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Background Metabolic complications, including type 2 diabetes mellitus (DM) and metabolic syndrome, are increasingly recognized among HIV-infected individuals. Low vitamin D levels increase the risk of type 2 DM, and vitamin D supplementation has been shown to decrease the risk of type 2 DM in patients without HIV infection. Objectives The primary objective was to determine whether vitamin D deficiency (serum 25-hyrdoxyvitamin D<20 ng/mL) was associated with type 2 DM among HIV-infected patients. Our secondary objective was to determine whether vitamin D deficiency was associated with metabolic syndrome in HIV. Methods We conducted a cross-sectional study among subjects enrolled in the prospective Modena (Italy) HIV Metabolic Clinic Cohort. Clinical and laboratory data, including history of type 2 DM, fasting blood glucose, components of metabolic syndrome, and 25-hydroxyvitamin D levels, were obtained for all subjects. Results After adjusting for vitamin D supplementation, sex, age, body mass index, and hepatitis C virus co-infection, vitamin D deficiency was associated with type 2 DM (adjusted OR, 1.85; 95% CI, 1.03–3.32; p=.038). The association between vitamin D deficiency and metabolic syndrome was not significant after adjusting for vitamin D supplementation, sex age and body mass index (adjusted OR 1.32; 95% CI, 1.00–1.75;p=.053). Conclusions Our study demonstrates an association between vitamin D deficiency and type 2 DM. Clinical trials are needed to better characterize the association between vitamin D deficiency and type 2 DM in HIV infection and to evaluate whether vitamin D is able to prevent or delay the onset of type 2 DM.

BackgroundCD4/CD8<0.8 is a surrogate marker of immune-activation/immunosenescence and independently predicts mortality in the HIV-infected patients due to non-AIDS related events. Most studies showed that patients on antiretroviral therapy (ART) often fail to normalize the CD4/CD8 ratio despite CD4 count normalization. Primary objective of the study was to explore the impact of CD4/CD8<0.8 as independent predictor of HIV-associated non-AIDS (HANA) conditions and multimorbidity (MM) in HIV patients. In patients with no previous history of cardiovascular disease (CVD) a particular insight is provided in the association between impact of CD4/CD8<0.8 and risk prediction of CVD or radiological markers of subclinical CVD.Materials and Methods914 consecutive patients attending Modena Metabolic HIV Clinic were evaluated in a cross-sectional retrospective study. Inclusion criteria: stable ART from ≥2 years; HIV-RNA plasma levels<40 copies/mL; stable CD4 count≥350/mmc. CD4/CD8 strata (0.8) was chosen as a cut off representing the median value of the cohort. MM was defined as the presence of≥2 HANA conditions including standard defined: chronic kidney disease, hypertension, previous CVD events, osteoporosis and diabetes mellitus. Calendar year of ART initiation was defined: “PreART” (<2000); “EarlyART” (2000–2005) and “LateART” (>=2006). High CVD risk was defined for Framingham Risk Score (FRS)≥6. Subclinical CVD was defined using cardiac CT scan for calcium score (CAC)≥100. Logistic univariate and multivariable adjusted analysis were performed to assess relationships between variables.ResultsDemographic and HIV-specific variables distribution in patients with and without MM are shown in Table 1. Figure 1 shows HANA distribution across CD4/CD8 strata: CVD prevalence only appeared to be higher in patients with no CD4/CD8>0.8.In multivariable analyses CD4/CD8<0.8 was not an independent predictor of MM (OR=1.225, CI 0.891; 1.681, p=0.211) after adjustment for age, gender and BMI. Patients with CD4/CD8<0.8 displayed higher CVD risk but not higher prevalence of subclinical CVD. At multivariable analyses CD4/CD8<0.8 remained predictor of higher CVD risk (OR=0.65, CI 0.47–0.917, p=0.014) after correction for sex, BMI, age strata and HIV infection duration.ConclusionsLow CD4/CD8 ratio was not associated with MM prevalence. Patients with CD4/CD8<0.8 ratio displayed higher prevalence of CVD. At multivariable logistic regression CD4/CD8<0.8 is an independent prepredictor of enhanced CVD risk. This may support role of immune-activation/senescence in the pathogenesis of CVD.

Objective: GH secretion is impaired in lipodystrophic human immunodeficiency virus (HIV) patients and inversely related to lipodystrophy-related fat redistribution in men. Less is known about the underlying mechanisms involved in reduced GH secretion in HIV-infected women. Design: A case-control, cross-sectional study comparing GH/IGF1 status, body composition, and metabolic parameters in 92 nonobese women with HIV-related lipodystrophy and 63 healthy controls matched for age, ethnicity, sex, and body mass index (BMI). Methods: GH, IGF1, IGF binding protein 3 (IGFBP3), GH after GHRH plus arginine (GHRHCArg), several metabolic variables, and body composition were evaluated. Results: GH response to GHRHCArg was lower in HIV-infected females than in controls. Using a cutoff of peak GH %7.5 mg/l, 20.6% of HIV-infected females demonstrated reduced peak GH response after GHRHCArg. In contrast, none of the control subjects demonstrated a peak GH response %7.5 mg/l. Bone mineral density (BMD), quality of life, IGF1, and IGFBP3 were lowest in the HIV-infected females with a GH peak %7.5 mg/l. BMI was the main predictive factor of GH peak in stepwise multiregression analysis followed by age, with a less significant effect of visceral fat in the HIV-infected females. Conclusions: This study establishes that i) GH response to GHRHCArg is lower in lipoatrophic HIVinfected women than in healthy matched controls, ii) BMI more than visceral adipose tissue or trunk fat influences GH peak in this population, and iii) HIV-infected women with a GH peak below or equal to 7.5 mg/l demonstrate reduced IGF1, IGFBP3, BMD, and quality of life.

The immunological mechanisms that modulate immune response to SARS-CoV-2 infection remain elusive. Little is known on the magnitude and the durability of antibody response against COVID-19. There is consensus that patients with immune dysfunction, such as dialysis patients, may be unable to mount a robust and durable humoral immunity after infections. Recent studies showed that dialysis patients seroconverted after COVID-19, but data on the durability of the immune response are missing. We reported the data of a durable anti-spike protein seroconversion after natural SARS-CoV-2 infection in three patients on hemodialysis with a mean age of 67.2 AE 13.8 years. A mean antibody titer of 212.6 AE 174.9 UA/ml (Liaison ® , DiaSorin) was found after one year (range, 366-374 days) from the diagnosis of COVID-19. In conclusion, this case series provided evidence that patients Modena COVID-19 Working Group (MoCo19) includes: