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)

A retrospective analysis was undertaken to better define the clinical presentation and therapy of patients with secondary hyperparathyroidism and the timing of surgical removal of the parathyroid glands in secondary hyperparathyroidism. Sixty-eight patients with end-stage renal disease (ESRD) underwent 74 parathyroid procedures over a 10-year period. There were 38 per cent women and 62 per cent men in this population--the same proportion of men and women with ESRD. These proportions are reversed when compared with patients with primary hyperparathyroidism. The mean time between initiation of dialytic therapy and parathyroidectomy was 5.4 years. Preoperative mean serum calcium and phosphorus levels were 10.1 +/- 0.2 and 6.1 +/- 0.2 mg/dl, respectively. All patients were symptomatic and 60 per cent of the patients had at least two symptoms before surgery. Renal osteodystrophy was the most common symptom (74%), whereas pruritus was noted in 65 per cent of this population. Patients underwent either subtotal (88%) or total (12%) parathyroidectomy with autotransplantation. Six patients required reoperation: five for recurrent disease (2 to 5 years after the initial surgery) and one for persistent disease. All patients were symptomatically improved after the surgery. Complications included the following: transient hoarseness (7%), hypocalcemia requiring calcium, and/or vitamin D therapy (32%) for 6 months after surgery. This analysis demonstrates that although the initial therapy of secondary hyperparathyroidism is medical, surgical therapy should be instituted before multiple symptoms develop in the ESRD population.
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PMID:Secondary hyperparathyroidism. The role of surgery. 272 73

In addition to the well-documented hyporesponsiveness of the kidney, resistance to parathyroid hormone (PTH) has been postulated for bone in pseudohypoparathyroidism type I (PHP). In some of these patients reduced bone density and even frank osteitis fibrosa suggest osteoclastic overactivity. To address the possibility that the skeletal system of patients with PHP may be affected by their increased PTH secretion we measured intact serum PTH and three biochemical markers of bone turnover in a large number of patients with PHP (n = 20). The results were compared with subjects with low (hypoparathyroidism, HP n = 29), normal (controls, n = 31) and high (primary hyperparathyroidism, 1 degree HPT, n = 13) PTH secretion. Both markers of osteoblastic bone formation, alkaline phosphatase activity and osteocalcin concentration in serum, and one index of osteoclastic bone degradation, the urinary hydroxyproline/creatinine ratio (OH-P/Cr), were decreased in HP and increased in 1 degree HPT, whereas only OH-P/Cr was elevated in patients with PHP. Although intact serum PTH was significantly more increased in PHP than in 1 degree HPT, the markers of bone turnover were not significantly different in these two groups, suggesting some bone resistance in the patients with PHP. In these subjects intact serum PTH was elevated even at normocalcaemia during vitamin D treatment with a negative correlation with the respective serum calcium concentration (r = -0.69, P less than 0.001), indicating an elevated set-point for the suppression of their parathyroid glands. OH-P/Cr was negatively related to serum calcium in PHP, it normalized in most patients during normocalcaemia induced by vitamin D treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biochemical markers of bone turnover, intact serum parathyroid horn and renal calcium excretion in patients with pseudohypoparathyroidism and hypoparathyroidism before and during vitamin D treatment. 274 15

Forty-nine patients with primary hyperparathyroidism were examined preoperatively and three months after parathyroid operation for their serum vitamin D metabolites and routine laboratory samples related to calcium metabolism. The preoperative serum 24,25-dihydroxyvitamin D level, mean (SE) was 1.86 (0.22) nmol/l and the postoperative level 5.35 (0.63) nmol/l, the difference being highly significant (P less than 0.001). Serum 1,25-dihydroxyvitamin D levels fell significantly (P less than 0.001) from a preoperative level of 175.5 (17.9) pmol/l to 102.8 (10.1) pmol/l postoperatively. The preoperative 25-hydroxyvitamin D level did not change significantly after surgery. The preoperative serum 24,25-dihydroxyvitamin D level was very low, especially in patients with bone disease while serum parathormone was significantly higher than in patients without bone disease.
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PMID:Serum vitamin D metabolite concentrations in primary hyperparathyroidism. 278 97

