No quantitative syntheses of these studies have been performed. A systematic review and meta-analysis were conducted to examine the prevalence of inherited AT, PC,

and PS deficiencies in these patients and to compare the prevalence with healthy subjects. PubMed, EMBASE, and Cochrane Library databases were employed to identify all studies in which inherited AT, PC, and PS deficiencies in PVST and/or BCS were evaluated by family study or gene analysis. Prevalence and odds ratios of these inherited deficiencies were pooled; heterogeneity www.selleckchem.com/products/forskolin.html among studies was evaluated. Nine studies were included in our meta-analysis. The pooled prevalence of inherited AT, PC, and PS deficiencies were 3.9%, 5.6%, and 2.6% in PVST, and 2.3%, 3.8%, and 3.0% in BCS, respectively. Heterogeneity among studies was not significant except for the analysis of inherited PC deficiency in BCS. Three studies compared the prevalence selleck kinase inhibitor of these inherited deficiencies between PVST patients and

healthy subjects. The pooled odds ratios of inherited AT, PC, and PS deficiencies for PVST patients were 8.89 (95% confidence interval [CI] 2.34–33.72, P = 0.0011), 17.63 (95% CI 1.97–158.21, P = 0.0032), and 8.00 (95% CI 1.61–39.86, P = 0.011), respectively. Only one study demonstrated that no inherited deficiency was found in both BCS patients and healthy subjects. Inherited AT, PC, and PS deficiencies are rare in PVST and BCS. These inherited deficiencies

increase the risk of PVST. “
“To the Editor: We enjoyed the well-written review by Ratziu et al.1 on the role of insulin sensitizers in nonalcoholic steatohepatitis (NASH). However, we would like to correct two minor errors regarding our study2 and share our ongoing efforts that address some of the knowledge gaps highlighted by the authors. Table 1 in Ratziu et al.’s review states that we recruited only patients with diabetes. As reported elsewhere,3, 4 this is incorrect. We designed the study in 2002, and within the context of the emerging liver toxicity associated with troglitazone, we felt that exposure to a thiazolidinedione (TZD) should be reserved for NASH patients with type 2 diabetes mellitus (T2DM), or nondiabetic patients at risk of developing T2DM (i.e., impaired glucose tolerance [IGT]), so that the risk/benefit ratio selleck chemicals of treatment would favor patients at least by improving glucose metabolism (the progression from IGT to T2DM is ≈6%-10% per year). Therefore, at study entry, patients were screened with an oral glucose tolerance test. Only 14% of all patients screened (n = 70) had known T2DM. Among those patients believed to have normal glucose metabolism (n = 60), 49% had IGT, and 30% were diagnosed with new-onset T2DM, whereas only 21% had normal glucose metabolism (the latter patients were excluded from the study). These results are similar to more recent work by our group.