RESUMO
Systemic lupus erythematosus (SLE) is an autoimmune disease that can affect multiple organ systems. Among these, the heart, including the pericardium, conduction system, myocardium, valves, and coronary arteries, can be affected. Hypertrophic cardiomyopathy (HCM) is a myocardial disease caused mainly by genetic mutation. The association between SLE and HCM is still unclear. We are reporting a case of a 25-year-old female with SLE with end-stage renal disease (ESRD) due to lupus nephritis, who was found to have hypertrophic obstructive cardiomyopathy (HOCM) on the echocardiogram and required septal myectomy. She presented to the hospital with dyspnea and was admitted as a hypertensive emergency with pulmonary edema, which required intubation and admission to the cardiac intensive care unit (CICU). She underwent urgent hemodialysis and blood pressure medication adjustment and then improved and was discharged home. Based on the literature review, 10 cases of SLE and HCM were reported, and the underlying mechanisms linking SLE and HCM remain unclear. Further studies are warranted for a better understanding of the association between SLE and HCM.
RESUMO
This report details cases of uterine fibroid-associated deep vein thrombosis leading to massive pulmonary embolism, as well as the likely associated physiology. Two women, aged 33 and 37, presented with fibroid-associated pulmonary embolism. They both had large uterine sizes and no underlying thrombophilia. Case 1 had an uncomplicated course, whereas Case 2 had a course complicated by cardiac arrest and prolonged recovery. The presence of fibroids enhances coagulation and platelet adhesion. Mechanical compression also plays a role in predisposing to thrombosis. There may be a role for preoperative screening, especially in those with an elevated estimated uterine weight.
RESUMO
Background: Hypertriglyceridemia is a common cause of acute pancreatitis (AP). This literature review compared the effectiveness and adverse events of insulin therapy, with or without heparin, and plasmapheresis, in reducing triglyceride levels in patients with hypertriglyceridemia-induced AP. Methods: Systematic reviews, meta-analyses, evidence syntheses, editorials, commentaries, protocols, abstracts, theses and preprints were excluded. Review Manager was used to conduct the meta-analysis. The literature search yielded 2765 articles, but only 5 were included in the systematic review and meta-analysis and the total number of participants in the review was 269. Results: From this study's analysis, insulin ± heparin was more successful in reducing triglyceride levels than plasmapheresis (standardized mean difference -0.37, 95% confidence interval [CI] 0.99 to 0.25; P=0.25). Insulin ± heparin therapy had a lower mortality rate than plasmapheresis (risk ratio [RR] 0.70, 95%CI 0.25-1.95). Hypotension, hypoglycemia, and acute renal failure were less common in the plasmapheresis therapy group than in insulin ± heparin therapy (RR 1.13, 95%CI 0.46-2.81, RR 3.90, 95%CI 0.45-33.78, and RR 0.48, 95%CI 0.02-13.98 for hypotension, hypoglycemia, and acute renal failure, respectively). Conclusions: This study found no significant difference in mortality between insulin ± heparin therapy and plasmapheresis used for the reduction in triglyceride levels. It is notable that no substantial differences were observed in the most common side-effects encountered during these therapies, thus indicating non-inferiority.