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

The first scientific understandings on the value of nutrition and the assimilation of food, in the Greek language "metabole" (metabolism), are published in the Corpus Hippocraticum. But the conception of metabolism was introduced in scientific literature not earlier than 1839 by Theodor Schwann (1810-1882) and 1842 by Justus von Liebig (1803-1873). The antique ideas were completed in the 17th century by the theory of ferments, introduced by the iatro-chemist Johann Baptist van Helmont (1577-1644), and the Italian priest Lazzaro Spallanzani (1729-1799) could proof the existence of such processes in the living organism by animal experiments in 1776. Then Schwann could discover in the gastric juice a substance in 1835 which he called "pepsin". In the time of the voyages of discovery new, not yet known malnutritions on the ships were known as scurvy, beriberi and in the northern countries rickets. Then it became clear that not only the three groups of food, but also supplementary materials, known in 1912 as vitamines by Casimir Funk (1884-1967), could develop determined effects. The starvation in the first and the second world war showed clearly, that deterioration of food supply diminished the condition of immunity. Failed food experiments with gelatin, synthetically produced citric acid and the discussions of malnutrition diseases, based on a deficiency of zinc, of toddlers, are discussed as the malnutrition illness kwashiorkor in the third world. In conclusion a citation of the famous American physiologist Graham Lusk (1866-1932) is mentioned from the year 1906, who praised the scientific priority of the German medical research.
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PMID:[Nutrition and individual defense--historical considerations]. 205 90

Technological advances in the intensive care of low birth weight (LBW) infants have resulted in major increases in their survival. New challenges in meeting their nutritional needs have emerged. Very low birth (VLBW) weight infants have very little body fat or glycogen reserves at birth, making them susceptible to starvation. If fed enterally, they require at least 120 calories/kg per day for growth. Numerous immaturities in the gastrointestinal tract and liver limit protein digestion, absorption, and metabolism. Several amino acids not considered essential to the older child or adult are essential to the VLBW infant. Supplying a high protein load with an inappropriate amino acid composition may lead to metabolic imbalances. The digestion and absorption of fats differs from the older child or adult. Lingual and gastric lipases are important, and the lack of bile acids limits fat absorption. Lipoprotein lipase deficiency causes problems when too much fat or fat of incorrect composition is provided. There are controversies regarding the most appropriate carbohydrate source, but research shows that lactose remains an important carbohydrate source for most of these infants. Calcium, magnesium, and phosphorus requirements pose questions in both enterally and parenterally nourished infants. Studies of iron usage suggest that VLBW infants fed either human milk or formula should receive iron supplements. Vitamin E may be helpful in preventing oxygen toxicity. Vitamin D deficiency contributes to bone demineralization and rickets. Controversy exists regarding the correlation between vitamin A nutrition and development of chronic lung disease. Guidelines have been developed for recommended intakes, but much needs to be learned to provide a sound scientific basis upon which to provide optimal nourishment for the high risk, LBW infant.
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PMID:Scientifically-based strategies for nutrition of the high-risk low birth weight infant. 212 45

Oral administration of manganese to young rats results in poorly mineralized primary spongiosa and an irregularly thickened growth plate with a histologic resemblance to that in vitamin D-deficiency rickets. In the present study, the rachitic lesions were characterized by stereologic methods at the light microscopic level. With increasing doses of Mn in the diet, the animals developed rachitic lesions of increasing severity, i.e., the total height of the growth plate and the relative volume of the hypertrophic zone increased. The experimental animals developed hypophosphatemia, which was dependent on the Mn dose. The observed serum concentrations of Mn and phosphorus are compatible with the idea that MnHPO4 is precipitated in the gut, leaving only small amounts of Mn and phosphate available for absorption. Furthermore, the severity of the rachitic lesions were inversely correlated to the concentration of phosphate in serum. The most important pathomechanism in Mn rickets is phosphate depletion, which per se causes similar rachitic changes, even though Mn also seems to have other effects. Starvation caused a decrease in the height of the growth plate and in the volume fraction of the hypertrophic zone, thus changes contrary to the rachitic lesions.
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PMID:The effect of manganese ingestion, phosphate depletion, and starvation on the morphology of the epiphyseal growth plate. A stereologic study. 401 42

