for YRTC Aftercare Pilot Projects to Healing Lodge of the Seven Nations in Spokane Valley, Washington, and Desert Sage Youth Wellness Center in Hemet, California. The awards are for 3 years. Both sites will develop innovative, collaborative strategies to improve the health of Native youth as they transition back to their communities.

A cardinal feature of Alzheimer disease is the way beta-amyloid—generally a metabolic waste product—clumps to form amyloid plaques. Now a National Institute on Alcohol Abuse and Alcoholism (NIAAA) study indicates that sleep may be an important link in that process. The researchers found that losing just 1 night of sleep led to an immediate increase in beta-amyloid.

Researchers used positron emission tomography to scan the brains of 20 healthy volunteers, aged 22 to 72 years, after a night of rested sleep and after being awake for 31 hours. They found beta-amyloid increases of about 5% after the sleep deprivation in the thalamus and hippocampus, regions especially vulnerable to damage in the early stages of Alzheimer disease, the researchers say. The study participants with larger increases also reported worse mood after sleep deprivation.

It is important to note, the researchers add, that the link between sleep disorders and Alzheimer risk is considered by many scientists to be bidirectional, since elevated beta-amyloid also may cause sleep disturbance.

It is unknown, the researchers say, whether the increase in beta-amyloid in the study participants would subside after a night of rest.

A cardinal feature of Alzheimer disease is the way beta-amyloid—generally a metabolic waste product—clumps to form amyloid plaques. Now a National Institute on Alcohol Abuse and Alcoholism (NIAAA) study indicates that sleep may be an important link in that process. The researchers found that losing just 1 night of sleep led to an immediate increase in beta-amyloid.

Researchers used positron emission tomography to scan the brains of 20 healthy volunteers, aged 22 to 72 years, after a night of rested sleep and after being awake for 31 hours. They found beta-amyloid increases of about 5% after the sleep deprivation in the thalamus and hippocampus, regions especially vulnerable to damage in the early stages of Alzheimer disease, the researchers say. The study participants with larger increases also reported worse mood after sleep deprivation.

It is important to note, the researchers add, that the link between sleep disorders and Alzheimer risk is considered by many scientists to be bidirectional, since elevated beta-amyloid also may cause sleep disturbance.

It is unknown, the researchers say, whether the increase in beta-amyloid in the study participants would subside after a night of rest.

A cardinal feature of Alzheimer disease is the way beta-amyloid—generally a metabolic waste product—clumps to form amyloid plaques. Now a National Institute on Alcohol Abuse and Alcoholism (NIAAA) study indicates that sleep may be an important link in that process. The researchers found that losing just 1 night of sleep led to an immediate increase in beta-amyloid.

Researchers used positron emission tomography to scan the brains of 20 healthy volunteers, aged 22 to 72 years, after a night of rested sleep and after being awake for 31 hours. They found beta-amyloid increases of about 5% after the sleep deprivation in the thalamus and hippocampus, regions especially vulnerable to damage in the early stages of Alzheimer disease, the researchers say. The study participants with larger increases also reported worse mood after sleep deprivation.

It is important to note, the researchers add, that the link between sleep disorders and Alzheimer risk is considered by many scientists to be bidirectional, since elevated beta-amyloid also may cause sleep disturbance.

It is unknown, the researchers say, whether the increase in beta-amyloid in the study participants would subside after a night of rest.

NIH researchers tested the common wisdom that opioids act only on the same surface receptors as endogenous opioids. They discovered that opioids, such as morphine and oxycodone, bind to receptors inside neurons—which are not the targets of naturally occurring opioids. The difference in the actions could help guide the design of pain relievers that do not produce addiction or other adverse opioid-related effects.

The researchers used a new type of antibody biosensor—a nanobody—that generates a fluorescent signal when certain proteins are activated. The signal allowed researchers to track chemicals as they move through cells and responded to stimuli.

The first discovery was that the opioid receptors were activated not only on the surface, but also in the endosome, where the mu-receptor remained activated over several minutes. The researchers also found that there are large differences across a range of opioid drugs in how strongly they induce receptor activation in the endosome. Yet another discovery was that the opioid drugs uniquely induce rapid nanobody signaling, within tens of seconds, in the Golgi apparatus. Therapeutic opioids also uniquely activated mu-opioid receptors in Golgi outposts, in the long, branched structures of neurons.

Based on those findings, the researchers hypothesize that current medically used opioids distort the normal time and spatial sequence of mu-opioid receptor activating and signaling. That distortion may provide the mechanistic link, they say, that explains the undesired adverse effects of opioid medicines.

