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CROI 2015: Cardiovascular Risk Factors for HIV-Positive People

Consistent with past research, an analysis from New York City has shown that people with HIV are at higher risk for death due to cardiovascular disease, although this risk is declining, according to a report at the recent 2015 Conference on Retroviruses and Opportunistic Infections (CROI). Several other studies looked at cardiovascular risk factors in this population, including inflammatory biomarkers, chronic kidney disease, gut bacteria, and use of abacavir.

altCardiovascular Mortality

Several previous observational studies have found that cardiovascular disease (CVD) and associated events such as heart attacks and strokes are more common among HIV-positive people compared to the HIV-negative general population. But the relationship between heart disease and HIV infection itself, inflammation and metabolic abnormalities, antiretroviral drug toxicities, and traditional risk factors such as smoking is not fully understood.

David Hanna from Albert Einstein College of Medicine and colleagues assessed changing CVD mortality rates among people with HIV in New Your City (abstract 729). The analysis included all HIV-positive people age 13 or older between 2001 and 2012, as reported to the New York City HIV Surveillance Registry. Surveillance data were linked with the city's Vital Statistics Registry and National Death Index to determine how many people with HIV died due to major CVD-related events.

The study included 145,009 HIV-positive people, who contributed nearly 1,227,000 total person-years of data; 71% were men and the median age was 49 years. Between 2001 and 2012, a total of 29,326 deaths occurred. Overall mortality declined over time, mostly due to fewer HIV/AIDS-related deaths.

During this period, about one-tenth of all deaths among people with HIV were attributed to major CVD events, including ischemic heart disease events such as myocardial infarction (42% of CVD deaths), hypertensive or high blood pressure disease (27%), and cerebrovascular events such as stroke (10%).

However, while the proportion of deaths due to CVD rose during this period from 7% to 13% -- because fewer people were dying of AIDS and other causes -- the actual cardiovascular mortality rate for people with HIV fell over time. Cardiovascular mortality in the general population declined as well, from 47% to 39%.

Overall, after adjusting for other factors including sex, race/ethnicity, and year, people with HIV had a 54% higher CVD death rate than HIV-negative people. CVD mortality was significantly higher for people with HIV in all age groups through age 65. Among older people, CVD mortality was similar or higher in the general population. While HIV-positive people with both detectable viral load and those with viral suppression had higher CVD death rates than HIV-negatives, those whose latest HIV RNA measurement was <400 copies/mL had a significantly lower rate than those with higher viral load (3.9 vs 7.7 per 1000 person-year, respectively).

"CVD deaths constitute an increasing share of deaths among HIV-diagnosed persons," the researchers concluded. "HIV care providers should emphasize preventive measures to reduce CVD risk such as smoking cessation, blood pressure control, and lipid management."

Inflammation and Gut Flora

In recent years there has been a growing emphasis on the detrimental effects of chronic inflammation and immune activation in people with HIV, even those with sustained viral suppression. As previously reported, this was the theme of a CROI plenary talk by Steven Grinspoon of Massachsuetts General Hospital and Harvard Medical School (abstract 134).

Inflammation and immune activation may result from low-level residual viral replication even in people with undetectable plasma viral load using standard clinical tests.

In an analysis of the large NA-ACCORD trial, Daniel Drozd from the University of Washington and colleagues (abstract 748) found that detectable HIV viral load, a history of AIDS-defining illness, and lower CD4 T-cell count were independent predictors of myocardial infarction, or heart attack. Similarly, Jorge Salinas from Emory University and colleagues (abstract 746) showed that cumulative HIV viremia and CD4 count over time -- not just at a single time-point -- predicted risk of myocardial infarction in the Veterans Aging Cohort Study.

Another potential trigger of inflammation is microbial translocation, or leakage of bacteria from the gut resulting from damage to the intestinal lining. Research has shown that this damage happens soon after HIV infection and may not be fully reversed even after starting effective antiretroviral therapy (ART).

Suman Srinivasa, a member of Grinspoon's team at Massachusetts General, and colleagues (abstract 138) prospectively compared therelationship between gut microbes and their metabolites in 155 HIV-positive and 67 HIV-negative people without known CVD at baseline. HIV-positive participants were relatively young (mean age 47 years), had been infected for 14 years and on ART for 8 years on average, and most had undetectable viral load.

