Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that lithium is a general inhibitor of hormone-activated adenylate cyclase, we infuse parathyroid hormone (PTH) into human subjects prior to and during lithium carbonate administration. PTH infusion caused a significant increase in urinary cyclic AMP and urinary phosphate excretion. There was no significant difference in these responses in the lithium compared to the control period. In four patients with primary hyperparathyroidism, lithium had no significant effect on serum calcium or phosphate or on tubular reabsorption of phosphate. The data do not substantiate the hypothesis that lithium (at therapeutic concentrations) is a general inhibitor of hormonally-activated adenylate cyclase, nor do they support its potential clinical utility in primary hyperparthyroidism.
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PMID:Lithium does not inhibit the parathyroid hormone-mediated rise in urinary cyclic AMP and phosphate in humans. 18 15

To investigate whether overall tubular dysfunction is encountered in a particular subgroup of patients with urolithiasis, the following parameters of renal tubular function have been measured in fasting morning urine in 124 male stone formers: excretion of lysozyme and gamma-glutamyl transpeptidase (gamma-GT), fractional excretion (FE) or glucose, insulin, bicarbonate after an alkali load, and theoretical phosphate threshold (TmP/GFR). The following have been diagnosed: primary hyperparathyroidism (n = 3), medullary sponge kidneys (n = 5), hyperuricemia (n = 8), cystinuria (n = 1), struvite nephrolithiasis (n = 2), idiopathic hypercalciuria of the absorptive (n = 16), dietary (n = 46) or renal (n = 5) type, and normocalciuric idiopathic urolithiasis (n = 38). Urinary excretion of lysozyme and of gamma-GT were elevated in 14% and 21% of patients respectively; FE glucose and FE insulin were elevated in 6% and 8% of patients respectively. In 62% of the patients TmP/GFR was below 0.95 mmol/l and in 52% of the patients FE HCO3 after alkali load was above normal. The findings show that a large number of stone formers have signs of renal tubular dysfunction; apparent renal leaks of phosphate and of bicarbonate are the most frequently encountered defects; while they are not specific for a given etiologic group of patients, they have been found in each group. The latter observation suggests that nephrolithiasis itself can damage renal tubular function.
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PMID:[Tubular dysfunction in renal lithiasis: cause or consequence?]. 285 24

To address whether a renal tubular dysfunction is encountered in a particular patient subgroup with urolithiasis, the following parameters of tubular function were measured in urine taken in the morning from 214 stone formers after fasting: pH, excretion of lysozyme and gamma-glutamyl transferase (gamma-GT); fractional excretion (FE) of glucose, insulin, Mg, K, and HCO3 after an alkali loading; and the renal threshold for phosphate (TmP/GFR). The following diagnoses were made in the patient group: primary hyperparathyroidism (N = 8), medullary sponge kidneys (N = 21), hyperuricemia (N = 10), cystinuria (N = 2), struvite stone disease (N = 6), idiopathic hypercalciuria of the absorptive (N = 25), dietary (N = 69) or renal (N = 7) type, and normocalciuric idiopathic urolithiasis (N = 66). In 31% of the patients TmP/GFR was below 0.80 mmole/liter and in 13% of the patients, FE HCO3 after alkali loading was above normal. Urinary excretion of lysozyme and that of gamma-GT both were elevated in 17% of the patients. FE glucose, FE insulin, FE Mg, and FE K were elevated in 8, 9, 3, and 7% of the patients, respectively. This study demonstrates that a significant number of stone formers present with signs of renal tubular dysfunction, primarily involving the proximal tubule since apparent leaks of phosphate and of bicarbonate were most frequently encountered. The defects were not specific for a given etiologic group of patients; on the other hand, occurrence was related to the presence of large stones in the pyelocaliceal system at the time data were gathered. Taken together these data suggest that the tubulopathy in nephrolithiasis is the consequence rather than the cause of the stone.
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PMID:Tubulopathy in nephrolithiasis: consequence rather than cause. 287 Dec 16