The effects of adjuvant treatment with tamoxifen on bone metabolism in a postmenopausal woman with primary hyperparathyroidism is presented. A 69-year-old woman with increased serum ionized calcium, parathyroid hormone, and 1,25-(OH)2 vitamin D levels and a normal bone scan received tamoxifen 10 mg three times daily for 1 year. During treatment bone turnover decreased whereas parathyroid hormone increased further. After cessation of treatment the calcium metabolic variables returned to pretreatment levels. The antiestrogen tamoxifen seems to behave as an estrogen on bone metabolism in primary hyperparathyroidism.
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PMID:Amelioration of postmenopausal primary hyperparathyroidism during adjuvant tamoxifen for breast cancer. 279 Jul 5

Pharmacokinetic properties of pharmacological doses of 24,25-dihydroxyvitamin-D3 [24,25(OH)2D3] were determined in healthy volunteers. Four male subjects received 25 micrograms of 24,25(OH)2D3 as an intravenous bolus injection. Plasma concentrations of 24,25(OH)2D3, 25-hydroxyvitamin D and 1,25-dihydroxy-vitamin D were monitored during 14 days. In addition, serum ionized calcium, total calcium, inorganic phosphate, albumin, creatinine and intact hPTH(1-84) were measured during 14 days. The concentration-time curve of 24,25(OH)2D3 could be described by a two-exponential curve with half-lives of 3.0 +/- 0.9 hrs and 8.2 +/- 2.9 days (mean +/- SD). The volume of distribution was 0.19 +/- 0.02 liters/kg. None of the mentioned biochemical parameters, except serum 24,25(OH)2D3, changed markedly. In 18 subjects suffering from primary hyperparathyroidism, taking 25 micrograms of 24,25(OH)2D3 daily during three months, an average plateau level of 39 +/- 12 nmol/l of serum was observed. Bioavailability as estimated from this plateau level was approximately 70%.
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PMID:Pharmacokinetics of 24,25-dihydroxyvitamin D3 in humans. 280 47

Self-rated psychiatric symptoms were investigated in 30 patients referred for surgery because of primary hyperparathyroidism (HPT) (serum calcium, 2.87 +/- 0.21 mmol/L) in 38 subjects detected in a health screening, with 15 years of mild hypercalcemia and probable HPT (serum calcium, 2.66 +/- 0.09 mmol/L), and in 38 normocalcemic control subjects. The psychiatric symptomatology was evaluated by use of the Hopkins Symptom Checklist (HSCL-56), a self-rating symptom scale. The patients with verified HPT had the highest mean HSCL score, 89.1 +/- 20.1 before surgery, compared with 76.6 +/- 17.0 (p less than 0.01) in the health survey hypercalcemic patients and 73.8 +/- 16.0 (p less than 0.001) in the controls. The factors for anxiety, depression, and cognitive symptoms were the most pronounced in the HPT patients and were also increased among the mildly hypercalcemic persons of the health survey, compared with the controls. Somatic symptoms such as headache, back pain, chest pain, and weakness were equally common in HPT and in the controls, and measurements of isometric muscle strength of knee extension did not demonstrate reduction of muscle strength in the health survey hypercalcemic patients. Follow-up of the HPT patients 1 year after parathyroid surgery revealed a marked improvement in mental health (HSCL score 73.2 +/- 13.7, p less than 0.001). In the health survey hypercalcemic patients, neither the psychiatric symptomatology nor the muscle strength were influenced by 6 months of oral vitamin D therapy (alphacalcidol). The results demonstrate that psychiatric symptoms are experienced frequently by patients with HPT and minimum to moderate increases in the serum calcium level and that these disturbances are reversed by parathyroid surgery.
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PMID:Self-rated psychiatric symptoms in patients operated on because of primary hyperparathyroidism and in patients with long-standing mild hypercalcemia. 291 6

