Sherry Boschert

SAN FRANCISCO — The use of acyclovir to suppress herpes simplex virus or to prevent herpes transmission failed to reduce transmission of HIV in several recent international studies.

Previous data have shown that type 2 herpes simplex virus (HSV-2) infection increases the risk for HIV acquisition and transmission. Investigators had hoped that medical suppression of HSV-2 reactivation might reduce HIV transmission rates in areas such as Africa, which has a very high (90%) seroprevalence of HSV, Dr. Diane V. Havlir said. The data, however, showed that HSV-2 suppression had no effect on HIV. “This particular strategy has been put on hold,” she said at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

A 2008 study randomized 3,172 HIV-negative, HSV-2 seropositive patients in Africa, Peru, and the United States to 800 mg acyclovir or matching placebo for 12–18 months (Lancet 2008;371:2109–19). Although acyclovir reduced the likelihood of developing genital ulcers compared with placebo, the incidence of HIV acquisition was similar between groups (3.9 and 3.3 cases per 100 person-years, respectively), noted Dr. Havlir, professor of medicine at the university and chief of the HIV/AIDS division at San Francisco General Hospital.

Some of the same investigators reported separate unpublished data at the 2009 International AIDS Society meeting in Cape Town, South Africa, showing similarly disappointing results in a study of 3,408 serodiscordant couples, Dr. Havlir added. She reported having no conflicts of interest related to these topics.

SAN FRANCISCO — The use of acyclovir to suppress herpes simplex virus or to prevent herpes transmission failed to reduce transmission of HIV in several recent international studies.

Previous data have shown that type 2 herpes simplex virus (HSV-2) infection increases the risk for HIV acquisition and transmission. Investigators had hoped that medical suppression of HSV-2 reactivation might reduce HIV transmission rates in areas such as Africa, which has a very high (90%) seroprevalence of HSV, Dr. Diane V. Havlir said. The data, however, showed that HSV-2 suppression had no effect on HIV. “This particular strategy has been put on hold,” she said at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

A 2008 study randomized 3,172 HIV-negative, HSV-2 seropositive patients in Africa, Peru, and the United States to 800 mg acyclovir or matching placebo for 12–18 months (Lancet 2008;371:2109–19). Although acyclovir reduced the likelihood of developing genital ulcers compared with placebo, the incidence of HIV acquisition was similar between groups (3.9 and 3.3 cases per 100 person-years, respectively), noted Dr. Havlir, professor of medicine at the university and chief of the HIV/AIDS division at San Francisco General Hospital.

Some of the same investigators reported separate unpublished data at the 2009 International AIDS Society meeting in Cape Town, South Africa, showing similarly disappointing results in a study of 3,408 serodiscordant couples, Dr. Havlir added. She reported having no conflicts of interest related to these topics.

SAN FRANCISCO — The use of acyclovir to suppress herpes simplex virus or to prevent herpes transmission failed to reduce transmission of HIV in several recent international studies.

Previous data have shown that type 2 herpes simplex virus (HSV-2) infection increases the risk for HIV acquisition and transmission. Investigators had hoped that medical suppression of HSV-2 reactivation might reduce HIV transmission rates in areas such as Africa, which has a very high (90%) seroprevalence of HSV, Dr. Diane V. Havlir said. The data, however, showed that HSV-2 suppression had no effect on HIV. “This particular strategy has been put on hold,” she said at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

A 2008 study randomized 3,172 HIV-negative, HSV-2 seropositive patients in Africa, Peru, and the United States to 800 mg acyclovir or matching placebo for 12–18 months (Lancet 2008;371:2109–19). Although acyclovir reduced the likelihood of developing genital ulcers compared with placebo, the incidence of HIV acquisition was similar between groups (3.9 and 3.3 cases per 100 person-years, respectively), noted Dr. Havlir, professor of medicine at the university and chief of the HIV/AIDS division at San Francisco General Hospital.

Some of the same investigators reported separate unpublished data at the 2009 International AIDS Society meeting in Cape Town, South Africa, showing similarly disappointing results in a study of 3,408 serodiscordant couples, Dr. Havlir added. She reported having no conflicts of interest related to these topics.

Major Finding: The integrase inhibitor raltegravir has joined the preferred first-line agents in combination therapy for HIV. S/GSK1349572 showed promise in a preliminary trial.

Source of Data: STARTMRK trial, a double-blind trial in 566 patients with HIV randomized to raltegravir or efavirenz. Also, unpublished data from a randomized, placebo-controlled trial of S/GSK1349572 in 30 subjects.

Disclosures: Dr. Havlir has no conflicts of interest. STARTMRK was funded by Merck, which makes raltegravir. The S/GSK1349572 trial was funded by the drug's developer, GlaxoSmithKline.

SAN FRANCISCO — For the first time, an integrase inhibitor is included in the preferred first-line antiretroviral regimens for adolescents and adults with HIV, and another integrase inhibitor may be starting phase II/III clinical trials.

Integrase inhibitors in recent years have become important tools for managing highly treated patients with drug-resistant HIV.

New data showing efficacy in previously untreated patients with HIV have moved the integrase inhibitor raltegravir into the starting lineup, Dr. Diane V. Havlir said at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

New guidelines released by the Department of Health and Human Services on Dec. 1, 2009, include a combination of raltegravir plus tenofovir and emtricitabine (TDF/FTC) as one of five preferred first-line antiretroviral therapy options for previously untreated patients with HIV.

The pivotal trial (called STARTMRK) that boosted raltegravir into first-line therapy randomized 566 treatment-naive patients with HIV to 48 weeks of TDF/FTC plus either raltegravir or efavirenz, said Dr. Havlir, professor of medicine at the university and chief of the HIV/AIDS division at San Francisco General Hospital.

Results for the raltegravir and efavirenz groups showed similar rates of viral suppression (82% and 86%, respectively) and of serious adverse events (less than 2% each), and viral suppression was more rapid in the raltegravir group (Lancet 2009;374:796–806).

Longer follow-up data out to 96 weeks now show sustained suppression of HIV RNA levels with raltegravir.

The Food and Drug Administration approved raltegravir for first-line combination antiretroviral therapy in August 2009.

A separate analysis suggested that raltegravir therapy avoids most of the increases in total cholesterol and triglyceride levels seen with efavirenz, she added, making the combination regimen containing raltegravir useful for HIV-infected patients with a history of lipid or cardiovascular problems.

The raltegravir plus TDF/FTC regimen involves more complex dosing and a higher pill burden than a once-a-day formulation of efavirenz combined with TDF/FTC (Atripla), which is one of the other preferred first-line regimens in the new federal guidelines.

An investigational integrase inhibitor that could be used in once-daily dosing might overcome that disadvantage, and the agent, S/GSK1349572, has showed promise in a preliminary trial in previously untreated patients with HIV, Dr. Havlir said.

A 10-day trial of various doses of the integrase inhibitor S/GSK1349572 in three cohorts of 10 patients each (with 8 patients on the active drug and 2 on placebo in each cohort) found that a 50-mg/day dose of S/GSK1349572 reduced HIV-1 RNA levels by 2.5 log₁₀ copies/mL, according to reports at an international AIDS meeting in South Africa earlier this year.

“It's my understanding that this is now going into phase II and III trials,” Dr. Havlir said. “We certainly look forward to more data on this particular agent.”

Major Finding: The integrase inhibitor raltegravir has joined the preferred first-line agents in combination therapy for HIV. S/GSK1349572 showed promise in a preliminary trial.

Source of Data: STARTMRK trial, a double-blind trial in 566 patients with HIV randomized to raltegravir or efavirenz. Also, unpublished data from a randomized, placebo-controlled trial of S/GSK1349572 in 30 subjects.

Disclosures: Dr. Havlir has no conflicts of interest. STARTMRK was funded by Merck, which makes raltegravir. The S/GSK1349572 trial was funded by the drug's developer, GlaxoSmithKline.

SAN FRANCISCO — For the first time, an integrase inhibitor is included in the preferred first-line antiretroviral regimens for adolescents and adults with HIV, and another integrase inhibitor may be starting phase II/III clinical trials.

Integrase inhibitors in recent years have become important tools for managing highly treated patients with drug-resistant HIV.

New data showing efficacy in previously untreated patients with HIV have moved the integrase inhibitor raltegravir into the starting lineup, Dr. Diane V. Havlir said at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

New guidelines released by the Department of Health and Human Services on Dec. 1, 2009, include a combination of raltegravir plus tenofovir and emtricitabine (TDF/FTC) as one of five preferred first-line antiretroviral therapy options for previously untreated patients with HIV.

The pivotal trial (called STARTMRK) that boosted raltegravir into first-line therapy randomized 566 treatment-naive patients with HIV to 48 weeks of TDF/FTC plus either raltegravir or efavirenz, said Dr. Havlir, professor of medicine at the university and chief of the HIV/AIDS division at San Francisco General Hospital.

Results for the raltegravir and efavirenz groups showed similar rates of viral suppression (82% and 86%, respectively) and of serious adverse events (less than 2% each), and viral suppression was more rapid in the raltegravir group (Lancet 2009;374:796–806).

Longer follow-up data out to 96 weeks now show sustained suppression of HIV RNA levels with raltegravir.

The Food and Drug Administration approved raltegravir for first-line combination antiretroviral therapy in August 2009.

A separate analysis suggested that raltegravir therapy avoids most of the increases in total cholesterol and triglyceride levels seen with efavirenz, she added, making the combination regimen containing raltegravir useful for HIV-infected patients with a history of lipid or cardiovascular problems.

