Thrombocytopenia (less than 100 × 109/L platelets) presents in around one quarter of patients with nonalcoholic fatty liver disease (NAFLD), the hepatic component of insulin resistance (IR). It is unknown whether IR, by itself, associates with thrombocytopenia. Persons with NAFLD and/or IR were prospectively accrued in the study after February 2018. Insulin resistance was defined by assessing α hydroxybutyrate, lynoleoyl glycerolphosphocoline, oleic acid, and insulin (Quantose IR), whereas the presence of NAFLD was defined by serologic determinations (Fibromax) and liver transient elastography (Fibroscan). In 78 patients with NAFLD, thrombocytopenia was identified in 22 (28%), whereas in 19 persons with IR, 14 (73%) were found to have NAFLD. In persons with IR + NAFLD, thrombocytopenia presented in 9 (64%). In the subset of patients with IR, the prevalence of thrombocytopenia was 52%. There was only 1 patient with IR/without NAFLD who displayed thrombocytopenia. Significant statistical association between NAFLD and thrombocytopenia was found (odds ratio [OR]: = 13, confidence interval [CI]: 1.5-162, P = .05), whereas there was no association between IR and thrombocytopenia (OR = 0.38, CI: 0.06-2.3, P = .61). Insulin resistance, by itself, was not found to be associated with diminished platelet counts. The presence of NAFLD, one of the consequences of IR, seems to be required to lead into thrombocytopenia.

Background Multiple sclerosis is an immune-mediated disease which has been associated to a great variety of mechanisms that could influence its pathogenesis. Numerous reports in the medical literature suggest that Helicobacter pylori may be a mediator of the disease. However, it is unknown if there is any clear association between MS and HP. Results We studied 144 persons with multiple sclerosis prospectively enrolled in our hematopoietic stem cell transplantation program. In 144 persons, 14% patients were positive for IgG-HP whereas 86% were negative, 8.3% pwMS were IgM-HP positive while 91.6% pwMS were negative, 18% patients were positive and 82% negative for IgA-HP. Significantly lower concentrations of anti-HP IgG were found in RRMS in comparison with SPMS (− 28.5, 95% CI 4.3–52.7). While concentrations of anti-HP IgA were significantly lower in SPMS in comparison with RRMS (0.54, 95% CI 0.1–0.9). In a multivariate analysis, positivity rate of anti-HP IgG was found to be higher in SPMS patients (OR 4.7, 95% CI 1.1–19.6). Conclusions There was a negative correlation between the presence of anti-HP antibodies and MS. Further larger studies with specific laboratory testing methods are needed to discard or confirm the potential role of anti-HP antibodies as protective for MS.