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)

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

Two acute quadriplegic adolescent boys with hypercalcemia had large increases in urine calcium during calcium-free, or nearly free, intravenous hyperalimentation. The calcium which spilled in the urine proved to be of endogenous origin since it was accompanied by proportional amounts of hydroxyproline. To limit the endogenous bone losses during hyperalimentation, it is recommended that calcium in an amount equal to that loss be added to the perfusate so that only exogenous calcium is spilled in the urine.
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PMID:Increased urine calcium during hyperalimentation in quadriplegia: report of 2 cases. 678 13

During the course of hospitalization for comprehensive rehabilitation, a 14-year-old boy with C4 spinal cord injury and hypercalcemia was treated with 5 different treatment regimens which were instituted to reduce the hypercalcemia and associated complications. These regimens included low calcium diet, steroids, oral phosphates, intravenous saline, diuretics, hyperalimentation, calcitonin and spironolactone in various combinations, and mobilization. Careful metabolic monitoring carried out throughout hospitalization permitted the evaluation in retrospect of the impact of each treatment regimen, and, to a lesser extent, the impact of their individual components. Among all the therapeutic modalities, the most effective variables in reducing hypercalcemia in this patient were mobilization in the form of wheelchair sitting for long-term effects, and saline, furosemide, and calcitonin for short-term effects.
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PMID:Spinal cord injury hypercalcemia: therapeutic profile. 680 36

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

A 55-year-old patient with hypercalcemic crisis due to gastric carcinoma with bone marrow metastasis was treated with bisphosphonate (pamidronate) and calcitonin. Urinary excretion of parathyroid hormone-related protein (PTHrP) was increased. When normocalcemia had been attained, intravenous hyperalimentation was started, in which 1,000 U vitamin D2 was inadvertently supplemented on days 5-18, On days 15-18, hypercalcemia rapidly recurred, accompanied by markedly increased serum levels of 25-OHD2 (9.1 ng/dl) and 1,25-(OH)2D2 (161 pg/ml). This clinical course suggests that PTHrP, like PTH, stimulated 1 alpha-hydroxylase activity and produced excessive 1,25-(OH)2D2. Vitamin D should not be administered to patients with malignancy-associated hypercalcemia, particularly that due to PTHrP-producing tumors.
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PMID:Increased 1,25-(OH)2D2 concentration in a patient with malignancy-associated hypercalcemia receiving intravenous hyperalimentation inadvertently supplemented with vitamin D2. 801 94

A 76-year-old female patient who had been taking vitamin D2 100,000 U/day for more than 14 years due to hypoparathyroidism following total throidectomy was admitted because of protracted hypercalcemia. On admission, the levels of serum vitamin D2 (99.8 ng/ml) and 25-OHD2 (356 ng/ml) were very high, and 1,25-(OH)2D2 was low (4.0-18.7 pg/ml). Serum D3' 25-OHD3 and 1,25-(OH)2D3 were below the normal range. Despite intensive hydration with saline, intravenous hyperalimentation with phosphate- and calcium-free nutrients, and administration of glucocorticoid and calcitonin, the hypercalcemia persisted, accompanied by hypoproteinemia, edema, pleural effusion and congestive heart failure. The serum D2 and 25-OHD2 concentrations remained high and were accompanied by a gradual increase in 1,25-(OH)2D2 (121 pg/ml), which further increased after the administration of bisphosphonate (pamidronate) to 183 pg/ml. Seventeen months later, serum calcium and 1,25-(OH)2D2 were normalized but serum D2 and 25-OHD2 remained high. The serum 24,25-(OH)2D2/25-OHD2 ratio was relatively constant throughout her clinical course, whereas the low serum 1,25-(OH)2D2/25-OHD2 ratio at admission gradually increased during admission, suggesting that the increase in serum 1,25-(OH)2D2 is due to increased production rather than decreased degradation. The administration of pamidronate further increased serum 1,25-(OH)2D2. These features of the clinical course demonstrate that the 1,25-dihydroxyvitamin D concentration in hypercalcemic patients with protracted vitamin D intoxication may be decreased, normal or increased. Possible factors responsible for a protracted increase in serum 1,25-(OH)2D2 are body weight loss, hypoproteinemia, and phosphate depletion. In addition, some bisphosphonates would certainly promote PTH-independent production of 1,25-(OH)2D2.
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PMID:Progressively increased serum 1,25-dihydroxyvitamin D2 concentration in a hypoparathyroid patient with protracted hypercalcemia due to vitamin D2 intoxication. 852 47

