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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

The ischemic myocardium utilizes glycogen as metabolic substrate. The effects of oral nutrition on the levels of glycogen in the myocardium and of myocardial glycogen content on myocardial tolerance to ischemia were studied. Rats were divided into groups and fed (a) rat chow, (b) rat chow plus 5% dextrose, and elemental diets (c) Flexical (Mead Johnson) or (d) Vital (Ross Laboratories). Another group was starved. All fed groups gained weight normally while the starved rats lost 23% of their body weight. Compared with the effect on rat chow, myocardial glycogen levels were elevated in the Flexical and starvation groups, while Vital depressed the level (P less than 0.01). Thus, both caloric intake and diet affected myocardial glycogen content. Elevation of myocardial glycogen content after starvation contrasted with glycogen disappearance from the liver. The level of myocardial glycogen and left ventricular function after global ischemia were correlated in dogs under cardiopulmonary bypass conditions. During 30 minutes of normothermic aortic cross-clamping, hearts with a preischemic myocardial glycogen content greater than 0.4 g% had less asystole or ventricular fibrillation. Their left ventricular function (stroke work index, myocardial contractility) upon reperfusion was substantially better than those with a myocardial glycogen level of less than 0.4 g%. Dietary manipulation and the nutritional status can thus affect the myocardial glycogen content and may be useful in protecting the myocardium from ischemia.
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PMID:Protection of ischemic myocardium: the roles of nutrition and myocardial glycogen. 711 54

Hunger strike is described as voluntary refusal of food and/or fluids. Prolonged starvation may produce many adverse events including even death in rare circumstances. Here, we present three fatal cases (all males, 25-38 years) died from hunger strike. In all corpses, obvious muscle wasting with reduced subcutaneous and internal fat deposits, and atrophy in some organs were demonstrated at autopsy. The extraordinary long starvation period before death could presumably be linked to the thiamine uptake in this period, which had been discontinued by all subjects before the death occurred. Prolonged caloric deficiency with subsequent complications such as multiple organ failure, severe sepsis and ventricular fibrillation could account as major causes of death in these subjects. The competence of the physicians working with hunger strikers about the processes and potential problems is of great importance since they have to acknowledge about them to their patients.
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PMID:Deaths due to hunger strike: post-mortem findings. 1548 19