Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

States of hypersecretion of PTH may occur primarily, or in response to other physiologic abnormalities. Primary hyperparathyroidism must be considered in the differential diagnosis of hypercalcemia, nephrolithiasis, metabolic bone disease, and pancreatitis and peptic-ulcer disease. The clinical manifestations of this disease have become more subtle with improved detection. The serum calcium level is almost always elevated, and when it it accompanied by relatively high serum PTH levels or increased urinary cAMP excretion, the diagnosis is usually secure. Findings of hypophosphatemia, decreased renal tubular reabsorption of phosphorus, hypercalciuria, and characteristic roentgenographic changes support the diagnosis of hyperparathyroidism, but are not prerequisites for that diagnosis. Most cases will come to operation, and experienced intraoperative assessment is necessary for the correct distinction between multiglandular disease and that involving only a single gland. We expect that a clearer understanding of the histopathologic features of these diseases, and improvement in the methods for measurement of PTH will be the main areas of advancement in the diagnosis of hyperparathyroidism in the next few years.
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PMID:Diagnosis of hyperparathyroidism. 19 30

We evaluated the turnover of the plasma 25-OH-vitamin D pool, acid, and mineral balances in paired balance studies of 6 normal subjects during normal acid base conditions and during stable chronic metabolic acidosis induced by NH4Cl. Positive acid balances and negative Ca balances due to hypercalciuria were observed as previously reported. Plasma 25-OH-D pool turnover averaged 6.1+/-0.4 nmol/day during control and did not change during acidosis (6.5 +/- 0.5 nmol/day) nor were any significant increments in net intestinal absorption of Ca, PO4, or Mg, the physiological expression of vitamin D action, observed during acidosis. In 3 other subjects, repetitive measurements of serum iPTH during 7 control days and 24 days of stable NH4Cl acidosis showed no changes. We interpret the data to support the hypothesis that neither PTH nor vitamin D and its metabolites mediates the increase in net bone resorption that must accompany chronic metabolic acidosis.
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PMID:The lack of effect of chronic metabolic acidosis on 25-OH-vitamin D metabolism and serum parathyroid hormone in humans. 99 11

The effects of acute and chronic metabolic acidosis on serum immunoreactive parathyroid hormone (iPTH) were studied. Acute metabolic acidosis induced by administration of ammonium chloride (NH4Cl) produced a barely detectable increase in serum iPTH. Chronic NH4Cl administration produced a marked elevation of serum iPTH that was well correlated with the magnitude of acid-induced hypercalciuria but not with the degree of acidosis. Acetazolamide administration produced an equivalent degree of acidosis, but hypercalciuria was minimal and iPTH increased only marginally. Methionine administration caused moderate hypercalciuria and a significant but moderate increase in iPTH. Chronic NH4Cl-induced acidosis produced no hypercalciuria when dietary sodium intake was rigidly restricted, and under these conditions serum iPTH remained normal. When sodium intake was suddenly increased while maintaining the acid load, hypercalciuria appeared and was followed by progressive rise in serum iPTH equivalent to that observed during chronic NH4Cl-induced acidosis in subjects consuming salt ad lib. These results indicate that chronic acidosis elevates iPTH mainly by producing hypercalciuria and that acidosis itself is not a primary stimulus to PTH secretion.
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PMID:Effect of acute and chronic metabolic acidosis on serum immunoreactive parathyroid hormone in man. 120 55

By use of histomorphometry and photon and physical, calcium homeostasis, bone morphology, bone mass and bone growth were studied in freely fed control, streptozotocin-induced diabetic, long-term and short-term insulin treated diabetic rats 14 weeks after the induction of diabetes. We conclude that untreated chronic streptozotocin-induced diabetic rat could result in abnormal bone and mineral metabolism, which is characterized by hypercalciuria, hyperphosphaturia and hyperphosphatemia, significant bone loss and growth arrest. The extent of bone loss correlated with the duration of the disease process. The anatomical basis of bone mass reduction is the diminution of osteoblasts activity which results in reduction of bone formation and insufficient bone calcification and relative increment of osteoclasts activity. Thus, bone resorption overweight bone formation leading to a negative balance of bone remodeling. The effect of PTH and CT on bone changes in diabetic rats can't be affirmed in our experiments. It is probable that metabolic disorder and/or insulin deficiency has a direct effect on bone changes. Insulin therapy started earlier in the course can prevent and somewhat later can completely normalize the altered skeletal morphology of diabetic rats. Whether this result is due to direct effect of insulin on skeletal tissue or through the correction of metabolic disorder remains to be resolved.
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PMID:[Effect of insulin therapy on abnormal bone and mineral metabolism in chronic streptozotocin-induced diabetic rat]. 130 70

