The effect of left ventricular remodelling on soluble ST2 in a cohort of hypertensive subjects.

Soluble ST2 is a biomarker of cardiomyocyte stretch that is useful in the diagnosis and prognosis of coronary artery disease. Its role in the field of hypertension and hypertensive heart failure (HHF) has not yet been well investigated. We studied the effect of left ventricular remodelling on the concentration of soluble ST2 in a cohort of 210 subjects with hypertension (HT). Left ventricular hypertrophy (LVH) was considered present when echocardiographic left ventricular mass indexed for height in metres (m) was greater than 46.2 g m(-1 2.7) in women and 49.2 g m(-1 2.7) in men. Subjects were subdivided into three groups: those without LVH (HT, n = 83); those with LVH (hypertension with left ventricular hypertrophy (HTLVH), n = 50) and those with HHF, n=77). Plasma ST2 and NT-pro BNP were measured using electrochemiluminescence type immunoassay. Subjects with HHF had higher plasma ST2 concentrations compared to HTLVH (134.7 ± 57.3 ng ml(-1) versus 23.0 ± 8.3 ng ml(-1), P < 0.001) and those with HT (134.7 ± 57.3 ng ml(-1) versus 14.5 ± 4.9 ng ml(-1), P < 0.0001). NT-pro BNP levels were similar when HTLVH was compared with HT (P = 0.68), but subjects with HHF had significantly higher NT-pro BNP compared to HTLVH (P < 0.0002). Soluble ST2 had strong correlation with clinical and echocardiograhic parameters, and correlated well with NT-pro BNP (r = 0.41, P < 0.0001). Plasma ST2 is a useful biomarker in not only differentiating HHF from HT with or without LVH, but also distinguishes hypertensive LVH from HT without LVH.

Association among vitamin D, oral candidiasis, and calprotectinemia in HIV.

Vitamin D deficiency is associated with negative health outcomes, including infections. Vitamin D modulates inflammation and down-regulates the expression of calprotectin, a molecule which influences neutrophil functions and which has been linked to oral candidiasis (OC), the most prevalent oral lesion in human immunodeficiency virus (HIV). We hypothesized a positive association between vitamin D deficiency and OC, and that this effect was partially modulated by calprotectinemia. Plasma calprotectin and serum 25 (OH) vitamin D levels were measured in stored samples from 84 HIV-seropositive Chicago women enrolled in the Oral Substudy of the Women's Interagency HIV Study (WIHS). OC and vitamin D deficiency were diagnosed in, respectively, 14 (16.7%) and 46 (54.8%) of those studied. Vitamin D deficiency was positively associated with OC (p = 0.011) and with higher calprotectinemia (p = 0.019) in univariate analysis. After adjustment for CD4, HIV viral load, HIV treatment, and tobacco and heroin/methadone use, vitamin D deficiency remained a significant predictor of OC (OR 5.66; 95% confidence interval 1.01-31.71). This association weakened after adjustment for calprotectinemia, supporting a role for calprotectinemia as a moderator of this effect. These findings support studies to examine the effect of vitamin D status on calprotectinemia, neutrophil functions, and opportunistic mucosal infections in HIV.

Serological markers of autoimmunity in patients infected with hepatitis C virus: impact of HIV co-infection.

OBJECTIVES: We sought to evaluate the prevalence, predictors and significance of autoantibody expression in patients with chronic hepatitis C (CHC) with or without HIV co-infection. METHODS: Retrospective review of laboratory and histologic data for all patients with CHC who had a liver biopsy available. HIV status was documented in all patients. Results analyzed in SPSS10, Chicago, IL, a p value <0.05 was considered significant. RESULTS: 170 patients with hepatitis C viremia, including 107 (63%) HIV co-infection, who had testing for anti-nuclear antibody (ANA) or anti-smooth muscle antibody (ASMA) and anti-mitochondrial antibody (AMA) were included in the study. Overall, 63% (74/117) of patients were ASMA seropositive and 6% (9/153) were positive for ANA. All 117 patients tested for AMA were negative. HIV co-infected patients were significantly more likely to be ASMA positive 71% (53/75) compared to those with hepatitis C alone (50%) [P=0.026]. There were no significant differences in age, gender, race, risk group, alanine aminotransferase (ALT) levels or grade of inflammation on histology between autoantibody positive and negative patients. ASMA positive patients had significantly higher globulin levels (P=0.036) and a trend towards more bridging fibrosis or cirrhosis. Patients with autoantibody expression rarely had histologic features of AIH. CONCLUSION: We found a high rate of ASMA seropositivity in our cohort of patients with chronic hepatitis C, and HIV co-infection was associated with significantly higher rates of ASMA expression. Autoantibody expression was not associated with demographic or clinical characteristics and does not necessarily preclude antiviral therapy.