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PubMed1988

Effects of calcitonin on plasma calcium and phosphate in the mudskipper, Periophthalmodon schlosseri (Teleostei), in water and during exposure to air.

After 7 days in air on wet filter paper mudskippers had normal body weight and normal levels of plasma sodium, potassium, and phosphate. They were, however, significantly hypercalcemic. The hypercalcemia could be reduced by the daily intraperitoneal injection of synthetic eel calcitonin (1.67 microgram kg-1 day-1) and this effect was dose dependent with a maximal response at a dose of 3.33 micrograms kg-1 day-1. Calcitonin had no effect on plasma calcium levels of fish held in water but did induce significant hyperphosphatemia whether the fish were held in water or in air on wet filter paper with this effect being greater under the latter conditions. The hypocalcemic action of calcitonin was restricted to conditions under which the fish displayed patent hypercalcemia. Under no conditions did calcitonin produce significant hypocalcemia so it appears that the action of synthetic eel calcitonin in the mudskipper, Periophthalmodon schlosseri, is dependent upon the presence of excess plasma calcium and is thus more accurately described as being anti-hypercalcemic rather than hypocalcemic.

Animals↗

PubMed1989

Influence of calcitonin administration of serum calcium and inorganic phosphate level of the frog, Rana tigrina.

The effect of salmon calcitonin (0.25 MRC mU/g body wt) was investigated on the serum calcium and inorganic phosphate levels of the frog. Rana tigrina. The hormone evokes hypocalcemia (on Day 1 and Day 3) which is followed by a significant hypercalcemia on Day 10. Thereafter, the level of calcium decreases again on Day 15. Calcitonin induces hypophosphatemia (on Day 3 and Day 5). Thereafter, hyperphosphatemia is recorded on Day 10. Normal serum phosphate value is achieved by Day 15. The results obtained in R. tigrina have been discussed in relation to the increased calcium deposits in the paravertebral lime sacs and to the possible enhanced secretion of the parathyroid glands.

Animals↗

PubMed1992

Effect of vitamin D3 administration on the serum calcium and inorganic phosphate levels of the freshwater catfish, Heteropneustes fossilis, maintained in artificial fresh water, calcium-rich fresh water, and calcium-deficient fresh water.

Freshwater catfish, Heteropneustes fossilis, were injected daily intraperitoneally either with vehicle (0.05 ml of 95% ethanol/100 g body wt) or vitamin D3 (50 I.U./100 g body wt) and maintained in artificial fresh water, calcium-rich fresh water, or calcium-deficient fresh water for 10 days. The specimens were sacrificed on Days 1, 3, 5, and 10 after initiation of the experiment. The blood samples were collected on these intervals and serum calcium and inorganic phosphate levels were analyzed. Vitamin D3 induced hypercalcemia and hyperphosphatemia in the freshwater catfish, H. fossilis. These effects of vitamin D3 are not dependent upon the calcium concentration of the different ambient media used in this study.

Animals↗

PubMed1988

Effect of acute reversal of experimentally-induced ketoacidosis with sodium bicarbonate on the plasma concentrations of phosphorus and potassium.

To determine if ketoacidosis per se, or its reversal with NaHCO3, predisposes to hypophosphatemia, six conditioned dogs were infused for two hours with 3.0 mmol/kg body wt/hour of beta-hydroxybutyric acid, followed by 1.5 mmol/kg/hour of NaHCO3 for two hours. Acid infusion caused moderate decrements in blood pH and [HCO3], a 23 +/- 4% increase in plasma [P] (p less than 0.005), and a 15 +/- 3% decrease in plasma [K] (p less than 0.005). NaHCO3 administration returned blood pH and [HCO3] levels to or slightly greater than baseline. Plasma [P] decreased, but not below baseline, whereas plasma [K] remained below baseline, and underwent an additional small decline (p less than 0.01). We conclude that acute correction of experimental ketoacidosis with NaHCO3 reverses the characteristic hyperphosphatemia but does not induce hypophosphatemia. On the other hand, NaHCO3 administration appeared to contribute to the perpetuation of hypokalemia.

3-Hydroxybutyric Acid↗

PubMed1976

The actions of parathyroid hormone on bone: relation to bone remodeling and turnover, calcium homeostasis, and metabolic bone disease. Part IV of IV parts: The state of the bones in uremic hyperaparathyroidism--the mechanisms of skeletal resistance to PTH in renal failure and pseudohypoparathyroidism and the role of PTH in osteoporosis, osteopetrosis, and osteofluorosis.