The raltegravir plus TDF/FTC regimen involves more complex dosing and a higher pill burden than a once-a-day formulation of efavirenz combined with TDF/FTC (Atripla), which is one of the other preferred first-line regimens in the new federal guidelines.

An investigational integrase inhibitor that could be used in once-daily dosing might overcome that disadvantage, and the agent, S/GSK1349572, has showed promise in a preliminary trial in previously untreated patients with HIV, Dr. Havlir said.

A 10-day trial of various doses of the integrase inhibitor S/GSK1349572 in three cohorts of 10 patients each (with 8 patients on the active drug and 2 on placebo in each cohort) found that a 50-mg/day dose of S/GSK1349572 reduced HIV-1 RNA levels by 2.5 log₁₀ copies/mL, according to reports at an international AIDS meeting in South Africa earlier this year.

“It's my understanding that this is now going into phase II and III trials,” Dr. Havlir said. “We certainly look forward to more data on this particular agent.”

Major Finding: The integrase inhibitor raltegravir has joined the preferred first-line agents in combination therapy for HIV. S/GSK1349572 showed promise in a preliminary trial.

Source of Data: STARTMRK trial, a double-blind trial in 566 patients with HIV randomized to raltegravir or efavirenz. Also, unpublished data from a randomized, placebo-controlled trial of S/GSK1349572 in 30 subjects.

Disclosures: Dr. Havlir has no conflicts of interest. STARTMRK was funded by Merck, which makes raltegravir. The S/GSK1349572 trial was funded by the drug's developer, GlaxoSmithKline.

SAN FRANCISCO — For the first time, an integrase inhibitor is included in the preferred first-line antiretroviral regimens for adolescents and adults with HIV, and another integrase inhibitor may be starting phase II/III clinical trials.

Integrase inhibitors in recent years have become important tools for managing highly treated patients with drug-resistant HIV.

New data showing efficacy in previously untreated patients with HIV have moved the integrase inhibitor raltegravir into the starting lineup, Dr. Diane V. Havlir said at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

New guidelines released by the Department of Health and Human Services on Dec. 1, 2009, include a combination of raltegravir plus tenofovir and emtricitabine (TDF/FTC) as one of five preferred first-line antiretroviral therapy options for previously untreated patients with HIV.

The pivotal trial (called STARTMRK) that boosted raltegravir into first-line therapy randomized 566 treatment-naive patients with HIV to 48 weeks of TDF/FTC plus either raltegravir or efavirenz, said Dr. Havlir, professor of medicine at the university and chief of the HIV/AIDS division at San Francisco General Hospital.

Results for the raltegravir and efavirenz groups showed similar rates of viral suppression (82% and 86%, respectively) and of serious adverse events (less than 2% each), and viral suppression was more rapid in the raltegravir group (Lancet 2009;374:796–806).

Longer follow-up data out to 96 weeks now show sustained suppression of HIV RNA levels with raltegravir.

The Food and Drug Administration approved raltegravir for first-line combination antiretroviral therapy in August 2009.

A separate analysis suggested that raltegravir therapy avoids most of the increases in total cholesterol and triglyceride levels seen with efavirenz, she added, making the combination regimen containing raltegravir useful for HIV-infected patients with a history of lipid or cardiovascular problems.

The raltegravir plus TDF/FTC regimen involves more complex dosing and a higher pill burden than a once-a-day formulation of efavirenz combined with TDF/FTC (Atripla), which is one of the other preferred first-line regimens in the new federal guidelines.

An investigational integrase inhibitor that could be used in once-daily dosing might overcome that disadvantage, and the agent, S/GSK1349572, has showed promise in a preliminary trial in previously untreated patients with HIV, Dr. Havlir said.

A 10-day trial of various doses of the integrase inhibitor S/GSK1349572 in three cohorts of 10 patients each (with 8 patients on the active drug and 2 on placebo in each cohort) found that a 50-mg/day dose of S/GSK1349572 reduced HIV-1 RNA levels by 2.5 log₁₀ copies/mL, according to reports at an international AIDS meeting in South Africa earlier this year.

“It's my understanding that this is now going into phase II and III trials,” Dr. Havlir said. “We certainly look forward to more data on this particular agent.”

SAN FRANCISCO — New federal guidelines recommend earlier initiation of antiretroviral therapy for adolescents and adults with HIV and come close to recommending therapy for nearly everyone with HIV.

“We're moving towards treating most people who are infected with HIV,” Dr. Diane V. Havlir said at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

She suggested, only somewhat tongue-in-cheek, that future guidelines may focus on which patients should not start antiretrovirals. Those future guidelines might look something like this: Do not start HIV therapy if there are no antiretroviral options due to drug intolerance, drug interactions, or transmitted multidrug resistance, and be cautious about starting antiretroviral therapy in a patient with a CNS lesion, said Dr. Havlir, professor of medicine at the university and chief of the HIV/AIDS division at San Francisco General Hospital.

Guidelines released Dec. 1, 2009, by the Department of Health and Human Services (HHS) recommend starting antiretrovirals for HIV in patients with CD4 counts of 350–500 cells/mm

Of the guidelines committee members, half favored starting antiretrovirals in patients with CD4 counts higher than 500 cells/mm

The new guidelines eclipse 2008 recommendations from the International AIDS Society–USA to start antiretroviral therapy in asymptomatic patients with CD4 cell counts less than 350 cells/mm

Shortly before the HHS announcement, the World Health Organization (WHO) changed its guidelines to advise starting antiretrovirals in adolescents and adults with AIDS or tuberculosis or when CD4 counts drop below 350 cells/mm

“Countries will have to weigh the pros and cons of the guidelines and their financial constraints to see if they will be able to adopt them,” Dr. Havlir said.

The move toward earlier antiretroviral therapy is due to “tectonic shifts in thinking about HIV as a disease,” she noted.

There is increasing recognition that HIV infection not only increases susceptibility to opportunistic infections, complications, and malignancies, but also damages the renal and cardiac systems and contributes to liver disease, CNS changes, and probably aging.

Antiretroviral therapy can prevent some of the newly recognized harms to organ systems as well as the classic AIDS complications, she said. Earlier treatment initiation also may result in less drug resistance and better cognitive function.

Two studies in particular prompted the guideline changes.

The North American AIDS Cohort Collaboration on Research and Design studied 17,517 people with asymptomatic HIV infection who had not taken antiretrovirals. Patients who deferred treatment until CD4 counts fell below 350 cells/mm

Another analysis of data on 21,247 antiretroviral-naive patients found a higher risk of death if treatment was deferred until CD4 counts fell to 350 cells/mm

Dr. Havlir reported no conflicts of interest related to these topics.

'We're moving towards treating most people who are infected with HIV.'

Source DR. HAVLIR

SAN FRANCISCO — New federal guidelines recommend earlier initiation of antiretroviral therapy for adolescents and adults with HIV and come close to recommending therapy for nearly everyone with HIV.

“We're moving towards treating most people who are infected with HIV,” Dr. Diane V. Havlir said at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

She suggested, only somewhat tongue-in-cheek, that future guidelines may focus on which patients should not start antiretrovirals. Those future guidelines might look something like this: Do not start HIV therapy if there are no antiretroviral options due to drug intolerance, drug interactions, or transmitted multidrug resistance, and be cautious about starting antiretroviral therapy in a patient with a CNS lesion, said Dr. Havlir, professor of medicine at the university and chief of the HIV/AIDS division at San Francisco General Hospital.

Guidelines released Dec. 1, 2009, by the Department of Health and Human Services (HHS) recommend starting antiretrovirals for HIV in patients with CD4 counts of 350–500 cells/mm

Of the guidelines committee members, half favored starting antiretrovirals in patients with CD4 counts higher than 500 cells/mm

The new guidelines eclipse 2008 recommendations from the International AIDS Society–USA to start antiretroviral therapy in asymptomatic patients with CD4 cell counts less than 350 cells/mm

Shortly before the HHS announcement, the World Health Organization (WHO) changed its guidelines to advise starting antiretrovirals in adolescents and adults with AIDS or tuberculosis or when CD4 counts drop below 350 cells/mm

“Countries will have to weigh the pros and cons of the guidelines and their financial constraints to see if they will be able to adopt them,” Dr. Havlir said.

The move toward earlier antiretroviral therapy is due to “tectonic shifts in thinking about HIV as a disease,” she noted.

There is increasing recognition that HIV infection not only increases susceptibility to opportunistic infections, complications, and malignancies, but also damages the renal and cardiac systems and contributes to liver disease, CNS changes, and probably aging.

Antiretroviral therapy can prevent some of the newly recognized harms to organ systems as well as the classic AIDS complications, she said. Earlier treatment initiation also may result in less drug resistance and better cognitive function.

Two studies in particular prompted the guideline changes.

The North American AIDS Cohort Collaboration on Research and Design studied 17,517 people with asymptomatic HIV infection who had not taken antiretrovirals. Patients who deferred treatment until CD4 counts fell below 350 cells/mm

Another analysis of data on 21,247 antiretroviral-naive patients found a higher risk of death if treatment was deferred until CD4 counts fell to 350 cells/mm

Dr. Havlir reported no conflicts of interest related to these topics.

'We're moving towards treating most people who are infected with HIV.'

Source DR. HAVLIR

SAN FRANCISCO — New federal guidelines recommend earlier initiation of antiretroviral therapy for adolescents and adults with HIV and come close to recommending therapy for nearly everyone with HIV.

