Gut microbiota,dysbiosis and colon lavage

Gut microbial dysbiosis is considered an alteration of diversity and abundance of intestinal microbes, which contributes to the onset of many disorders. Several factors cause dysbiosis, depending on life-style (nutrition, stress, environment, smoking, physical activity) or particular diseases (inflammatory, autoimmune, chronic diseases). Drugs (i.e. antibiotics, anticancer drugs), as well as medical and surgical procedures, can often cause dysbiosis. Mechanical bowel preparations (MBP) and the so called "bowel cleansing" have an immediate impact on intestinal microbial composition. Whether these "acute" changes may lead to any clinical consequences is still unknown. It is tempting to speculate that such dysbiosis fostering events, at least in patients already presenting abdominal complaints, such as irritable bowel syndrome (IBS), or inflammatory bowel disease (IBD) patients, may drive additional or more severe symptoms. Recently, the possibility of using probiotic supplementation has been addressed in the literature, with the purpose to counteract intestinal dysfunctional changes observed in relation to a dysbiotic state. Whereas probiotics are recognized to be effective and safe in restoring gut microbiota dysbiosis, preliminary evidence suggest that this approach may prove helpful even in case of transient dysbiotic states related to colonoscopy bowel preparation.     

Bacterial salivary microbiome associates with asthma among african american children and young adults

Several studies have shown that the airways of asthma patients contain higher diversity of bacteria and are enriched in pathogenic species. However, sampling the airways in children is challenging. Here we aimed to identify differences in the salivary bacterial composition between African Americans children with and without asthma. Saliva samples from 57 asthma cases and 57 healthy controls were analyzed by means of 16S ribosomal RNA amplicon profiling. Measurements of bacterial diversity and genus relative abundance were compared between cases and controls using the nonparametric Wilcoxon test and multivariate regression models. A total of five phyla and a mean of 56 genera were identified. Among them, 15 genera had a relative abundance greater than 1%, being Prevotella, Haemophilus, Streptococcus, and Veillonella the most abundant genera. Differences between cases and controls were found in terms of diversity, as well as in relative abundance for Streptococcus genus (13.0% in cases vs 18.3% in controls; P = .003) and Veillonella genus (11.1% in cases vs 8.0% in controls; P = .002). These differences remained significant after correction for multiple comparisons and when potential confounders were taken into account in logistic regression models. In conclusion, we identified changes in the salivary microbiota associated with asthma among African Americans.     

Low molecular weight heparin for treatment of acute myocardial infarction (FAMI): Fragmin (dalteparin sodium) in acute myocardial infarction

The benefit of using subcutaneous low molecular weight heparin for the treatment of acute myocardial infarction is not known. The aim of this study was to determine the efficacy of a low molecular weight heparin (dalteparin sodium) for the treatment of acute myocardial infarction in patients not treated with thrombolytic therapy. Twenty-nine cardiological centres from leading hospitals in India participated in this prospective, multicentre, double-blind, placebo-controlled study in two phases which included 1128 patients with acute myocardial infarction. In the acute phase (between day 1 and 3 of admission) all the patients received a weight-adjusted dose of subcutaneous dalteparin (120 IU/kg twice daily). In the second, double-blind phase of acute myocardial infarction, patients were randomised to receive a fixed dose of dalteparin (7,500 IU) or an identical placebo injection for 30 days. A composite primary endpoint of death, reinfarction, recurrence of angina and emergency revascularisation was used. All the 1128 patients with acute myocardial infarction were included in the trial. In the acute phase, the composite primary endpoint was observed in 58 (5.1%) patients. Of 1037 paients who were randomly assigned to receive a fixed dose of dalteparin (n=519) or placebo (n=518), the composite primary event rate was 6.7 percent and 7.0 percent, respectively (RR 0.97; 95% CI 0.62-1.52; p=0.90). To conclude, treatment with dalteparin administered subcutaneously in a weight-adjusted dose of 120 IU/kg twice daily resulted in a lower than expected mortality during the acute phase of myocardial infarction. A lower fixed once daily dose of 7,500 IU during the chronic phase did not confer additional protection.     

