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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypophosphatemia with or without phosphorus depletion can be observed in various diseases--particularly diabetic ketoacidosis, respiratory alkalosis, alcoholism, parenteral nutrition and hyperalimentation--and may cause serious neurologic, muscular, and hematologic disorders. This review summarizes the knowledges about hypophosphatemia--etiological mechanisms, pathophysiology and therapeutic modalities--and suggests that some place be reserved for serum phosphate in systematic and emergency panels of blood tests.
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PMID:[Hypophosphatemia. A review (author's transl)]. 11 83

Too often neglected, dosage of phosphatemia should yet be kept on mind. The role of phosphorus in bone mineralisation and regulation of acid-base balance is well known. Phosphorus is also an energy purveyor during numerous biologic reactions, and depp deprivation may lead to a lot of pathologic situations, sometimes severe. Mild hypophosphatemia is not rare and occurs in various clinical or therapeutic circumstances; deep hypophosphatemia is rather uncommon, occuring chiefly during hyperalimentation or realimentation of starving patients, especially alcoolics. Deep hypophosphatemia (by depletion or transfert) mainly induces clinical and pathological manifestations; they are subsequent to alterations of glucose metabolism, leading to a failure in ATP and 2,3 DPG synthesis. these metabolic events particularly explain muscular and hematological manifestations of hypophosphatemia. Phosphorus loading per os, or in severe cases intravenously corrects the biological abnormalities and improves clinical manifestations.
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PMID:[Hypophosphatemia (author's transl)]. 39 93

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.
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PMID:Hypophosphatemia and rhabdomyolysis. 74 77

Acute areflexic paralysis associated with diffuse sensory loss, cranial nerve paisies, and respiratory insufficiency occurred in two patients who developed hypophosphatemia during hyperalimentation. Prompt recovery followed replacement of serum phosphorus in both cases. An electromyogram performed on one patient revealed only decreased insertional activity. A muscle biopsy specimen from the same patient showed minor, nonspecific neurogenic changes.
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PMID:Acute areflexic paralysis. Association with hyperalimentation and hypophosphatemia. 81 Jan 19

Patient L.A. (f., 20 yrs), affected by bulimia and self-induced vomiting, was hospitalized because of severe malnutrition (BMI 13.1), hypopotassemia (2.8 mEq/l) and prolonged QTc interval (0.469"). Intensive care treatment aimed to normalize mineral balance mainly serum potassium, consisted of administering e.v. potassium (mg 2346/day), magnesium (mg 72/day), calcium (mg 80/day), phosphorus (mg 769/day), chloride (mg 710/day), iron (mg 40/day). Dietary treatment was deliberately chosen to be slightly above minimum energy requirements in order to avoid possible side effects of forced hyperalimentation. The patient, immediately after hospitalization, interrupted vomiting and 2 wks later weight increased by 5 kg (from 34.9 kg to 40.0 kg). On the other hand normalization of serum potassium levels was slow and QTc interval reached normal range only after the 10th day of treatment (0.447"). This case supports the hypothesis that major ECG abnormalities may be present in severe malnutrition due to anorexia nervosa or bulimia with self-induced vomiting. The dangers of these complications were substantiated by the fact that intensive care treatment allowed prompt body weight recovery but normalization of electrolytic balance and cardiac function was very slow. For such patients, electrocardiographic monitoring should be routine.
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PMID:[Hypopotassemia and prolongation of the Q-T interval in a patient with severe malnutrition caused by bulimia and post-prandial vomiting]. 237 4

Too often neglected, dosage of phosphatemia should yet be kept on mind. The role of phosphorus in bone mineralization and regulation of acid-base balance is well known. Phosphorus is also an energy purveyor during numerous biologic reactions, and deep deprivation may lead to a lot of pathologic situations, sometimes severe. Mild hypophosphatemia is not rare and occurs in various clinical or therapeutic circumstances; deep hypophosphatemia is rather uncommon, occuring chiefly during hyperalimentation or realimentation of starving patients, especially alcoholics. Deep hypophosphatemia (by depletion or transfer) mainly induces clinical and pathological manifestations; they are subsequent to alterations of glucose metabolism, leading to a failure in ATP and 2,3 DPG synthesis. These metabolic events particularly explain muscular and hematological manifestations of hypophosphatemia. Phosphorus loading per os, or in severe cases intravenously corrects the biological abnormalities and improves clinical manifestations.
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PMID:[Hypophysphatemia (author's transl)]. 624 3

