Massive Pulmonary Embolism from worsening of Gouty Arthritis due to the COVID-19 Pandemic

Abstract: Gout is the most common inflammatory arthritis in men and is associated with increased mortality and is an independent risk factor for cardiovascular disease such as myocardial infarction and stroke. In addition, several other types of inflammatory arthritis have been linked to increased risk of venous thromboembolism (VTE). VTE is associated high mortality of around 9.7% for PE and 4.6% for DVT. However, only a handful of studies have been conducted to estimate the risk of VTE in patients with gout before or after diagnosis. Most recent study in Canada concluded that patients with gout have around a 20% increase in risk compared to the general population for VTE. However, they stated not all gout patients carry the same risk and further research is needed to identify high risk factors and implement prophylactic therapy. In addition to that, multiple studies have concluded that alcohol sales, mental health illness, and drug use has increased dramatically during the COVID-19 pandemic. We present an interesting case of a 64-year-old patient with history of chronic gout which worsened within the last six months, first leading to DVT and a few months later a massive pulmonary embolism (PE). The patient had multiple high-risk factors for PE including chronic gout with worsening flare ups due to the excessive alcohol drinking since the COVID-19 pandemic and recent non-adherence to DVT anticoagulant medication for a month. We highlight the importance to monitor for high-risk factors such as excessive alcohol use and immobility in patients with inflammatory condition such as gout especially during the COVID pandemic

BMPR2 expression is suppressed by signaling through the estrogen receptor

<p>Abstract</p> <p>Background</p> <p>Studies in multiple organ systems have shown cross-talk between signaling through the bone morphogenetic protein receptor type 2 (BMPR2) and estrogen pathways. In humans, pulmonary arterial hypertension (PAH) has a female predominance, and is associated with decreased BMPR2 expression. The goal of this study was to determine if estrogens suppress BMPR2 expression.</p> <p>Methods</p> <p>A variety of techniques were utilized across several model platforms to evaluate the relationship between estrogens and BMPR2 gene expression. We used quantitative RT-PCR, gel mobility shift, and luciferase activity assays in human samples, live mice, and cell culture.</p> <p>Results</p> <p>BMPR2 expression is reduced in lymphocytes from female patients compared with male patients, and in whole lungs from female mice compared with male mice. There is an evolutionarily conserved estrogen receptor binding site in the BMPR2 promoter, which binds estrogen receptor by gel-shift assay. Increased exogenous estrogen decreases BMPR2 expression in cell culture, particularly when induced to proliferate. Transfection of increasing quantities of estrogen receptor alpha correlates strongly with decreasing expression of BMPR2.</p> <p>Conclusions</p> <p>BMPR2 gene expression is reduced in females compared to males in live humans and in mice, likely through direct estrogen receptor alpha binding to the BMPR2 promoter. This reduced BMPR2 expression may contribute to the increased prevalence of PAH in females.</p

Visceral adipose tissue visfatin in nonalcoholic fatty liver disease

Background. Visfatin is a novel adipocytokine predominantly expressed and secreted by visceral adipose tissue. It is realized for its multiple functions of central importance in NAD biosynthesis, innate immunity and inflammation. Its phosphoribosyl transferase activity regulates cellular energetics and NAD dependent enzymes such as SIRTUINS. Although its expression in various tissues and circulating levels are documented, visceral visfatin levels in Nonalcoholic fatty liver disease (NAFLD) patients have not been reported.Objective. The aim of the present study was to assess visceral adipose tissue visfatin levels in NAFLD.Materials and methods. A total of 115 patients undergoing diagnostic laparoscopy were recruited in the study and categorized into two groups based on standard criteria for NAFLD. Visceral adipose tissue TNF-α, IL-6 and visfatin levels were measured by ELISA. Blood glucose, lipids, liver enzymes and non esterified fatty acids (NEFA) were estimated using standard procedures. Formalin fixed, Hematoxylene Eosin stained liver biopsy specimens were examined for the presence of steatosis and the degree of steatosis was ascertained as per Brunt’s classification.Results. The visceral visfatin level declined significantly (P < 0.001) in all groups of NAFLD as compared to non NAFLD group, while plasma NEFA level increased with progressive steatosis (P < 0.02). Significant increase in TNF a was observed in all groups of NAFLD, while IL-6 increased in NASH only.Conclusion. A significant decline in visceral adipose tissue visfatin level was found to be associated with degree of steatosis in NAFLD patients