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)

Of 351 patients treated for primary hyperparathyroidism from 1966 to 1981, 70 (20%) had grossly evident nodular thyroid disease at the time of subtotal parathyroidectomy. These patients have been reviewed to determine if prior radiation exposure may play a role in their coexistence and if combined subtotal parathyroidectomy and thyroidectomy are safe and efficacious. Thirty-three of the 70 patients (47%) had received prior radiation therapy for benign conditions of the head and neck. Nine of 15 patients with nonmedullary thyroid carcinoma had received previous irradiation. In addition to subtotal parathyroidectomy, 28 patients underwent total thyroidectomy, 14 underwent bilateral subtotal thyroidectomy, and 28 underwent unilateral lobectomy. There were no deaths and no permanent recurrent laryngeal nerve injury from combined subtotal parathyroidectomy and thyroidectomy. Two patients in whom parathyroid tissue was not autotransplanted required calcium and vitamin D supplementation. This study shows that (1) primary hyperparathyroidism and nodular thyroid disease occur simultaneously with sufficient frequency to warrant careful preoperative and intraoperative evaluation of both glands, (2) radiation probably does play a role in the pathogenesis of coexistent primary hyperparathyroidism and nodular thyroid disease, and (3) in experienced hands combined subtotal parathyroidectomy and thyroidectomy can be safely performed.
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PMID:Simultaneous primary hyperparathyroidism and nodular thyroid disease. 689 72

The intestinal absorption of magnesium (Mg) was estimated from the increment in urinary Mg following oral administration of 25 mmol of Mg. Fasting urinary Mg did not differ between the control group and patient groups (absorptive hypercalciuria, primary hyperparathyroidism, and hypoparathyroidism). As compared to the value in the control group, the increment in urinary Mg above the fasting value was not significantly different in absorptive hypercalciuria. However, it was significantly increased in primary hyperparathyroidism and significantly reduced in hypoparathyroidism. In control subjects, the increment in urinary Mg was much higher during a low than during a high calcium diet. The results suggest that 1,25-(OH)2-vitamin D stimulates Mg absorption, since Mg absorption was elevated in situations associated with stimulated 1,25-(OH)2-vitamin D synthesis (primary hyperparathyroidism and low calcium diet) and reduced in a condition characterized by low 1,25-(OH)2-vitamin D production (hypoparathyroidism). Moreover, the data indicate that 1,25-(OH)2-vitamin D may not be pathogenetically important in absorptive hypercalciuria, since Mg absorption was normal.
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PMID:Oral magnesium load test for the assessment of intestinal magnesium absorption. Application in control subjects, absorptive hypercalciuria, primary hyperparathyroidism, and hypoparathyroidism. 689 41

1. Plasma membranes were prepared from parathyroid adenomas in patients with primary hyperparathyroidism and from hyperplastic glands obtained from patients with chronic renal insufficiency. The basal and isoproterenol- or sodium fluoride-stimulated adenylate cyclase activities were measured in membranes in the presence of several vitamin D3 metabolites. 2. 24,25-Dihydroxycholecalciferol (10 and 1000 pmol/l) decreased isoproterenol- and sodium fluoride-stimulated adenylate cyclase activities in membranes prepared from parathyroid glands. 1,25-Dihydroxycholecalciferol (1000 pmol/l) inhibited the isoproterenol-stimulated adenylate cyclase activity. 25-Hydroxycholecalciferol and vitamin D3 had no effect on adenylate cyclase activities. Basal adenylate cyclase activity was not affected by any of th vitamin D3 metabolites tested. 3. These results indicate that 24,25-dihydroxycholecalciferol inhibits the isoproterenol- and sodium fluoride-stimulated adenylate cyclase activities in parathyroid tissues. Such an inhibition could explain the very rapid decrease in parathyroid hormone secretion after 24,25-dihydroxycholecalciferol administration that has been previously reported.
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PMID:Human parathyroid gland adenylate cyclase activity: inhibition by 24,25-dihydroxycholecalciferol in vitro. 697 85

