Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

PMS is probably a group of entities which include various symptoms that occur during the 7 to 10 days before menstruation and disappear a few hours after the onset of menstruation. The definition of PMS lacks objective criteria. The most common symptoms are irritability, bloating, aggressiveness, mastodynia, and headaches. The prevalence of PMS is estimated at 30 to 40 per cent. PMS is more prevalent among women working outside the home, alcoholics, women of high parity, and women with toxemic tendency; it probably runs in families. The etiology of PMS is no less obscure to us than when it was first described by Frank in 1931. No single theory has been established to explain the entire diversity of PMS symptomatology. The multitude of possible etiologic factors includes psychosocial bases, progesterone deficiency, prolactin excess, thyroid hypofunction, renin angiotensin alternations, antidiuretic hormone excess, decreased colloidosmotic pressure, endorphin activity alternations, serotonin metabolism alternations, prostaglandin action, vitamin deficiency, and such unconventional theories as the ovarian infection or the "yeast overgrowth" theory. A partial resolution of this divergence of hypotheses comes from the biopsychosocial model developed by Keye and Trunnel. According to this model, a biologic, perhaps genetically determined, predisposition to PMS is realized when past and present life experiences, attitudes, beliefs, coping styles, and social forces interact to stress a woman. The diagnosis of PMS is based on establishing a relationship between the luteal phase of the cycle and the symptoms. The evaluation of PMS patients includes the use of a monthly diary to scale the symptoms, a physical examination, and biochemical studies to rule out other disorders. Management includes education, reassurance, and drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The premenstrual syndrome. 218 58

Half a century after the elucidation of its molecular structure, aldosterone is generating the greatest interest, not in the fields of endocrinology or renal medicine but in cardiology-where aldosterone over-activation is now perceived as detrimental in heart failure (HF) and ischaemic heart disease. Clinically, excess aldosterone is associated with higher morbidity and mortality after myocardial infarction (MI) and HF. The Randomised Aldactone Evaluation Study (RALES) study in severe chronic heart failure and the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival (EPHESUS) study in post-MI heart failure have shown that use of non-selective and selective aldosterone receptor antagonists, respectively, improves prognosis. The pathophysiological mechanisms underpinning these damaging aldosterone-mediated cardiovascular effects are still being elucidated, but prime candidates include cardiomyocyte necrosis and apoptosis, and myocardial fibrosis resulting in adverse cardiac remodelling, coronary vasculopathy, tachyarrhythmia and positive feedback activation of the renin-angiotensin-aldosterone system. Practical points for consideration when instigating therapy include preferential use of aldosterone receptor antagonists to maintain electrolyte balance whenever loop or thiazide diuretics are used (vulnerable HF patients require higher ranges of potassium and magnesium to minimise propensity for tachyarrthythmia), for renoprotection and for counteracting aldosterone breakthrough despite adequate ACE inhibition; use of the minimum doses of loop diuretics required to lessen activation of the renin-angiotensin-aldosterone system in HF; use of selective aldosterone receptor antagonists to avoid gynaecomastia/mastalgia and impotence; and prophylactic use of aldosterone receptor antagonists to improve prognosis.
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PMID:Fiftieth anniversary of aldosterone: from discovery to cardiovascular therapy. 1531 May 30