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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 50% small bowel bypass was performed in diabetic rats (streptozotocin-treated) and in normal rats. Normal rats and diabetic rats were used as controls. Values of fasting blood glucose and oral glucose tolerance test showed a normalization and the disappearance of glycosuria, polyuria, polydipsia and hyperphagia in diabetic rats after surgery. Mean loss of weight 3 months after surgery was 9.1% in normal bypassed rats and 60.5% in the diabetic controls. After an initial postoperative weight loss of 33.4%, the diabetic bypassed rats gained subsequently their previous weight plus an increase of 7.2%. Improvement in carbohydrate metabolism appears to be independent of loss of weight and decrease in food intake in lean diabetic rats. Amelioration of diabetes after jejunoileal bypass is the result of several metabolic consequences, particularly the malabsorption of carbohydrates, fats and amino acids.
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PMID:Observations on the metabolic effects of partial jejunoileal bypass in streptozotocin-treated rats. 397 2

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
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PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44

Diencephalic syndrome (DS) is a complex of signs and symptoms related to hypothalamic dysfunction. Its main features are emaciation despite normal energy intake and an alert appearance. This syndrome has been described in association with space-occupying lesions of the hypothalamic-optic chiasm region, mainly low-grade glioma, and less often with tumors in the proximity of the IV ventricle. Two patients with DS are reported. The first patient was an 8-month old boy with classical features of DS. Extensive investigation of malabsorption revealed no abnormalities and the first neurologic sign was a rotatory nystagmus. Magnetic resonance imaging (MRI) showed evidence of a hypothalamic tumor, which was identified after surgical resection as a pilocytic astrocytoma. The second patient was an adolescent boy who presented a 20-kg weight loss over a 6-month period and psychological disturbances. Gastrointestinal disease was ruled out as a cause of malnutrition. Because of a polydipsia-polyuria syndrome, manifest while the patient was hospitalized with a suspected diagnosis of anorexia nervosa, MRI of the brain was performed. Multiple intracranial lesions were revealed, mainly in the hypothalamus, and were identified as a disseminated disgerminoma. No neurologic signs or symptoms were present. The patients died 2 years and 1 year after diagnosis, respectively. Although DS is rare, it should be considered in severe failure to thrive or emaciation despite adequate food intake and normal absorptive function of the small bowel.
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PMID:[Diencephalic syndrome: An uncommon cause of malnutrition]. 1204 23

Hyperparathyroidism is a disease characterized by hypercalcemia with hypophosphoremia resulting from increased secretion of parathyroid hormone (PTH). The disease may be divided into 3 forms: a) primary, b) secondary, c) tertiary (secondary refractory form). Primary hyperparathyroidism is rare in children; hyperplasia is more frequent during the early years of life (neonates and infants) and is difficult to distinguish from adenoma in children. The disease may be asymptomatic; elevated calcemia levels (>12 <13.5 mg/dl) are accompanied by anorexia, asthenia and persistent stipsis; severely elevated concentrations (>13.5 mg/dl) are accompanied by nausea, vomiting, polyuria due to osmosis, with dehydration and progressive onset of lethargy, stupor and coma. Osteopenia or osteitis fibrosa cystica may be present due to augmented bone resorption. Height and weight increases are altered due to anorexia and dehydration. Differential diagnosis includes iatrogenic causes of hypercalcemia (excessive vitamin D intake, prolonged immobilization, etc.) and idiopathic familial hypercalcemia. Emergency treatment is required in cases of extremely elevated hypercalcemia (Ca >13.5-14 mg/dl), due to risk of injury to the heart, the central nervous system, the gastrointestinal tract and the kidneys. The 4 cardinal points of treatment are: hydration, calciuresis, inhibition of bone calcium resorption, treatment of the cause underlying hyperparathyroidism. Secondary hyperparathyroidism is found in cases where chronic hypocalcemia is present, particularly in chronic renal failure, untreated deficiency rickets, chronic intestinal malabsorption, hepatobiliary disease, types I and II vitamin D-dependent rickets, tubular acidosis or Fanconi's syndrome. The tertiary form is distinguished by the autonomous nature of the parathyroid glands which have become hypertrophic/hyperplastic due to uncontrollable, chronic severe renal failure. It can also be of iatrogenic origin due to excessive intake of inorganic phosphates in familial hypophosphatemic rickets or chronic vitamin D deficiency.
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PMID:Hyperparathyroidism. 1524 24