A twenty-four year old patient showed severe hypophosphataemia after emergency surgery for colectasia. A critical study of the case isolated the factors which had favoured the development of this metabolic complication. The necessity for great care in the nutrition of emaciated patients as well as that of a phosphorus supply adapted to the metabolic status of the patient were emphasized. Frequent measurement of serum phosphate was recommended for patients undergoing intravenous hyperalimentation.
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PMID:[Severe hypophosphoremia in a patient on parenteral nutrition with phosphorus enrichment]. 642 18

Previous reports have described a syndrome of paresthesias, weakness, seizures and hypophosphatemia in patients and animals receiving intravenous hyperalimentation. In this report we describe a group of five patients who developed this syndrome while on oral caloric intake and three patients who received only modest amounts of hyperalimentation therapy. As an experimental corollary, studies were performed in starved and normal dogs with calories infused via an intragastric catheter. The serum inorganic phosphorus (Pi) fell slightly in normal animals from 4.8-2.5 mg. %. In the starved dogs with diarrhea or vomiting the Pi fell gradually from 4.8-1.6. In starved dogs without gastrointestinal symptoms the Pi fell precipitously from 3.7-1.4 mg % on the first day of infusion and remained at that level. Approximately 50% of the starved animals developed the neurological syndrome; none of the normal animals had neurological symptoms.
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PMID:Hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of hyperalimentation syndrome. 677 12

Because protein-calorie undernutrition is common in patients with neoplastic disease, nutritional support is often recommended. It is uncertain, however, that methods of supplemental alimentation successful in noncancerous subjects are suitable in cancer patients. We measured elemental balances, serum proteins, anthropometrics (triceps skinfold and mid-arm muscle area), and creatinine/height ratio in 15 undernourished patients with advanced cancer and in 10 noncancer undernourished controls during central venous or enteral hyperalimentation and found the following. (a) During central venous hyperalimentation, cancer patients showed significantly less improvement than the noncancerous controls in body weight (median increment, 5 kg in cancer patients and 8.5 kg in noncancerous), albumin (0.1 g/dl in cancer patients and 0.5 g/dl in noncancerous patients), creatinine/height ratio (4% of standard in cancer and 10% of standard in noncancer), and mid-arm muscle area (4% of standard in cancer and 11% of standard in noncancer). During enteral hyperalimentation, gains in body weight and albumin by cancer patients were significantly inferior to those in noncancerous subjects. Triceps skinfold increments, in contrast, were similar during both central venous and enteral hyperalimentation for cancer and noncancerous patients. (b) While nitrogen retention was similar in cancer and noncancer patients, the cancer group retained significantly less magnesium and phosphorus (delta Mg in cancer patients, 3.2 mEq/day central, -2.7 mEq/day enteral; delta Mg in noncancer patients, 11.9 mEq/day central, 10.1 mEq/day enteral; delta P in cancer patients, 0.13 g/day central, 0.07 g/day enteral; delta P in noncancer patients, 0.27 g/day central, 0.33 g/day enteral). The poorer balances of cancer patients were caused by increased urinary, not fecal, loss. These findings indicate a partial block in repletion of lean body mass or abnormal composition of newly deposited lean body mass when undernourished patients with advanced cancer receive hyperalimentation.
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PMID:Hyperalimentation of the cancer patient with protein-calorie undernutrition. 678 32

Copper deficiency has been described in premature infants on hyperalimentation. The bony abnormalities are generalized and are usually associated with anemia and neutropenia. These changes present with normal serum levels of iron, ascorbic acid, calcium, phosphorus, and magnesium, as well as with depressed levels of copper and ceruloplasmin. They appear at about three to nine months of age in infants with a low birth weight who are receiving total parenteral nutrition, but can be prevented by greater than normal maintenance levels of copper supplements. Established bone changes improve rapidly after the administration of therapeutic supplements.
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PMID:Skeletal changes associated with copper deficiency. 680 88


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