NIH researchers tested the common wisdom that opioids act only on the same surface receptors as endogenous opioids. They discovered that opioids, such as morphine and oxycodone, bind to receptors inside neurons—which are not the targets of naturally occurring opioids. The difference in the actions could help guide the design of pain relievers that do not produce addiction or other adverse opioid-related effects.

The researchers used a new type of antibody biosensor—a nanobody—that generates a fluorescent signal when certain proteins are activated. The signal allowed researchers to track chemicals as they move through cells and responded to stimuli.

The first discovery was that the opioid receptors were activated not only on the surface, but also in the endosome, where the mu-receptor remained activated over several minutes. The researchers also found that there are large differences across a range of opioid drugs in how strongly they induce receptor activation in the endosome. Yet another discovery was that the opioid drugs uniquely induce rapid nanobody signaling, within tens of seconds, in the Golgi apparatus. Therapeutic opioids also uniquely activated mu-opioid receptors in Golgi outposts, in the long, branched structures of neurons.

Based on those findings, the researchers hypothesize that current medically used opioids distort the normal time and spatial sequence of mu-opioid receptor activating and signaling. That distortion may provide the mechanistic link, they say, that explains the undesired adverse effects of opioid medicines.

NIH researchers tested the common wisdom that opioids act only on the same surface receptors as endogenous opioids. They discovered that opioids, such as morphine and oxycodone, bind to receptors inside neurons—which are not the targets of naturally occurring opioids. The difference in the actions could help guide the design of pain relievers that do not produce addiction or other adverse opioid-related effects.

The researchers used a new type of antibody biosensor—a nanobody—that generates a fluorescent signal when certain proteins are activated. The signal allowed researchers to track chemicals as they move through cells and responded to stimuli.

The first discovery was that the opioid receptors were activated not only on the surface, but also in the endosome, where the mu-receptor remained activated over several minutes. The researchers also found that there are large differences across a range of opioid drugs in how strongly they induce receptor activation in the endosome. Yet another discovery was that the opioid drugs uniquely induce rapid nanobody signaling, within tens of seconds, in the Golgi apparatus. Therapeutic opioids also uniquely activated mu-opioid receptors in Golgi outposts, in the long, branched structures of neurons.

Based on those findings, the researchers hypothesize that current medically used opioids distort the normal time and spatial sequence of mu-opioid receptor activating and signaling. That distortion may provide the mechanistic link, they say, that explains the undesired adverse effects of opioid medicines.

Seasonal flu vaccines mainly target an influenza surface protein called hemagglutinin (HA). But new research from National Institute of Health (NIH) studies suggest that it might be better to target a surface protein called neuraminidase (NA) for broader protection.

Researchers analyzed blood samples from people vaccinated against influenza and people who were diagnosed with the 2009 H1N1 virus or H3N2 viruses. The analyses indicated that influenza vaccines rarely induce NA-reactive antibodies, whereas natural influenza infection induces these types of antibodies at least as often as it induces HA-reactive antibodies, the researchers say.

Additional laboratory experiments showed the NA-reactive antibodies induced during natural flu infection were “broadly reactive,” meaning they could potentially protect against diverse strains. To test that theory, the researchers isolated NA-reactive monoclonal antibodies from the patients  with H3N2 and H1N1, then administered 13 N2-reactive antibodies to mice and infected the mice with a different H3N2 virus strain. Eleven of the N2-reactive antibodies partially or fully protected the mice. In a similar test of N1-reactive antibodies versus H1N1 virus and H5N1-like virus, 4 of 8 antibodies completely protected against both strains.

Seasonal flu vaccines mainly target an influenza surface protein called hemagglutinin (HA). But new research from National Institute of Health (NIH) studies suggest that it might be better to target a surface protein called neuraminidase (NA) for broader protection.

Researchers analyzed blood samples from people vaccinated against influenza and people who were diagnosed with the 2009 H1N1 virus or H3N2 viruses. The analyses indicated that influenza vaccines rarely induce NA-reactive antibodies, whereas natural influenza infection induces these types of antibodies at least as often as it induces HA-reactive antibodies, the researchers say.

Additional laboratory experiments showed the NA-reactive antibodies induced during natural flu infection were “broadly reactive,” meaning they could potentially protect against diverse strains. To test that theory, the researchers isolated NA-reactive monoclonal antibodies from the patients  with H3N2 and H1N1, then administered 13 N2-reactive antibodies to mice and infected the mice with a different H3N2 virus strain. Eleven of the N2-reactive antibodies partially or fully protected the mice. In a similar test of N1-reactive antibodies versus H1N1 virus and H5N1-like virus, 4 of 8 antibodies completely protected against both strains.