HIV-positive people weresignificantly more likely than their HIV-negative counterparts to have coronary plaque (53% vs 35%), as well as higher plaque volume. Among people with HIV, but not those without, higher levels of serum trimethylamine (TMA) -- a microbe-derived precursor of trimethylamine N-oxide (TMAO), which plays a role in cholesterol metabolism -- were associated with more plaque and higher levels of lipopolysaccharide (a bacterial toxin). TMAO has previously been linked to CVD in the HIV-negative population.

Based on these findings, the researchers concluded, "Our data demonstrate that serum, not serum TMAO, is associated with the presence of calcified and total coronary plaque burden in HIV-infected patients," an association largely independent of traditional CVD risk factors.

Several other studies at CROI looked at biomarkers of inflammation and immune activation and their association with CVD in people with HIV.

Álvaro Borges and fellow investigators with the INSIGHT SMART and ESPRIT study groups (abstract 761) found that the pro-inflammatory cytokine interleukin 6 (IL-6) was a strong predictor of non-AIDS-related clinical events and deaths, and also of CVD, among HIV-positive participants in these 2 trials -- stronger, in fact, than C-reactive protein and D-dimer were in the earlier SMART study.

A related study by Denise Hsu fromthe National Institute of Allergy and Infectious Diseases and colleagues (abstract 752), looking at 149 HIV-positive patients on suppressive ART in the SCOPE cohort, saw a link between elevated IL-6 and carotid intimal thickness, indicating buildup of plaque in the arteries supplying the brain. Likewise, Dominic Chow from the University of Hawaii and colleagues (abstract 754) found that HIV-positive people on suppressive ART had elevated levels of non-classical monocytes (characterized by unusual CD cell-surface markers) and of the pro-inflammatory cytokine MCP-1, which were associated with progression of carotid intima-media thickening. 


Researchers from the National Institutes of Health (abstract 928) reported that artery plaque build-up was greater even in adolescents and young adults (age 15-29) infected with HIV early in life compared with age-matched HIV-negative people, and was associated with CD8 T-cell activation and elevated levels of the cell adhesion molecule E-selectin.

Chronic Kidney Disease

Two research groups reported findings from studies looking at the association between CVD and kidney disease in people with HIV -- a link that is well-established in the HIV-negative general population.

Lene Ryom from the University of Copenhagen and fellow investigators with theD:A:D study group (abstract 742) assessed nearly 35,000 HIV-positive D:A:D participants  who had at least 2 estimated glomerular filtration rate (eGFR) measurements, a marker of kidney function. Over a median follow-up period of 6 years, 1033 people experienced CVD events (myocardial infarction, stroke, or related surgical procedures) during follow-up, for a rate of 5.1 events per 1000 person-years.

They found a "clear relationship" between confirmed eGFR at baseline and incidence of CVD events. While just 1.7% of people with eGFR >90 mL/min/1.73m2 progressed to CVD within 5 years, this rose to 23.4% of those with eGFR <30. While this was largely explained by age -- as older people are at higher risk for both kidney and heart disease -- a "strong trend" remained after adjusting for age, largely driven by a high CVD rate among people with eGFR <30.

"In a large contemporary cohort of HIV-positive individuals we observed a strong relationship between baseline and current confirmed impaired renal function and incident CVD," the researchers concluded. "These findings highlight the need for an intensified monitoring for all types of emerging CVD, in particular in older individuals with continuously low eGFR levels, and calls for an increased focus on applying different renal and cardiovascular preventive measures in HIV-positive individuals." 


Drozd and colleagues' analysis of more than 25,000 NA-ACCORD participants also saw a significant association between advanced chronic kidney disease (eGFR <30) and primary myocardial infarction.

What About Abacavir?

Frank Palella from Northwestern University and colleagues (abstract 749LB) presented findings another NA-ACCORD analysis looking at the association between heart attacks and use of abacavir (Ziagen, also in the Epzicom coformulation) -- a topic of ongoing debate as prior studies have produced conflicting results.

Looking at 16,733 HIV-positive adults in 7 U.S. cohorts, a total of 301 new myocardial infarctions occurred over more than 64,600 person-years of follow-up. Focusing on a subgroup of 6485 treatment-naive people starting ART that mirrored a previous D:A:D analysis, recent use of abacavir (within the past 6 months) was associated with a 71% adjusted increased risk of myocardial infarction -- approaching the nearly 2-fold risk seen in D:A:D.

However, a significant association was no longer apparent in an adjusted analysis of the full study population. Further, people who started an abacavir-containing ART regimen were more likely to have traditional and HIV-associated CVD risk factors, and the link between abacavir and myocardial infarction was diminished after taking these into account.