In early chronic renal failure, the state of the bones resembles that of type II primary hyperparathyroidism. Cortical bone becomes thinner and more porous, and there is increased extent of surface remodeling. These changes are followed in turn by osteomalacia and osteitis fibrosa, although sometimes these may be alternate rather than successive stages. Bone turnover is less than would be expected for the elevation of PTH level, probably because of 1,25 (OH)2D3 deficiency. The resorption velocity and lamellar bone appositional rates are depressed, but woven bone appositional rate may be increased, possibly because of hyperphosphatemia. Bone mass reflects the summation of three independent processes: loss of lamellar bone due to hyperparathyroidism (depending on the extent of insulation by osteoid); accumulation of partly mineralized osteoid because of osteomalacia; accumulation of woven bone because of osteitis fibrosa. Osteosclerosis may be growth-related metaphyseal, subchondral or diffuse axial, and periosteal neostosis may also occur. Some patients on hemodialysis lose bone because of planing rather than lacunar or dissecting resorption, combined with depression of both lamellar and woven bone formation. Hyperparathyroid bone disease tends to improve slowly after renal transplantation. Persistent hypocalcemia reflects a defect in the calcium homeostatic system and cannot be explained solely by the known stimuli to secondary hyperparathyroidism. The increment in plasma calcium in response to PTH infusion is subnormal, both in early chronic and in acute renal failure, probably because of 1,25(OH)2D3 deficiency. This is also the most likely explanation for the depressed level of blood-bone equilibrium. The activity of all three of the PTH responsive cell systems in bone is depressed in renal failure, probably because all three require 1,25(OH)2D3 in order to function normally. In pseudohypoparathyroidism, as in chronic renal failure, hypocalcemia results from a defect in the regulation of the blood-bone equilibrium. The bone-remodeling system shows all gradations of response, from slight depression of bone turnover to overt osteitis fibrosa, but bone turnover is never as low as in PTH deficiency. These differences may reflect the presence or absence of resistance to PTH of the osteoprogenitor cell as well as of the calcium homeostatic system, or may be due to varying degrees of 1,25(OH)2D3 deficiency, as in chronic renal failure. An increase in plasma calcium in response to PTH can occur either in the untreated state or after treatment with vitamin D because either the error-correcting or remodeling system remains responsive to PTH. Pseudohypoparathyroidism may be subdivided into three types, depending on whether the urinary cyclic-AMP response to PTH remains defective despite treatment with vitamin D, improves with treatment, or is normal before treatment. Only the former is associated with the genetic syndrome of Albright's hereditary osteodystrophy...

Bone Diseases↗

PubMed1982

Variation of rat serum biochemical values following decapitation or anesthesia with ether, halothane or Innovar-VetR: rapid Innovar-VetR-induced hyperuricemia and hyperglycemia.

True reference values (TRV) should ultimately be determined in blood from inactive, unstimulated rats but in practice, acceptable reference values (ARV) may be established using blood from decapitated or anesthetized animals if one is cognizant of variations associated with blood sampling procedures. Data reported here illustrate some variations in serum biochemical values following decapitation or anesthesia. Decapitation does not provide serum in which ARV for sodium, potassium or lactate dehydrogenase can be found but ARV can be determined for glucose, insulin and several other parameters. It is suggested that both TRV and ARV for serum electrolytes be determined using serum from cannulated rats. All three anesthetics raised glucose levels and ether and halothane increased alkaline phosphatase activity. Both halothane and Innovar-VetR decreased insulin:glucose ratios suggesting inhibition of insulin release from the pancreas. Innovar-VetR also produced hypoxia due to severe respiratory depression and bradycardia as well as hyperuricemia, hyperglycemia and hyperphosphatemia. Techniques most likely to provide ARV should be of the shortest possible duration, afford least respiratory and cardiovascular suppression and minimize stimulation of the sympathetic nervous system.

Anesthetics↗

PubMed1986

Induction of metallothionein after lead administration by three injection routes in mice.

The amount of induced hepatic metallothionein (MT) and the alterations of calcium (Ca) and lead (Pb) concentrations in plasma, liver, kidney, and spleen were compared in male mice after iv, ip, and sc injections of lead acetate at a dose of 30 mg Pb/kg body wt. The amount of hepatic MT at 1 day was in the order of ip greater than iv greater than sc injection approximately 0, despite the hepatic Pb concentration in the order of iv greater than ip greater than sc injection. Heat-stable Pb-binding MT was not detected following any injection route. After the iv injection, a transitory hypercalcemia with hyperphosphatemia was observed. As for the tissue Pb concentration after the iv and ip injections, liver and spleen showed a high concentration, while kidney concentration was relatively low. The high tissue Pb was accompanied by an increase of tissue Ca in most cases. Only 10 to 15% of the total Pb accumulated in the liver at 1 day was recovered from the supernatant fraction after ultracentrifugation. The increase of hepatic Ca was ascribed to that in the sediment fraction. After the sc injection, the tissue Pb concentration was very low and no alterations were observed in tissue Ca concentrations.