“We're moving towards treating most people who are infected with HIV,” Dr. Diane V. Havlir said at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

She suggested, only somewhat tongue-in-cheek, that future guidelines may focus on which patients should not start antiretrovirals. Those future guidelines might look something like this: Do not start HIV therapy if there are no antiretroviral options due to drug intolerance, drug interactions, or transmitted multidrug resistance, and be cautious about starting antiretroviral therapy in a patient with a CNS lesion, said Dr. Havlir, professor of medicine at the university and chief of the HIV/AIDS division at San Francisco General Hospital.

Guidelines released Dec. 1, 2009, by the Department of Health and Human Services (HHS) recommend starting antiretrovirals for HIV in patients with CD4 counts of 350–500 cells/mm

Of the guidelines committee members, half favored starting antiretrovirals in patients with CD4 counts higher than 500 cells/mm

The new guidelines eclipse 2008 recommendations from the International AIDS Society–USA to start antiretroviral therapy in asymptomatic patients with CD4 cell counts less than 350 cells/mm

Shortly before the HHS announcement, the World Health Organization (WHO) changed its guidelines to advise starting antiretrovirals in adolescents and adults with AIDS or tuberculosis or when CD4 counts drop below 350 cells/mm

“Countries will have to weigh the pros and cons of the guidelines and their financial constraints to see if they will be able to adopt them,” Dr. Havlir said.

The move toward earlier antiretroviral therapy is due to “tectonic shifts in thinking about HIV as a disease,” she noted.

There is increasing recognition that HIV infection not only increases susceptibility to opportunistic infections, complications, and malignancies, but also damages the renal and cardiac systems and contributes to liver disease, CNS changes, and probably aging.

Antiretroviral therapy can prevent some of the newly recognized harms to organ systems as well as the classic AIDS complications, she said. Earlier treatment initiation also may result in less drug resistance and better cognitive function.

Two studies in particular prompted the guideline changes.

The North American AIDS Cohort Collaboration on Research and Design studied 17,517 people with asymptomatic HIV infection who had not taken antiretrovirals. Patients who deferred treatment until CD4 counts fell below 350 cells/mm

Another analysis of data on 21,247 antiretroviral-naive patients found a higher risk of death if treatment was deferred until CD4 counts fell to 350 cells/mm

Dr. Havlir reported no conflicts of interest related to these topics.

'We're moving towards treating most people who are infected with HIV.'

Source DR. HAVLIR

Major Finding: Postponing antiretroviral therapy until CD4 counts are less than 200 copies/mm

Source of Data: Expert opinion.

Disclosures: Dr. Deeks has been an adviser to GlaxoSmithKline and has received research funds from Pfizer, Merck, Gilead, and Bristol-Myers Squibb. Dr. Maurer and Dr. Brooks reported having no conflicts of interest.

SAN FRANCISCO — Antiretroviral therapy has allowed many HIV-infected people to live long enough to grow old, yet their immune systems seem to age rapidly for their chronologic age, a factor that appears to be contributing to increased risks for non-HIV diseases of aging in middle-aged patients, according to several speakers at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

“There are striking similarities between the immune systems of some of our patients in their 50s and [those of] their parents,” said Dr. Steven G. Deeks, professor of medicine at the university.

In 2007, 28% of people living with HIV were aged 50 years or older; that proportion will grow to 50% by 2015, Dr. Richard Brooks, also of the university, said in a separate presentation.

Also at the meeting, Dr. Toby Maurer reported that her clinic is seeing more HIV-infected patients with skin diseases associated with aging, including disseminated herpes zoster and indolent Kaposi's sarcoma, despite relatively healthy CD4 counts ranging between 300 and 700 cells/mm

Disseminated zoster is “very unusual with a CD4 count of 350 cells/mm

The Kaposi's sarcoma cases are not the aggressive variety seen 20 years ago in HIV-infected patients, she said, but are the type typically found in older Mediterranean men.

To preserve immune function, Dr. Deeks advocates starting highly active antiretroviral therapy (HAART) in any HIV-infected patient who is motivated to begin treatment—a more aggressive approach than called for in treatment guidelines.

HAART reduces but does not eliminate T-cell activation and inflammation. Persistent, residual inflammation while on HAART is more extensive when patients start therapy at CD4 counts less than 200 copies/mm

Previous attempts to reduce HIV-associated inflammation and immunosenescence through the use of prednisone, hydroxyurea, cyclosporin, or mycophenolic acid were “like treating a subtle problem with sledgehammers,” and patients did not fare well, Dr. Deeks said.

“We need to reduce inflammation in a safe way” through the use of statins, aspirin, exercise, omega-3 fatty acids, vitamins, and immunomodulators, he said.

Newer strategies could include investigational drugs that enhance recovery of CD4 cells or that fully eradicate the subtle levels of persistent or replicating virus.

An “overwhelming amount of data” show that even those patients with undetectable virus and increased CD4 counts on HAART are more likely than people without HIV to develop heart disease, non-AIDS cancer, bone disease and fractures, left ventricular dysfunction, liver or kidney failure, frailty, and possibly cognitive dysfunction, Dr. Deeks said.

After controlling for the effects of other factors, including lipids or hypertension, HIV-infected patients have a 75% higher risk for cardiovascular events than do uninfected people, several studies suggest.

Dr. Brooks noted that frailty was 11 times more common in HIV-positive men, compared with HIV-negative men, in one study (J. Gerontol. A Biol. Sci. Med. Sci. 2007;62:1279–86). HIV infection of 4 years' duration or less conferred a risk for frailty in a 55-year-old man that compared with risks for a 65-year-old HIV-negative man, “confirming our impression that HIV-positive men are aging faster than their HIV-negative counterparts,” Dr. Brooks said.

To help HIV-infected patients stay healthy longer, he advised focusing on modification of traditional risk factors for non-HIV comorbidities of aging—smoking, hypertension, dyslipidemia, weight gain, diet, and exercise.

When possible, avoid HIV medications that can exacerbate illnesses associated with aging and check for drug-drug interactions, Dr. Brooks added. Older protease inhibitors and zidovudine increase the risk for insulin resistance. Tenofovir increases risk for renal dysfunction. Abacavir, didanosine, and protease inhibitors increase risk for cardiovascular disease. Zidovudine, protease inhibitors, and nonnucleoside reverse transcriptase inhibitors increase risk for dyslipidemia.

Dr. Brooks recommended the Beers Criteria, which lists medications to avoid in anyone older than 65 years or in older people with different disease states (Arch. Intern. Med. 2003;163:2716–24).

For iPhone users who subscribe to Epocrates, the criteria also are accessible in the Tables section of the program, he added.

Most physicians can check the top 30–40 medication interactions in their heads, “but I think you'd be surprised if we did it in a much more methodical way,” Dr. Brooks said.

Major Finding: Postponing antiretroviral therapy until CD4 counts are less than 200 copies/mm

Source of Data: Expert opinion.

Disclosures: Dr. Deeks has been an adviser to GlaxoSmithKline and has received research funds from Pfizer, Merck, Gilead, and Bristol-Myers Squibb. Dr. Maurer and Dr. Brooks reported having no conflicts of interest.

SAN FRANCISCO — Antiretroviral therapy has allowed many HIV-infected people to live long enough to grow old, yet their immune systems seem to age rapidly for their chronologic age, a factor that appears to be contributing to increased risks for non-HIV diseases of aging in middle-aged patients, according to several speakers at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

“There are striking similarities between the immune systems of some of our patients in their 50s and [those of] their parents,” said Dr. Steven G. Deeks, professor of medicine at the university.

In 2007, 28% of people living with HIV were aged 50 years or older; that proportion will grow to 50% by 2015, Dr. Richard Brooks, also of the university, said in a separate presentation.

Also at the meeting, Dr. Toby Maurer reported that her clinic is seeing more HIV-infected patients with skin diseases associated with aging, including disseminated herpes zoster and indolent Kaposi's sarcoma, despite relatively healthy CD4 counts ranging between 300 and 700 cells/mm

Disseminated zoster is “very unusual with a CD4 count of 350 cells/mm

The Kaposi's sarcoma cases are not the aggressive variety seen 20 years ago in HIV-infected patients, she said, but are the type typically found in older Mediterranean men.

To preserve immune function, Dr. Deeks advocates starting highly active antiretroviral therapy (HAART) in any HIV-infected patient who is motivated to begin treatment—a more aggressive approach than called for in treatment guidelines.

HAART reduces but does not eliminate T-cell activation and inflammation. Persistent, residual inflammation while on HAART is more extensive when patients start therapy at CD4 counts less than 200 copies/mm

Previous attempts to reduce HIV-associated inflammation and immunosenescence through the use of prednisone, hydroxyurea, cyclosporin, or mycophenolic acid were “like treating a subtle problem with sledgehammers,” and patients did not fare well, Dr. Deeks said.

“We need to reduce inflammation in a safe way” through the use of statins, aspirin, exercise, omega-3 fatty acids, vitamins, and immunomodulators, he said.

Newer strategies could include investigational drugs that enhance recovery of CD4 cells or that fully eradicate the subtle levels of persistent or replicating virus.

An “overwhelming amount of data” show that even those patients with undetectable virus and increased CD4 counts on HAART are more likely than people without HIV to develop heart disease, non-AIDS cancer, bone disease and fractures, left ventricular dysfunction, liver or kidney failure, frailty, and possibly cognitive dysfunction, Dr. Deeks said.

After controlling for the effects of other factors, including lipids or hypertension, HIV-infected patients have a 75% higher risk for cardiovascular events than do uninfected people, several studies suggest.