Seasonal flu vaccines mainly target an influenza surface protein called hemagglutinin (HA). But new research from National Institute of Health (NIH) studies suggest that it might be better to target a surface protein called neuraminidase (NA) for broader protection.

Researchers analyzed blood samples from people vaccinated against influenza and people who were diagnosed with the 2009 H1N1 virus or H3N2 viruses. The analyses indicated that influenza vaccines rarely induce NA-reactive antibodies, whereas natural influenza infection induces these types of antibodies at least as often as it induces HA-reactive antibodies, the researchers say.

Additional laboratory experiments showed the NA-reactive antibodies induced during natural flu infection were “broadly reactive,” meaning they could potentially protect against diverse strains. To test that theory, the researchers isolated NA-reactive monoclonal antibodies from the patients  with H3N2 and H1N1, then administered 13 N2-reactive antibodies to mice and infected the mice with a different H3N2 virus strain. Eleven of the N2-reactive antibodies partially or fully protected the mice. In a similar test of N1-reactive antibodies versus H1N1 virus and H5N1-like virus, 4 of 8 antibodies completely protected against both strains.

A National Institute of Health (NIH) research team that may have found the explanation for why iron supplements can sometimes worsen malaria infection. “Our study helps solve a long-standing mystery,” says Tracey Rouault, MD, a member of the team.

The researchers say the answer may lie with ferroportin, a protein that prevents iron from building to toxic levels in red blood cells and helps prevent malaria infection. Red blood cells use ferroportin to remove excess iron (a food source for malaria parasites). When the researchers fed mice a high-iron diet, they found that a hormone called hepcidin regulates ferroportin in erythroid cells. The hormone, which is more abundant in high-iron environments, not only lowered ferroportin levels in erythroblasts and red blood cells, but physically bound to ferroportin, preventing iron from being removed from cells.  

Findings from 2 malaria studies suggest that Q248H, a ferroportin mutation often found in malaria-endemic regions, protects against malaria. In 1 study, nearly 20% of 66 children hospitalized for malaria in Zambia had the mutation; these children also tended to have fewer malarial parasites in the blood and tolerated their fevers for a longer period before coming to the hospital.

In the other study, of 290 pregnant women in Ghana, nearly 9% had the mutation. Those women were significantly less likely to have pregnancy-associated malaria.

Rouault says the findings may help explain why iron supplements can sometimes worsen malaria infection and why, conversely, iron deficiency can sometimes be protective. The findings also may help researchers develop strategies to prevent and treat malarial infections, which numbered nearly 216 million in 2016.

A National Institute of Health (NIH) research team that may have found the explanation for why iron supplements can sometimes worsen malaria infection. “Our study helps solve a long-standing mystery,” says Tracey Rouault, MD, a member of the team.

The researchers say the answer may lie with ferroportin, a protein that prevents iron from building to toxic levels in red blood cells and helps prevent malaria infection. Red blood cells use ferroportin to remove excess iron (a food source for malaria parasites). When the researchers fed mice a high-iron diet, they found that a hormone called hepcidin regulates ferroportin in erythroid cells. The hormone, which is more abundant in high-iron environments, not only lowered ferroportin levels in erythroblasts and red blood cells, but physically bound to ferroportin, preventing iron from being removed from cells.  

Findings from 2 malaria studies suggest that Q248H, a ferroportin mutation often found in malaria-endemic regions, protects against malaria. In 1 study, nearly 20% of 66 children hospitalized for malaria in Zambia had the mutation; these children also tended to have fewer malarial parasites in the blood and tolerated their fevers for a longer period before coming to the hospital.

In the other study, of 290 pregnant women in Ghana, nearly 9% had the mutation. Those women were significantly less likely to have pregnancy-associated malaria.

Rouault says the findings may help explain why iron supplements can sometimes worsen malaria infection and why, conversely, iron deficiency can sometimes be protective. The findings also may help researchers develop strategies to prevent and treat malarial infections, which numbered nearly 216 million in 2016.

A National Institute of Health (NIH) research team that may have found the explanation for why iron supplements can sometimes worsen malaria infection. “Our study helps solve a long-standing mystery,” says Tracey Rouault, MD, a member of the team.

The researchers say the answer may lie with ferroportin, a protein that prevents iron from building to toxic levels in red blood cells and helps prevent malaria infection. Red blood cells use ferroportin to remove excess iron (a food source for malaria parasites). When the researchers fed mice a high-iron diet, they found that a hormone called hepcidin regulates ferroportin in erythroid cells. The hormone, which is more abundant in high-iron environments, not only lowered ferroportin levels in erythroblasts and red blood cells, but physically bound to ferroportin, preventing iron from being removed from cells.  