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

In 6 of 8 adults with severe hypocalcemia and osteomalacia due to vitamin D depletion, basal excretion of nephrogenous cAMP (NcAMP) was increased, but the mean renal phosphate threshold (TmP/GFR) was normal, indicating that the steady state phosphaturic response to cAMP generated by endogenous PTH was impaired, as in pseudohypoparathyroidism type II. In all 6 patients, correction of hypocalcemia by administration of vitamin D and calcium restored the normal relationship between NcAMP and TmP/GFR. By contrast, in 13 patients with normocalcemic osteomalacia due to vitamin D depletion, TmP/GFR was reduced, with a significant negative regression on NcAMP, and rose to normal after treatment. Bone histomorphometry after double tetracycline labeling did not differ significantly between the 2 groups. In 72 patients with primary hyperparathyroidism, the slope of the negative regression of TmP/GFR on NcAMP was the same as in normocalcemic secondary hyperparathyroidism, but the adjusted mean for TmP/GFR was significantly lower. We conclude that the effect of endogenous PTH on phosphate reabsorption varies with the level of plasma calcium, and that dissociation between this effect and the generation of cAMP is nonspecific and can be a consequence of hypocalcemia. Exclusion of vitamin D depletion should be an additional diagnostic criterion for pseudohypoparathyroidism type II.
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PMID:Dissociation between the effects of endogenous parathyroid hormone on adenosine 3',5'-monophosphate generation and phosphate reabsorption in hypocalcemia due to vitamin D depletion: an acquired disorder resembling pseudohypoparathyroidism type II. 298 17

Previous studies have demonstrated a spectrum of parathyroid responsivity to alterations in the extracellular calcium concentration in patients with primary hyperparathyroidism, but studies employing physiologic amounts of calcium have not, to our knowledge, been reported. We studied 18 unselected patients with primary hyperparathyroidism at the lower (400 mg) and upper (1000 mg) limits of a normal dietary intake of calcium. The diet containing high-normal amounts of calcium induced only a slight increase in 24-hour calcium excretion (from 281 to 337 mg per day) yet was associated with significant reductions in fasting serum levels of immunoreactive parathyroid hormone (from 60 to 50 nleq per milliliter; P less than 0.001), nephrogenous cyclic AMP (from 3.52 to 2.63 nmol per deciliter of glomerular filtrate; P less than 0.001), and plasma levels of 1,25-dihydroxyvitamin D (from 74 to 58 pg per milliliter; P less than 0.001). A wide spectrum of responses was observed, with some patients appearing to have essentially autonomous parathyroid function and others having marked suppressibility (up to 50 per cent) of the parathyroid hormone-vitamin D axis. We conclude that parathyroid function may be suppressed by dietary calcium in some patients with primary hyperparathyroidism.
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PMID:Sensitivity of the parathyroid hormone-1,25-dihydroxyvitamin D axis to variations in calcium intake in patients with primary hyperparathyroidism. 299 10

We found that a few patients with urolithiasis had normal parathyroid hormone levels but high cyclic AMP excretion. The purpose of this paper was to study the endocrinological mechanism. Male rats were given intraperitoneally dibutyryl cyclic AMP (DBcAMP), a derivative of cyclic AMP, per 100 gm of body weight for 50 days. Feed and water were supplied ad libitum. Crystal formation or calcification in mainly the dystal tubules and collecting system were found in 3 out of 10 rats, and renal calcium stones in 2 rats. The cyclic AMP of the renal parenchyma, especially the renal medulla, was elevated by more than 100 times after DBcAMP administration. Serum calcium levels, urinary calcium and phosphate excretion, and the adrenaline levels of the renal parenchyma were significantly increased. Serum parathyroid hormone was slightly enhanced, but vitamin D and the noradrenaline levels of the renal parenchyma were not changed. Based on these findings, it is suspected that stone formation in rats injected DBcAMP occurs through the action of DBcAMP on the renal tubules to increase urinary calcium excretion and to make renal stones as a form of primary hyperparathyroidism.
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PMID:[Studies on the endocrinological metabolism of the parathyroid. I. The production of renal calcinosis by cyclic AMP injection in rat]. 300 37


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