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

Progressive deterioration of the failing heart is now recognized to be a major cause of disability and death in patients with congestive heart failure. It appears that although the normal human heart functions for at least 90-100 years, overload-induced hypertrophy shortens the heart's life span to about 5 years. This accelerated deterioration of the failing heart can be viewed as a cardiomyopathy of overload in which chronic overloading causes changes in the myocardial cells that, while increasing cell mass, reduce their long-term viability. Although the pathogenesis of this putative cardiomyopathy remains poorly understood, chronic energy starvation and altered myocardial cell growth and composition appear to be contributing factors. Preferential expression of fetal isoforms of key muscle proteins, which accompanies accelerated growth of the overloaded heart, may contribute to this cardiomyopathy. The hypothesis that the cardiomyopathy of overload is due in part to a growth abnormality is supported by evidence that deterioration of the failing heart is slowed by the converting enzyme inhibitors, which may attenuate important effects of angiotensin II to stimulate cellular growth.
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PMID:The cardiomyopathy of overload: a hypothesis. 172 47

It is well known that changes in serum potassium cause ventricular arrhythmias as a result of clearly documented changes in the electrophysiological characteristics of single fibers. Hypopotassemia induced by thiazide and loop diuretics may contribute to the incidence of sudden cardiac death in patients with hypertension and those with congestive heart failure. In addition, hypopotassemia appears to be an independent risk factor for lethal ventricular arrhythmias occurring in the setting of acute myocardial infarction and contributes significantly to arrhythmias associated with starvation and alcoholism. The increase in myocardial extracellular potassium that occurs in the ischemic zone after coronary occlusion is clearly a major factor in the genesis of lethal ventricular arrhythmias that occur in this setting. A decrease in serum magnesium is also believed to be arrhythmogenic, and magnesium depletion is thought to play a role in many of the arrhythmias associated with hypopotassemia. Moreover, the administration of magnesium salts may be effective in the management of life-threatening ventricular arrhythmias. However, definite evidence establishing a causal relation between ventricular arrhythmias and hypomagnesemia or intracellular magnesium depletion is lacking. Changes in intracellular calcium contribute to the arrhythmias associated with acute ischemia and with reperfusion and may be important in the genesis of ventricular tachycardia induced by exercise and by digitalis. Thus, electrolyte and metabolic abnormalities clearly underlie lethal ventricular arrhythmias in a wide variety of clinical situations and should be routinely considered as potential etiologic factors in patients with life-threatening ventricular arrhythmias, particularly those with hypertension and congestive heart failure who are receiving thiazide and loop diuretics.
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PMID:Electrolyte abnormalities underlying lethal and ventricular arrhythmias. 172 8

Long-term overloading of the heart gives rise to myocardial abnormalities that play an important role in determining prognosis in patients with congestive cardiac failure. This myocardial response, which can be viewed as a cardiomyopathy of overload, results in part from energy-starvation and altered gene expression in the chronically overloaded heart. The role of vasodilator therapy in reducing symptoms and prolonging life in these patients may be due in part to reduced cardiac energy expenditure; however, the beneficial effects of some vasodilators, notably the converting enzyme inhibitors, may be due to additional effects on the cells of the hypertrophied, failing heart. Improved therapeutic strategies to slow myocardial deterioration in patients with congestive cardiac failure can be expected to come from new knowledge of the pathophysiology, biochemistry and molecular biology of the failing heart.
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PMID:The heart in congestive failure. 215 11

The internist plays a critical role in the care of eating disorder patients, especially in the management of the life-threatening medical complications of these conditions. In anorexia nervosa, the immediate danger is related to the effects of voluntary starvation, including hypophosphatemia, bone marrow failure, cardiac decompensation, and shock. Patients with bulimia nervosa more often experience severe fluid and electrolyte abnormalities resulting in hypovolemia, secondary hyperaldosteronism, depletion of total body potassium, and cardiac arrhythmias. Immediate management of medical complication and correction of nutritional deficits are necessary before patients can benefit from psychotherapy. The need for continued involvement of the internist in the ongoing care of the eating disorder patient is stressed. The high mortality and the likelihood of chronicity without early intervention underscore the need for early recognition and skilled management of eating disorders.
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PMID:Medical complications of anorexia nervosa and bulimia nervosa. 220 58

Anorexia nervosa is a common psychiatric disorder predominantly affecting young women, associated with significant morbidity and mortality, much involving the cardiovascular system. In contrast, protein-calorie malnutrition, while not strictly analogous to the protein-sparing characteristics often noted in anorexia nervosa, is a problem of global stature. Physiologic consequences of anorexia nervosa include rhythm disturbances, mitral valve prolapse, plus both systolic and diastolic ventricular dysfunction. Diminished exercise capacity occurs in both states, with marked blunting of the heart rate and blood pressure response. Congestive heart failure may appear, especially during refeeding. In addition to the myofibrillar destruction associated with protein-calorie malnutrition, hypophosphatemia, particularly when exacerbated by unrestricted glucose-rich refeedings or hyperalimentation, may be one additional cause of ventricular dysfunction. A high level of suspicion for cardiovascular complications is, therefore, warranted in the evaluation and therapy of weight loss conditions such as starvation and anorexia nervosa.
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PMID:Weight loss and the heart. Effects of anorexia nervosa and starvation. 265 Jun 47

