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)

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90

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

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

Postoperative phosphate dynamics were studied in 30 patients who underwent radical surgery for thoracic esophageal cancer and who were postoperatively nourished by total parenteral nutrition. There was a significant fall in the serum phosphate level on the 2nd and 3rd postoperative days in all patients. Postoperative hypophosphatemia was due to an increase in urinary phosphate excretion which was indicated by the fall in TRP% and TmPO4/GFR. A highly significant positive correlation was observed between the increase in urinary phosphate loss and the enhanced secretion of parathyroid hormone which was possibly triggered by surgical stress, a decrease in the serum level of calcium, the action of phosphate buffer or diuretics. All the patients except for those with postoperative pulmonary complications responded to the drop in serum phosphate by renal conservation of phosphate. A slight decrease in the serum level of phosphate was also found on the 6th postoperative day in most patients who were receiving parenteral hyperalimentation. The second fall in phosphate was due to transcellular shifts of phosphate. It is concluded that patients with postoperative pulmonary complications develop severe hypophosphatemia which should be prevented by replacement therapy with phosphate in the immediate postoperative period.
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PMID:[Postoperative hypophosphatemia in patients with cancer of the thoracic esophagus]. 846 25

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