Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235886 (leg edema)
 674 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first case of isolated thyrotropin (TSH) deficiency with Cushing's syndrome was reported. A 46-year-old female was admitted to our hospital because of fatigability, puffy eye-lids, leg edema and petechia. She was treated with thyroid hormone. A low free triiodothyronine continued. Serum TSH was undetectable and serum thyrotropin releasing hormone (TRH) was elevated. No response of serum TSH and normal response of serum prolactin after administration of exogenous TRH suggested the abnormalities of anterior pituitary gland. The secretion of growth hormone and gonadotropin were intact, but the secretion of adrenocorticotropic hormone (ACTH) was impaired. A high level of serum cortisol, no response of serum ACTH by metyrapone test and a tumor mass of abdomen detected by computed tomography led to the diagnosis of Cushing's syndrome. Histological examination of the tumor revealed adrenal adenoma. Twenty two months after the surgery, serum ACTH level was normalized, but the secretion of serum TSH to exogenous TRH was still absent. The results indicated that hypothyroidism in our patient was due to isolated TSH deficiency.
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PMID:A case of isolated thyrotropin deficiency with Cushing's syndrome. 263 42

Peripartum cardiomyopathy (PPCM) is a potentially life-threatening condition typically presenting as heart failure with reduced ejection fraction (HFrEF) in the last month of pregnancy or in the months following delivery in women without another known cause of heart failure. This updated position statement summarizes the knowledge about pathophysiological mechanisms, risk factors, clinical presentation, diagnosis and management of PPCM. As shortness of breath, fatigue and leg oedema are common in the peripartum period, a high index of suspicion is required to not miss the diagnosis. Measurement of natriuretic peptides, electrocardiography and echocardiography are recommended to promptly diagnose or exclude heart failure/PPCM. Important differential diagnoses include pulmonary embolism, myocardial infarction, hypertensive heart disease during pregnancy, and pre-existing heart disease. A genetic contribution is present in up to 20% of PPCM, in particular titin truncating variant. PPCM is associated with high morbidity and mortality, but also with a high probability of partial and often full recovery. Use of guideline-directed pharmacological therapy for HFrEF is recommended in all patients respecting contraindications during pregnancy/lactation. The oxidative stress-mediated cleavage of the hormone prolactin into a cardiotoxic fragment has been identified as a driver of PPCM pathophysiology. Pharmacological blockade of prolactin release using bromocriptine as a disease-specific therapy in addition to standard therapy for heart failure treatment has shown promising results in two clinical trials. Thresholds for devices (implantable cardioverter-defibrillators, cardiac resynchronization therapy and implanted long-term ventricular assist devices) are higher in PPCM than in other conditions because of the high rate of recovery. The important role of education and counselling around contraception and future pregnancies is emphasised.
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PMID:Pathophysiology, diagnosis and management of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Study Group on peripartum cardiomyopathy. 3124 66