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)

Aluminum exposure in man is unavoidable. The occurrence of dialysis dementia, vitamin D-resistant osteomalacia, and hypochromic microcytic anemia in dialysis patients underscores the potential for aluminum toxicity. Although exposure via dialysate and hyperalimentation leads to significant tissue aluminum accumulation, the ubiquitous occurrence of aluminum and the severe pathology associated with large aluminum burdens suggest that smaller exposures via the gastrointestinal tract and lungs could represent an important, though largely unrecognized, public health problem. It is clear that some aluminum absorption occurs with the ingestion of small amounts of aluminum in the diet and medicines, and even greater aluminum absorption is seen in individuals consuming large amounts of aluminum present in antacids. Aluminum absorption is enhanced in the presence of elevated circulating parathyroid hormone. In addition, elevated PTH leads to the preferential deposition of aluminum in brain and bone. Consequently, PTH is likely to be involved in the pathogenesis of toxicities in those organs. PTH excess also seems to lead to the deposition of aluminum in the parathyroid gland. The in vitro demonstration that aluminum inhibits parathyroid hormone release is consistent with the findings of a euparathyroid state in dialysis patients with aluminum related vitamin D-resistant osteomalacia. Nevertheless, it seems likely that hyperparathyroidism is at least initially involved in the pathogenesis of aluminum neurotoxicity and osteomalacia; the increases in tissue aluminum stores are followed by suppression of parathyroid hormone release, which is required for the evolution of osteomalacia. Impaired renal function is not a prerequisite for increased tissue aluminum burdens, nor for aluminum-related organ toxicity. Consequently, it is likely that these diseases will be observed in populations other than those with chronic renal disease.
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PMID:Aluminum, parathyroid hormone, and osteomalacia. 642 72

A case of hypophosphatemia-induced hypercalcemia during post-traumatic acute renal failure is described. Proposed causes for the hypophosphatemia include changes in tissue distribution of phosphate associated with hyperalimentation and phosphate losses during hemodialysis. In the absence of hyperparathyroidism the hypercalcemia as well as changes in osteoclast morphology found on bone biopsy are ascribed to a direct effect of hypophosphatemia on bone.
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PMID:Hypophosphatemia-induced hypercalcemia during acute renal failure. 667 51

Plasma concentrations of 25 essential (EAA) and nonessential (NEAA) amino acids were measured pre- and postdialysis in 46 chronic hemodialysis therapy (CDT) patients. Sixteen of these patients with prior weight loss of 14.5 +/- 2.37 pounds in 24 months were administered a GAA solution (EAA + NEAA + glucose) for 20 weeks during each dialysis. Eight of these patients (group 1) responded with improved appetite and weight gain; the remaining eight patients (group 2) with clinically advanced metabolic bone disease continued to lose weight. Five other patients (group 14), biochemically similar to group 1 but with shorter prior dialysis experience, who received EAA (plus glucose) hyperalimentation (including oral I-histidine), experienced weight gain similar to group 1 but displayed significantly different plasma aminograms indicating a deficit of NEAA. When EAA and glucose hyperalimentation was administered without histidine (1 patient) no weight gain occurred and aminograms differed significantly from other groups. Plasma aminograms of 25 weight-stable, nonhyperalimented CDT patients were obtained for comparison. Results indicate GAA hyperalimentation can promote weight gain in catabolic CDT patients with inadequate prior nutritional intake (as in groups 1 and 14) but cannot reverse weight loss when the primary clinical setting is advanced metabolic bone disease and myopathy due to hyperparathyroidism (group 2). Hyperalimentation with glucose and an amino acid solution specifically tailored to the needs of CDT patients may improve results. Plasma phosphoethanolamine levels, normal for weight-stable and elevated in catabolic CDT patients, suggest a possible role for phosphoethanolamine as a marker for catabolism.
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PMID:Prolonged hyperalimentation in catabolic chronic dialysis therapy patients. 680 Dec 81

Hypercalcemia associated with head and neck malignancy is not an uncommon occurrence; its causes are multiple. Eight hypercalcemic patients with head and neck malignancy were studied. Serum calcium, serum phosphorus, tubular phosphorus threshold, fasting calcium excretion, plasma 1,25-dihydroxyvitamin D, nephrogenous cyclic adenosine monophosphate (AMP), and immunoreactive parathyroid hormone were measured. Excessive dietary calcium administration in the form of an oral hyperalimentation preparation appeared to be the cause of hypercalcemia in 2 patients. Six patients demonstrated humorally mediated hypercalcemia. These patients resembled patients with primary hyperparathyroidism in having elevated nephrogenous cyclic AMP excretion and reduced proximal tubular phosphorus reabsorption, but they differed from patients with primary hyperparathyroidism by having normal levels of immunoreactive parathyroid hormone, markedly increased fasting calcium excretion, and strikingly reduced mean plasma levels of 1,25-dihydroxyvitamin D. These data strongly suggest that the humoral factor responsible for hypercalcemia in patients with head and neck cancer is not parathyroid hormone, and that patients with hyperparathyroidism can now be distinguished with confidence from those with malignancy-associated hypercalcemia.
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PMID:Mechanisms of hypercalcemia in patients with head and neck cancer. 716 31

The simultaneous occurrence of hyperthyroidism and hyperparathyroidism was previously reported to be rare, but it was recognised more and more clearly by effective evaluations. Recent studies also mentioned the coexistence of parathyroid adenoma and papillary thyroid carcinoma (PTC). The potential mechanism is still unknown. We report a case of a 46-year-old man coexisted with primary hyperparathyroidism, Graves' hyperthyroidism and occult PTC. The patient had a 6-month history of polyphagia and irritability. Blood examinations showed elevated serum calcium and parathyroid hormone levels. Serum phosphate was lower. Thyroid function evaluation indicted Graves' hyperthyroidism. Ultrasound showed a solitary hyperchoic thyroid nodule in the right gland. Parathyroid radioisotope scanning found a mild enhancement of 99mTc absorption in the lower part of the right parathyroid gland. A surgical exploration was carried out and the parathyroid adenoma resection was performed. An occult micro-PTC with BRAF(V600E) mutation was also detected.
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PMID:Incidental finding of papillary thyroid carcinoma with BRAFV600E mutation in a patient with coexistent primary hyperparathyroidism and Graves' hyperthyroidism. 2487 26