We describe an adult patient who developed persistent hypercalcemia while bedridden for more than three months with pancreatitis and sepsis. On the basis of hypercalciuria, suppressed serum intact PTH, suppressed serum 1,25-dihydroxy vitamin D3 and no clinical evidence of malignancy, the diagnosis of immobilization hypercalcemia was established His hypercalcemia improved during treatment with saline, calcitonin and/or etidronate. With active mobilization and weight-bearing exercises, serum calcium finally normalized. We discuss clinical and laboratory features as well as current modalities of treatment of this rare form of hypercalcemia in adults.
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PMID:Immobilization hypercalcemia in an adult patient with pancreatitis and sepsis: case report. 148 89

In order to clarify the pathogenesis of hypercalciuria, the response to extrinsic human parathyroid hormone (h-PTH) was studied the 21 patients with calcium containing urinary stone(s) and 5 normal controls (NO). The stone patients were classified into 3 groups from the result of the oral calcium loading test, i.e. Non-hypercalciura (NH, n = 8) and absorptive hypercalciuria (AH, n = 8) and renal hypercalciuria (RH, n = 5). Only in the AH group, urinary excretion of calcium (u-Ca) was strongly correlated to that of sodium (u-Na) in pre-load of h-PTH, and both increments were also correlated in post-load of h-PTH. As of this fact the increase in Na excretion seems to be responsible for a cause of hypercalciuria in the AH group. There was a significant correlation between the value of %TRP in pre-load of h-PTH and the rate of urinary phosphorus (P) increment between pre-load and post-load of h-PTH in the NO and NH groups. However, this relationship was not found in the AH and RH groups. These findings indicate that there is response disorder of P to h-PTH. In addition, serum P was low, plasma 1,25 (OH)2D was high, N-c-AMP was low in the AH group, whereas both serum P and %TRP were low in the RH group in pre-load of h-PTH. These findings are compatible with the primary renal P leak.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The pathogenesis of hypercalciuria from the aspect of the response to human parathyroid hormone in Ca containing stone formers]. 150 27

To elucidate the pathophysiology of dietary calcium independent hypercalciuria, 42 calcium stone formers (Ca SF) were selected because they had on free diet a calciuria greater than 0.1 mmol/kg/day. For four days they were put on a diet restricted in calcium (Ca RD) by exclusion of the dairy products. They collected 24 hour urines on free diet and on day 4 of Ca RD as well as the two-hour fasting urines on the morning of the day 5 and the four-hour urines passed after an oral calcium load of 1 g, for measurement of creatinine, Ca, PO4, urea and total hydroxyprolinuria (THP). On day 5 fasting plasma concentrations of Ca, PO4, intact PTH, Gla protein, calcidiol and calcitriol were measured. The patients were firstly classified into dietary hypercalciuria (DH, 18 patients) and dietary calcium-independent hypercalciuria (IH, 24 patients) on the basis of the disappearance or not of hypercalciuria on Ca RD. Then the patients with IH were subclassified into absorptive hypercalciuria (AH) because of normal fasting calciuria (8 patients) and into fasting hypercalciuria (16 patients). Fasting hypercalciuric patients were subsequently divided according to the PTH levels into renal hypercalciuria (RH, 1 patient) with elevated fasting PTH becoming normal after the Ca load and undetermined hypercalciuria (UH, 15 patients) with normal PTH levels. Furthermore, their vertebral mineral density (VMD) was measured by quantitative computerized tomography which was normal in DH (91 +/- 6% of the normal mean for age and sex) but was decreased in IH to 69 +/- 4%. No difference in VMD was observed between AH and UH. Urinary excretions of urea, phosphate and THP was higher in IH than in DH and comparable in AH and UH. Sodium excretion Ca RD was the same in all groups and subgroups as well as the plasma parameters. Plasma calcitriol was increased in IH and DH comparatively to normal in spite of normal plasma calcidiol. Calciuria increase after oral calcium load, an index of Ca absorption, was higher in IH than in controls and comparable in IH and DH as well as in the three subgroups of IH. From these data and correlation studies in IH it is concluded: (1.) VMD is decreased in Ca stone formers with IH but not in those with DH, making the distinction of these two groups of hypercalciuria patients clinically relevant.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diet, vitamin D and vertebral mineral density in hypercalciuric calcium stone formers. 189 73

