November 27, 2012
Gilles Wandeler et al. Clinical Infectious Diseases 2012;55(10):1408-16. Read the abstract.
You do not have to be that old to recall when hepatitis C (HCV) was known as "non-A non-B hepatitis" and was considered an emergent stalker of blood banks, tissue banks and dialysis machines. Even after the wastepaper-basket moniker was traded for the next available letter in the alphabet, we continued to consider this virus as either a nosocomial infection or one that was spread outside of clinical settings by needle sharing and tattooing.
More recently, we have come to understand that HCV can be transmitted sexually -- particularly by MSM. Investigators from the Swiss HIV Cohort Study examined data collected from 1998 to 2011 to gauge HCV incidence among HIV-infected MSM, heterosexuals and IDU, excluding IDU in the other categories. Since 1998, HCV antibody testing has been conducted every other year during cohort study visits on everyone not already known to be HCV infected.
At first test, 3% of the 4,629 MSM, 11% of the 4,530 heterosexuals and a whopping 92% of the 2,678 IDU screened positive for HCV infection. A total of 6,534 patients, of whom 3,333 were MSM, 123 were IDU and 3,078 were heterosexuals, were included in the HCV incidence analyses.
Over a total follow-up period of 23,707 patient-years (py) for the MSM group, 733 py for the IDU group and 20,752 py for the heterosexual group, 101 (3.0%), 41 (33.3%) and 25 (0.8%) patients, respectively, experienced an HCV seroconversion during follow-up. Incidence rates increased among MSM by 18-fold (!), while they fell for IDU from 1998 to 2011; there were very few cases among heterosexuals overall.
Predictors of HCV infection among the MSM included past syphilis and hepatitis B (HBV) infection, as well as inconsistent condom use.
These results punctuate a few important points:
Jennifer H. Han et al. AIDS 2012; 26:2087-2095. Read the abstract.
There are mixed data regarding the presence of a heightened risk of diabetes mellitus for persons living with HIV. As with other metabolic conditions, there can be considerable confounding factors that make associations difficult to establish. Certainly, HIV does not protect against the development of diabetes in those destined to this fate.
In a clever paper from the Centers for AIDS Research Network of Integrated Clinical Systems (CNICS) cohort, a study of HIV-infected patients in clinical care nationwide, responses to type-2 diabetes therapies were assessed in 286 HIV-infected patients and 858 age- and sex-matched controls without HIV infection. The HIV-infected cases were those in care at any of the 8 CNICS sites, while the controls were enrolled in a large cohort study out of Philadelphia. For both cases and controls, ICD-9 codes and prescriptions of diabetes-specific medications were used to establish prevalent disease, and the initial date of first-ever diabetes therapy was ascertained.
The main outcome was change in HbA1c over the first year of therapy. The patients with HIV infection had lower mean baseline HbA1c values: 7.82% (standard deviation [SD] 2.3) versus 8.62% (SD 2.4), respectively; P < .001. The most common diabetes treatment was metformin, followed by sulfonylureas. HIV-infected patients achieved significantly smaller decreases in HbA1c compared to patients without HIV infection, with an absolute mean difference in HbA1c reduction of -0.17% during the first year of treatment (95% CI, -0.28 to -0.06; P < .003), after adjustment for baseline HbA1c. However, in adjusted subgroup analyses, the difference in the change in HbA1c with therapy between HIV-infected and HIV-uninfected patients was seen in those on a protease inhibitor, but was not seen in those on regimens excluding this class of antiretrovirals.
Interestingly, despite the observed smaller decrease in HbA1c for the HIV-infected patients, they were more likely to achieve a value that is below the American Diabetes Association goal of 7% for this parameter. This finding is partly explained by the fact that the HIV-infected folks started with a lower HbA1c. In addition, others have described an HbA1c-glycemia disconnect in HIV, wherein the HbA1c underestimates the level of hyperglycemia. A paper by Peter S. Kim et al in Diabetes Care associated elevated mean corpuscular volume and abacavir (Ziagen) use with this disconnect.
Overall, these data show that there was a small but significant difference in response rates, and that protease inhibitor therapy was implicated as a culprit. It is unclear whether these drugs are having a direct effect on glycemic control or whether those taking protease inhibitors were different in some other ways (e.g., more advanced HIV disease, longer duration of treatment, higher number of risk factors for diabetes).
The results also suggest that treatment of diabetes and other cardiovascular disease risks may need to be more aggressive among those living with HIV.
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