Findings from 2 malaria studies suggest that Q248H, a ferroportin mutation often found in malaria-endemic regions, protects against malaria. In 1 study, nearly 20% of 66 children hospitalized for malaria in Zambia had the mutation; these children also tended to have fewer malarial parasites in the blood and tolerated their fevers for a longer period before coming to the hospital.

In the other study, of 290 pregnant women in Ghana, nearly 9% had the mutation. Those women were significantly less likely to have pregnancy-associated malaria.

Rouault says the findings may help explain why iron supplements can sometimes worsen malaria infection and why, conversely, iron deficiency can sometimes be protective. The findings also may help researchers develop strategies to prevent and treat malarial infections, which numbered nearly 216 million in 2016.

A reanalysis of 2 National Institutes of Health (NIH)-funded studies refutes the conclusions of PROMISE (Promoting Maternal and Infant Survival Everywhere), which found tenofovir disoproxil fumarate (TDF) combination treatment raised the risk of adverse outcomes.

The PROMISE study compared several treatments in pregnant women with HIV in India and Africa. According to those researchers, women on TDF regimens were twice as likely as those on zidovudine to have a very preterm infant, and their infants were more likely to die within the first 2 weeks. 

Those results surprised the current researchers, given that other, earlier studies had found TDF combinations safe for use during pregnancy. In fact, the World Health Organization recommends that all adults with HIV, including pregnant women, receive TDF combination therapy.

In the current study, NIH researchers compared outcomes from 2 US studies, reviewing records on more than 4,600 infants born to 3,847 women. The women were on either a combination regimen including zidovudine or 1 containing TDF.

The researchers found no significant differences in the risk of preterm birth or low birth weight, nor did they find any significant difference in severe birth outcomes, including infant death, in the first 2 weeks. “Notably,” they add, comparing women on zidovudine combination treatment with TDF/emtricitabine/atazanavir/ritonavir, the researchers found the TDF group had a 10% lower chance of preterm birth, low birth weight, and infant death.

Source:

National Institutes of Health. https://www.nih.gov/news-events/news-releases/anti-hiv-drug-combination-does-not-increase-preterm-birth-risk-study-suggests. Published April 25, 2018. Accessed May 24, 2018.

A reanalysis of 2 National Institutes of Health (NIH)-funded studies refutes the conclusions of PROMISE (Promoting Maternal and Infant Survival Everywhere), which found tenofovir disoproxil fumarate (TDF) combination treatment raised the risk of adverse outcomes.

The PROMISE study compared several treatments in pregnant women with HIV in India and Africa. According to those researchers, women on TDF regimens were twice as likely as those on zidovudine to have a very preterm infant, and their infants were more likely to die within the first 2 weeks. 

Those results surprised the current researchers, given that other, earlier studies had found TDF combinations safe for use during pregnancy. In fact, the World Health Organization recommends that all adults with HIV, including pregnant women, receive TDF combination therapy.

In the current study, NIH researchers compared outcomes from 2 US studies, reviewing records on more than 4,600 infants born to 3,847 women. The women were on either a combination regimen including zidovudine or 1 containing TDF.

The researchers found no significant differences in the risk of preterm birth or low birth weight, nor did they find any significant difference in severe birth outcomes, including infant death, in the first 2 weeks. “Notably,” they add, comparing women on zidovudine combination treatment with TDF/emtricitabine/atazanavir/ritonavir, the researchers found the TDF group had a 10% lower chance of preterm birth, low birth weight, and infant death.

Source:

National Institutes of Health. https://www.nih.gov/news-events/news-releases/anti-hiv-drug-combination-does-not-increase-preterm-birth-risk-study-suggests. Published April 25, 2018. Accessed May 24, 2018.

A reanalysis of 2 National Institutes of Health (NIH)-funded studies refutes the conclusions of PROMISE (Promoting Maternal and Infant Survival Everywhere), which found tenofovir disoproxil fumarate (TDF) combination treatment raised the risk of adverse outcomes.

The PROMISE study compared several treatments in pregnant women with HIV in India and Africa. According to those researchers, women on TDF regimens were twice as likely as those on zidovudine to have a very preterm infant, and their infants were more likely to die within the first 2 weeks. 

Those results surprised the current researchers, given that other, earlier studies had found TDF combinations safe for use during pregnancy. In fact, the World Health Organization recommends that all adults with HIV, including pregnant women, receive TDF combination therapy.