Dr. Brooks noted that frailty was 11 times more common in HIV-positive men, compared with HIV-negative men, in one study (J. Gerontol. A Biol. Sci. Med. Sci. 2007;62:1279–86). HIV infection of 4 years' duration or less conferred a risk for frailty in a 55-year-old man that compared with risks for a 65-year-old HIV-negative man, “confirming our impression that HIV-positive men are aging faster than their HIV-negative counterparts,” Dr. Brooks said.

To help HIV-infected patients stay healthy longer, he advised focusing on modification of traditional risk factors for non-HIV comorbidities of aging—smoking, hypertension, dyslipidemia, weight gain, diet, and exercise.

When possible, avoid HIV medications that can exacerbate illnesses associated with aging and check for drug-drug interactions, Dr. Brooks added. Older protease inhibitors and zidovudine increase the risk for insulin resistance. Tenofovir increases risk for renal dysfunction. Abacavir, didanosine, and protease inhibitors increase risk for cardiovascular disease. Zidovudine, protease inhibitors, and nonnucleoside reverse transcriptase inhibitors increase risk for dyslipidemia.

Dr. Brooks recommended the Beers Criteria, which lists medications to avoid in anyone older than 65 years or in older people with different disease states (Arch. Intern. Med. 2003;163:2716–24).

For iPhone users who subscribe to Epocrates, the criteria also are accessible in the Tables section of the program, he added.

Most physicians can check the top 30–40 medication interactions in their heads, “but I think you'd be surprised if we did it in a much more methodical way,” Dr. Brooks said.

Major Finding: Postponing antiretroviral therapy until CD4 counts are less than 200 copies/mm

Source of Data: Expert opinion.

Disclosures: Dr. Deeks has been an adviser to GlaxoSmithKline and has received research funds from Pfizer, Merck, Gilead, and Bristol-Myers Squibb. Dr. Maurer and Dr. Brooks reported having no conflicts of interest.

SAN FRANCISCO — Antiretroviral therapy has allowed many HIV-infected people to live long enough to grow old, yet their immune systems seem to age rapidly for their chronologic age, a factor that appears to be contributing to increased risks for non-HIV diseases of aging in middle-aged patients, according to several speakers at a meeting on the medical management of HIV and AIDS sponsored by the University of California, San Francisco.

“There are striking similarities between the immune systems of some of our patients in their 50s and [those of] their parents,” said Dr. Steven G. Deeks, professor of medicine at the university.

In 2007, 28% of people living with HIV were aged 50 years or older; that proportion will grow to 50% by 2015, Dr. Richard Brooks, also of the university, said in a separate presentation.

Also at the meeting, Dr. Toby Maurer reported that her clinic is seeing more HIV-infected patients with skin diseases associated with aging, including disseminated herpes zoster and indolent Kaposi's sarcoma, despite relatively healthy CD4 counts ranging between 300 and 700 cells/mm

Disseminated zoster is “very unusual with a CD4 count of 350 cells/mm

The Kaposi's sarcoma cases are not the aggressive variety seen 20 years ago in HIV-infected patients, she said, but are the type typically found in older Mediterranean men.

To preserve immune function, Dr. Deeks advocates starting highly active antiretroviral therapy (HAART) in any HIV-infected patient who is motivated to begin treatment—a more aggressive approach than called for in treatment guidelines.

HAART reduces but does not eliminate T-cell activation and inflammation. Persistent, residual inflammation while on HAART is more extensive when patients start therapy at CD4 counts less than 200 copies/mm

Previous attempts to reduce HIV-associated inflammation and immunosenescence through the use of prednisone, hydroxyurea, cyclosporin, or mycophenolic acid were “like treating a subtle problem with sledgehammers,” and patients did not fare well, Dr. Deeks said.

“We need to reduce inflammation in a safe way” through the use of statins, aspirin, exercise, omega-3 fatty acids, vitamins, and immunomodulators, he said.

Newer strategies could include investigational drugs that enhance recovery of CD4 cells or that fully eradicate the subtle levels of persistent or replicating virus.

An “overwhelming amount of data” show that even those patients with undetectable virus and increased CD4 counts on HAART are more likely than people without HIV to develop heart disease, non-AIDS cancer, bone disease and fractures, left ventricular dysfunction, liver or kidney failure, frailty, and possibly cognitive dysfunction, Dr. Deeks said.

After controlling for the effects of other factors, including lipids or hypertension, HIV-infected patients have a 75% higher risk for cardiovascular events than do uninfected people, several studies suggest.

Dr. Brooks noted that frailty was 11 times more common in HIV-positive men, compared with HIV-negative men, in one study (J. Gerontol. A Biol. Sci. Med. Sci. 2007;62:1279–86). HIV infection of 4 years' duration or less conferred a risk for frailty in a 55-year-old man that compared with risks for a 65-year-old HIV-negative man, “confirming our impression that HIV-positive men are aging faster than their HIV-negative counterparts,” Dr. Brooks said.

To help HIV-infected patients stay healthy longer, he advised focusing on modification of traditional risk factors for non-HIV comorbidities of aging—smoking, hypertension, dyslipidemia, weight gain, diet, and exercise.

When possible, avoid HIV medications that can exacerbate illnesses associated with aging and check for drug-drug interactions, Dr. Brooks added. Older protease inhibitors and zidovudine increase the risk for insulin resistance. Tenofovir increases risk for renal dysfunction. Abacavir, didanosine, and protease inhibitors increase risk for cardiovascular disease. Zidovudine, protease inhibitors, and nonnucleoside reverse transcriptase inhibitors increase risk for dyslipidemia.

Dr. Brooks recommended the Beers Criteria, which lists medications to avoid in anyone older than 65 years or in older people with different disease states (Arch. Intern. Med. 2003;163:2716–24).

For iPhone users who subscribe to Epocrates, the criteria also are accessible in the Tables section of the program, he added.

Most physicians can check the top 30–40 medication interactions in their heads, “but I think you'd be surprised if we did it in a much more methodical way,” Dr. Brooks said.

SAN DIEGO — Prophylactic use of a proton pump inhibitor plus clopidogrel after percutaneous coronary revascularization was associated with significantly greater risk for cardiovascular events, compared with clopidogrel alone, a small retrospective study found.

After percutaneous coronary intervention (PCI), 40 (56%) of 72 patients who were discharged on concomitant clopidogrel and proton pump inhibitor (PPI) therapy developed major adverse coronary events over a mean follow-up of 50 months, compared with 92 (38%) of 243 patients discharged on clopidogrel alone, Dr. Ekta Gupta and her associates reported at the annual meeting of the American College of Gastroenterology.

After adjustment for baseline characteristics including the type of stent, patients in the combination-therapy group had a 95% excess risk for major adverse coronary events, said Dr. Gupta of the University of Arkansas, Little Rock.

“Our study suggests that 'routine' use of prophylactic PPIs to prevent gastrointestinal bleeding should be avoided” until results of prospective, randomized, controlled studies become available, she said.

The adverse coronary events studied included cardiac or noncardiac death, MI, and target vessel failure (defined as a composite of cardiac death, MI, or target vessel revascularization).

Most patients who got a PPI used rabeprazole, with a minority getting omeprazole or lansoprazole. The study excluded patients who received pantoprazole or esomeprazole because previous studies found no association between these two drugs and an impaired response to clopidogrel seen with the other PPIs, suggesting that the adverse PPI-clopidogrel interaction may not apply to the whole class of drugs, she said.

If a PPI is needed after PCI, it may be preferable to use esomeprazole or pantoprazole, Dr. Gupta said. Alternatively, clinicians may want to consider separating the dosing of clopidogrel and the PPI to avoid any potential drug-drug interaction, she said.

Dr. Gupta had no conflicts of interest related to this study.

SAN DIEGO — Prophylactic use of a proton pump inhibitor plus clopidogrel after percutaneous coronary revascularization was associated with significantly greater risk for cardiovascular events, compared with clopidogrel alone, a small retrospective study found.

After percutaneous coronary intervention (PCI), 40 (56%) of 72 patients who were discharged on concomitant clopidogrel and proton pump inhibitor (PPI) therapy developed major adverse coronary events over a mean follow-up of 50 months, compared with 92 (38%) of 243 patients discharged on clopidogrel alone, Dr. Ekta Gupta and her associates reported at the annual meeting of the American College of Gastroenterology.

After adjustment for baseline characteristics including the type of stent, patients in the combination-therapy group had a 95% excess risk for major adverse coronary events, said Dr. Gupta of the University of Arkansas, Little Rock.

“Our study suggests that 'routine' use of prophylactic PPIs to prevent gastrointestinal bleeding should be avoided” until results of prospective, randomized, controlled studies become available, she said.

The adverse coronary events studied included cardiac or noncardiac death, MI, and target vessel failure (defined as a composite of cardiac death, MI, or target vessel revascularization).

Most patients who got a PPI used rabeprazole, with a minority getting omeprazole or lansoprazole. The study excluded patients who received pantoprazole or esomeprazole because previous studies found no association between these two drugs and an impaired response to clopidogrel seen with the other PPIs, suggesting that the adverse PPI-clopidogrel interaction may not apply to the whole class of drugs, she said.

If a PPI is needed after PCI, it may be preferable to use esomeprazole or pantoprazole, Dr. Gupta said. Alternatively, clinicians may want to consider separating the dosing of clopidogrel and the PPI to avoid any potential drug-drug interaction, she said.

Dr. Gupta had no conflicts of interest related to this study.

SAN DIEGO — Prophylactic use of a proton pump inhibitor plus clopidogrel after percutaneous coronary revascularization was associated with significantly greater risk for cardiovascular events, compared with clopidogrel alone, a small retrospective study found.