We have studied the metabolic response to changes in calcium in 15 hypercalciuric essential hypertensives, in 8 normotensive hypercalciuric stone formers and in 11 normotensive healthy subjects matched for age and sex. At variance with hypercalciuric stone formers, at low calcium intake hypercalciuric hypertensives did not appropriately reduce urinary calcium excretion and developed mild hypocalcemia. Furthermore, the PTH response to calcium deprivation was not appropriately enhanced in these patients. The data indicate that different mechanisms prevail in these two forms of hypercalciuria: the renal in essential hypertension and the intestinal in urolithiasis.
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PMID:Mechanism of hypercalciuria in essential hypertension and in primary nephrolithiasis. 195 54

Nifedipine has been shown to lower urinary calcium in "essential" hypercalciuria. However, the mechanism(s) by which this action takes place is completely unknown. This study describes the effect of nifedipine on some calcium-controlling hormones in essential hypercalciuria. Nifedipine (20 mg/day) was administered to ten essential hypercalciuric patients, and urinary PgE2, plasma bicyclic PgE2, 1,25 vitamin D3, and PTH were assayed before and after drug administration. Nifedipine promoted a significant fall in urinary calcium (352.1 +/- 87.67 SD vs. 231.2 +/- 74.62 mg/hr; t = 7.35, p less than .0001) and PgE2 (343.92 +/- 42.71 vs. 245.03 +/- 35.41 SD ng/24 hr; t = 6.18, p less than .0002), as well as in plasma bicyclic PgE2 (310.00 +/- 30.91 vs. 200.00 +/- 31.62 SD pg/ml; t = 9.86, p less than .0001) and 1,25 (OH)2 vitamin D3 (32.77 +/- 3.23 vs. 26.94 +/- 2.94 SD pg/ml; t = 6.53, p less than .0001), while PTH remained unaltered (18.50 +/- 3.63 vs. 19.50 +/- 4.09 SD ng/ml; t = 0.85, p, ns). Urinary calcium and PgE2 correlated positively before (r = 0.81, p less than .005) but not after treatment. The fall in urinary PgE2 brought about by nifedipine seems to be due to an inhibition of PgE2 synthesis, since the absolute decrements in both urinary PgE2 and plasma PgE2 metabolites were positively correlated (r = 0.79, p less than .007). No correlation was found between the absolute decrements of plasma bicyclic PgE2 and 1,25 (OH)2 vitamin D3. These data seem to suggest that the fall in urinary calcium brought about by nifedipine is in some way related to PgE2 synthesis inhibition and to uncoupling of 1,25 (OH)2 vitamin D3 and PTH action.
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PMID:Effect of nifedipine on urinary excretion of calcium and calcium-controlling hormones in essential hypercalciuria. 207 11

Because of the bone remodelling it induces, hyperthyroidism modifies the parameters of calcium-phosphorus metabolism. For a better determination of the mechanism involved, we studied 13 patients with Graves' disease compared with 13 controls. We measured the various parameters of calcium-phosphorus metabolism, notably the levels of parathormone, 25-hydroxycholecalciferol, 1-25 dihydroxycholecalciferol and ostocalcin; 8 patients were re-examined in euthyroidism. Total and corrected values of calcaemia (P less than 0.05 and P less than 0.01), phosphoreamie (P less than 0.01), alkaline phosphatase (P less than 0.01), calciuria (P less than 0.01) and hydroxyprolinuria (P less than 0.01) were significantly higher in patients with hyperthyroidism. Osteocalcin also was significantly increased (P less than 0.01) and correlated with thyroid hormone levels, thus confirming its usefulness as marker of bone remodelling in hyperthyroidism. Creatininaemia was significantly lowered (P less than 0.01). The intestinal absorption of calcium after injection of 1 g of calcium was reduced. Parathormone and 25-hydroxycholecalciferol levels were not significantly different in patients and in controls. In patients who were re-examined in euthyroidism, there was a significant increase in parathormone and in 1-25 dihydroxycholecalciferol levels (P less than 0.05). Thus, in situations of hyperthyroidism 2 elements contribute to a deficit in calcium balance: (a) a fall in parathormone level, consecutive to a rise in calcaemia, induces hypercalciuria; and (b) a fall in 1-25 dihydroxycholecalciferol level, consecutive to functional hypoparathyroidism and hyperphosphoraemia, results in a decrease of intestinal calcium absorption.
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PMID:[Phosphorus-calcium metabolism in hyperthyroidism]. 213 61


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