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Background: Human immunodeficiency virus (HIV) infection and antiretroviral therapy have been associated with non-alcoholic fatty liver disease (NAFLD), but few studies have evaluated whether HIV infection is an independent risk factor for the development of hepatic steatosis and advanced liver fibrosis. Objectives: To study the prevalence and severity of hepatic steatosis and advanced fibrosis in people living with HIV and control outpatients. Methods: We conducted a cross-sectional analysis of relevant data from 875 pairs of individuals belonging to an HIV-dedicated outpatient clinic and an adult primary care clinic of an inner-city hospital. Hepatic Steatosis Index (HSI) and FIB-4 index were calculated as non-invasive measures of steatosis and fibrosis, respectively. A multivariate logistic regression analysis was performed to assess predictors of steatosis and advanced fibrosis. Results: The prevalence of hepatic steatosis, determined by HSI ≥36, was higher in HIV-negative subjects (71.5% vs. 65.4%, p=0.006). The prevalence of advanced fibrosis, determined by FIB-4 index ≥3.25, was higher in the HIV-positive group (7% vs. 1.7%, p Conclusions: In this cohort, hepatic steatosis was more prevalent in non-HIV infected patients, while advanced fibrosis had a higher prevalence in people living with HIV. HIV infection was not found to be an independent risk factor for either hepatic steatosis or fibrosis.

Dysphagia is a symptom with diverse etiologies including luminal narrowing of the esophagus and motility disorders. Arterial vessels are known to compress the esophagus and cause luminal narrowing. However, identifying a pulmonary venous compression of the esophagus rarely occurs in a patient with dysphagia. The technology available at the time of the few prior case reports published more than three decades ago limited the analysis of the pulmonary vessels. We report a case that utilized CT-angiography as well as multiplanar reconstructions and three-dimensional imaging to demonstrate that esophageal compression in the patient presenting with dysphagia was caused by a large left common pulmonary vein.

Background Clostridium difficile infection (CDI) is a leading cause of community-onset and healthcare–associated infection, with high recurrence rates, and associated high morbidity and mortality. We report national rates, leading causes, and predictors of hospital readmission for CDI. Methods Retrospective study of data from the 2013 Nationwide Readmissions Database of patients with a primary diagnosis of CDI and re-hospitalization within 30-days. A multivariate regression model was used to identify predictors of readmission. Results Of 38,409 patients admitted with a primary diagnosis of CDI, 21% were readmitted within 30-days, and 27% of those patients were readmitted with a primary diagnosis of CDI. Infections accounted for 47% of all readmissions. Female sex, anemia/coagulation defects, renal failure/electrolyte abnormalities and discharge to home (versus facility) were 12%, 13%, 15%, 36%, respectively, more likely to be readmitted with CDI. Conclusions We found that 1-in-5 patients hospitalized with CDI were readmitted to the hospital within 30-days. Infection comprised nearly half of these readmissions, with CDI being the most common etiology. Predictors of readmission with CDI include female sex, history of renal failure/electrolyte imbalances, anemia/coagulation defects, and being discharged home. CDI is associated with a high readmission risk, with evidence of several predictive risks for readmission.

Eosinophilic gastroenteritis is an uncommon condition characterized by focal or diffuse infiltration of eosinophils in the gastrointestinal tract in the absence of secondary causes. The pathogenesis of this condition is not well understood and its clinical presentation depends on the segment and layer of the gastrointestinal tract affected. The definition of eosinophilic gastroenteritis may be difficult, as the normal ranges of eosinophil numbers in normal and abnormal gastric and intestinal mucosa are not standardized. We present the case of a 59-year-old male who came to the hospital with hypovolemic shock and lethargy secondary to severe diarrhea. Laboratory analysis was significant for peripheral eosinophilia, and pathology from both the duodenum and colon showed marked eosinophilic infiltration.

In a previous report of HIV-infected patients with fat redistribution, we found that recombinant human growth hormone (rhGH) therapy reduced visceral adipose tissue (VAT) but increased insulin resistance, and that the addition of rosiglitazone reversed the negative effects of rhGH on insulin sensitivity. In this study, we sought to determine the effects of rhGH and rosiglitazone therapy on an array of inflammatory and fibrinolytic markers.72 patients with HIV-associated abdominal obesity and insulin resistance were randomized to treatment with rhGH, rosiglitazone, the combination of rhGH and rosiglitazone, or placebo for 12 weeks. Subjects with plasma and serum samples available at weeks 0 (n=63) and 12 (n=46-48) were assessed for adiponectin, C-reactive protein, homocysteine, interleukin-1, interleukin-6, tumor necrosis factor alpha, interferon gamma, fibrinogen, plasminogen activator inhibitor-1 antigen, and tissue plasminogen activator antigen.Treatment with both rosiglitazone alone and the combination of rosiglitazone and rhGH for 12 weeks resulted in significant increases in adiponectin levels from baseline. Adiponectin levels did not change significantly in the rhGH arm alone . There were no significant changes in the other biomarkers among the different treatment groups.In this study of HIV-infected patients with altered fat distribution, treatment with rosiglitazone had beneficial effects on adiponectin concentrations, an effect that was also seen with a combination of rosiglitazone and rhGH. RhGH administration alone, however, did not demonstrate any significant impact on adiponectin levels despite reductions in VAT.

A young male with quiescent hepatitis B presented with sub-acute onset of lower limb weakness found to have an incidental hepatoma that had metastasized to the vertebrae causing an oncologic emergency in the form of spinal cord compression, a rare initial presentation in HBV-related hepatocellular carcinoma (HCC).