After percutaneous coronary intervention (PCI), 40 (56%) of 72 patients who were discharged on concomitant clopidogrel and proton pump inhibitor (PPI) therapy developed major adverse coronary events over a mean follow-up of 50 months, compared with 92 (38%) of 243 patients discharged on clopidogrel alone, Dr. Ekta Gupta and her associates reported at the annual meeting of the American College of Gastroenterology.

After adjustment for baseline characteristics including the type of stent, patients in the combination-therapy group had a 95% excess risk for major adverse coronary events, said Dr. Gupta of the University of Arkansas, Little Rock.

“Our study suggests that 'routine' use of prophylactic PPIs to prevent gastrointestinal bleeding should be avoided” until results of prospective, randomized, controlled studies become available, she said.

The adverse coronary events studied included cardiac or noncardiac death, MI, and target vessel failure (defined as a composite of cardiac death, MI, or target vessel revascularization).

Most patients who got a PPI used rabeprazole, with a minority getting omeprazole or lansoprazole. The study excluded patients who received pantoprazole or esomeprazole because previous studies found no association between these two drugs and an impaired response to clopidogrel seen with the other PPIs, suggesting that the adverse PPI-clopidogrel interaction may not apply to the whole class of drugs, she said.

If a PPI is needed after PCI, it may be preferable to use esomeprazole or pantoprazole, Dr. Gupta said. Alternatively, clinicians may want to consider separating the dosing of clopidogrel and the PPI to avoid any potential drug-drug interaction, she said.

Dr. Gupta had no conflicts of interest related to this study.

SAN FRANCISCO — Modern diets full of fructose may be a driving force in the epidemic of cardiovascular disease, according to Dr. Richard J. Johnson.

Both human and animal studies have shown that high levels of fructose intake induce features of the metabolic syndrome, which in turn can lead to the development of diabetes and hypertension, he said at the sixth annual World Congress on the Insulin Resistance Syndrome.

Each year, Americans ingest an average of 150 pounds of sugar, and 25% of the U.S. population eats more than 200 pounds of sugar, data from the National Health and Nutrition Examination Survey (NHANES) suggest.

“In modern societies, we're on high sugar,” said Dr. Johnson, professor of medicine and chief of the division of renal diseases and hypertension at the University of Colorado, Denver.

Sugar consists of sucrose and fructose. Fructose- and purine-rich foods increase uric acid levels, induce oxidative stress, decrease nitric oxide in cells, and raise blood pressure, he said. Fructose consumption can raise uric acid levels within a 30-minute period. At least 17 published studies have shown that hyperuricemia is an independent risk factor for hypertension.

“If uric acid is driving hypertension, it would be most likely to be elevated in newly diagnosed hypertension,” he said at the conference, which was sponsored by the International Committee for Insulin Resistance.

Dr. Johnson and his associates randomized 30 adolescents with newly diagnosed stage 1 essential hypertension and serum uric acid levels at or greater than 6 mg/dL to treatment with allopurinol or placebo for 4 weeks, followed by a 2-week washout period, after which they were switched to the other treatment group.

The 24-hour ambulatory systolic blood pressure decreased by an average of 6.3 mm Hg on allopurinol and increased by 0.8 mm Hg on placebo.

Mean 24-hour ambulatory diastolic measurements decreased by 4.6 mm Hg on allopurinol and by 0.3 mm Hg on placebo. The differences between the groups were statistically significant (JAMA 2008;300:924–32).

“The results were dramatic,” he said. Only 1 of the 30 teenagers became normotensive on placebo, but 20 became normotensive on allopurinol. “In those who lowered the uric acid to less than 5 ng/dL, 86% became normotensive.”

Two subsequent, unpublished studies confirmed the findings. The National Institutes of Health have invited Dr. Johnson and his associates to conduct a multicenter trial to see if lowering uric acid can prevent the development of hypertension in adolescents, he said.

In a study to be published February in the International Journal of Obesity, Dr. Johnson and his associates gave 200 g/day of fructose with or without allopurinol to 76 healthy overweight men for 2 weeks. Fructose intake without allopurinol increased daytime and night-time systolic blood pressure, raised triglyceride levels, lowered HDL cholesterol levels, increased uric acid levels, and added a pound in weight on average. “We could induce metabolic syndrome in 30% of individuals in just 2 weeks with fructose,” he said.

Taking allopurinol with the fructose blocked the increase in blood pressure but did not significantly affect changes in lipids, Dr. Johnson said.

Dr. Johnson and his associates also published their case for excessive fructose as a driver in the diabetes and cardiovascular disease epidemics in a recent review of the literature (Endocr. Rev. 2009;30:96–116).

Dr. Johnson has been a speaker for Merck & Co. and coauthored (with Timothy Gower) a book about the effect of fructose on health.

SAN FRANCISCO — Modern diets full of fructose may be a driving force in the epidemic of cardiovascular disease, according to Dr. Richard J. Johnson.

Both human and animal studies have shown that high levels of fructose intake induce features of the metabolic syndrome, which in turn can lead to the development of diabetes and hypertension, he said at the sixth annual World Congress on the Insulin Resistance Syndrome.

Each year, Americans ingest an average of 150 pounds of sugar, and 25% of the U.S. population eats more than 200 pounds of sugar, data from the National Health and Nutrition Examination Survey (NHANES) suggest.

“In modern societies, we're on high sugar,” said Dr. Johnson, professor of medicine and chief of the division of renal diseases and hypertension at the University of Colorado, Denver.

Sugar consists of sucrose and fructose. Fructose- and purine-rich foods increase uric acid levels, induce oxidative stress, decrease nitric oxide in cells, and raise blood pressure, he said. Fructose consumption can raise uric acid levels within a 30-minute period. At least 17 published studies have shown that hyperuricemia is an independent risk factor for hypertension.

“If uric acid is driving hypertension, it would be most likely to be elevated in newly diagnosed hypertension,” he said at the conference, which was sponsored by the International Committee for Insulin Resistance.

Dr. Johnson and his associates randomized 30 adolescents with newly diagnosed stage 1 essential hypertension and serum uric acid levels at or greater than 6 mg/dL to treatment with allopurinol or placebo for 4 weeks, followed by a 2-week washout period, after which they were switched to the other treatment group.

The 24-hour ambulatory systolic blood pressure decreased by an average of 6.3 mm Hg on allopurinol and increased by 0.8 mm Hg on placebo.

Mean 24-hour ambulatory diastolic measurements decreased by 4.6 mm Hg on allopurinol and by 0.3 mm Hg on placebo. The differences between the groups were statistically significant (JAMA 2008;300:924–32).

“The results were dramatic,” he said. Only 1 of the 30 teenagers became normotensive on placebo, but 20 became normotensive on allopurinol. “In those who lowered the uric acid to less than 5 ng/dL, 86% became normotensive.”

Two subsequent, unpublished studies confirmed the findings. The National Institutes of Health have invited Dr. Johnson and his associates to conduct a multicenter trial to see if lowering uric acid can prevent the development of hypertension in adolescents, he said.

In a study to be published February in the International Journal of Obesity, Dr. Johnson and his associates gave 200 g/day of fructose with or without allopurinol to 76 healthy overweight men for 2 weeks. Fructose intake without allopurinol increased daytime and night-time systolic blood pressure, raised triglyceride levels, lowered HDL cholesterol levels, increased uric acid levels, and added a pound in weight on average. “We could induce metabolic syndrome in 30% of individuals in just 2 weeks with fructose,” he said.

Taking allopurinol with the fructose blocked the increase in blood pressure but did not significantly affect changes in lipids, Dr. Johnson said.

Dr. Johnson and his associates also published their case for excessive fructose as a driver in the diabetes and cardiovascular disease epidemics in a recent review of the literature (Endocr. Rev. 2009;30:96–116).

Dr. Johnson has been a speaker for Merck & Co. and coauthored (with Timothy Gower) a book about the effect of fructose on health.

SAN FRANCISCO — Modern diets full of fructose may be a driving force in the epidemic of cardiovascular disease, according to Dr. Richard J. Johnson.

Both human and animal studies have shown that high levels of fructose intake induce features of the metabolic syndrome, which in turn can lead to the development of diabetes and hypertension, he said at the sixth annual World Congress on the Insulin Resistance Syndrome.

Each year, Americans ingest an average of 150 pounds of sugar, and 25% of the U.S. population eats more than 200 pounds of sugar, data from the National Health and Nutrition Examination Survey (NHANES) suggest.

“In modern societies, we're on high sugar,” said Dr. Johnson, professor of medicine and chief of the division of renal diseases and hypertension at the University of Colorado, Denver.

Sugar consists of sucrose and fructose. Fructose- and purine-rich foods increase uric acid levels, induce oxidative stress, decrease nitric oxide in cells, and raise blood pressure, he said. Fructose consumption can raise uric acid levels within a 30-minute period. At least 17 published studies have shown that hyperuricemia is an independent risk factor for hypertension.

“If uric acid is driving hypertension, it would be most likely to be elevated in newly diagnosed hypertension,” he said at the conference, which was sponsored by the International Committee for Insulin Resistance.

Dr. Johnson and his associates randomized 30 adolescents with newly diagnosed stage 1 essential hypertension and serum uric acid levels at or greater than 6 mg/dL to treatment with allopurinol or placebo for 4 weeks, followed by a 2-week washout period, after which they were switched to the other treatment group.

The 24-hour ambulatory systolic blood pressure decreased by an average of 6.3 mm Hg on allopurinol and increased by 0.8 mm Hg on placebo.

Mean 24-hour ambulatory diastolic measurements decreased by 4.6 mm Hg on allopurinol and by 0.3 mm Hg on placebo. The differences between the groups were statistically significant (JAMA 2008;300:924–32).