In the current study, NIH researchers compared outcomes from 2 US studies, reviewing records on more than 4,600 infants born to 3,847 women. The women were on either a combination regimen including zidovudine or 1 containing TDF.

The researchers found no significant differences in the risk of preterm birth or low birth weight, nor did they find any significant difference in severe birth outcomes, including infant death, in the first 2 weeks. “Notably,” they add, comparing women on zidovudine combination treatment with TDF/emtricitabine/atazanavir/ritonavir, the researchers found the TDF group had a 10% lower chance of preterm birth, low birth weight, and infant death.

Source:

National Institutes of Health. https://www.nih.gov/news-events/news-releases/anti-hiv-drug-combination-does-not-increase-preterm-birth-risk-study-suggests. Published April 25, 2018. Accessed May 24, 2018.

Other cardiovascular disease outcomes, such as kidney disease and dementia, are less known than the “tradional” outcomes, such as heart attack, heart failure, and stroke. In a Centers for Disease Control and Prevention (CDC) study of 4,166 adults, only 38.5% of those with self-reported hypertension were aware of the risk of kidney disease, versus 24.8% of normotensive adults. Awareness of the risk of dementia was “markedly low”: 8.7% and 7.9%, respectively.

The researchers found “notable” socioeconomic and racial/ethnic differences in awareness of risks. For example, high-income respondents had greater awareness of the association between uncontrolled hypertension and kidney disease, stroke, and dementia, when compared with low-income respondents. Non-Hispanic whites had greater awareness of risk than non-Hispanic blacks (who have a higher prevalence of hypertension and uncontrolled hypertension).

Nearly 35 million people have uncontrolled hypertension, the researchers note. To educate more diverse patient populations about the risks, they recommend expanding current initiatives such as the “Mind Your Risks” program (https://mindyourrisks.nih.gov), promoted by the National Institute of Neurological Disorders and Stroke; and the “Measure Up/Pressure Down (www.measureuppressuredown.com) program, sponsored by the American Medical Group Association.

Other cardiovascular disease outcomes, such as kidney disease and dementia, are less known than the “tradional” outcomes, such as heart attack, heart failure, and stroke. In a Centers for Disease Control and Prevention (CDC) study of 4,166 adults, only 38.5% of those with self-reported hypertension were aware of the risk of kidney disease, versus 24.8% of normotensive adults. Awareness of the risk of dementia was “markedly low”: 8.7% and 7.9%, respectively.

The researchers found “notable” socioeconomic and racial/ethnic differences in awareness of risks. For example, high-income respondents had greater awareness of the association between uncontrolled hypertension and kidney disease, stroke, and dementia, when compared with low-income respondents. Non-Hispanic whites had greater awareness of risk than non-Hispanic blacks (who have a higher prevalence of hypertension and uncontrolled hypertension).

Nearly 35 million people have uncontrolled hypertension, the researchers note. To educate more diverse patient populations about the risks, they recommend expanding current initiatives such as the “Mind Your Risks” program (https://mindyourrisks.nih.gov), promoted by the National Institute of Neurological Disorders and Stroke; and the “Measure Up/Pressure Down (www.measureuppressuredown.com) program, sponsored by the American Medical Group Association.

Other cardiovascular disease outcomes, such as kidney disease and dementia, are less known than the “tradional” outcomes, such as heart attack, heart failure, and stroke. In a Centers for Disease Control and Prevention (CDC) study of 4,166 adults, only 38.5% of those with self-reported hypertension were aware of the risk of kidney disease, versus 24.8% of normotensive adults. Awareness of the risk of dementia was “markedly low”: 8.7% and 7.9%, respectively.

The researchers found “notable” socioeconomic and racial/ethnic differences in awareness of risks. For example, high-income respondents had greater awareness of the association between uncontrolled hypertension and kidney disease, stroke, and dementia, when compared with low-income respondents. Non-Hispanic whites had greater awareness of risk than non-Hispanic blacks (who have a higher prevalence of hypertension and uncontrolled hypertension).

Nearly 35 million people have uncontrolled hypertension, the researchers note. To educate more diverse patient populations about the risks, they recommend expanding current initiatives such as the “Mind Your Risks” program (https://mindyourrisks.nih.gov), promoted by the National Institute of Neurological Disorders and Stroke; and the “Measure Up/Pressure Down (www.measureuppressuredown.com) program, sponsored by the American Medical Group Association.

