Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Corticosteroid myopathy was studied in young, mature New Zealand white rabbits given daily injections of betamethasone (0.3 mg/kg body weight/day) for two weeks. Control rabbits were pair-fed and received saline injections. Bethamethasone treatment caused significant wasting of type 2 gluteus medius and psoas muscles but did not cause any atrophy of type 1 soleus and gluteus minimus muscles. The Mg2+- and Ca2+-activated myofibrillar ATPase activities of the corticosteroid-treated rabbits did not differ from controls despite a 30% reduction in muscle wet weight and pronounced reduction in cross-sectional area of fibers. SDS-polyacrylamide gel electrophoresis profiles of myofibrillar proteins did not differ quantitatively or qualitatively between experimental and control rabbits. Studies of net muscle protein degradation (using 3H-leucine) in betamethasone-treated and control rabbits indicate that both type 1 and type 2 muscle fiber proteins are degraded several times faster in the corticosteroid-treated group. This suggests that a compensatory mechanism exists for those type 1 and mixed fiber type muscles which have increased degradation but do not undergo wasting.
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PMID:Experimental corticosteroid myopathy: effect on myofibrillar ATPase activity and protein degradation. 15 6

Urine excretion of magnesium (Mg), calcium (Ca) and sodium(Na) was studied in patients with renal Ca stones having normal kidney function (n= 60), and in matched controls (n= 60), on a free diet following an overnight fasting period. In some formers, Mg was lower than in normals, whereas Ca was unusually high resulting in a significantly higher molar Ca/Mg ratio (p less than 0.001). 2. In 3 out of 4 stone groups Na excretion was significantly elevated because of reduced tubular reabsorption. In normals, fractional Na excretion varied between 0.44 and 0.54% of endogenous creatinine clearance, whereas it exceeded 1% in the stone patients. Conversely, the molar ratio Na/Ca was equal in all groups. 3. Fasting urinary cyclic AMP was comparable in both populations supporting the assumption that in the majority of patients Ca- or Mg- wasting via urine may not be responsible for secondary hyperparathyroidism. In small selected groups, losses of divalent cations may act in concert, leading to stimulation of the parathyroid glands. 4. Correlations between minerals and Na reveal a close relationship between Na, Ca and Mg in terms of clearance and excretion rate in patients and controls. Fractional Na and Ca excretion are correlated in patients but not in normals. This suggests that in the absence of phosphaturia, factors other than extracellular volume expansion and/or hyperparathyroidism are operative in stone disease. 5. The origin of fasting natriuresis and relative hypercalciuria may be ascribed to a change, as yet not causally identified, in distal tubular Na reabsorption.
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PMID:Fasting urine excretion of magnesium, calcium, and sodium in patients with renal calcium stones. 18 86

The pathogenesis of the association of medullary sponge kidney and hyperparathyroidism from parathyroid adenoma remains obscure. This unusual case of medullary sponge kidney and secondary hyperparathyroidism due to renal-leak hypercalciuria gives insight into a possible mechanism for the occurrence of medullary sponge kidney with parathyroid adenoma. Suppressible hyperparathyroidism due to renal calcium wasting could represent an intermediate stage in the development of unsuppressible parathyroid hormone secretion. Thus, parathyroid adenoma occurring with medullary sponge kidney may represent a consequence of disordered renal calcium excretion rather than a primary abnormality.
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PMID:Medullary sponge kidney and renal-leak hypercalciuria. A link to the development of parathyroid adenoma? 43 Jun 89

The benzothiadiazide diuretics are known to cause magnesium and potassium wasting and retention of calcium and uric acid. The effect of magnesium replacement on diuretic-induced changes in sodium, potassium, calcium, and magnesium balance, weight, and blood pressure was studied in 12 normal subjects and 13 hypertensive patients to determine whether oral magnesium would reduce thiazide-induced kaliuresis. The groups differed in their response to diuresis in that the normotensive subjects did not show a fall in blood pressure (despite an equivalent weight loss), returned to a state of sodium balance earlier, and developed a greater net negative potassium balance over 12 days of diuretic therapy. Both groups displayed calcium and uric acid retention and magnesium wasting during diuretic therapy. The addition of oral magnesium replacement during diuretic therapy had no effect on any measured values beyond that seen in subjects who took diuretics without magnesium replacement. Thus, magnesium replacement did not reduce urinary potassium loss. However, urinary calcium losses increased when magnesium was given to subjects who were not receiving diuretics. The data provide the first report that small doses of oral magnesium enhance calcium excretion in hypertensive subjects.
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PMID:Interrelationships among thiazide diuretics and calcium, magnesium, sodium, and potassium balance in normal and hypertensive man. 72 50

