Gastroesophageal Reflux and Idiopathic Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) and Gastroesophageal reflux disease (GERD) commonly co-exist. Pathophysiological mechanisms causing IPF are still not well understood, and GERD has been implicated in both as a probable causative and disease-promoting entity. Although not conclusively proven, this relationship has been the subject of several studies, including therapeutic interventions aimed at treating GERD and its resultant effect on IPF and related outcomes. Our review aims to present the current concepts and understanding of these two disease processes, which are multifaceted. Their complex interaction includes epidemiology, pathophysiology, diagnosis, treatment, review of research studies conducted to date, and future directions for research

Effect of atorvastatin and pioglitazone on plasma levels of adhesion molecules in non-diabetic patients with hypertension or stable angina or both

Background: It was to study the effect of atorvastatin, pioglitazone and their combination on plasma levels of adhesion molecules in patients with hypertension or stable angina or both. Methods: It was an open-label, randomized parallel-group study. Forty-five atorvastatin-naive patients with hypertension or stable angina or both, were randomized to receive either atorvastatin (19 patients; 10 mg OD for 12 weeks) or pioglitazone (26 patients; 30 mg OD for 12 weeks). Another group of 30 patients who were already on atorvastatin were put on add-on pioglitazone therapy (pioglitazone (15 mg OD) + atorvastatin (10 mg OD) for 12 weeks). Plasma high-sensitivity C-reactive protein (hsCRP), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) levels were measured at baseline and after 12 weeks of therapy. Results: Atorvastatin monotherapy significantly reduced plasma sICAM-1, but pioglitazone monotherapy did not produce any significant effect. Addition of pioglitazone in patients already receiving atorvastatin also significantly reduced plasma sICAM-1 level. However, there was no significant change in plasma hsCRP and sVCAM-1 levels in any of the groups after 12 weeks of therapy. Conclusion: There is therapeutic advantage of combining pioglitazone and atorvastatin on plasma sICAM-1 levels

Daily Intake and Serum Levels of Copper, Selenium and Zinc According to Glucose Metabolism: Cross-Sectional and Comparative Study

Trace elements play an important role in metabolism. We compared the daily intake and serum concentrations of copper (Cu), selenium (Se), and zinc (Zn) across a spectrum of glucose tolerance status in a representative U.S. population. Daily intake and serum concentrations of Cu, Zn and Se in 5087 adults from the 2011–2016 National Health and Nutrition Examination Survey (NHANES) were examined and compared to normal (NGT) and abnormal (AGT) glucose tolerance and the presence of diabetes mellitus (DM). Other than Zn deficiency (21.15%), the prevalence of Zn, Se, and Cu excess and Se and Cu deficiency were low (<4.00%). As compared to the NGT group, Cu and Se supplementation was higher in the AGT and DM groups (p < 0.0001 for all). Serum Se and Zn, but not Cu, concentrations were highly correlated with daily intake (p < 0.0001 for both). As compared to the NGT group, serum Cu concentration was highest in the AGT group (p = 0.03), serum Se concentration was highest in the DM group (p < 0.0001), and serum Zn concentration was highest in the AGT group (p < 0.0001). Serum Se and Zn concentration was correlated with daily Se and Zn intake. Even within the reference range for serum Cu, Se, and Zn concentrations, a higher serum concentration of Cu, Se, and Zn was associated with abnormal glucose metabolism. Although the casual relationship remains to be elucidated, these data suggest caution in Cu, Se and Zn supplementation in non-deficient individuals

Transaldolase exchange and its effects on measurements of gluconeogenesis in humans

The deuterated water method is used extensively to measure gluconeogenesis in humans. This method assumes negligible exchange of the lower three carbons of fructose 6-phsophate via transaldolase exchange since this exchange will result in enrichment of carbon 5 of glucose in the absence of net gluconeogenesis. The present studies tested this assumption. 2H2O and acetaminophen were ingested and [1-13C]acetate infused in 11 nondiabetic subjects after a 16-h fast. Plasma and urinary glucuronide enrichments were measured using nuclear magnetic resonance spectroscopy before and during a 0.35 mU·kg FFM−1·min−1 insulin infusion. Rates of endogenous glucose production measured with [3-3H]- and [6,6-2H2]glucose did not differ either before (14.0 ± 0.7 vs. 13.8 ± 0.7 μmol·kg−1·min−1) or during the clamp (10.4 ± 0.9 vs. 10.9 ± 0.7 μmol·kg−1·min−1), consistent with equilibration and quantitative removal of tritium during triose isomerase exchange. Plasma [3-13C] glucose-to-[4-13C]glucose and urinary [3-13C] glucuronide-to-[4-13C]glucuronide ratios were <1.0 (P < 0.001) in all subjects both before (0.66 ± 0.04 and 0.60 ± 0.04) and during (059 ± 0.05 and 0.56 ± 0.06) the insulin infusion, respectively, indicating that ∼35–45% of the labeling of the 5th carbon of glucose by deuterium was due to transaldolase exchange rather than gluconeogenesis. When corrected for transaldolase exchange, rates of gluconeogenesis were lower (P < 0.001) and glycogenolysis higher (P < 0.001) than uncorrected rates both before and during the insulin infusion. In conclusion, assuming negligible dilution by glycerol and near-complete triose isomerase equilibration, these data provide strong experimental evidence that transaldolase exchange occurs in humans, resulting in an overestimate of gluconeogenesis and an underestimate of glycogenolysis when measured with the 2H2O method. Use of appropriate 13C tracers provides a means of correcting for transaldolase exchange

Acute Exacerbation of Idiopathic Pulmonary Fibrosis

Episodes of Acute exacerbation (AE) of Idiopathic Pulmonary fibrosis (IPF) are important events in the disease trajectory of IPF, associated with punctuated decline in lung function with significant mortality and morbidity associated with it. These episodes are idiosyncratic, and often unpredictable and may have triggers. Our diagnostic criteria for these events, etiology, pathogenesis, risk factors and management continue to evolve over the years, with limited availability of qualitative research data to help guide management. Outcome in general is poor with no well-defined therapy but prevention may be possible with use of Nintedanib. Our chapter aims to explore the contemporary knowledge of the key aspects of this disease entity