Adipose Tissue, Bile Acids, and Gut Microbiome Species Associated With Gallstones After Bariatric Surgery.

Several risk factors are associated with gallstone disease after bariatric surgery, but the underlying pathophysiological mechanisms of gallstone formation are unclear. We hypothesize that gallstone formation after bariatric surgery is induced by different pathways compared with gallstone formation in the general population, since postoperative formation occurs rapidly in patients who did not develop gallstones in preceding years. To identify both pathophysiological and potentially protective mechanisms against postoperative gallstone formation, we compared the preoperative fasting metabolome, fecal microbiome, and liver and adipose tissue transcriptome obtained before or during bariatric surgery of obese patients with and without postoperative gallstones. In total, 88 patients were selected from the BARIA longitudinal cohort study. Within this group, 32 patients had postoperative gallstones within 2 years. Gut microbiota metagenomic analyses showed group differences in abundance of 41 bacterial species, particularly abundance of Lactobacillaceae and Enterobacteriaceae in patients without gallstones. Subcutaneous adipose tissue transcriptomic analyses revealed four genes that were suppressed in gallstone patients compared with patients without gallstones. These baseline gene expression and gut microbiota composition differences might relate to protective mechanisms against gallstone formation after bariatric surgery. Moreover, baseline fasting blood samples of patients with postoperative gallstones showed increased levels of several bile acids. Overall, we revealed different genes and bacteria associated with gallstones than those previously reported in the general population, supporting the hypothesis that gallstone formation after bariatric surgery follows a different trajectory. Further research is necessary to confirm the involvement of the bile acids, adipose tissue activity, and microbial species observed here.

Vitamin B6 requirements in chronic renal failure.

According to our results the long-term daily oral supplementation of 6 mg vitamin B6 was sufficient for prevention of vitamin B6 deficiency in chronic renal failure, regular dialysis treatment and CAPD groups of patients. Haemodialysis and charcoal haemoperfusion have led to non-significant decrease of erythrocyte vitamin B6. A favourable effect was found of daily oral administration of 50 mg pyridoxine on electrophoretic mobility of peripheral blood lymphocytes and cellular immunity.

Subacute (de Quervain's) thyroiditis: association with HLA-Bw35 antigen and abnormalities of the complement system, immunoglobulins and other serum proteins.

The HLA antigens in 40 patients with subacute thyroiditis were investigated. An association between subacute thyroiditis and HLA-Bw35 antigen as previously reported, was confirmed. Further immunological observations included a decrease in Serum Clq, C4 and C3 activator levels; conversely, there was an increase in serum C3, IgM, alpha1-acid glycoprotein and alpha1-antitrypsin levels. Serum IgA levels were decreased in those patients who were Bw35 negative, but were normal in the patients who were Bw-35 positive, with serum alpha2-macroglobulin levels the opposite was found. These studies support the view that a genetic factor(s), viz., the major histocompatibility system, plays a role in the pathogenesis of subacute thyroiditis. A "nosological clustering" around the Bw35 antigen as a marker for viral susceptibility is suggested.