To investigate the safety of rapid infusion of alendronate, we used alendronate therapy for 11 breast cancer patients with bone metastasis. Of the 11 patients, only 1 had hypercalcemia and the remaining 10 normocalcemia. Rapid infusion of alendronate consisted of an administration of alendronate 10 mg diluted in 100 ml saline in 30 minutes, and was repeated every two weeks. Each patient underwent 1 to 9 alendronate treatments. During alendronate therapy, only one patient complained of general fatigue, and the remaining 10 showed no alendronate-induced clinical symptoms. Rapid infusion of alendronate caused an increase in BUN level in two patients receiving intravenous hyperalimentation (IVH), a mild increase of GOT level in one, and a decrease of serum phosphorus level in two receiving IVH. However, no increase was found in serum creatinine and GOT levels. In addition, no patients showed alendronate-induced hypocalcemia. In conclusion, rapid infusion of alendronate brings about no major adverse effects, and makes it easier for many patients with bone metastasis to receive alendronate therapy on an outpatient basis.
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PMID:[A study of the safety of rapid infusion of alendronate]. 1006 98

A 9-year-old, spayed female domestic shorthair cat presented for polyphagia, polydipsia, and polyuria following chronic methylprednisolone acetate therapy for pruritus. Initial diagnostics were consistent with uncomplicated diabetes mellitus. Serum calcium was within reference range. Within 12 hours the cat developed depression, anorexia, vomiting, and severe dehydration. Laboratory analysis indicated marked hypercalcemia as measured by both ionized and total calcium concentration. No underlying neoplastic or inflammatory process was identified. An adrenocorticotropic hormone stimulation test was indicative of adrenocortical insufficiency. The hypercalcemia resolved with glucocorticoid supplementation and correction of the dehydration. The diabetes mellitus and adrenal insufficiency both resolved within 9 weeks.
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PMID:Hypercalcemia due to latrogenic secondary hypoadrenocorticism and diabetes mellitus in a cat. 1180 13

From point of view of physiology, the metabolic syndrome is a syndrome of overeating when an optimal by the content of fatty acids in food is too much a physologically. This condition forms an omental variant of increase of body mass. The oleic triglycerides cumulate in fatty cells of omentum and after activation of lypolisis at the level of paracrinically regulating associations of cells and organs release into blood many non-etherifying fatty acids. The albumin has no possibilities to bind them all. The polar fatty acids-free fatty acids which are not bind by albumin form in blood direct heterogeneous micelles which spontaneously incorporate into plasmatic membrane of monolayer of endothelium. At that, the hydrophilic lipid pores are formed through which Ca2+, Na+ and water get into cytosol and K+ gets out. The hydration of cytosol and hypercalcinemia increase dimensions, thickness of monolayer of epithelium, narrow lumen of arterioles of muscular type and increase resistance to blood flow in distal section of arterial channel. The hydrodynamic pressure increases compensatory in proximal section of arterial channel along with the development of arterial hypertension. The late in phylogenesis insulin has no possibilities to block lipolysis in fatty cells of omentum hence these cells have no receptors to this insulin. While in blood plasma the concentration of non-etherifying acids is increased the cell will not absorb and oxidize glucose. The non-etherifying form the resistance too late in phylogenesis insulin, hyperglycemia and hyperinsulinemia. The concentration of oleic triglycerides increases in blood. The increase in omentum of number of fatty cells of loose connective tissue forms biological reaction of inflammation right up to destruction of overloaded oleic triglycerides cells on the type of apoptosis. This occurrence increases the concentration of C-reactive protein in blood plasma. All symptoms of syndrome of overeating (metabolic syndrome) are formed in the framework of integrated pathogenesis.
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PMID:[The non-etherifying and free fatty acids of blood plasma. Pathogenesis of arterial hypertension and symptoms of syndrome of overeating-metabolic syndrome: a lecture]. 2475 63