Animals↗

PubMed1995

Tophaceous pseudogout (tumoral calcium pyrophosphate dihydrate crystal deposition disease).

Most cases of calcium deposition seen radiologically in soft tissues are caused by calcium hydroxyapatite and occur either as a complication of trauma with associated necrosis (eg, fat necrosis), generalized connective tissue diseases (eg, scleroderma), metabolic disturbances (eg, hyperparathyroidism, familial hyperphosphatemia), sarcoidosis, myeloma, or metastases. Hydroxyapatite deposits are seen at many soft tissue sites, including joint capsules, ligaments, blood vessels, dermis, etc. On the other hand, deposits of calcium pyrophosphate are seen typically in the meniscus, articular cartilage, ligamentum flavum, and intervertebral disc. They usually are punctate or linear in distribution within the meniscus or parallel to the subchondral bone end plate. We report seven cases of massive focal calcium pyrophosphate dihydrate (CPPD) crystal deposition disease (tophaceous pseudogout) that occurred in atypical locations for CPPD. The ages of the patients ranged from 31 to 86 years (average, 60.7 years). One patient was male and six were female. The temporomandibular joint was involved in three patients and the metatarsophalangeal joint of the great toe was involved in two patients. The hip joint and cervical spine were involved in one patient each. A mass or swelling with or without pain was a common symptom. None of the patients in our series had clinical or radiographic evidence of CPPD crystal deposition disease in any other joints. Roentgenograms showed calcified lesions with a granular or fluffy pattern. Histologically, the lesions showed small or large deposits of intensely basophilic calcified material containing needle shaped and rhomboid crystals with weakly positive birefringence characteristic of CPPD. Foreign body granulomatous reaction to the CPPD deposition was constantly found. Chondroid metaplasia around and in the areas of CPPD deposition was observed commonly. Some of the chondroid areas showed cellular atypia in chondrocytes suggestive of a malignant cartilage tumor. It is important to recognize this rare form of CPPD crystal deposition disease and to identify the CPPD crystals in the calcified deposits, thus avoiding the misdiagnosis of benign or malignant cartilaginous lesions.

Adult↗

PubMed1988

The medical and metabolic consequences of administration of sodium acetate.

1. The standard total parenteral nutrition, peritoneal dialysis, hemodialysis and many surgical fluids in use today contain 36 to 45 mM D,L-lactate or 2 to 140 mM acetate whereas the normal blood level of D-lactate is 0.02 mM L-lactate 0.5 to 5 mM and acetate 0.1 nM. The reasons for the continued use in patients of such unphysiological concentrations of these anions appear to be historic. 2. Administration of similar concentrations of these anions to the rat causes widespread metabolic disturbances which mimic many of the untoward complications associated with current parenteral and dialysis therapy. Understanding of the mechanisms attendant upon the metabolism of these anions may serve as a guide for designing improved parenteral fluids for human patients. 3. Elevation of blood D-lactate to 5 mM is associated with cerebral dysfunction in human patients. 4. Acetate stimulates the release of the inflammatory leukokine, interleukin-1 from human monocytes. Use of 35 to 45 mM acetate in peritoneal dialysis fluids led to peritoneal fibrosis. Patients exposed to acetate containing hemodialysis fluids have 12-fold elevation in their plasma interleukin-1 levels. 5. Administration of 20 mM sodium acetate to rats leads to a number of metabolic disturbances similar to those seen in human dialysis patients: (a) Acetate elevates blood glucose in the rat and may contribute to the exacerbation of the carbohydrate intolerance seen in uremic patients. (b) Acetate increases the levels of hepatic malonyl CoA, the rate controlling substrate of fatty acid synthesis and may exacerbate the hypertriglyceridemia characteristic of dialysis patients. (c) Acetate administration in the rat leads to a decrease in the cytosolic phosphorylation potential, reduction of the redox state of the free cytosolic NAD couple and paradoxical oxidation of the mitochondrial NAD couple in a pattern analogous to that produced by uncouplers of oxidative phosphorylation and may account in part for the elevation of temperature reported in patients undergoing hemodialysis with acetate. (d) Acetate administration in the rat leads to an increase in intracellular phosphorylated intermediates, adenine nucleotides, inorganic phosphate, inorganic pyrophosphate, calcium and magnesium. On cessation of acetate metabolism, the inorganic phosphate and calcium accumulated intracellularly leave the intracellular space. In patients undergoing hemodialysis, the blood phosphate returns to predialysis levels, within 6 hr after the completion of treatment, leaving significant numbers of patients with chronic hyperphosphatemia and the multiple complications attendant to that state.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetates↗

PubMed1985

Urolithiasis in acromegaly.