“The results were dramatic,” he said. Only 1 of the 30 teenagers became normotensive on placebo, but 20 became normotensive on allopurinol. “In those who lowered the uric acid to less than 5 ng/dL, 86% became normotensive.”

Two subsequent, unpublished studies confirmed the findings. The National Institutes of Health have invited Dr. Johnson and his associates to conduct a multicenter trial to see if lowering uric acid can prevent the development of hypertension in adolescents, he said.

In a study to be published February in the International Journal of Obesity, Dr. Johnson and his associates gave 200 g/day of fructose with or without allopurinol to 76 healthy overweight men for 2 weeks. Fructose intake without allopurinol increased daytime and night-time systolic blood pressure, raised triglyceride levels, lowered HDL cholesterol levels, increased uric acid levels, and added a pound in weight on average. “We could induce metabolic syndrome in 30% of individuals in just 2 weeks with fructose,” he said.

Taking allopurinol with the fructose blocked the increase in blood pressure but did not significantly affect changes in lipids, Dr. Johnson said.

Dr. Johnson and his associates also published their case for excessive fructose as a driver in the diabetes and cardiovascular disease epidemics in a recent review of the literature (Endocr. Rev. 2009;30:96–116).

Dr. Johnson has been a speaker for Merck & Co. and coauthored (with Timothy Gower) a book about the effect of fructose on health.

SAN FRANCISCO — Pain is common in breast cancer patients—painkillers less so, according to results of an online survey.

In all, 65% of 335 breast cancer patients reported they suffered from pain during the course of their disease or treatment, yet 28% of the 218 patients reporting pain did not use an analgesic.

The top reasons given for lack of analgesic use were not having a recommendation for analgesic use from their health care provider (83%), fear of addiction or dependency (77%), and inability to pay for medication (74%), Dr. Charles B. Simone II and his associates reported in an award-winning poster at a breast cancer symposium sponsored by the American Society of Clinical Oncology.

Some of those who reported pain but no analgesic use tried physical therapy (86%), massage therapy (8%), or other alternative measures for pain control, but still reported having pain on a regular basis, said Dr. Simone, a clinical fellow at the National Cancer Institute's Radiation Oncology Branch.

The findings highlight a need for additional education of health care providers on cancer pain evaluation and management, the investigators said. Clinicians should make pain management a priority, perform a standardized assessment of pain at every visit, and regularly discuss pain symptoms and pain treatment with breast cancer patients in order to break down the barriers to pain management, they suggested.

The survey was posted on the University of Pennsylvania's OncoLink Web site, the oldest and one of the largest online cancer information sources. Respondents were 97% female, 77% white, and predominantly educated beyond high school (82%). Of the entire cohort, 92% had undergone surgery, 74% had been treated with chemotherapy, and 62% underwent radiation therapy.

Acute or inconsistent analgesic use may be inadequate. Many breast cancer patients could benefit from analgesic use throughout the course of their disease and treatment, Dr. Simone and his associates suggested.

The researchers reported having no conflicts of interest related to the survey.

Acute or inconsistent analgesic use may be inadequate.

Source DR. SIMONE

SAN FRANCISCO — Pain is common in breast cancer patients—painkillers less so, according to results of an online survey.

In all, 65% of 335 breast cancer patients reported they suffered from pain during the course of their disease or treatment, yet 28% of the 218 patients reporting pain did not use an analgesic.

The top reasons given for lack of analgesic use were not having a recommendation for analgesic use from their health care provider (83%), fear of addiction or dependency (77%), and inability to pay for medication (74%), Dr. Charles B. Simone II and his associates reported in an award-winning poster at a breast cancer symposium sponsored by the American Society of Clinical Oncology.

Some of those who reported pain but no analgesic use tried physical therapy (86%), massage therapy (8%), or other alternative measures for pain control, but still reported having pain on a regular basis, said Dr. Simone, a clinical fellow at the National Cancer Institute's Radiation Oncology Branch.

The findings highlight a need for additional education of health care providers on cancer pain evaluation and management, the investigators said. Clinicians should make pain management a priority, perform a standardized assessment of pain at every visit, and regularly discuss pain symptoms and pain treatment with breast cancer patients in order to break down the barriers to pain management, they suggested.

The survey was posted on the University of Pennsylvania's OncoLink Web site, the oldest and one of the largest online cancer information sources. Respondents were 97% female, 77% white, and predominantly educated beyond high school (82%). Of the entire cohort, 92% had undergone surgery, 74% had been treated with chemotherapy, and 62% underwent radiation therapy.

Acute or inconsistent analgesic use may be inadequate. Many breast cancer patients could benefit from analgesic use throughout the course of their disease and treatment, Dr. Simone and his associates suggested.

The researchers reported having no conflicts of interest related to the survey.

Acute or inconsistent analgesic use may be inadequate.

Source DR. SIMONE

SAN FRANCISCO — Pain is common in breast cancer patients—painkillers less so, according to results of an online survey.

In all, 65% of 335 breast cancer patients reported they suffered from pain during the course of their disease or treatment, yet 28% of the 218 patients reporting pain did not use an analgesic.

The top reasons given for lack of analgesic use were not having a recommendation for analgesic use from their health care provider (83%), fear of addiction or dependency (77%), and inability to pay for medication (74%), Dr. Charles B. Simone II and his associates reported in an award-winning poster at a breast cancer symposium sponsored by the American Society of Clinical Oncology.

Some of those who reported pain but no analgesic use tried physical therapy (86%), massage therapy (8%), or other alternative measures for pain control, but still reported having pain on a regular basis, said Dr. Simone, a clinical fellow at the National Cancer Institute's Radiation Oncology Branch.

The findings highlight a need for additional education of health care providers on cancer pain evaluation and management, the investigators said. Clinicians should make pain management a priority, perform a standardized assessment of pain at every visit, and regularly discuss pain symptoms and pain treatment with breast cancer patients in order to break down the barriers to pain management, they suggested.

The survey was posted on the University of Pennsylvania's OncoLink Web site, the oldest and one of the largest online cancer information sources. Respondents were 97% female, 77% white, and predominantly educated beyond high school (82%). Of the entire cohort, 92% had undergone surgery, 74% had been treated with chemotherapy, and 62% underwent radiation therapy.

Acute or inconsistent analgesic use may be inadequate. Many breast cancer patients could benefit from analgesic use throughout the course of their disease and treatment, Dr. Simone and his associates suggested.

The researchers reported having no conflicts of interest related to the survey.

Acute or inconsistent analgesic use may be inadequate.

Source DR. SIMONE

SAN DIEGO — Isotretinoin use was associated with a 68% increased risk for subsequent development of inflammatory bowel disease, particularly ulcerative colitis, in a retrospective case-control study of 30,021 patients.

The odds ratio of 1.68 for inflammatory bowel disease (IBD) in isotretinoin users compared with nonusers had a 95% confidence interval (CI) of 0.98-2.86, Dr. Seth Crockett and his associates reported in a poster presentation at the annual meeting of the American College of Gastroenterology.

The findings add to ongoing controversy that IBD risk with isotretinoin may have been a factor in the decision by Roche to pull the best-known brand of isotretinoin, Accutane, off the market in June 2009.

The current study examined a large administrative claims database with records on 55 million patients from more than 70 U.S. health plans. The investigators compared 8,189 patients with at least 12 months of continuous health plan enrollment and diagnoses of ulcerative colitis, Crohn's disease, or indeterminate IBD with three non-IBD control patients per IBD patient, matched by age, gender, and geographic region. They looked at exposure to isotretinoin in the 21,832 control patients during the first 12 months of health plan enrollment.

Results pointed to a possible dose-response effect: The risk for IBD increased with the number of isotretinoin prescriptions. Having four or more isotretinoin prescriptions was associated with an odds ratio of 2.67 for development of IBD (CI, 1.32-5.41), reported Dr. Crockett of the University of North Carolina, Chapel Hill.

Subgroup analyses showed a strong association between isotretinoin use and ulcerative colitis (odds ratio, 4.36; CI, 1.98-9.66) but no association between isotretinoin exposure and Crohn's disease (odds ratio, 0.68).

“The flip side of all this is that there are patients who desperately need isotretinoin,” Dr. Stephen P. Stone commented in an interview. “Those of us who care for people with acne and are aware of the physical and psychosocial aspects of it find it an indispensable drug,” said Dr. Stone, chair of the American Academy of Dermatology's task force on retinoids and professor at Southern Illinois University, Carbondale. The drug also is helpful for less common problems such as cutaneous lupus that do not respond to other treatments, he added.

The possible association between isotretinoin and IBD has long been included in label warnings, but it drew increased interest after a 2006 study by gastroenterologists at the University of Chicago. That study looked at all 85 cases of IBD in isotretinoin users reported to the Food and Drug Administration in 1997-2002 and graded the strength of causality using the Naranjo adverse drug reaction probability scale. Mean scores suggested that the oral retinoid was a “probable” cause of IBD (Am. J. Gastroenterol. 2006;101:1569-73). Some dermatologic experts criticized the study's methodology, saying that a one-point adjustment for accuracy in the probability ratings would downgrade the mean score to “possible.”

A separate study by gastroenterologists at the University of Manitoba, Winnipeg, found no significant association between isotretinoin use and IBD. Using a large government database and drug registry, they found that 1.2% of patients with IBD and 1.1% of matched patients without IBD used isotretinoin before IBD diagnosis, an insignificant difference (Am. J. Gastroenterol. 2009;104:2774-8).

Dr. Crockett and his associates reported having no conflicts of interest related to their study. Dr. Stone reported no conflicts of interest.

