Calcium abnormal metabolism

Anomalously high Ca concentrations in hair samples (up to 8285 (xgg-1) which correlate with high P concentrations (up to 4720 jxg g-1) from a group of women from Rio de Janeiro were detected by ICP-MS measurements.87 These abnormal hair compositions were related to endocrinological pathologies affecting calcium/bone metabolism. Very low Ca concentrations were observed in older women and were related to senile osteoporosis.87... 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Patients with tumor lysis syndrome experience a wide range of metabolic abnormalities. The massive cell lysis that occurs leads to the release of intracellular electrolytes, resulting in hyperkalemia and hyperphosphatemia. High concentrations of phosphate bind to calcium, leading to hypocalcemia and calcium phosphate precipitation in the renal tubule. Purine nucleic acids are also released that are subsequently metabolized to uric acid... 

Iron appeared to reduce the effects of orally or subcutaneously administered lead on blood enzyme and liver catalase activity (Bota et al. 1982). Treatment of pregnant hamsters with iron- or calcium-deficient diets in conjunction with orally administered lead resulted in embryonic or fetal mortality and abnormalities (ranting, edema) in the litters, while treatment with complete diets and lead did not (Carpenter 1982). Inadequate levels of iron in association with increased body burdens of lead enhanced biochemical changes associated with lead intoxication (Waxman and Rabinowitz 1966). Ferrous iron was reported to protect against the inhibition of hemoglobin synthesis and cell metabolism by lead it has been speculated that iron competes with lead uptake by the cell (Waxman and Rabinowitz 1966). In... 

Electrolyte or metabolic abnormalities (calcium or sodium fluctuations, hyper- or hypoglycemia)... 

Long-term anticonvulsive therapy with diphenylhydantoin or phenobarbital is known to cause osteomalacia by influencing calcium metabolism (24,25). Alteration in the metabolism of vitamin D, presumably secondary to induction of hepatic microsomal enzymes, leads to the calcium and bone abnormalities (26). Patients on anticonvulsive therapy with phenytoin exhibit a decrease in serum 25-hydroxyvitamin D (27). Adequate dietary amounts of vitamin precursors or microsomal enzyme stimulators might prevent these effects of long-term therapy. 

In light of the increased number of man-6-P/IGF-II receptors in I-cell fibroblasts, the above interactions of IGF could have far-reaching effects. For example, I-cell disease has not been typically associated with abnormalities in phos-phorous/calcium metabolism. The extensive skeletal deformities could involve impairment of mechanisms of orderly calcium deposition. Rather than resulting from a primary disorder of calcium metabolism, it is possible that the bone lesions in I-cell disease are secondary to altered lysosomal processing events in the kidney or liver. 

Vitamin D is necessary to allow the body to metabolize calcium and phosphorus effectively. Independent of the formation of vitamin D, it must be emphasized that excessive uptake of UV sunlight can lead to abnormal skin cell division and the possibility of skin cancer. 

Our interest in the role of trace elements in bone metabolism developed in a rather bizarre fashion. Ve became interested in the orthopedic problems of a prominent professional basketball player. Bill Walton. Several years ago he was plagued by frequent broken bones, pains in his joints and an inability to heal bone fractures. We hypothesized that he might be deficient in trace elements as a result of his very limited vegetarian diet. In cooperation with his physician, we were able to analyze Walton s serum. We found no detectable manganese (Mn). His serum concentrations of copper (Cu) and zinc (Zn) were below normal values. Dietary supplementation with trace elements and calcium (Ca) was begun. Over a period of several months his bones healed and he returned to professional basketball (1,2). In cooperation with several other orthopedic physicians, we analyzed serum from other patients with slow bone healing. Several of these patients also had abnormally low Zn, Cu and Mn levels. 

Not all calcium present in the diet is absorbed by the small intestine and mechanisms are present to ensure only amounts appropriate to body needs are absorbed. These processes are complex and involve the interaction of special transport protein, vitamin D and parathormone. Thus, abnormalities of calcium metabolism may result from many different disease processes. Diseases affecting the bowel may prevent normal absorption, diseases of the parathyroid gland may result in inappropriate levels of parathormone for calcium requirement and a nutritionally inadequate diet may cause vitamin D deficiency with consequent disordered calcium absorption. 

Partial results of studies of normal newborns and children with abnormalities of calcium metabolism are given ... 

The power of this modeling technique might be better appreciated by considering a case of abnormal calcium metabolism, such as fibroplasia ossificans progressiva (FOP) The shape of the isotope dilution curves for this subject are notably different in the period of 1-2 days into the study as Figure 5 shows They have a flattening in the first 20 hours that is not... 

For the authors (PIO) the simplest explanation of the data on tryptophan metabolism in these 3 patients would be as follows in scleroderma (acrosclerosis) there was an abnormal urinary excretion of kynurenine and its metabolites after oral ingestion of tryptophan. The administration of pyridoxine or pyridoxine plus nicotinamide partially corrected the metabolic abnormality. The efficacy of pyridoxine plus Na2EDTA could be explained on the basis of a decrease in tissue calcium and zinc (and possibly other cations), enabling the metal ions, normally functioning with pyridoxal phosphate, as magnesium ions, to be utilized more advantageously. 

Von Ruecker AA, Bertele R, Harms HK. Calcium metabolism and cystic fibrosis mitochondrial abnormalities suggest a modification of the mitochondrial membrane. Pediatr Res 18 (1984) 594-9. 

Metabolic bone disease in children receiving parenteral nutrition manifests primarily as osteopenia and, on occasion, fractures (5). The etiology is multifactorial calcium and phosphate deficiency play a major role in the preterm infant but the part played by aluminium toxicity in this population is unknown. Lack of reference values of bone histomorphometry in the premature infant, as well as lack of reference data for biochemical markers of bone turnover in these patients, contributes to the uncertainty. Other factors that may play a role in the pathogenesis of bone disease associated with parenteral nutrition include lack of periodic enteral feeding underljdng intestinal disease, including malabsorption and inflammation the presence of neoplasms and drug-induced alterations in calcium and bone metabohsm. However, the true incidence and prevalence of parenteral nutrition-associated bone abnormalities in pediatric patients are unknown. 

Since there is an abnormality of calcium metabolism in scurvy, it has been reasoned that supplementary ascorbic acid in the hen ration might help to resolve the problem of thin eggshell during summer heat. Some reports show improved shell soundness during high environmental temperatures others do not. According to Thorton (164,165) and Thorton... 

Effective antihypertensive therapy should include agents that do not adversely affect carbohydrate metabolic abnormalities. Commonly used antihypertensive agents, such as thiazide, thiazide-like diuretics and /3-blockers, are associated with glucose intolerance and increased insulin resistance (Sowers, 1991). In contrast, calcium antagonists and peripheral a-blockers (such as prazosin and terazosin) do not adversely affect glucose tolerance or insulin sensitivity. 

In general, the hypertrophied heart seems to be more susceptible to the deleterious effects of ischemia and reperfusion (reviewed by Friehs and Del Nido200). This may be attributed to alterations in myocardial energy metabolism and calcium handling or to anatomic and functional abnormalities of the coronary bed, such as reduced capillary density and coronary flow reserve. 

---