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)

The clinical peculiarities, and the etiological and pathogenetic factors of urolithiasis in 296 patients suffering from spontaneous stone elimination were studied. It was established that 209 patients eliminated stones consisting of uric acid, sodium salts and ammonium salts. Moderate hypocalcemia and hyperphosphatemia and also hyperuricemia and hyperuricuria were present. There were 39 'eliminators' of calcium stones. Their blood calcium content was higher, hypercalciuria, inorganic phosphorus and normal uric acid, were noted. Compound stones were present in 48 observations. When carrying out additional biochemical tests in 57 patients with calcium and compound stones, primary hyperparathyroidism was diagnosed in 34 observations; and parathyroidectomy was successfully performed.
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PMID:On the pathogenesis of stone formation in stone-eliminating patients. 42 6

Two patients with primary hyperparathyroidism had hyperuricemia due to the decrease in urate clearance. In analysis by 4-component model system, the tubular secretion of urate commonly decreased without changes in either filtered urate or presecretory reabsorption of urate. Both patients had a reduction of urea clearance, and both parathyroidectomy in the former case and intravenous infusion of saline in the latter case could reduce the serum urate level associated with the increase in the ratio of urate clearance to creatinine clearance. It is of interest that the former case with a higher serum urate level had a relatively higher postsecretory reabsorption, even with the decrease in tubular secretion of urate. However, the latter patient with a lower serum urate level had a decrease in postsecretory reabsorption of urate in proportion to the decrease in tubular secretion. These results suggest that in hyperuricemia patients with primary hyperparathyroidism, the reduction of tubular urate secretion via hypoperfusion of the capillary network is typically present, however, the severity of the hyperuricemia might be dependent on the dysfunction of the postsecretory reabsorption of urate.
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PMID:Renal handling of urate in two patients with hyperuricemia and primary hyperparathyroidism. 139 85

Serum urate and the renal handling of urate were measured in 37 patients with primary hyperparathyroidism and in normal sex- and age-matched subjects. Serum urate was increased in the hyperparathyroid group compared to the control group (6.23 +/- 1.46 versus 4.64 +/- 1.24 mg/100 ml; p less than 0.005), whereas the fractional excretion of urate was decreased in hyperparathyroid patients compared to the controls (6.80 +/- 2.69 versus 8.73 +/- 3.47%; p less than 0.005). Twenty-four of these hyperparathyroid patients were studied 6 months after surgical correction of their disease. Serum urate decreased after surgery (5.14 +/- 1.65 mg/100 ml) compared to the preoperative state (5.92 +/- 1.46 mg/100 ml) and was no longer different from the normal values. The possible mechanisms of hyperuricemia associated with the hyperparathyroid state are discussed.
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PMID:Hyperuricemia and renal handling of urate in primary hyperparathyroidism. 260 2

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

In order to elucidate the influence of the parathyroid function on the uric acid metabolism, 24 patients (14 males, 10 females) with primary hyperparathyroidism (PHP) and 17 patients (9 males, 8 females) with idiopathic hypoparathyroidism (IHP) were extensively studied. The mean age was not significantly different between these groups, being 40.3 +/- 2.8 and 39.0 +/- 3.5 respectively. Hyperuricemia was found in 4 patients with PHP, but none of the patients had experienced gout. The serum uric acid levels were significantly higher and uric acid clearances were significantly lower in PHP than in IHP. There was no difference in daily urinary excretion of uric acid and in creatinine clearance between the two groups. In PHP, a positive correlation was observed between the levels of serum uric acid and calcium, both of which negatively correlated to renal uric acid clearance. Although the serum uric acid levels did not correlate to serum PTH levels in PHP, the removal of parathyroid adenoma resulted in a significant fall of serum uric acid levels. In IHP, the administration of PTH induced a small but significant decrease in serum uric acid levels with a coincidental increase in urinary uric acid excretion. Four hours of calcium infusion had no effect on the serum uric acid levels and urinary uric acid excretion. Treatment of IHP with 1 alpha-OH D3 to restore normal serum calcium levels caused significant increase in serum uric acid levels. These data indicate that the parathyroid function influences uric acid metabolism, even in the absence of renal insufficiency, mainly through changes of uric acid clearance. Levels of active vitamin D or chronically abnormal calcium levels in the circulation may be major determinant for uric acid metabolism in parathyroid disorders.
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PMID:[Parathyroid function and uric acid metabolism]. 666 55

A series of 38 cases of primary hyperparathyroidism seen at a single hospital within a four a half year period is reported. The importance of hypercalcemia in the diagnosis of this syndrome and its screening in cases of arterial hypertension, gout, osteoporosis, and families with type I multiple endocrine neoplasia are underlined. The patients in the present series had a florid clinical history with a mean duration of 14 years. Main symptoms were urolithiasis (52%), arterial hypertension (28.9%), bone involvement and pain (23.7%), and peptic ulcer (18.4%). There were a high proportion of patients with hyperuricemia (26.3%), some with classical symptoms of gout. One patient presented simultaneous pituitary and pancreatic involvement. Surgical therapy was undertaken in 25 patients, of whom 24 (96%) were cured, one of them after reoperation. There were no cases of relapse, hypoparathyroidism, or postoperative death. Surgery is the only rational and definitive form of treatment of hyperparathyroidism; both experienced surgeons and pathologists are necessary to deal with the anatomic and histologic subtleties of this interesting endocrine disorder.
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PMID:[Comments on a series of 38 cases of primary hyperparathyroidism (author's transl)]. 724 69

The case of an 81-year-old woman with persistent post-traumatic pain of the knee linked to tophaceous gout of the patella is presented. This gout was associated with adenomatous primary hyperparathyroidism. The relationship between hyperuricemia, hyperparathyroidism and chronic renal failure is discussed.
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PMID:Tophaceous gout of the patella with primary hyperparathyroidism. 765 76