The US goal is to get Tuberculosis (TB) rates down to > 1 case per 1 million people, but in 2017 there were 28 cases per million. After years of decline, TB rates have stagnated among people born in the US. The TB rate dropped slightly (–2.5%) from 2016 to 2017. Another even slighter decrease was seen in 2017 (–1.8%). Moreover, < 1 in 10 TB cases occurred among children aged < 15 years (a “key marker” of recent transmission, the CDC says). Half of all cases were reported in California, New York, Texas, and Florida, all 4 corners of the country.

As many as 13 million people in the US have latent TB infection but the vast majority do not know it. On average, 5% - 10% of people with latent TB infection progress to infectious TB. More than 80% of US TB cases are associated with long-standing, untreated latent TB infections.

The CDC says reaching the elimination goal will take an “intensified, dual approach” that strengthens existing systems to prevent transmission of infectious TB disease and increases efforts to detect and treat latent infection before it progresses to infectious TB.

It is essential to ensure that every active case of TB disease is effectively detected and treated, the CDC says. Treatments can be difficult to complete; however, not completing treatment can lead to drug-resistant bacteria, and even lengthier and more expensive treatment. CDC research has identified a shorter regimen for people with latent infection: 12 once-weekly doses of isoniazid and rifapentine, a simpler treatment compared with other regimens that include a 270-dose,  and 9-month daily regimen of isoniazid.

Over the past 20 years, health departments and CDC TB control efforts have prevented an estimated 300,000 cases of TB disease. “Challenges remain,” says Philip LoBue, MD, director of CDC’s Division of Tuberculosis Elimination. But “[t]he good news is that the path to accelerated progress is clear.” In addition to the shorter treatment regimen, recent advances include electronic directly observed therapy (eDOT), which makes TB treatment less expensive and more convenient; and a diagnostic blood test that can provide accurate results in a single medical visit.

The US goal is to get Tuberculosis (TB) rates down to > 1 case per 1 million people, but in 2017 there were 28 cases per million. After years of decline, TB rates have stagnated among people born in the US. The TB rate dropped slightly (–2.5%) from 2016 to 2017. Another even slighter decrease was seen in 2017 (–1.8%). Moreover, < 1 in 10 TB cases occurred among children aged < 15 years (a “key marker” of recent transmission, the CDC says). Half of all cases were reported in California, New York, Texas, and Florida, all 4 corners of the country.

As many as 13 million people in the US have latent TB infection but the vast majority do not know it. On average, 5% - 10% of people with latent TB infection progress to infectious TB. More than 80% of US TB cases are associated with long-standing, untreated latent TB infections.

The CDC says reaching the elimination goal will take an “intensified, dual approach” that strengthens existing systems to prevent transmission of infectious TB disease and increases efforts to detect and treat latent infection before it progresses to infectious TB.

It is essential to ensure that every active case of TB disease is effectively detected and treated, the CDC says. Treatments can be difficult to complete; however, not completing treatment can lead to drug-resistant bacteria, and even lengthier and more expensive treatment. CDC research has identified a shorter regimen for people with latent infection: 12 once-weekly doses of isoniazid and rifapentine, a simpler treatment compared with other regimens that include a 270-dose,  and 9-month daily regimen of isoniazid.

Over the past 20 years, health departments and CDC TB control efforts have prevented an estimated 300,000 cases of TB disease. “Challenges remain,” says Philip LoBue, MD, director of CDC’s Division of Tuberculosis Elimination. But “[t]he good news is that the path to accelerated progress is clear.” In addition to the shorter treatment regimen, recent advances include electronic directly observed therapy (eDOT), which makes TB treatment less expensive and more convenient; and a diagnostic blood test that can provide accurate results in a single medical visit.

The US goal is to get Tuberculosis (TB) rates down to > 1 case per 1 million people, but in 2017 there were 28 cases per million. After years of decline, TB rates have stagnated among people born in the US. The TB rate dropped slightly (–2.5%) from 2016 to 2017. Another even slighter decrease was seen in 2017 (–1.8%). Moreover, < 1 in 10 TB cases occurred among children aged < 15 years (a “key marker” of recent transmission, the CDC says). Half of all cases were reported in California, New York, Texas, and Florida, all 4 corners of the country.

As many as 13 million people in the US have latent TB infection but the vast majority do not know it. On average, 5% - 10% of people with latent TB infection progress to infectious TB. More than 80% of US TB cases are associated with long-standing, untreated latent TB infections.

The CDC says reaching the elimination goal will take an “intensified, dual approach” that strengthens existing systems to prevent transmission of infectious TB disease and increases efforts to detect and treat latent infection before it progresses to infectious TB.