SAN DIEGO — Isotretinoin use was associated with a 68% increased risk for subsequent development of inflammatory bowel disease, particularly ulcerative colitis, in a retrospective case-control study of 30,021 patients.

The odds ratio of 1.68 for inflammatory bowel disease (IBD) in isotretinoin users compared with nonusers had a 95% confidence interval (CI) of 0.98-2.86, Dr. Seth Crockett and his associates reported in a poster presentation at the annual meeting of the American College of Gastroenterology.

The findings add to ongoing controversy that IBD risk with isotretinoin may have been a factor in the decision by Roche to pull the best-known brand of isotretinoin, Accutane, off the market in June 2009.

The current study examined a large administrative claims database with records on 55 million patients from more than 70 U.S. health plans. The investigators compared 8,189 patients with at least 12 months of continuous health plan enrollment and diagnoses of ulcerative colitis, Crohn's disease, or indeterminate IBD with three non-IBD control patients per IBD patient, matched by age, gender, and geographic region. They looked at exposure to isotretinoin in the 21,832 control patients during the first 12 months of health plan enrollment.

Results pointed to a possible dose-response effect: The risk for IBD increased with the number of isotretinoin prescriptions. Having four or more isotretinoin prescriptions was associated with an odds ratio of 2.67 for development of IBD (CI, 1.32-5.41), reported Dr. Crockett of the University of North Carolina, Chapel Hill.

Subgroup analyses showed a strong association between isotretinoin use and ulcerative colitis (odds ratio, 4.36; CI, 1.98-9.66) but no association between isotretinoin exposure and Crohn's disease (odds ratio, 0.68).

“The flip side of all this is that there are patients who desperately need isotretinoin,” Dr. Stephen P. Stone commented in an interview. “Those of us who care for people with acne and are aware of the physical and psychosocial aspects of it find it an indispensable drug,” said Dr. Stone, chair of the American Academy of Dermatology's task force on retinoids and professor at Southern Illinois University, Carbondale. The drug also is helpful for less common problems such as cutaneous lupus that do not respond to other treatments, he added.

The possible association between isotretinoin and IBD has long been included in label warnings, but it drew increased interest after a 2006 study by gastroenterologists at the University of Chicago. That study looked at all 85 cases of IBD in isotretinoin users reported to the Food and Drug Administration in 1997-2002 and graded the strength of causality using the Naranjo adverse drug reaction probability scale. Mean scores suggested that the oral retinoid was a “probable” cause of IBD (Am. J. Gastroenterol. 2006;101:1569-73). Some dermatologic experts criticized the study's methodology, saying that a one-point adjustment for accuracy in the probability ratings would downgrade the mean score to “possible.”

A separate study by gastroenterologists at the University of Manitoba, Winnipeg, found no significant association between isotretinoin use and IBD. Using a large government database and drug registry, they found that 1.2% of patients with IBD and 1.1% of matched patients without IBD used isotretinoin before IBD diagnosis, an insignificant difference (Am. J. Gastroenterol. 2009;104:2774-8).

Dr. Crockett and his associates reported having no conflicts of interest related to their study. Dr. Stone reported no conflicts of interest.

SAN DIEGO — Isotretinoin use was associated with a 68% increased risk for subsequent development of inflammatory bowel disease, particularly ulcerative colitis, in a retrospective case-control study of 30,021 patients.

The odds ratio of 1.68 for inflammatory bowel disease (IBD) in isotretinoin users compared with nonusers had a 95% confidence interval (CI) of 0.98-2.86, Dr. Seth Crockett and his associates reported in a poster presentation at the annual meeting of the American College of Gastroenterology.

The findings add to ongoing controversy that IBD risk with isotretinoin may have been a factor in the decision by Roche to pull the best-known brand of isotretinoin, Accutane, off the market in June 2009.

The current study examined a large administrative claims database with records on 55 million patients from more than 70 U.S. health plans. The investigators compared 8,189 patients with at least 12 months of continuous health plan enrollment and diagnoses of ulcerative colitis, Crohn's disease, or indeterminate IBD with three non-IBD control patients per IBD patient, matched by age, gender, and geographic region. They looked at exposure to isotretinoin in the 21,832 control patients during the first 12 months of health plan enrollment.

Results pointed to a possible dose-response effect: The risk for IBD increased with the number of isotretinoin prescriptions. Having four or more isotretinoin prescriptions was associated with an odds ratio of 2.67 for development of IBD (CI, 1.32-5.41), reported Dr. Crockett of the University of North Carolina, Chapel Hill.

Subgroup analyses showed a strong association between isotretinoin use and ulcerative colitis (odds ratio, 4.36; CI, 1.98-9.66) but no association between isotretinoin exposure and Crohn's disease (odds ratio, 0.68).

“The flip side of all this is that there are patients who desperately need isotretinoin,” Dr. Stephen P. Stone commented in an interview. “Those of us who care for people with acne and are aware of the physical and psychosocial aspects of it find it an indispensable drug,” said Dr. Stone, chair of the American Academy of Dermatology's task force on retinoids and professor at Southern Illinois University, Carbondale. The drug also is helpful for less common problems such as cutaneous lupus that do not respond to other treatments, he added.

The possible association between isotretinoin and IBD has long been included in label warnings, but it drew increased interest after a 2006 study by gastroenterologists at the University of Chicago. That study looked at all 85 cases of IBD in isotretinoin users reported to the Food and Drug Administration in 1997-2002 and graded the strength of causality using the Naranjo adverse drug reaction probability scale. Mean scores suggested that the oral retinoid was a “probable” cause of IBD (Am. J. Gastroenterol. 2006;101:1569-73). Some dermatologic experts criticized the study's methodology, saying that a one-point adjustment for accuracy in the probability ratings would downgrade the mean score to “possible.”

A separate study by gastroenterologists at the University of Manitoba, Winnipeg, found no significant association between isotretinoin use and IBD. Using a large government database and drug registry, they found that 1.2% of patients with IBD and 1.1% of matched patients without IBD used isotretinoin before IBD diagnosis, an insignificant difference (Am. J. Gastroenterol. 2009;104:2774-8).

Dr. Crockett and his associates reported having no conflicts of interest related to their study. Dr. Stone reported no conflicts of interest.

SAN DIEGO — Among 366 patients with Barrett's esophagus, 82% were alive 5 years after diagnosis, a rate that was essentially no different than the overall survival rate seen in a matched control group from the general population.

The retrospective study is one of the first on survival in a large cohort of patients with Barrett's esophagus in the United States, Dr. Ganapathy A. Prasad said at the annual meeting of the American College of Gastroenterology.

Among previous studies, some found decreased survival in patients with Barrett's esophagus, compared with matched controls, while others showed comparable overall survival rates.

Those data came predominantly from Europe, said Dr. Prasad of the Mayo Clinic, Rochester, Minn.

Dr. Prasad and his associates identified 401 patients with Barrett's esophagus in the Rochester Epidemiology Project who were diagnosed between January 1976 and January 2007, and excluded 35 who had some evidence of cancer or who developed cancer within 6 months of diagnosis.

The 366 patients in the study were followed for a mean of 7.1 years. They had a mean age of 62 years at baseline, 70% were male, and more than 85% were white.

The investigators compared the study cohort's survival rate with survival data from an age- and gender-matched cohort from the U.S. Census for the white population in Minnesota.

At diagnosis, the mean segment length of the Barrett's esophagus was 4.8 cm, and 59% of patients had long-segment Barrett's esophagus. No dysplasia was apparent in 84% of patients.

The only predictors of death were older age and higher scores on the Charlson Comorbidity Index at the time of Barrett's esophagus diagnosis, a multivariate analysis showed. Neither male gender nor the presence of dysplasia affected survival significantly.

Only 5% of the 104 patients who died during follow-up died of esophageal adenocarcinoma.

Dr. Prasad reported having no conflicts of interest.

SAN DIEGO — Among 366 patients with Barrett's esophagus, 82% were alive 5 years after diagnosis, a rate that was essentially no different than the overall survival rate seen in a matched control group from the general population.

The retrospective study is one of the first on survival in a large cohort of patients with Barrett's esophagus in the United States, Dr. Ganapathy A. Prasad said at the annual meeting of the American College of Gastroenterology.

Among previous studies, some found decreased survival in patients with Barrett's esophagus, compared with matched controls, while others showed comparable overall survival rates.

Those data came predominantly from Europe, said Dr. Prasad of the Mayo Clinic, Rochester, Minn.

Dr. Prasad and his associates identified 401 patients with Barrett's esophagus in the Rochester Epidemiology Project who were diagnosed between January 1976 and January 2007, and excluded 35 who had some evidence of cancer or who developed cancer within 6 months of diagnosis.

The 366 patients in the study were followed for a mean of 7.1 years. They had a mean age of 62 years at baseline, 70% were male, and more than 85% were white.

The investigators compared the study cohort's survival rate with survival data from an age- and gender-matched cohort from the U.S. Census for the white population in Minnesota.

At diagnosis, the mean segment length of the Barrett's esophagus was 4.8 cm, and 59% of patients had long-segment Barrett's esophagus. No dysplasia was apparent in 84% of patients.

The only predictors of death were older age and higher scores on the Charlson Comorbidity Index at the time of Barrett's esophagus diagnosis, a multivariate analysis showed. Neither male gender nor the presence of dysplasia affected survival significantly.

Only 5% of the 104 patients who died during follow-up died of esophageal adenocarcinoma.

Dr. Prasad reported having no conflicts of interest.

