Background Prior mortality estimates of air pollution from coal-fired power plants in India use PM2.5 exposure-response functions from settings that may not be representative, and do not include other potentially harmful effects of these plants, such as fly ash pollution and heavy freshwater consumption. Methods We use a national, district level dataset to assess the impact of coal-fired power plants on all-cause mortality (15-69 years) in 2014. We compare districts with coal-fired power plants (total capacity >1000 MW) to districts without a coal-fired power plant, estimating the effect of these power plants on all-cause mortality within districts that have these plants. Results Out of 597 districts in India in 2014, 60 districts had a coal-fired power plant. When compared to districts without a coal-fired power plant, districts with a coal-fired power plant (>1000 MW) had higher rates of age-standardized mortality in both women (0.38, 95% CI: -0.14 - 0.90) and men (0.55, -0.17 - 1.27). Similarly, these districts had higher rates of conditional probability of premature death in both women (2.22, -0.13 - 4.56) and men (2.12, -0.54 - 4.77). The point estimates for total excess deaths were 19,320 for women and 27,727 for men. In affected districts, the proportion of premature adult deaths attributable to coal-fired power plants was 5.8% (-0.3% – 11.9%) in women and 4.3% (-1.1% – 9.6%) in men. Conclusions We estimate that ~47,000 premature adult deaths can be attributed to large coal-fired power plants in India in 2014. These deaths are concentrated in the ~10% of districts that have the nation’s power plants, where they are associated with 1 out of 20 premature adult deaths. Effective regulation of emissions from these plants, coupled with a phaseout of coal-fired power plants, can help decrease this burden of inequitable and premature adult mortality.
Cardiovascular events caused by dyslipidemia are one of the leading causes of death in patients with Chronic Kidney Disease (CKD). Statins are the first line of treatment for patients with hyperlipidemia and in the treatment regimen for patients with CKD. Therefore, the introduction of Proprotein Convertase Subtilisin-Kexin type 9 inhibitors (PCSK9 inhibitors) is a viable and possibly effective treatment option for patients who, despite high doses of statins, struggle to lower their low-density lipoprotein cholesterol (LDL-C) levels. Our paper's objective is to explore the safety of these biological agents, particularly in patients with varying stages of impaired kidney function, and the correlating effectiveness in lowering their LDL-C levels, thereby reducing cardiovascular risks in these patients.We methodically retrieved relevant articles from PubMed, PubMed Central, Medline, and Google scholar in April 2022. We used the Medical Subject Heading (MeSH) Strategy and used the relevant keyword, then applied our inclusion and exclusion criteria; the initial search gave 10,542 results; with the removal of duplicates, irrelevant articles, and application of quality assessments done, we finally included 15 papers for our review with 37,188 patients. PCSK9 inhibitors are reliable, safe, and efficient therapy in lowering LDL-C levels in patients with CKD. However, its safety and efficacy in severe and end-stage kidney disease are grey, as other factors such as infections lead to morbidity and mortality. Future trials on chronic kidney disease and PCSK9 inhibitors should investigate the inhibitors' ability to improve kidney functions at all stages of kidney disease while lowering lipid levels and finally analyze the safety in patients with end-stage kidney disease.
Non-alcoholic fatty liver disease (NAFLD) represents one of the leading causes of chronic liver disease globally, perhaps because of the drastic increase in prevalence around the world during the last 20 years and continues growing. The disease starts from simple steatosis (NAFL) that can progress to non-alcoholic steatohepatitis (NASH) and, in some patients, progress to cirrhosis and hepatocellular carcinoma (HCC). The pathogenesis and pathophysiology of NAFLD are complex and involve different factors (genetic, metabolic, endocrinopathies, and others). One of the concerns that appeared in recent years is hypothyroidisminduced NAFLD. The pathogenesis is compound and not well understood, and an association between hypothyroidism and NAFLD remains controversial because of insufficient studies that can confirm it. More research is needed to determine the association between hypothyroidism and NAFLD and the underlying mechanisms. In this review, we will discuss a more in-depth analysis of the physiology of thyroid hormones (TH) as well as the pathophysiology of hypothyroidism-induced NAFLD and, based on the recent metaanalyses, the association of thyroid hormones and NAFLD.
Inflammatory bowel disease (IBD) is a globally rising chronic intestinal disease that affects individuals in many parts of the world. Immunosuppressive medications such as corticosteroids are used to manage flareups and to induce remission in IBD. Corticosteroids are said to cause several systemic symptoms, but they are also associated with drug-induced neuropsychiatric disorders. This article examines the existing data on psychiatric and cognitive effects associated with corticosteroid therapy in relation to IBD. Many studies have found that corticosteroids appear to cause mood disturbances such as mania, hypomania, depression, and cognitive problems in the first few weeks of therapy, but these effects are dose-dependent and often mild. The purpose of this literature review is to shed light on the impact corticosteroids can have on individuals' mental health, which will aid physicians in the future when treating patients with IBD. Healthcare professionals should advise patients of this risk and assess the need for intervention. While there is evidence that corticosteroids can elicit neuropsychiatric symptoms, more data on people with IBD who are on corticosteroid therapy is needed to determine the prevalence of glucocorticoid-induced mood changes in this population.
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