The patient recovered from severe preeclampsia after resection of a hemorrhagic parathyroid adenoma and was fully rehabilitated after 3 months.
CONCLUSION: This patient exhibited a concealed hyperparathyroidism with acute hypertensive crisis, probably attributable to hemorrhagic
parathyroid adenoma. The presentation mimics acute late-onset preeclampsia and requires vigilant diagnosis followed by surgery. (Obstet Gynecol 2011;117:498-500) DOI: 10.1097/AOG.0b013e3182061fc2″
“Purpose of review Pulmonary hypertension and right ventricular failure (RVF) in left ventricular systolic dysfunction (LVSD) is associated with high morbidity and mortality. This review presents an overview of the classification, pathophysiology, natural history, clinical features, prevention and treatment of this common clinical problem with a focus on the most recent studies. Many of the current evidence-based therapeutic agents GS-9973 supplier for pulmonary hypertension in the absence of systolic or diastolic heart failure (e. g. prostaglandins, endothelin antagonists) are not efficacious in pulmonary hypertension with LVSD.
Recent findings Recent clinical evidence strongly supports an evolving role for phosphodiesterase type 5 (PDE5) inhibition in patients with pulmonary hypertension and LVSD. Chronic PDE5 inhibition
in the short to intermediate duration studies to date significantly reduces pulmonary pressures and pulmonary vascular resistance (PVR), effects reverse right ventricle and left ventricle remodeling, improves ventilator efficiency, improves peak exercise capacity and improves quality of life in selected patients with stable, moderately symptomatic FK228 order LVSD and pulmonary hypertension.
Summary Although long-term outcome studies are currently lacking, chronic PDE5 inhibition should
be considered in carefully selected LVSD patients who manifest persistent learn more significant elevation of pulmonary hypertension or PVR or uncontrolled RVF after aggressive management with all standard current evidence-based LVSD therapies (neurohormonal antagonists, diuretics and cardiac resynchronization in appropriate candidates).”
“Background: Heatstroke is generally considered as a syndrome of hyperthermia associated with systemic inflammation leading to multiorgan dysfunction. High mobility group box-1 protein (HMGB1) has recently been identified as a late mediator of systemic inflammation inducing multiorgan dysfunction. Elevation of plasma HMGB1 in heatstroke has been observed in animals, but there is no data available about its changes in heatstroke patients. The objectives of this study are to observe the time course of plasma HMGB1 changes and assess its prognostic value in patients with exertional heatstroke.
Methods: Blood samples were taken from the patients with exertional heatstroke. Plasma HMGB1 level was detected by the enzyme-linked immunosorbent assay. C-reactive protein level was measured using a fully automated IMMAGE Immunochemistry System.