OBJECTIVES

The study compared health care utilization and costs among homeless veterans randomly assigned to peer mentors or usual care and described contacts with peer mentors.

METHODS

Homeless patients at four Department of Veterans Affairs clinics were randomly assigned to a peer mentor (N=195) or to usual care (N=180). Administrative data on utilization and costs over a six-month follow-up were combined with peer mentors' reports of patient contacts.

RESULTS

Most patients (87%) in the peer mentor group had at least one peer contact. Patients in this group spent the largest proportions of time discussing housing and health issues with peer mentors and had more outpatient encounters than those in usual care, although differences were not significant. No other between-group differences were found in utilization or costs.

CONCLUSIONS

Although significant impacts of peer mentors on health care patterns or costs were not detected, some patients had frequent contact with peer mentors.

BACKGROUND

Hepatic steatosis is increasing worldwide. Whether HIV and its associated metabolic perturbations exacerbate steatosis is unclear. Sex differences in adipose tissue distribution may also affect steatosis risk. We examined the contribution of HIV and sex to steatosis.

METHODS

Using MRI and spectroscopy, visceral adipose tissue (VAT) and liver fat fraction (LFF) were measured in 121 HIV-infected and 107 uninfected men and women without viral hepatitis. Differences in LFF by HIV status and sex were evaluated using multivariable linear regression, adjusting for demographic, lifestyle, VAT, homeostasis model assessment-estimated insulin resistance, and HIV-related factors.

RESULTS

HIV-infected women had lower LFF than uninfected women (demographic-adjusted mean: 1.9 vs. 3.1%; P = 0.028); LFF was similar in HIV-infected and uninfected men (4.6 vs. 4.1%; P = 0.78). HIV-infected and uninfected women had less VAT than men (median: 139 and 161 vs. 201 cm and 188 cm, respectively). After adjustment, HIV-infected women had 34% [95% confidence interval (CI): -54%, -5.5%] lower LFF than uninfected women, whereas there was little difference in men (-5.5%; 95% CI: -26%, 21%). Among HIV-infected persons, greater VAT and homeostasis model assessment-estimated insulin resistance were associated with greater LFF. HIV-related factors (CD4 cell count, HIV RNA level, or antiretroviral therapy use) had little association with LFF. Although HIV-infected men had 81% (95% CI: 32%, 148%) greater LFF than HIV-infected women, the association was attenuated after multivariable adjustment (25%; 95% CI: -9.1%, 73%).

CONCLUSION

Contrary to expectation, HIV infection is not associated with greater steatosis compared with uninfected adults. It is possible that less fat is stored in the liver to maintain subcutaneous fat (which is reduced in HIV) and the effect is magnified in HIV-infected women, who also have less VAT.

OBJECTIVES

HIV/hepatitis C virus (HCV) coinfection is associated with insulin resistance, but the mechanism is unclear. We hypothesized that intestinal epithelial damage and the consequent monocyte/macrophage activation and inflammation explain this perturbation.

DESIGN

Cross-sectional study of 519 adults (220 HIV+/HCV-; 64 HIV-/HCV+; 89 HIV+/HCV+; 146 HIV-/HCV-).

METHODS

We used multivariable linear regression to evaluate associations of HIV and HCV with the homeostasis model assessment of insulin resistance (HOMA-IR) and if intestinal fatty (FA) acid binding protein (I-FABP, a marker of gut epithelial integrity), soluble CD14 (sCD14) and soluble CD163 (sCD163) (markers of monocyte/macrophage activation), and IL-6 (an inflammatory cytokine) mediated this association.

RESULTS

HIV+/HCV+ and HIV-/HCV+ had greater demographic-adjusted HOMA-IR [mean (95% confidence interval (CI)): 1.96 (1.51, 2.54) and 1.65 (1.22, 2.24)] than HIV+/HCV- and HIV-/HCV-[1.41 (1.18, 1.67) and 1.44 (1.17, 1.75), respectively]. After additional adjustment for lifestyle and metabolic factors, HIV+/HCV+ remained associated with 36% (95% CI: 4, 80%) greater HOMA-IR relative to HIV-/HCV-, whereas HIV-/HCV+ and HIV+/HCV- had smaller differences. Adjustment for sCD163 substantially attenuated the difference between HIV+/HCV+ and HIV-/HCV-; adjustment for I-FABP, sCD14, and IL-6 had little effect. Higher sCD163 was independently associated with 19% (95% CI: 7, 33%), 26% (95% CI: 15, 39%), 25% (95% CI: 14, 37%), and 23% (95% CI: 11, 36%) greater HOMA-IR in HIV+/HCV+, HIV-/HCV+, HIV+/HCV-, and HIV-/HCV- (all estimates per doubling of sCD163). I-FABP, sCD14, and IL-6 were not associated with HOMA-IR.

CONCLUSION

HIV/HCV coinfection is associated with greater HOMA-IR, even after controlling for demographic, lifestyle, and metabolic factors. sCD163, which appears independent of intestinal epithelial damage and inflammation, partly explains this association. Our findings that the association of sCD163 with HOMA-IR occurred even in the absence of HIV and HCV, indicate that viral and nonviral factors affect sCD163 levels. Its role in insulin resistance needs elucidation.