Hypercalcemia, hypercalciuria, and hyperphosphatemia are common findings in acromegaly, yet there are only a few reports on the occurrence of urinary stones in these patients. We reviewed the files of 64 patients with acromegaly. A total of 8 patients had evidence of renal calculi: 4 patients underwent nephrolithotomy, 3 had stones which were seen on intravenous pyelography, and 1 patient voided a stone. Moreover, 2 other patients suffered from recurrent typical episodes of renal colic. In view of the high incidence of urolithiasis in our series we believe that more attention should be paid to detection of urinary stones in acromegalics to avoid further complications and suffering.

Acromegaly↗

PubMed1992

Physiologic concentrations of inorganic phosphate accelerate fructosamine synthesis.

The effect of physiologic concentrations of inorganic phosphate (Pi) on fructosamine (FRA) synthesis was studied. After 75 g oral glucose administration (OGTT), 'delta FRA/24 h', defined as delta FRA after incubating serum or other specimens at 37 degrees C for 24 h after adding 1000 mg/dl glucose, was significantly decreased in parallel to the decrease of plasma Pi concentrations. 'The FRA index', defined as the FRA value divided by the corresponding glucose concentration, both at fasting, correlated significantly with plasma Pi concentrations. In vitro incubation of serum total protein (TP), albumin (ALB), gamma-globulin (GLB), free lysine (Lys), and free valine (Val) with glucose at different concentrations of Pi showed a Pi-dependent increase of FRA synthesis throughout 48 h of incubation. The accelerating effect of 5 mg/dl Pi on FRA synthesis from TP, ALB, GLB, Lys, and Val at pH 7.4 was, respectively, as great as 48, 20, 24, 13 or 25% of those without Pi. Increase of pH from 6 to 10 logarithmically increased delta FRA/24 h in contrast to a logarithmic decrease of the accelerating effect of Pi on delta FRA/24 h. These data show that physiologic concentrations of Pi accelerate protein glycation by accelerating dehydrogenation during the Amadori rearrangement through the negative charge of Pi. Because this accelerating effect of physiologic Pi presumably exists in vivo, Pi concentration must be taken into account as an accelerating factor for FRA synthesis in evaluating diabetic control, and further studies must be carried out to elucidate whether hyperphosphatemia accelerates glycation-induced diabetic complications.

Adult↗

PubMed1990

Hypocalcemia in cancer.

Hypocalcemia based on total calcium measurement is frequent in certain cancers (especially prostate) in association with osteosclerotic bone metastases. In a majority of these patients hypocalcemia is related to the low serum albumin and/or renal failure. True ionized hypocalcemia may be seen as a toxic effect of certain chemotherapeutic agents or as a consequence of hyperphosphatemia due to rapid tumor lysis. In addition, tumors may produce osteoblast-stimulating factor(s) which cause massive accretion of calcium by the skeleton. Isolation and purification of these factors may provide us with unique osteoblast-stimulating factors which may have therapeutic applications.

Antineoplastic Agents↗

PubMed1991

Influence of parathyroidectomy, 1,25-dihydroxyvitamin D3 and high dietary calcium intake on demineralized bone matrix powder-induced bone formation in the rat.

Demineralized bone matrix induces ectopic endochondral bone formation. We used this model to study the effect of parathyroidectomy (PTX), 1,25-dihydroxyvitamin D3 treatment, and calcium enriched diet on bone formation in the rat. Hypocalcemia and hyperphosphatemia in PTX rats were corrected by 1,25-dihydroxyvitamin D3 treatment (2 x 12.5 ng/day) or by calcium enriched diet (3% calcium). Serum 1,25-dihydroxyvitamin D3 concentration was decreased in PTX rats and in intact rats with high dietary calcium intake. Calcium content of ectopic new bones (42 days after bone matrix implantation) was reduced in PTX rats compared with intact control rats. This could be prevented by 1,25-dihydroxyvitamin D3 treatment. In contrast, calcium enriched diet led to diminished mineralization of ectopic bones both in intact and PTX rats. We conclude that the effect of parathyroidectomy on bone formation may be mediated by 1,25-dihydroxyvitamin D3. 1,25-Dihydroxyvitamin D3 directly stimulates bone formation in this model and this effect is not simply the result of increasing serum calcium concentration.

