Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rates of recurrent venous thromboembolism (RVTE) vary widely, and its causes still need to be elucidated. Statistical multivariate methods can be used to determine disease predictors and improve current methods for risk calculation. The objective of this study was to apply principal component analysis to a set of data containing clinical records of patients with previous venous thromboembolism and extract the main factors that predict recurrent thrombosis. Records of 39 factors including blood and lipid parameters, hereditary thrombophilia, antiphospholipid syndrome, clinical data regarding previous thrombosis and treatment, and Doppler ultrasound results were collected from 235 patients. The results showed that 13 principal components were associated with RVTE and that 18 of 39 factors are the important for the analysis. These factors include red blood cell, white blood cell, hematocrit, red cell distribution width, glucose, lipids, natural anticoagulant, creatinine, age, as well as first deep vein thrombosis data (distal/proximal, d-dimer, and time of anticoagulation). The results demonstrated that simple clinical parameters easy to be collected can be used to predict rates of recurrence and to develop new clinical decision support systems to predict the rates of RVTE.
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PMID:Principal Component Analysis on Recurrent Venous Thromboembolism. 3185 29

Risk factors for COVID-19 patients with poorer outcomes include pre-existing conditions: obesity, type 2 diabetes mellitus, cardiovascular disease (CVD), heart failure, hypertension, low oxygen saturation capacity, cancer, elevated: ferritin, C reactive protein (CRP) and D-dimer. A common denominator, hyperinsulinaemia, provides a plausible mechanism of action, underlying CVD, hypertension and strokes, all conditions typified with thrombi. The underlying science provides a theoretical management algorithm for the frontline practitioners.Vitamin D activation requires magnesium. Hyperinsulinaemia promotes: magnesium depletion via increased renal excretion, reduced intracellular levels, lowers vitamin D status via sequestration into adipocytes and hydroxylation activation inhibition. Hyperinsulinaemia mediates thrombi development via: fibrinolysis inhibition, anticoagulation production dysregulation, increasing reactive oxygen species, decreased antioxidant capacity via nicotinamide adenine dinucleotide depletion, haem oxidation and catabolism, producing carbon monoxide, increasing deep vein thrombosis risk and pulmonary emboli. Increased haem-synthesis demand upregulates carbon dioxide production, decreasing oxygen saturation capacity. Hyperinsulinaemia decreases cholesterol sulfurylation to cholesterol sulfate, as low vitamin D regulation due to magnesium depletion and/or vitamin D sequestration and/or diminished activation capacity decreases sulfotransferase enzyme SULT2B1b activity, consequently decreasing plasma membrane negative charge between red blood cells, platelets and endothelial cells, thus increasing agglutination and thrombosis.Patients with COVID-19 admitted with hyperglycaemia and/or hyperinsulinaemia should be placed on a restricted refined carbohydrate diet, with limited use of intravenous dextrose solutions. Degree/level of restriction is determined by serial testing of blood glucose, insulin and ketones. Supplemental magnesium, vitamin D and zinc should be administered. By implementing refined carbohydrate restriction, three primary risk factors, hyperinsulinaemia, hyperglycaemia and hypertension, that increase inflammation, coagulation and thrombosis risk are rapidly managed.
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PMID:Relationships between hyperinsulinaemia, magnesium, vitamin D, thrombosis and COVID-19: rationale for clinical management. 3293 58


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