It is essential to ensure that every active case of TB disease is effectively detected and treated, the CDC says. Treatments can be difficult to complete; however, not completing treatment can lead to drug-resistant bacteria, and even lengthier and more expensive treatment. CDC research has identified a shorter regimen for people with latent infection: 12 once-weekly doses of isoniazid and rifapentine, a simpler treatment compared with other regimens that include a 270-dose,  and 9-month daily regimen of isoniazid.

Over the past 20 years, health departments and CDC TB control efforts have prevented an estimated 300,000 cases of TB disease. “Challenges remain,” says Philip LoBue, MD, director of CDC’s Division of Tuberculosis Elimination. But “[t]he good news is that the path to accelerated progress is clear.” In addition to the shorter treatment regimen, recent advances include electronic directly observed therapy (eDOT), which makes TB treatment less expensive and more convenient; and a diagnostic blood test that can provide accurate results in a single medical visit.

When interpreting tacrolimus levels, it is important to monitor changes in red blood cells (RBC). A patient who had hepatitis C virus (HCV) genotype 3A lesson reinforced that lesson for clinicians in the dialysis unit at Fraser Health in Abbotsford, Canada who authored a recent case report. Ribavirin-induced anemia reduced the level of tacrolimus in the patien, the authors reported.

The patient, a 37-year-old man, developed renal failure and received a kidney transplant, which subsequently failed (due to complications likely related to HCV). He had been started on tacrolimus while waiting to go back on the transplant list. Eight years later, the patient restarted hemodialysis (HD), with a regimen of sofosbuvir and ribavirin (SOF/RBV). His whole-blood tacrolimus level was 6.6 ng/mL (target 4–6); his hemoglobin (Hb) level was 10.3 g/dL. Two months later, the patient left for a 1-month vacation. When he returned, his Hb was “dramatically low,” at 3.7 g/dL.

The clinicians put the ribavirin on hold and increased darbepoetin. The patient was given packed RBCs; a bone marrow biopsy ruled out myeloproliferative disorder. Two weeks later, the tacrolimus level was 1.0 mg/mL and then dropped to an undetectable level 5 days later. The clinicians increased the dose. During the next month, the patient’s Hb “gradually bounced back,” to > 10 g/dL, whereupon the clinicians restarted RBV. When the tacrolimus level reached 7.2 ng/mL, the dosages were gradually cut back.  Sofosbuvir and RBV were stopped a couple of months later. The patient’s HCV RNA level was undetectable 12 weeks after therapy finished.

Practitioners are always facing the dilemma of risk (anemia) vs benefit (efficacy) in deciding whether and how much RBV should be reduced in renal impairment, the case report authors say. They note that the guidelines for treatment-naïve genotype 3 patients have changed. The recommendation for SOF/RBV has been replaced by one for glecaprevir/pibrentasvir or SOF/velpatasvir.

With the availability of newer direct antivirals, they add, the case again supports the abandoning of RBV-containing regimens. In the “very unlikely instance” that RBV is warranted in a patient on HD, the clinicians advise careful monitoring of Hb, especially 1 month after RBV therapy has started. Consider increasing the dosage of erythropoietin-stimulating agents if the patient’s Hb is at the lower end of the target range.

The decision to increase tacrolimus dosage based on a lower tacrolimus whole-blood concentration induced by anemia is “debatable,” the clinicians say. Nevertheless, this case reminds practitioners to take account of changes in RBC counts when interpreting tacrolimus levels—especially when a drastic change is not expected.

Source:

Liu HY, Cheung CYS, Cooper SE. BMJ Case Rep. 2018;2018. pii: bcr-2017-222477.
doi: 10.1136/bcr-2017-222477.

When interpreting tacrolimus levels, it is important to monitor changes in red blood cells (RBC). A patient who had hepatitis C virus (HCV) genotype 3A lesson reinforced that lesson for clinicians in the dialysis unit at Fraser Health in Abbotsford, Canada who authored a recent case report. Ribavirin-induced anemia reduced the level of tacrolimus in the patien, the authors reported.

The patient, a 37-year-old man, developed renal failure and received a kidney transplant, which subsequently failed (due to complications likely related to HCV). He had been started on tacrolimus while waiting to go back on the transplant list. Eight years later, the patient restarted hemodialysis (HD), with a regimen of sofosbuvir and ribavirin (SOF/RBV). His whole-blood tacrolimus level was 6.6 ng/mL (target 4–6); his hemoglobin (Hb) level was 10.3 g/dL. Two months later, the patient left for a 1-month vacation. When he returned, his Hb was “dramatically low,” at 3.7 g/dL.

