Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phosphate depletion occurring during total parenteral nutrition has been frequently reported during the part 4 years. Hypophosphatemia may be associated with confusion, hyperventilation, and neuromuscular irritability, suggesting a total body phosphate deficiency. If inorganic phosphate levels fall below 1.0 mg %, diminished red cell glycolysis occurs with low erythrocyte levels of 2,3 diphosphoglycerate and adenosine triphosphate. Lowered red cell organic phosphates are associated with increased hemoglobin oxygen affinity. If severe hypophosphatemia occurs, hemolytic anemia, which is correctible by phosphate infusion, may result. In addition, leucocyte function is impaired by low levels of serum inorganic phosphate. While recognized as a needed additive, recommended phosphate supplements vary. Different infusion regimens have been suggested over the past 4 years, based primarily on assumed daily requirements. In the 19 trauma patients described who received hyperalimentation as part of their treatment, phosphate administration was calculated retrospectively and prospectively as a function of non-protein calories infused. Four different groups were studied. Group A received no phosphate additive and quickly became severely hypophosphatemic. Group B received from one to 15 meg of potassium acid phosphate per 1,000 K cal and developed a more gradual lowering of serum inorganic phosphate levels. Group C received 15 to 25 meg of potassium acid phosphate per 1,000 K cal and maintained normal phosphate levels throughout the course of treatment. Group D received greater than 25 meq of potassium acid phosphate per 1,000 K cal and gradually increased their serum inorganic phosphate levels. A significant positive correlation was found between serum inorganic phosphate levels, 2,3 diphosphoglycerate levels, adenosine triphosphate levels, and P50 of the oxy-hemoglobin dissociation curve. No patients developed hemolytic or neuromuscular syndromes which were attributable to hypophosphatemia. This study describes a simple method for the maintenance of adequate phosphate levels in patients whose dextrose-protein solutions may vary from day to day, by relating it to non-protein calories. Provision of 20 to 25 meq of potassium dihydrogen phosphate per 1,000 K cal will maintain normal serum levels of inorganic phosphate during total parenteral nutrition.
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PMID:Phosphate depletion and repletion: relation to parenteral nutrition and oxygen transport. 81 Nov 82

A 69-year-old woman was admitted with apoplexy after operation of mitral valve stenosis and gastrectomy due to a gastric ulcer. In June 1994, her condition gradually worsened after acute pneumoniae in her right lung. Intravenous hyperalimentation with cimetidine administration was started to improve her undernourishment, because she had a history of gastric ulcer. However, after 10 days from the start of cimetidine therapy, anemia progressed rapidly. Biochemical examinations revealed that the serum indirect bilirubin and LDH levels were elevated and no serum haptoglobin was detected. These results indicated the development of hemolytic anemia, but at that time we could not clarify the reason. In October 1994, thrombocytopenia gradually progressed, and we halted the administration of cimetidine to ranitidine. Both hemolytic anemia and thrombocytopenia was dramatically improved after cessation of cimetidine administration. We then changed the drug from cimetidine, however the same phenomena have appeared again. The patient was in stable condition, after cessation of H2-blockers administration. The complication of hemolytic anemia and thrombocytopenia associated with H2-blocker administration in Japan.
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PMID:[Hemolytic anemia and thrombocytopenia induced by cimetidine: recurrence with ranitidine administration]. 905 66