Traditional Risk Factors

Finally, traditional cardiovascular risk factors such as older age, smoking, abnormal blood lipid levels, diabetes, and obesity also play a role in people with HIV.

Perhaps stating the obvious, Drozd's NA-ACCORD analysis found that tobacco smoking was an independent risk factor for atherosclerosis, or build-up of plaque in arteries that can rupture and cause blockages in the heart (causing myocardial infarction) or brain (causing stroke).

A study by Sean Kelly and fellow investigators with the Multicenter AIDS Cohort Study (abstract 743) reported that cigarette smoking was the major independent risk factor for atherosclerosis. This analysis also found that HIV-positive gay and bisexual men in MACS were more likely to smoke than a group of similar at-risk HIV-negative men (31% vs 22%). Use of other substances, including alcohol and marijuana, had an inconsistent relationship with atherosclerosis.

"Our findings underscore the value of effective smoking cessation strategies targeting HIV+ persons to decrease cardiovascular disease burden," the researchers concluded.

Turning to management of elevated CVD risk, Sahera Dirajlal-Fargo from Case Western Reserve University School of Medicine and colleagues (abstract 745) looked at the relationship between physical activity and markers of cardiovascular and metabolic health and inflammation among people with HIV.

This analysis included 147 participants on ART (80% men, median age 46 years) in SATURN-HIV, a trial of rosuvastatin (Crestor) for people with HIV.They found that physical activity was significantly associated with several markers of cardio-metabolic health and inflammation. After adjusting for other factors, exercise remained independently associated with markers of cardiovascular disease including carotid intima-media thickness and endothelial function, as well as insulin resistance.

"[O]ver the 96 week study period, exercise was associated with multiple measures of subclinical vascular disease, suggesting that exercise in HIV-infected patients may improve vascular structure as well as function," the researchers concluded. "This association was evident even when accounting for statin use."

A large multicenter trial known as REPRIEVE is now underway to learn more about cardiovascular disease, its predictors and outcomes, and the benefits of statins for people with HIV.

SEE ALSO:

Predicting Cardiovascular Disease in People with HIV -- Can We Do Better?

Statins May Reduce Risk of Heart Disease in People with HIV

4/22/15

References

DB Hanna, C Ramaswamy, CP Kaplan, et al. Cardiovascular Disease Mortality Among HIV-Infected Persons, New York City, 2001-2012. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 729.

SGrinspoon. Cardiovascular Disease in HIV Patients: An Emerging Paradigm and Call to Action. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 134.

D Drozd, M Kitahata, S Heckbert, et al. Incidence and Risk of Myocardial Infarction (MI) by Type in the NA-ACCORD. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 748.

J Salinas, V Marconi, D Rimland, et al. Cumulative HIV Care Measures Highly Associated With Acute Myocardial Infarction. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 746.

S Srinivasa, V Fitch, J Lo, et al. Calcified Plaque Burden Is Associated With Serum Gut Microbiota-Generated TMA in HIV. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 138.

AH Borges, JL O'Connor, AN Phillips, et al (INSIGHT SMART and ESPRIT Study Groups). IL-6 Is a Stronger Predictor of Clinical Events Than hsCRP or D-Dimer in HIV Disease. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 761.

D Hsu, Z Hu, I Sereti, et al. IL-6 and CD8 Senescence Independently Associate With Atherosclerosis in Treated HIV. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 752.

DC Chow, JM Kagihara, GG Zhang, et al. Non-Classical Monocytes Predict Progression of Carotid Intima-Media Thickness. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 754.

JB Purdy, A Unsal, S Abd-Elmoniem, et al. T-Cell Activation and E-Selectin Associated With Coronary Plaque in HIV-Infected Youth. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 928.

L Ryom, JD Lundgren, P Reiss, et al. (D:A:D Study Group). Relationship Between Confirmed eGFR and Cardiovascular Disease in HIV-Positive Persons. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 742.

FJ Palella, KN Althoff, R Moore, et al. Abacavir Use and Risk for Myocardial Infarction in the NA-ACCORD. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 749LB.

SG Kelly, M Plankey, W Post, FJ Palella, et al. Smoking, Other Substance Use and Coronary Atherosclerosis Among HIV-Infected and Uninfected Men. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 743.