Metformin is the key factor in elevated plasma growth differentiation factor-15 levels in type 2 diabetes: A nested,case–control study

Produced as a tissue defence response to hypoxia and inflammation, growth differentiation factor-15 (GDF-15) is elevated in people receiving metformin treatment. To gain insight into the relationship of GDF-15 with metformin and major cardiovascular risk factors, we analysed the data from the SUMMIT cohort (n = 1438), a four-centre, nested, case–control study aimed at verifying whether biomarkers of atherosclerosis differ according to the presence of type 2 diabetes and cardiovascular disease. While in univariate analysis, major cardiovascular risk factors, with the exception of gender and cholesterol, increased similarly and linearly across GDF-15 quartiles, the independent variables associated with GDF-15, both in participants with and without diabetes, were age, plasma creatinine, N-terminal pro-brain natriuretic peptide, diuretic use, smoking exposure and glycated haemoglobin. In participants with diabetes, metformin treatment was associated with a 40% rise in GDF-15 level, which was independent of the other major factors, and largely explained their elevated GDF-15 levels. The relatively high GDF-15 bioavailability might partly explain the protective cardiovascular effects of metformin.     

Effects of hydroxymethylglutaryl coenzyme A reductase inhibitor simvastatin on smooth muscle cell proliferation in vitro and neointimal formation in vivo after vascular injury

OBJECTIVES: We sought to evaluate the effects of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors on vascular smooth muscle cell (VSMC) proliferation in vitro and neointimal formation in vivo after vascular injury. BACKGROUND: Neointimal hyperplasia after vascular injury is responsible for restenosis after arterial stenting, whereas arterial remodeling and neointimal formation are the causes of restenosis after percutaneous transluminal coronary angioplasty. METHODS: We assessed the effect of simvastatin on in vitro VSMC proliferation. To study the effects of simvastatin in vivo, balloon injury and stent deployment were performed in the common carotid artery of rats. Neointimal area was measured two weeks later in the balloon injury model and three weeks after stent deployment. RESULTS: Simvastatin markedly inhibits VSMC proliferation in vitro. In vivo, simvastatin reduced, in a dose-dependent manner, the neointimal area and the neointima-media ratio after balloon injury from 0.266 +/- 0.015 mm2 to 0.080 +/- 0.026 mm2 and from 1.271 +/- 0.074 to 0.436 +/- 0.158 (p < 0.001 vs. control rats) at the highest dose. Simvastatin also significantly reduced the neointimal formation and the neointima-media ratio after stenting from 0.508 +/- 0.035 mm2 to 0.362 +/- 0.047 mm2 (p < 0.05 vs. control rats) and from 2.000 +/- 0.136 to 1.374 +/- 0.180 (p < 0.05 vs. control rats). The vessel thrombosis rate after stent deployment was 30% in the control group and 11.1% in the treated group (p = NS). Moreover, the systemic administration of simvastatin did not affect hepatic and renal functions, blood pressure or heart rate. CONCLUSIONS: Simvastatin potently inhibits VSMC proliferation in vitro and reduces neointimal formation in a rat model of vascular injury.     

CASE REPORT: Pancreatic Ascites in an Infant: Lack of Symptoms and Normal Amylase

A 4-month-old boy presented with 9 days of abdominal distension. The abdomen was tense, distended, and nontender, with a fluid wave. Hypoalbuminemia, hyponatremia, high lipase, normal amylase, high ascitic fluid: lipase, amylase, and serum-ascites albumin gradient < 1.1 were present. Abdominal CT showed large ascites, edema, and pancreatic cyst. No improvement was noted with bowel rest, TPN, albumin, furosemide, octreotide, and paracentesis. Endoscopic retrograde cholangiopancreatography showed disrupted pancreatic duct and a cyst. Pancreatic duct stenting was complicated by early outward migration of the stent and was thus ineffective. An exploratory laporatomy revealed a cyst. Cystogastrostomy resolved the pancreatitis and ascites. The patient was discharged off TPN and tolerating enteral nutrition. Pancreatic ascites is rare, producing few or no symptoms in infants. In conclusion, our patient may have had viral pancreatitis, complicated by a disrupted duct and/or ruptured pseudocyst with ascites formation. Medical management was ineffective. Surgery appears to have been curative.     

How fat is obese?

The aim of the study was a comparison between body fat measurements and body mass index. We analyzed the data of 890 subjects, 596 females and 294 males, ranging in age from 18 to 83 years, in body mass index (BMI) from 14 to 54 kg/m(2), and in body fat percentage (BF%) from 4% to 57%. A considerable number of subjects, both males and females, could not be classified as obese based on their BMI alone. Such a misclassification is undesirable, especially in general practice, and it calls for diagnostic criteria other than the BMI alone to be used for obesity.