A 12-year-old boy developed renal wasting of magnesium, calcium, and potassium, with secondary hypomagnesaemia, hypocalcaemia, and hypokalaaemia (without hyperaldosteronism) after treatment with 14 400 mg gentamicin over 4 months. Gentamicin should not be given for prolonged courses if less toxic antibiotics are suitable. If it used, plasma magnesium, calcium, and potassium levels should be monitored during and after treatment.
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PMID:Hypomagnesaemic hypocalcaemia with hypokalaemia caused by treatment with high dose gentamicin. 72 98

A proximal renal tubular acidosis (RTA) is the mechanism underlying the systemic acidosis found in vitamin D deficiency rickets. Acidotic subjects have high levels of PTH. In non-acidotic subjects proximal bicarbonate wasting can be induced by exogenous PTH injection. Carbonic anhydrase activity is not involved in this process. Calcium infusion is able to suppress both the spontaneous and the PTH-induced bicarbonate leak. The development of RTA in vitamin D deficiency is related to a particular equilibrium between two antagonizing factors at tubular level, parathyroid hormone and calcium.
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PMID:Proximal renal tubular acidosis in vitamin D deficiency rickets. 81 Jan 89

Two patients developed severe hypomagnesemia, hypocalcemia, and hypokalemia as a result of renal wasting of magnesium and potassium shortly after being treated with large doses of gentamicin. When therapy with gentamicin was discontinued renal loss of magnesium and potassium ceased, and serum calcium, magnesium, and potassium returned toward normal. Serum immunoreactive parathyroid hormone levels were inappropriately low during the episodes of hypocalcemia. Both patients represent examples of hypomagnesemic hypocalcemia induced by inappropriate magnesuria, possibly caused by gentamicin. These observations suggest that serum calcium, magnesium, and potassium should be monitored during gentamicin therapy.
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PMID:Hypomagnesemic hypocalcemia secondary to renal magnesium wasting. 113 60

The identification of marginal magnesium deficit, such as we have detected in a patient with anxiety, depression, and psychomatic complaints, is a difficult diagnostic problem. Electromyography of a limb, rendered acutely ischemic either just before or after hyperventilation, can elicit latent tetany in this condition, as well as in calcium deficiency. We have demonstrated iterative electrical activity in our patient, whose magnesium deficit is attributable to renal wasting of magnesium. We have elicited similar patterns in several other patients, who had marginally low serum magnesium and who also exhibited weakness, anxiety, and psychosomatic disorders. This preliminary report suggests the need for further consideration of the possibility that chronic magnesium-deficit may contribute to the syndrome of latent tetany, psychosomatic complaints, and weakness.
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PMID:Latent tetany and anxiety, marginal magnesium deficit, and normocalcemia. 116 68

Cestrum diurnum poisoning was described in a Florida bull. Clinical signs included chronic wasting and progressive lameness. Plasma calcium was elevated for long periods of time but decreased toward low normal values. There was pronounced C-cell hyperplasia. Osteopetrosis was very severe and reflected retarded osteocytic osteolysis and chondrolysis. Further negative effects on the osteocytes eventually lead to osteonecrosis. Soft tissue calcinosis involved tendons and ligaments, major arteries and veins but kidneys and lungs were spared. Whereas the osteopetrosis could be explained by hypercalcitoninism, the osteonecrosis was believed to result from direct action by the Cestrum diurnum factor, previously shown to have an action similar to that of 1,25-dihydroxy-cholecalciferol, which is the biologically active metabolite of vitamin D3.
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PMID:Cestrum diurnum poisoning in Florida cattle. 119 49

Inotropic agents alter myocardial oxygen consumption by influencing heart rate, by influencing preload and afterload due to vasodilation, and by direct effects on the myocardium. The latter critically depend on the pharmacologic mode of action. Inotropic agents which act by increasing cyclic AMP in the failing human myocardium increase myocardial energy turnover by their effects on excitation-contraction coupling, resulting in a considerable increase in the amount of calcium cycling. Glycosides, which increase contractile force independent of cyclic AMP, increase calcium cycling moderately and do not influence myocardial energy turnover significantly. Calcium-sensitizers, by increasing calcium-affinity of contractile proteins, may increase contractile force and decrease myocardial energy turnover. Peripheral vasodilation following the application of inotropic agents decreases myocardial oxygen consumption due to a decrease in systolic stress-time integral. The energy-saving effect of reduced preload and afterload may counterbalance a direct myocardial energy-wasting effect of some inotropic agents. An increase in heart rate due to inotropic interventions is unfavorable since 1) oxygen consumption increases in proportion to heart rate, and 2) contractile force of the failing human myocardium decreases. The latter was obvious from experimental and clinical studies showing that increasing heart rate increases contractile force and cardiac output in nonfailing human myocardium, but decreases cardiac performance in the failing human heart. In light of the inverse force-frequency relation in failing human myocardium, negative chronotropic drugs may represent a new class of "positive inotropic" agents. Agents reducing heart rate may be beneficial from an energetic point of view by reducing myocardial oxygen consumption and by improving myocardial perfusion due to a prolongation of diastole.
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PMID:[New cardiotonic/inodilator agents: energetic aspects]. 129 Mar 7


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