The purpose of this paper is to review clinical studies on hypophosphatemia in pediatric intensive care unit patients with a view to verifying prevalence and risk factors associated with this disorder. We searched the computerized bibliographic databases Medline, Embase, Cochrane Library, and LILACS to identify eligible studies. Search terms included critically ill, pediatric intensive care, trauma, sepsis, infectious diseases, malnutrition, inflammatory response, surgery, starvation, respiratory failure, diuretic, steroid, antiacid therapy, mechanical ventilation. The search period covered those clinical trials published from January 1990 to January 2004. Studies concerning endocrinological disorders, genetic syndromes, rickets, renal diseases, anorexia nervosa, alcohol abuse, and prematurity were not included in this review. Out of 27 studies retrieved, only 8 involved pediatric patients, and most of these were case reports. One clinical trial and one retrospective study were identified. The prevalence of hypophosphatemia exceeded 50%. The commonly associated factors in most patients with hypophosphatemia were refeeding syndrome, malnutrition, sepsis, trauma, and diuretic and steroid therapy. Given the high prevalence, clinical manifestations, and multiple risk factors, the early identification of this disorder in critically ill children is crucial for adequate replacement therapy and also to avoid complications.
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PMID:Hypophosphatemia in critically ill children. 1554 5

THE FOLLOWING INFERENCES MAY BE MADE FROM THE FOREGOING STUDY: 1. The lesions resulting from fat starvation, at least in the case of pigs, do not resemble or even suggest those of rickets. 2. Prolonged fat starvation leads to the entire disappearance of fat from the adipose tissues. The form of fat atrophy observed as the result of experimental fat starvation corresponds to the serous fat atrophy described by Flemming, and is essentially the same type of fat atrophy as that found in the epicardial and perirenal fat in the human subject as the result of wasting disease. 3. The. lecithins of the brain and the fat of the liver are not materially reduced by fat starvation. 4. Fat starvation does not lead to advanced serous fat atrophy of the subcutaneous fat if the animal be given a large excess of carbohydrate food or a considerable excess of the carbohydrate and proteid constituents of milk. 5. Fat starvation causes a very imperfect absorption of the salts of P(2)O(5) from the intestine.
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PMID:AN EXPERIMENTAL STUDY OF FAT STARVATION WITH ESPECIAL REFERENCE TO THE PRODUCTION OF SEROUS ATROPHY OF FAT. 1986 73

Hypophosphatemia can be acute or chronic. Acute hypophosphatemia with phosphate depletion is common in the hospital setting and results in significant morbidity and mortality. Chronic hypophosphatemia, often associated with genetic or acquired renal phosphate-wasting disorders, usually produces abnormal growth and rickets in children and osteomalacia in adults. Acute hypophosphatemia may be mild (phosphorus level, 2-2.5 mg/dL), moderate (1-1.9 mg/dL), or severe (<1 mg/dL) and commonly occurs in clinical settings such as refeeding, alcoholism, diabetic ketoacidosis, malnutrition/starvation, and after surgery (particularly after partial hepatectomy) and in the intensive care unit. Phosphate replacement can be given either orally, intravenously, intradialytically, or in total parenteral nutrition solutions. The rate and amount of replacement are empirically determined, and several algorithms are available. Treatment is tailored to symptoms, severity, anticipated duration of illness, and presence of comorbid conditions, such as kidney failure, volume overload, hypo- or hypercalcemia, hypo- or hyperkalemia, and acid-base status. Mild/moderate acute hypophosphatemia usually can be corrected with increased dietary phosphate or oral supplementation, but intravenous replacement generally is needed when significant comorbid conditions or severe hypophosphatemia with phosphate depletion exist. In chronic hypophosphatemia, standard treatment includes oral phosphate supplementation and active vitamin D. Future treatment for specific disorders associated with chronic hypophosphatemia may include cinacalcet, calcitonin, or dypyrimadole.
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PMID:Approach to treatment of hypophosphatemia. 2286 86