S Dirajlal-Fargo, AR Webel, B Kinley, et al. The Effect of Physical Activity on Cardiometabolic Health and Inflammation in HIV. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 745.

NIH Launches Large Trial of Cardiovascular Disease Among People with HIV

The U.S. National Heart, Lung, and Blood Institute and National Institute of Allergy and Infectious Diseases have started enrolling participants in the REPRIEVE trial, a large international study looking at cardiovascular disease risk factors, outcomes, and statin therapy for people living with HIV. A substudy of 800 participants will focus on the effects of pitavastatin (Livalo) on coronary artery disease and inflammatory biomarkers in this population.

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CROI 2015: Screening Finds High Prevalence of Early-Stage Lung Cancer in Smokers with HIV

Using low-dose computed tomography to screen selected people living with HIV who smoke led to early lung cancer diagnoses at younger ages than normally seen in the general population, according to findings from the ANRS EP48 HIV CHEST study reported last week at the 2015 Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle.

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CROI 2015: Cardiovascular Risk Factors for HIV-Positive People

Consistent with past research, an analysis from New York City has shown that people with HIV are at higher risk for death due to cardiovascular disease, although this risk is declining, according to a report at the recent 2015 Conference on Retroviruses and Opportunistic Infections (CROI). Several other studies looked at cardiovascular risk factors in this population, including inflammatory biomarkers, chronic kidney disease, gut bacteria, and use of abacavir.

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CROI 2015: Varenicline Helps People with HIV Stop Smoking, but Success Rate Remains Low

The smoking cessation drug varenicline (Chantix) helped more people with HIV to stop smoking than counseling alone, but less than 20% were able to remain abstinent for a year, according to the results of a French study presented at the 2015 Conference on Retroviruses and Opportunistic Infections (CROI) last week in Seattle.The smoking cessation rates in this study were comparable to those previously seen for HIV-negative people using varenicline or other methods -- across the board only a minority manage to quit long-term.

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CROI 2015: Cardiovascular Disease Among People with HIV

People living with HIV are at greater risk for cardiovascular disease (CVD) and events such as heart attacks. Several presentations at the recent 2015 Conference on Retroviruses and Opportunistic Infections (CROI) looked at CVD risk factors, how to better predict it, and approaches to risk reduction.

Predicting Cardiovascular Disease in People with HIV -- Can We Do Better?

Cardiovascular Risk Factors for HIV-Positive People

Statins May Reduce Risk of Heart Disease in People with HIV

4/10/15

 

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CROI 2015: Smoking and Its Detrimental Outcomes for People with HIV

Smoking and its consequences was a major topic at the 2015 Conference on Retroviruses and Opportunistic Infections (CROI) last week in Seattle. Researchers presented findings on smoking as a risk factor for cancer, CT scans to detect early lung cancer, and varenicline for smoking cessation.

Smoking Outweighs HIV-Related Risk Factors for Non-AIDS Cancers

Screening Finds High Prevalence of Early-Stage Lung Cancer in Smokers with HIV

Varenicline Helps People with HIV Stop Smoking

3/4/15

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CROI 2015: Predicting Cardiovascular Disease in People with HIV -- Can We Do Better?

Four existing models used to predict risk of cardiovascular disease (CVD) underestimated that risk in large cohorts of people living with HIV, according to research presented at the recent 2015 Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle. Other studies suggested that even without that underestimation being taken into account, many HIV-positive people are currently undertreated with statins, which could protect them from cardiovascular events like myocardial infarction.

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CROI 2015: Study Finds High Rates of Cancer Among Elderly People with HIV

Elderly people living with HIV (over the age of 65) are at greatly increased risk of HIV-associated cancers, though many of the most commonly diagnosed cancers may be related more to aging than to HIV itself, according to a study reported last week at the at the 2015 Conference on Retroviruses and Opportunistic Infections (CROI).

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CROI 2015: Stopping Co-trimoxazole During ART Raises Risk of Bacterial Illness and Malaria

Stopping trimethoprim/sulfamethoxazole (Co-trimoxazole) prophylaxis increases the risk of serious bacterial infections and malaria, even at high CD4 cell counts, among people with HIV taking antiretroviral therapy (ART) in Uganda, according to results of a randomized trial presented by Jonathan Levin of the UK Medical Research Council at the recent 2015 Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle.

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Coverage of the 2015 Conference on Retroviruses and Opportunistic Infections

HIVandHepatitis.com coverage of the 2015 Conference on Retroviruses and Opportunistic infections (CROI 2015), February 23-26, 2015, in Seattle.