Animals↗

PubMed1990

Calcifying panniculitis associated with polycystic kidney disease and chronic renal failure.

Tender erythematous nodules and plaques developed on the abdomen and legs of two women, 45 and 48 years of age, with hyperparathyroidism as a result of chronic renal failure caused by polycystic kidney disease. The histopathologic findings of these lesions were characterized by a calcifying panniculitis. Laboratory tests disclosed normal calcium levels and hyperphosphatemia with an elevated level of calcium phosphate product. Calciphylaxis appeared to be the mechanism of soft tissue calcification in these patients.

Calcinosis↗

PubMed1984

Dystrophic calcification, cataracts, and enamel hypoplasia due to long-standing, privational vitamin D deficiency.

A 19-year-old Indian girl presenting with intermittent tetany, enamel hypoplasia, bilateral cataracts, and calcification of the basal ganglia is described. Dental evidence suggested a calcification defect had been present from the age of 2-3 years. Hypocalcemia, hyperphosphatemia, and low levels of immunoassayable parathyroid hormone (iPTH), urinary cAMP, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D were documented, suggesting hypoparathyroidism with vitamin D deficiency. A bone biopsy showed osteomalacia. Following ultraviolet irradiation and oral calciferol therapy, a symptomatic and biochemical response typical of privational vitamin D deficiency occurred. iPTH levels rose to normal and remained normal following withdrawal of treatment, indicating that the clinical features were entirely due to long-standing vitamin D deficiency.

Adult↗

PubMed1995

A patient with carpotarsal osteolysis and nephropathy treated with long-term hemodialysis.

We describe a type III carpotarsal osteolysis patient with nephropathy who has been maintained on chronic hemodialysis for 12 years. The diagnosis of osteolysis was based on x-ray findings and bone biopsy. At the age of 12 years, she developed renal disease that progressed; she was placed on chronic dialysis at the age of 18 years. Blood pressure was controlled by a medical regimen, and her anemia has benefitted from erythropoietin up to a level of 28% to 30%. Her osteolysis has stabilized since the age of 20 years; she is presently 30 years old. The major problem affecting the patient's clinical outcome is hyperphosphatemia.

Adolescent↗

PubMed1995

Secondary hyperparathyroidism in renal failure: the trade-off hypothesis revisited.

Our understanding of the mechanism responsible for secondary hyperparathyroidism (HPTH) has advanced significantly since the "trade-off" hypothesis was formulated. It appears that in early renal failure a deficit of calcitriol synthesis is an important factor. However, additional factors, such as a defect of the vitamin D receptor or the newly cloned calcium sensor receptor (BoPCaR1), may be present in the parathyroid cells. As renal failure progresses, the lack of calcitriol becomes more pronounced, inducing HPTH. With advanced chronic renal failure, hyperphosphatemia is an additional important factor in worsening HPTH. In addition, resistance of the parathyroids to calcitriol due to a reduced density of calcitriol receptors also may contribute to HPTH. Finally, uremia per se not only may cause a receptor abnormality in the parathyroid but at the level of the bone it may aggravate the impaired calcemic response to PTH. In conclusion, after reviewing the "trade-off" hypothesis, although some of the original concepts may have been simplistic, most of the factors postulated 30 years ago are still operative in the pathogenesis of secondary HPTH in renal failure.

Calcitriol↗

PubMed1985

Aluminum intake from non-prescription drugs and sucralfate.

The use of non-prescription antacids to control hyperphosphatemia has been implicated as a primary cause of aluminum intoxications in patients with reduced renal function. Additional reports suggest that oral aluminum intake may have adverse effects on mineral metabolism of patients with normal renal function. The non-prescription drugs that contain substantial quantities of aluminum salts include some antacids, buffered aspirins, antidiarrheals, and vaginal douches. Sucralfate, an anti-ulcer drug available by prescription, is the aluminum salt of sucrose sulfate. If taken as directed, the daily aluminum intake from the antacids can be as much as 5,000 mg. When aluminum buffered aspirins are used as part of the drug therapy for rheumatoid arthritis, aluminum intake can be elevated by 700 mg/day. Although aluminum intoxications have been reported among patients with reduced renal function, existing reports are not sufficient to estimate whether the chronic elevation of aluminum intake from drugs is causing adverse health effects among other patient populations.

Aluminum↗