A patient with acute myelogenous leukemia developed severe hypophosphatemia manifesting by extreme weakness, confusion, loss of sphincter control, nuchal rigidity, hyperesthesia, hemolysis, congestive heart failure and liver dysfunction. The possible causes for this condition were starvation, parenteral glucose and saline administration, sepsis, hypokalemia and treatment with acetazolamide. A dramatic improvement was noted following phosphate administration.
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PMID:Life-threatening hypophosphatemia in a patient with acute myelogenous leukemia. 677 68

Weight loss is a frequent sequela in patients with congestive heart failure and is commonly referred to as cardiac cachexia. This weight loss is unlike that seen in simple starvation because it preferentially involves the depletion of lean body mass. In addition, the presence of cardiac cachexia can have profound clinical implications for patients in terms of complications, clinical outcome, and overall cost. The mechanism for the alterations in body composition is multifactorial, but a major cause may be the cytokine-mediated host response to the underlying disease. This article reviews the syndrome of cardiac cachexia in light of recent evidence regarding the role of cytokines, as well as potential therapies.
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PMID:The nutrition implications of cardiac cachexia. 781 51

The improved cardiac function in patients with congestive heart failure treated with coenzyme Q10 supports the hypothesis that this condition is characterized by mitochondrial dysfunction and energy starvation, so that it may be ameliorated by coenzyme Q10 supplementation. However, the main clinical problems in patients with congestive heart failure are the frequent need of hospitalization and the high incidence of life-threatening arrhythmias, pulmonary edema, and other serious complications. Thus, we studied the influence of coenzyme Q10 long-term treatment on these events in patients with chronic congestive heart failure (New York Heart Association functional class III and IV) receiving conventional treatment for heart failure. They were randomly assigned to receive either placebo (n = 322, mean age 67 years, range 30-88 years) or coenzyme Q10 (n = 319, mean age 67 years, range 26-89 years) at the dosage of 2 mg/kg per day in a 1-year double-blind trial. The number of patients who required hospitalization for worsening heart failure was smaller in the coenzyme Q10 treated group (n = 73) than in the control group (n = 118, P < 0.001). Similarly, the episodes of pulmonary edema or cardiac asthma were reduced in the control group (20 versus 51 and 97 versus 198, respectively; both P < 0.001) as compared to the placebo group. Our results demonstrate that the addition of coenzyme Q10 to conventional therapy significantly reduces hospitalization for worsening of heart failure and the incidence of serious complications in patients with chronic congestive heart failure.
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PMID:Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study. 824 97

Nutritionists, including those involved in famine relief, have learned in the last 25 years that certain deficiency diseases arise from the high protein foods used to rehabilitate starving populations. Other, sometimes inappropriate relief foods starving populations. Other, sometimes inappropriate relief foods include unprocessed or inappropriate grains and unfortified dry skimmed milk. Yet, relief workers do not always receive the most appropriate food for distribution to certain populations. Millions of dollars are appropriated to protect relief supplies for starving people in Somalia, but money is not spent to develop and evaluate simple foods that might save the lives of starving people. There are several items relief agencies and governments should consider when deciding on the most appropriate foods to prevent starvation in famine situations. During kwashiorkor, intestinal mucous produce grossly defective cells, resulting in considerable lactose malabsorption. Thus, using milk to rehabilitate people, especially children, poses a considerable hazard. High carbohydrate diets to rehabilitate starving people can cause gross edema and fatal congestive heart failure. Generally, clinically apparent vitamin or mineral deficiencies do not occur during famines, because the amount of vitamins or minerals needed to small to maintain a very shrunken body. Yet, when the body demand increases as a result of a rehabilitation diet poor in vitamins and minerals but high in protein or calories, clinical deficiency symptoms emerge, e.g., pellagra in Mozambique. Common food combinations used in relief situations consists of corn, soy, and milk fortified with vitamins and minerals (Bal'ahar mixture, India). Both mixtures require the addition of vegetable oils to make it easier for infants and small children to digest the mixtures.
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PMID:Starvation in the modern world. 845 Aug 73

The effect of high molecular weight water-soluble chitosan (WSC) on serum starvation-induced apoptosis in human astrocytes (CCF-STTG1 Cells) was investigated. WSC, having an average molecular weight of 300 kDa and a degree of deacetylation over 90%, can be produced using a simple multi-step membrane separation process. Serum starvation led to growth arrest, rounding up of cells and appearance of p53 bands. Prolonged (48 h) incubation in serum starved medium led to cell detachment and death. WSC significantly protected the serum starvation-induced cellular rounding up and protected the serum starvation-induced cell death as tested by flow cytometry. WSC also protected serum starvation-induced p53 activation as determined by Western blot. These results suggest that WSC may prevent serum starvation-induced apoptosis of CCF-STTG1 cells via p53 inactivation.
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PMID:High molecular weight water-soluble chitosan protects against apoptosis induced by serum starvation in human astrocytes. 1198 7


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