Lithium carbonate is known to alter calcium metabolism by lowering urinary calcium excretion and increasing serum calcium concentrations. Several investigators have reported increases in serum immunoreactive PTH (iPTH) values after a few weeks or months of lithium treatment, and several cases of primary hyperparathyroidism developing during lithium treatment have been reported. To determine whether the increases in serum iPTH might be the result of increased renal retention of inactive PTH fragments rather than stimulation of parathyroid function, we measured plasma intact PTH by immunoradiometric assay and estimated parathyroid size by ultrasonography in men who had received short term (less than 6 months) or long term (greater than 3 yr) lithium treatment and in normal subjects. Serum ionized calcium was higher by 0.03-0.04 mmol/L in subjects treated short term (mean, 1.7 months) with lithium than in normal subjects, but plasma intact PTH and serum midregion iPTH values were not different. The absence of a reciprocal decrease in PTH values is compatible with a lithium-induced shift in the set-point for the inhibition of PTH secretion by calcium toward a higher calcium value. Both plasma intact PTH and serum midregion PTH values were higher in subjects during longer term (mean, 103 months) lithium treatment, and estimated parathyroid volume was 3-fold higher. Serum phosphate was lower, and serum chloride and plasma 1,25-dihydroxy-vitamin D values were higher in those treated with lithium long term, probably from the biological action of the increased PTH. We conclude that long term lithium treatment increases circulating biologically active PTH and causes parathyroid enlargement. Whether this chronic stimulus to parathyroid growth might lead to adenoma formation in certain susceptible individuals and whether a PTH-induced increase in skeletal remodelling occurs that might hasten the appearance of osteopenia remain to be determined.
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PMID:Lithium treatment increases intact and midregion parathyroid hormone and parathyroid volume. 291 61

The hypothesis that chronic metabolic acidosis encountered in some patients with primary hyperparathyroidism is due to inhibition of proximal HCO3 reabsorption has recently been challenged. Indeed, this action of parathyroid hormone (PTH) has only been observed in acute studies, whereas in animal models of chronic hyperparathyroidism a metabolic alkalosis has been induced, probably owing to the release of alkaline salts from bone tissue, and to the stimulation of tubular acid secretion by hypercalcaemia. Studies were, therefore, performed to determine the effect of PTH on the renal handling of HCO3 in an animal model in which changes in plasma calcium and phosphate, and nephrocalcinosis, all known to affect tubular acidification, did not occur. Thyroparathyroidectomized (TPTX) rats were infused with synthetic bovine hormone fragment bPTH 1-34 via Alzet minipumps at the rate of 0.7 U h-1 to simulate normal endogenous production of PTH (group I) and at the three-fold higher rate of 2.1 U h-1 (group II). In order to prevent changes in serum calcium and phosphate, and nephrocalcinosis, animals of group II were fed a Ca- and P-free diet prior to TPTX (compared with a regular diet for group I) and both groups were treated with dichloromethylene-diphosphonate (Cl2MDP, 10 mg kg-1 day-1) and a Ca-free diet during PTH infusion. During the course of PTH infusion both groups of animals had stable and normal levels of plasma calcium and phosphate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid hormone directly inhibits tubular reabsorption of bicarbonate in normocalcaemic rats with chronic hyperparathyroidism. 312 45

A 64 year old woman had been on lithium carbonate for 12 years for manico-depressive psychosis. Mild asthenia leads to the diagnosis of primary hyperparathyroidism based on the findings of hypercalcemia up to 2.85 mmol/l inappropriate levels of parathormone and a non-suppressive rise of nephrogenic cyclic AMP. These symptoms were not relieved by removal of a chief cell adenoma of the left inferior parathyroid; surgical reexploration leads to the removal of an adenoma in a high, ectopic situation. Further venous samplings were collected during cervico mediastinal phlebography because of persistent hypercalcemia: parathormone levels were high in a thymic vein and a new cervicotomy revealed a fifth gland with an adenoma in the high mediastinum. After removal of the third adenoma, the patient became hypocalcemic. Lithium was not discontinued according to the patient's wishes. Eighteen months later she was well and normocalcemic on alfacalcidol therapy. Multiple adenomas of the parathyroids are rare (1.7 p. 100 to 5 p. 100) and the recurrence of an adenoma on a supernumerary gland is exceptional. Eighteen clinical cases of primary hyperparathyroidism under lithium therapy have been reported, but mild asymptomatic hypercalcemia with inappropriate increased parathormone levels seems to be more common. Duration of treatment is very variable: 1 day to 12 years, and serum calcium levels or up to 3.9 mmol have been observed. Ten patients underwent cervicotomy with removal of an adenoma 6 of them remaining under treatment, with 2 recurrences in our case. Five of the 8 non-operated patients remained on lithium therapy and showed mild hypercalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Multiple hypersecreting lesions of the parathyroid glands during treatment with lithium]. 371 17