The clinicians put the ribavirin on hold and increased darbepoetin. The patient was given packed RBCs; a bone marrow biopsy ruled out myeloproliferative disorder. Two weeks later, the tacrolimus level was 1.0 mg/mL and then dropped to an undetectable level 5 days later. The clinicians increased the dose. During the next month, the patient’s Hb “gradually bounced back,” to > 10 g/dL, whereupon the clinicians restarted RBV. When the tacrolimus level reached 7.2 ng/mL, the dosages were gradually cut back.  Sofosbuvir and RBV were stopped a couple of months later. The patient’s HCV RNA level was undetectable 12 weeks after therapy finished.

Practitioners are always facing the dilemma of risk (anemia) vs benefit (efficacy) in deciding whether and how much RBV should be reduced in renal impairment, the case report authors say. They note that the guidelines for treatment-naïve genotype 3 patients have changed. The recommendation for SOF/RBV has been replaced by one for glecaprevir/pibrentasvir or SOF/velpatasvir.

With the availability of newer direct antivirals, they add, the case again supports the abandoning of RBV-containing regimens. In the “very unlikely instance” that RBV is warranted in a patient on HD, the clinicians advise careful monitoring of Hb, especially 1 month after RBV therapy has started. Consider increasing the dosage of erythropoietin-stimulating agents if the patient’s Hb is at the lower end of the target range.

The decision to increase tacrolimus dosage based on a lower tacrolimus whole-blood concentration induced by anemia is “debatable,” the clinicians say. Nevertheless, this case reminds practitioners to take account of changes in RBC counts when interpreting tacrolimus levels—especially when a drastic change is not expected.

Source:

Liu HY, Cheung CYS, Cooper SE. BMJ Case Rep. 2018;2018. pii: bcr-2017-222477.
doi: 10.1136/bcr-2017-222477.

When interpreting tacrolimus levels, it is important to monitor changes in red blood cells (RBC). A patient who had hepatitis C virus (HCV) genotype 3A lesson reinforced that lesson for clinicians in the dialysis unit at Fraser Health in Abbotsford, Canada who authored a recent case report. Ribavirin-induced anemia reduced the level of tacrolimus in the patien, the authors reported.

The patient, a 37-year-old man, developed renal failure and received a kidney transplant, which subsequently failed (due to complications likely related to HCV). He had been started on tacrolimus while waiting to go back on the transplant list. Eight years later, the patient restarted hemodialysis (HD), with a regimen of sofosbuvir and ribavirin (SOF/RBV). His whole-blood tacrolimus level was 6.6 ng/mL (target 4–6); his hemoglobin (Hb) level was 10.3 g/dL. Two months later, the patient left for a 1-month vacation. When he returned, his Hb was “dramatically low,” at 3.7 g/dL.

The clinicians put the ribavirin on hold and increased darbepoetin. The patient was given packed RBCs; a bone marrow biopsy ruled out myeloproliferative disorder. Two weeks later, the tacrolimus level was 1.0 mg/mL and then dropped to an undetectable level 5 days later. The clinicians increased the dose. During the next month, the patient’s Hb “gradually bounced back,” to > 10 g/dL, whereupon the clinicians restarted RBV. When the tacrolimus level reached 7.2 ng/mL, the dosages were gradually cut back.  Sofosbuvir and RBV were stopped a couple of months later. The patient’s HCV RNA level was undetectable 12 weeks after therapy finished.

Practitioners are always facing the dilemma of risk (anemia) vs benefit (efficacy) in deciding whether and how much RBV should be reduced in renal impairment, the case report authors say. They note that the guidelines for treatment-naïve genotype 3 patients have changed. The recommendation for SOF/RBV has been replaced by one for glecaprevir/pibrentasvir or SOF/velpatasvir.

With the availability of newer direct antivirals, they add, the case again supports the abandoning of RBV-containing regimens. In the “very unlikely instance” that RBV is warranted in a patient on HD, the clinicians advise careful monitoring of Hb, especially 1 month after RBV therapy has started. Consider increasing the dosage of erythropoietin-stimulating agents if the patient’s Hb is at the lower end of the target range.

The decision to increase tacrolimus dosage based on a lower tacrolimus whole-blood concentration induced by anemia is “debatable,” the clinicians say. Nevertheless, this case reminds practitioners to take account of changes in RBC counts when interpreting tacrolimus levels—especially when a drastic change is not expected.

Source:

Liu HY, Cheung CYS, Cooper SE. BMJ Case Rep. 2018;2018. pii: bcr-2017-222477.
doi: 10.1136/bcr-2017-222477.