SAN DIEGO — Among 366 patients with Barrett's esophagus, 82% were alive 5 years after diagnosis, a rate that was essentially no different than the overall survival rate seen in a matched control group from the general population.

The retrospective study is one of the first on survival in a large cohort of patients with Barrett's esophagus in the United States, Dr. Ganapathy A. Prasad said at the annual meeting of the American College of Gastroenterology.

Among previous studies, some found decreased survival in patients with Barrett's esophagus, compared with matched controls, while others showed comparable overall survival rates.

Those data came predominantly from Europe, said Dr. Prasad of the Mayo Clinic, Rochester, Minn.

Dr. Prasad and his associates identified 401 patients with Barrett's esophagus in the Rochester Epidemiology Project who were diagnosed between January 1976 and January 2007, and excluded 35 who had some evidence of cancer or who developed cancer within 6 months of diagnosis.

The 366 patients in the study were followed for a mean of 7.1 years. They had a mean age of 62 years at baseline, 70% were male, and more than 85% were white.

The investigators compared the study cohort's survival rate with survival data from an age- and gender-matched cohort from the U.S. Census for the white population in Minnesota.

At diagnosis, the mean segment length of the Barrett's esophagus was 4.8 cm, and 59% of patients had long-segment Barrett's esophagus. No dysplasia was apparent in 84% of patients.

The only predictors of death were older age and higher scores on the Charlson Comorbidity Index at the time of Barrett's esophagus diagnosis, a multivariate analysis showed. Neither male gender nor the presence of dysplasia affected survival significantly.

Only 5% of the 104 patients who died during follow-up died of esophageal adenocarcinoma.

Dr. Prasad reported having no conflicts of interest.

SAN DIEGO — The risk for gastric cancer was more than 200 times higher in patients with gastric intestinal metaplasia on initial or repeat upper endoscopy, compared with the control population, in a retrospective study of 11,600 male veterans.

In all, 3% of the cohort (354 veterans) were diagnosed with gastric intestinal metaplasia (GIM) over a 19-year period; the investigators compared their records with those of 355 randomly selected patients who were seen at the GI clinic of the Brooklyn campus of the Veterans Affairs New York Harbor Healthcare System.

Of the veterans with GIM, 6% (21 patients) were diagnosed with gastric cancer, a rate that was 200-fold higher than the gastric cancer rate seen in the control group, Dr. Naveen Anand and his associates reported at the annual meeting of the American College of Gastroenterology.

Half of the cancer diagnoses were made on the initial endoscopy, and half were made on follow-up endoscopy, said Dr. Anand, a chief resident at the State University of New York Downstate Medical Center, Brooklyn. Repeat endoscopies were performed on 53% of the cohort (including 11% who underwent four or more endoscopies), and 47% underwent initial endoscopy only.

Gastric cancer was more likely to be diagnosed in patients with GIM who were older and black, or who had more severe gastritis on histology.

Patients with GIM—especially patients in these higher-risk subgroups—should undergo regular endoscopic surveillance with careful histologic diagnosis of GIM based on biopsies at multiple gastric locations, Dr. Anand suggested.

He acknowledged that increased surveillance has cost implications, but noted that the gastric cancer rate in patients with GIM is similar to that seen in patients with severe dysplasia. “If patients have severe dysplasia on biopsy, we will bring these patients back for follow-up. So, if we're seeing similar rates of progression to cancer from GIM, these patients probably should be followed up.

“We need a prospective study looking at these patients followed over time,” he said.

He and his associates were surprised to find that having a history of Helicobacter pylori infection did not significantly influence pathology results, compared with patients with no history of H. pylori. He attributed that to early intervention (that is, treatment that was initiated whenever H. pylori was diagnosed by histology).

Patients with GIM were more likely to be 70-90 years old, whereas those without GIM were more likely to be aged 50-70 years. About half of patients in the GIM and control groups were black and half were white, and there were small numbers of veterans of other races or ethnicities. Because the mean age in blacks was significantly older than in whites (75 vs. 71 years), blacks accounted for 67% of patients who developed gastric cancer, Dr. Anand said.

“We believe there is a long lead time between the premalignant lesion and intestinal metaplasia and intestinal-type gastric carcinoma, similar to what we see in colon cancer and cervical cancer, which gives us an opportunity for possible surveillance and even possible intervention,” Dr. Anand said.

The investigators reported no conflicts of interest.

SAN DIEGO — The risk for gastric cancer was more than 200 times higher in patients with gastric intestinal metaplasia on initial or repeat upper endoscopy, compared with the control population, in a retrospective study of 11,600 male veterans.

In all, 3% of the cohort (354 veterans) were diagnosed with gastric intestinal metaplasia (GIM) over a 19-year period; the investigators compared their records with those of 355 randomly selected patients who were seen at the GI clinic of the Brooklyn campus of the Veterans Affairs New York Harbor Healthcare System.

Of the veterans with GIM, 6% (21 patients) were diagnosed with gastric cancer, a rate that was 200-fold higher than the gastric cancer rate seen in the control group, Dr. Naveen Anand and his associates reported at the annual meeting of the American College of Gastroenterology.

Half of the cancer diagnoses were made on the initial endoscopy, and half were made on follow-up endoscopy, said Dr. Anand, a chief resident at the State University of New York Downstate Medical Center, Brooklyn. Repeat endoscopies were performed on 53% of the cohort (including 11% who underwent four or more endoscopies), and 47% underwent initial endoscopy only.

Gastric cancer was more likely to be diagnosed in patients with GIM who were older and black, or who had more severe gastritis on histology.

Patients with GIM—especially patients in these higher-risk subgroups—should undergo regular endoscopic surveillance with careful histologic diagnosis of GIM based on biopsies at multiple gastric locations, Dr. Anand suggested.

He acknowledged that increased surveillance has cost implications, but noted that the gastric cancer rate in patients with GIM is similar to that seen in patients with severe dysplasia. “If patients have severe dysplasia on biopsy, we will bring these patients back for follow-up. So, if we're seeing similar rates of progression to cancer from GIM, these patients probably should be followed up.

“We need a prospective study looking at these patients followed over time,” he said.

He and his associates were surprised to find that having a history of Helicobacter pylori infection did not significantly influence pathology results, compared with patients with no history of H. pylori. He attributed that to early intervention (that is, treatment that was initiated whenever H. pylori was diagnosed by histology).

Patients with GIM were more likely to be 70-90 years old, whereas those without GIM were more likely to be aged 50-70 years. About half of patients in the GIM and control groups were black and half were white, and there were small numbers of veterans of other races or ethnicities. Because the mean age in blacks was significantly older than in whites (75 vs. 71 years), blacks accounted for 67% of patients who developed gastric cancer, Dr. Anand said.

“We believe there is a long lead time between the premalignant lesion and intestinal metaplasia and intestinal-type gastric carcinoma, similar to what we see in colon cancer and cervical cancer, which gives us an opportunity for possible surveillance and even possible intervention,” Dr. Anand said.

The investigators reported no conflicts of interest.

SAN DIEGO — The risk for gastric cancer was more than 200 times higher in patients with gastric intestinal metaplasia on initial or repeat upper endoscopy, compared with the control population, in a retrospective study of 11,600 male veterans.

In all, 3% of the cohort (354 veterans) were diagnosed with gastric intestinal metaplasia (GIM) over a 19-year period; the investigators compared their records with those of 355 randomly selected patients who were seen at the GI clinic of the Brooklyn campus of the Veterans Affairs New York Harbor Healthcare System.

Of the veterans with GIM, 6% (21 patients) were diagnosed with gastric cancer, a rate that was 200-fold higher than the gastric cancer rate seen in the control group, Dr. Naveen Anand and his associates reported at the annual meeting of the American College of Gastroenterology.

Half of the cancer diagnoses were made on the initial endoscopy, and half were made on follow-up endoscopy, said Dr. Anand, a chief resident at the State University of New York Downstate Medical Center, Brooklyn. Repeat endoscopies were performed on 53% of the cohort (including 11% who underwent four or more endoscopies), and 47% underwent initial endoscopy only.

Gastric cancer was more likely to be diagnosed in patients with GIM who were older and black, or who had more severe gastritis on histology.

Patients with GIM—especially patients in these higher-risk subgroups—should undergo regular endoscopic surveillance with careful histologic diagnosis of GIM based on biopsies at multiple gastric locations, Dr. Anand suggested.

He acknowledged that increased surveillance has cost implications, but noted that the gastric cancer rate in patients with GIM is similar to that seen in patients with severe dysplasia. “If patients have severe dysplasia on biopsy, we will bring these patients back for follow-up. So, if we're seeing similar rates of progression to cancer from GIM, these patients probably should be followed up.

“We need a prospective study looking at these patients followed over time,” he said.

He and his associates were surprised to find that having a history of Helicobacter pylori infection did not significantly influence pathology results, compared with patients with no history of H. pylori. He attributed that to early intervention (that is, treatment that was initiated whenever H. pylori was diagnosed by histology).

Patients with GIM were more likely to be 70-90 years old, whereas those without GIM were more likely to be aged 50-70 years. About half of patients in the GIM and control groups were black and half were white, and there were small numbers of veterans of other races or ethnicities. Because the mean age in blacks was significantly older than in whites (75 vs. 71 years), blacks accounted for 67% of patients who developed gastric cancer, Dr. Anand said.

“We believe there is a long lead time between the premalignant lesion and intestinal metaplasia and intestinal-type gastric carcinoma, similar to what we see in colon cancer and cervical cancer, which gives us an opportunity for possible surveillance and even possible intervention,” Dr. Anand said.

The investigators reported no conflicts of interest.