Pulmonary Embolism in COVID-19 Patients: Facts and Figures

COVID-19 infection affects many systems in the body including the coagulation mechanisms. Imbalance between pro-coagulant and anticoagulant activities causes a roughly nine times higher risk for pulmonary embolism (PE) in COVID-19 patients. The reported incidence of PE in COVID-19 patients ranges from 3 to 26%. There is an increased risk of PE in hospitalized patients with lower mobility and patients requiring intensive care therapy. Obesity, atrial fibrillation, raised pro-inflammatory markers, and convalescent plasma therapy increases the risk of PE in COVID-19 patients. Endothelial injury in COVID-19 patients causes loss of vasodilatory, anti-adhesion and fibrinolytic properties. Viral penetration and load leads to the release of cytokines and von Willebrand factor, which induces thrombosis in small and medium vessels. D-dimers elevation gives strong suspicion of PE in COVID-19 patients, and normal D-dimer levels effectively rule it out. Point of care echocardiogram may show right heart dilatation, thrombus in heart or pulmonary arteries. DVT increases the risk of developing PE. The gold standard test for the diagnosis of PE is CTPA (computerized tomographic pulmonary angiography) which also gives alternative diagnosis in the absence of PE. Therapeutic anticoagulation is the corner stone in the management of PE and commonly used anticoagulants are LMWH (low molecular weight heparin) and UFH (unfractionated heparin). Mortality in COVID-19 patients with PE is up to 43% compared to COVID patients without PE being around 3%

Iron intake and markers of iron status and risk of Barrett's esophagus and esophageal adenocarcinoma

OBJECTIVE: To investigate the association between iron intake and iron status with Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC). METHODS: 220 BE patients, 224 EAC patients, and 256 frequency-matched controls completed a lifestyle and food frequency questionnaire, and provided serum and toenail samples between 2002 and 2005. Using multiple logistic regression, odds ratios (OR) and 95% confidence intervals (95%CI) were calculated within quartiles of intake/status. RESULTS: Comparing the fourth to the first quartile, ferritin (OR 0.47; 95%CI: 0.23, 0.97) and transferrin saturation (OR 0.41; 95%CI: 0.20, 0.82) were negatively associated with BE; whilst total iron binding capacity was positively associated per 50 µg/dl increment (OR 1.47; 95%CI: 1.12, 1.92). Comparing the fourth to the first quartile, iron intake (OR 0.50; 95%CI: 0.25, 0.98), non-heme iron intake per 10 mg/day increment (OR 0.29; 95%CI: 0.08, 0.99), and toenail iron (OR 0.40; 95%CI: 0.17, 0.93) were negatively associated with EAC; whilst heme iron intake was positively associated (OR 3.11 95%CI: 1.46, 6.61). PRINCIPAL CONCLUSION: In contrast to the hypothesis that increased iron intakes and higher iron stores are a risk factor for BE and EAC, this study suggests that higher iron intakes and stores may have a protective association with BE and EAC, with the exception of what was found for heme iron intake