Conference highlights include PrEP and HIV treatment as prevention, hepatitis C treatment for HIV/HCV coinfected people, new antiretroviral drugs, HIV cure research, HIV-related conditions, TB, Ebola virus, and access to care.

HIVandHepatitis.com coverage by topic

CROI website

3/2/15

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CROI 2015: FRAX Fracture Prediction Tool Underestimates Fracture Risk in Men with HIV

The Fracture Risk Assessment Tool (FRAX), an online tool developed by the World Health Organization and used to help guide decisions about who to screen or treat in order to prevent bone fractures, underestimates overall risk of fracture in people living with HIV -- even with an adjustment experts have recommended to improve its accuracy for people with HIV -- according to an analysis of the Veterans Aging Cohort Study Virtual Cohort (VACS-VC) reported at the recent 2015 Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle.

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CROI 2015: Retrovirus Conference Now Underway in Seattle

The 2015 Conference on Retroviruses and Opportunistic Infections (CROI) takes place this week, February 23-26, at the Washington State Convention Center in Seattle. CROI focuses on HIV treatment, prevention, and basic science. For the past several years it has also included substantial hepatitis C content, and this year will feature presentations on Ebola virus. HIVandHepatitis.com is on site in Seattle all week bringing you news coverage and Twitter updates (@HIVandHepatitis).

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CROI 2015: Does HIV Make You Fat? Study Connects Viral Load with Fat Gains

HIV infection or inflammatory changes associated with it may be responsible for fat accumulation and body fat redistribution, rather than antiretroviral drugs, according to a study presented at the recent 2015 Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle.

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[Produced in collaboration with Aidsmap]

Grace McComsey of Case Western University in Cleveland said that although the association of subcutaneous fat loss (lipoatrophy) with mitochondrial damage caused by certain HIV drugs is well-established -- and most of the world no longer uses the drugs like stavudine (d4T) that are most strongly associated with it -- 2 decades of research had failed to establish a cause for the distinctive fat gain(lipohypertrophy), especially in the trunk and within the abdomen, seen in some people with HIV on antiretroviral therapy (ART).

Initially these fat gains were associated with protease inhibitors (PIs) but switching from PIs to non-nucleoside reverse transcriptase inhibitors (NNRTIs) or to integrase inhibitors did not reverse fat gains. One study found greater fat gain in people taking boosted atazanavir (Reyataz) rather than efavirenz (Sustiva), but a general association with any drug or class of drugs had not been demonstrated. Given that untreated HIV infection usually results in weight loss, fat gains when people started ART, once it became available, may have understandably been associated with treatment rather than HIV.

The study McComsey presented, ACTG A5260s, compared changes in limb fat, trunk fat, visceral adipose tissue (central abdominal fat), and lean muscle mass in 1809 ART-naive patients starting either of the 2 boosted PIs atazanavir or darunavir (Prezista), or the integrase inhibitor raltegravir (Isentress), all combined with tenofovir/emtricitabine (Truvada).

DEXA and CAT scans measured fat and muscle distribution at baseline and nearly 2 years (96 weeks) later. They were then assessed for associations with drug regimen, baseline HIV viral load, Framingham risk score (a measure of the likelihood of cardiovascular disease), and a number of hormones, cytokines (cell messenger chemicals), and markers of inflammation: leptin (higher in obese people), adiponectin (lower in obese people), D-dimer (a coagulation marker), C-reactive protein (an inflammation indicator), and the cytokines or cytokine receptors interleukin 6 (IL-6), CD14, and CD163.

In terms of demographics, the study participants' average age was 36, 90% were men, and 44% were white (slightly more taking atazanavir). Their average pre-ART viral load was 34,150 copies/mL and their average CD4 count was 351 cells/mm3.  Those taking atazanavir had slightly, but not significantly, more limb and trunk fat, but not more visceral fat or muscle.

Limb, trunk, and visceral fat all increased during the 96 weeks on ART. Limb fat increased by 15% (20% on raltegravir), trunk fat by 22% (16% on atazanavir and 29% on raltegravir), and visceral fat by 31%; the differences between drugs were not statistically significant. Lean muscle mass increased slightly, by 2%, in people on atazanavir or raltegravir, and by 1.2% in patients taking darunavir; this was a significant difference but probably does not reflect any real difference between the drugs.

