Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-nine-day-old female Wistar rats that had been made diabetic 9 days earlier by an intraperitoneal injection of streptozotocin were studied by a combination radioisotope and balance technique that evaluates calcium absorption, excretion, and bone calcium deposition and resorption rates. Streptozotocin-induced diabetes was associated with a marked drop in calcium absorption and a threefold rise in urinary calcium excretion, changes that greatly exceeded the expected effects from the hyperphagia and increased calcium intake of the experimental animals. Bone calcium deposition was halved in the diabetic rats, with bone resorption unchanged and equal to the deposition rate. As a result, the bone and body calcium balances were zero in the experimental animals. To maintain plasma calcium near normal under these circumstances, the diabetic animals turned over their skeletal calcium in relationship to the central pool much more rapidly than the controls. Although the skeleton in the normal animals serves as both storehouse and regulator of the plasma calcium, in short-term streptozotocin-induced diabetes there is no calcium storage in bone, with the skeleton only playing the role of regulator of calcium homeostasis.
 ...
PMID:Regulation of calcium metabolism in streptozotocin-induced diabetes. 674 21

Preterm infants require large amounts of calcium and phosphate to maintain skeletal mineralization during prolonged hyperalimentation. It is impossible to supply the amount of calcium and phosphate normally acquired transplacentally (150 mg/kg/day of calcium and 80 mg/kg/day of phosphate) with reasonable volumes of a single hyperalimentation solution of a physiological pH. We recently encountered calcium phosphate precipitates plugging our hyperalimentation catheters as we tried to raise the calcium concentration above 20 mEq of calcium per liter of hyperalimentation solution. Such a solution supplies 50 mg/kg/day of calcium when run at 125 mL/kg/day. In an attempt to circumvent this problem, we are currently using two hyperalimentation solutions--one high in calcium and the other high in phosphates--run alternately for 12-hour periods. This regimen supplies 80 mg/kg/day of calcium.
 ...
PMID:Calcium and phosphate requirements of preterm infants who require prolonged hyperalimentation. 676 42

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.
 ...
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.
 ...
PMID:Spinal cord injury hypercalcemia: therapeutic profile. 680 36

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.
 ...
PMID:Skeletal changes associated with copper deficiency. 680 88

The metabolic and nutritional effects of long-term parenteral and enteral nutrition were studied in two infants and one child with severe growth failure due to chronic renal failure (two patients) and congenital nephrosis (one patient). Six periods of treatment were analyzed. Both the parenteral nutrition and continuous enteral nutrition were found efficient in enhancing growth and correcting the metabolic abnormalities of uremia. The beneficial effects of this intensive nutrition were smaller in congenital nephrosis, although growth accelerated. Nitrogen balance studies confirmed effective nutrient utilization. The serum levels of calcium and phosphate were normalized as anabolism was achieved in the uremia. In fact, the rapid development of severe hypophosphatemia in one of the patients proved that the "fatal hyperalimentation syndrome" appears to be a specific threat in parenteral nutrition applied in uremia.
 ...
PMID:Growth failure due to uremia and congenital nephrosis: growth enhancement by aggressive nutritional therapy. 681 67

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.
 ...
PMID:Mechanisms of hypercalcemia in patients with head and neck cancer. 716 31

Intracellular free calcium activity is in part determined by a calmodulin-regulated plasma membrane Ca(2+)-pump. Since changes in Ca2+ permeability have been implicated in atherosclerotic plaque formation, we initiated a lipid hyperalimentation protocol during which we measured various erythrocyte calcium flux parameters and early atheroma development. Adolescent New Zealand White rabbits were fed a diet with 0.5% cholesterol and 2.5% lard over a 3-month period. Plasma cholesterol and triacylglycerols increased on average 18.7- and 13.9-fold respectively, while erythrocyte membrane cholesterol content decreased 18% and total phospholipids by 54%. After 3 months of lipid hyperalimentation, 22% of the aortic arch was covered with large, early-stage, raised atheroma. Basal and calmodulin-activated (Ca2+ + Mg2+)-ATPase activities in erythrocyte membranes increased by 31% and 123%, respectively at 2 months, with a concomitant increase in calmodulin affinity (Km) from 15.6 to 4.2 nM. These differences were transient on account of changes in the control animals which exhibited a slowly developing sensitivity to calmodulin during maturation. Basal Ca2+ transport and passive Ca2+ permeability increased about 7-fold during the hyperlipidemic phase. This suggests that overt hyperlipidemia, leading to atherosclerotic plaque development, alters plasma membrane Ca2+ regulatory mechanisms including passive Ca2+ permeability. The changes in enzymatic function, membrane composition, and Ca2+ permeability seen in this red cell model system may be a reflection of early changes in cells that are directly involved in the development of atherosclerotic plaques.
 ...
PMID:Regulation of rabbit erythrocyte Ca(2+)-pump sensitivity to calmodulin in experimental hyperlipidemia. 763 51

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.
 ...
PMID:[Postoperative hypophosphatemia in patients with cancer of the thoracic esophagus]. 846 25

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.
 ...
PMID:Progressively increased serum 1,25-dihydroxyvitamin D2 concentration in a hypoparathyroid patient with protracted hypercalcemia due to vitamin D2 intoxication. 852 47


<< Previous 1 2 3 4 5 6 Next >>