The chronic renal and systemic acid-base effects of hyperparathyroidism in humans remain controversial and unresolved. The present studies evaluated the acid-base response of normal human subjects to a 13-day intravenous infusion of synthetic b(1-34) PTH sufficient to result in sustained hypercalcemia and hypophosphatemia. The acid-base response was biphasic: an initial transient renal acidosis developed on the first day of PTH infusion, followed by a prompt increase in net acid excretion and plasma [HCO3-] of sufficient magnitude to result in a steady state of mild metabolic alkalosis. The results indicate that: 1) sustained, continuous, experimentally produced hyperparathyroidism results in a steady state of mild metabolic alkalosis; 2) the alkalosis is both generated and maintained, at least in part, by renal mechanisms; and 3) reported renal acidosis in sustained clinical conditions of primary hyperparathyroidism is not attributable to either direct or indirect effects of PTH excess when present for a 2-week period, an interval sufficient to re-establish a new steady state of renal and systemic acid-base equilibrium.
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PMID:Acid-base homeostasis during chronic PTH excess in humans. 383 29

In both normal volunteers and in patients with primary hyperparathyroidism, the induction of a metabolic alkalosis by infusion of sodium bicarbonate results in a decrease in serum calcium ion and in an increase of circulating parathyroid hormone concentrations. Bicarbonate infusion may serve in man as a new provocative test for release of parathyroid hormone. Furthermore, we speculate that the metabolic alkalosis which is found at times in patients with the Zollinger-Ellison syndrome and severe peptic ulcer disease may result in parathyroid gland stimulation.
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PMID:Ulcer disease, metabolic alkalosis and hyperparathyroidism: A mechanism of interrelationship? 441 67

Phosphate stones are divided in two groups: I. Infection stones = triple phosphate stones (struvite and carbonate apatite). II. Calcium phosphate stones = Hydroxy apatite. Ad I. For the formation of this stone, infection with urease-producing bacteria is essential. It is important to look for factors that cause infection and for metabolic abnormalities. Three possibilities for treatment are discussed: Acidifying the urine: orally with NH4NO3 or NH4Cl; dosage is possible up to 12 g a day (metabolic acidosis!). Irrigation for instance with Renacidin ; when using a nephrostomy-tube, one can start 5 days after the operation. It is important to look for fever and flank pain. Especially useful in cases with small residual stones. Reduction of phosphate excretion in urine ( Shorr -regimen). Some aluminium combinations reduce the intestinal phosphate absorption as a result of the formation of a nonabsorbable aluminium-phosphate combination. This can be combined with a low calcium- and phosphate diet. In several publications good results are shown. Also when using a less rigid regimen, satisfactory results are seen: decrease of the phosphate excretion from 30 to 17 mmol/24 h (own investigation). Urease-inhibitors result in a lower urine-pH and a decrease of the ammonium-concentration. there are only a few publications with results, but AHA seems able to reduce the stone size in 24% of the patients. Ad II. This stone is concerning formation and treatment much like the calcium oxalate stone. In case of an alkaline urine one must look for primary hyperparathyroidism and renal tubular acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Conservative therapy of phosphate calculi]. 653 26

The cortisone suppression test and some biochemical tests were evaluated in 13 patients with hypercalcemia due to primary hyperparathyroidism (PHP) and in 10 with hypercalcemia due to a malignant disease. The biochemical tests revealed that serum chloride was significantly raised in patients with PHP compared to patients with malignant diseases, whereas no differences were observed with regard to the serum values of corrected calcium, serum phosphate, chloride/phosphate ratio, HCO3-. Although serum values of parathyroid hormone were higher in patients with PHP, a consider-able overlap was observed between values in the two patient groups. Corrected serum calcium values were significantly suppressed during cortisone administration in patients with malignant disease compared to patients wit PHP, whereas prednisolone had no suppressive effect. The positive predictive value of the test was 80.0% and the negative predictive value 66.7%. We conclude that there is still no entirely reliable method to distinguish between hypercalcemia due to PHP or malignant disease.
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PMID:Hypercalcemia due to primary hyperparathyroidism or malignant disease. Evaluated by means of biochemical tests and the steroid suppression test. 714 7


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