Increases in visceral fat were associated with lower leptin and higher adiponectin levels, but this probably is effect rather than cause, as adiponectin is secreted by fatty tissue. Subcutaneous limb fat gain was also associated with higher IL-6 and lean body mass gain with higher D-dimer and lower baseline CD4 -- the latter not unexpected, as lean body mass falls with AIDS.

However by far the strongest association with fat gain was with high viral load. There were mean increases of at least 25% and up to 35% in both subcutaneous and visceral fat in people who had a baseline viral load over 100,000 copies/mL, whichever drug they were taking. In patients with a baseline viral load below 100,000 copies/mL, the fat gains were below 10%, apart from a gain in visceral fat of about 14% in people taking raltegravir. She noted that even when adjusted for inflammatory markers, HIV viral load was still significantly associated with fat gain.

McComsey said that the fat gains observed were not necessarily those associated with health improvement due to control of HIV. "A 30% gain in visceral adipose tissue in just 2 years is pretty bad," she said. "Even limb fat increased by 1.5 kilos from a baseline of 7 kilos (21%). There was an average increase in 3.0 to 3.5 in people’s BMI [body mass index] score." Although people in general may be getting fatter, it does not happen as fast as this, she added.

3/17/15

Reference

GA McComsey, C Moser, JS Currier, et al. Body Composition Changes After Initiation of Raltegravir or Protease Inhibitors. 2015 Conference on Retroviruses and Opportunistic Infections. Seattle, February 23-24, 2015. Abstract 140.

CROI 2015: Retrovirus Conference Starts Monday in Seattle

The 2015 Conference on Retroviruses and Opportunistic Infections (CROI) takes place next week, February 23-26, at the Washington State Convention Center in Seattle. CROI focuses on HIV treatment, prevention, and basic science. For the past several years it has also included substantial hepatitis C content, and this year will feature presentations on Ebola virus. HIVandHepatitis.com will be on site in Seattle all week bringing you news coverage and Twitter updates (@HIVandHepatitis).

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CROI 2015: Tenofovir, Atazanavir & Lopinavir Associated with Raised Risk of Chronic Kidney Disease

Three antiretroviral drugs are associated with a slowly increasing rate of chronic kidney disease over time, researchers reported at the recent 2015 Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle. Although the risk of developing chronic kidney disease was low for people with normal kidney function -- with fewer than 1% of patients in the large D:A:D cohort developing it -- the use of any of these drugs was associated with 2 to 3 times higher risk of kidney disease developing over the course of 5 years on the drug.

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Screening for Bone Fracture Risk Should Be Routine for HIV+ People over 40

Screening for fracture risk should be a routine part of HIV care for all people over 40, and all postmenopausal women, all men over 50, and people at high risk for fractures of any age should undergo DEXA screening (a type of X-ray) to assess bone mineral density and their need for treatment, experts on bone disorders recommend in new guidelines published in the January 21 online edition of Clinical Infectious Diseases.

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CROI 2015: Statins May Reduce Risk of Heart Disease in People with HIV

Evidence is mounting that statin therapy can prevent the progression of coronary atherosclerosis (hardening and narrowing of the arteries supplying the heart) in people living with HIV, according to the results of 2 randomized clinical trials reported last week at the 2015 Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle.

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HIV May Cause Cognitive Impairment by Disrupting Brain's Garbage Disposal

HIV's Tat protein interferes with autophagy, a process by which damaged or unneeded cell components are broken down and eliminated, according to research published in the February 4 Journal of Neuroscience. This disruption can lead to neuron damage, but the immunosuppressant drug rapamycin was able to reverse this process in a study of mice.

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CROI 2015: Smoking Outweighs HIV-Related Risk Factors for Non-AIDS Cancers

Smoking appears to contribute most to the burden of non-AIDS-defining cancers diagnosed in people living with HIV in the U.S., out of all the potential modifiable risk factors -- including hepatitis B or C, low CD4 cell count, an AIDS diagnosis, or having an unsuppressed viral load -- according to a study reported last week at the 2015 Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle.

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HIV Rebound Linked to Liver Fibrosis Progression in HIV/HCV Coinfected

HIV-positive people with hepatitis C virus (HCV) experienced progression to liver fibrosis if their HIV viral load rebounded above 1000 copies/mL or remained detectable on 2 consecutive tests, researchers reported in the January edition of HIV Medicine. Smaller transient HIV "blips," however, were not associated with worsening fibrosis. Optimized antiretroviral therapy, the study authors suggested, may protect the liver.

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