Vitamin D appears to influence parathyroid function indirectly through its effects on calcium metabolism rather than by a direct action of its metabolites on the parathyroid glands. In states of both secondary and primary hyperparathyroidism, the quantitative production of 1,25-(OH)2D may be determined by the prevailing concentration of serum 25-(OH)D but there appears to be some constraint that limits the formation of 1,25-0(OH)2D when the provision of its precursor exceeds the physiological. From the absence of this constraint in 'type 2 vitamin D dependency' it is inferred that it may operate through 'self-inhibition' of the renal production of 1,25-(OH)2D. It is shown that the level of serum 25-(OH)D may always exert some influence on the production of 1,25-(OH)2D and that this effect is facilitated by hyperparathyroidism. In developing vitamin D deficiency the reactive secondary hyperparathyroidism may thus function as an adaptive mechanism that sustains the level of serum 1,25-(OH)2D in the face of a diminishing serum 25-(OH)D. Failure of this adaptation and the development of a critical deficiency of 1,25-(OH)2D is regarded as the direct cause of defective mineralisation of bone. This concept would explain the absence of osteomalacia in some patients with very low levels of serum 25-(OH)D and the occurrence of defective osseous mineralisation in hypoparathyroidism.
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PMID:Vitamin D and hyperparathyroidism: the Lumleian Lecture 1981. 697 36

The basal values of plasma vitamin D metabolites were evaluated in patients with primary hyperparathyroidism (1 degree HPT, n = 31), hypoparathyroidism (HP, n = 7), pseudohypoparathyroidism (PHP, n = 4) and normal controls (n = 21). Plasma 25-hydroxyvitamin D (25-OH-D) in 1 degree HPT (9.0 +/0 7.3 ng/ml, mean SD) was significantly lower than that of normal controls (17.9 +/- 5.5ng/ml)(p less than 0.001), and in particular 1 degree HPT classified as the skeletal type showed extremely low value (4.7 +/- 4.6 ng/ml). Plasma 1, 25-dihydroxyvitamin D [1, 25-(OH)2D] was significantly higher in 1 degree HPT (69.1 +/- 31.4pg/ml)(p less than 0.001) and significantly lower in Hp (15.2 +/- 11.0 pg/ml) (p less than 0.001) compared to normal controls (37.2 +/- 13.8pg/ml), although there was no significant difference in PHP (22.3 +/- 17.5 pg/ml). Plasma 24, 25-dihydroxyvitamin D [24,, 25-(OH)2D] in 1 degree HPT (1.06 +/- 0.55 ng/ml) was significantly lower than that of normal controls (1.73 +/- 0.62 ng/ml) (p less than 0.05), and particularly 1 degree HPT classified as the skeletal type showed a marked low value (0.85 +/- 0.27 ng/ml), whereas no significant differences were seen in HP (1.84 +/- 0.46 ng/ml) or PHP (1.34 +/- 0.22 ng/ml). There were slight but significant correlations between either plasma 25-OH-D and 1, 25-(OH)2D (r = -0.350, p less than 0.05), or plasma 25-OH-D and 24, 25-(OH)2D (r = 0.356, p less than 0.05), or plasma 1, 25-(OH)2D and 24, 25-(OH)2D (r = -0.444, p less than 0.01) in all subjects. In addition, relationships between plasma vitamin D metabolites and other indicators of parathyroid function in all subjects were analyzed. There were positive correlations between plasma 1, 25-(OH)2D and serum Ca (r = -0.621, p less than 0.001) or urinary cAMP (r = -0.671, p less than 0.001) or nephrogenous cAMP (r = -0.689, p less than 0.001), while negative correlations were seen between plasma 1, 25-(OH)2D and serum P (r = -0.680, p less than 0.001) or %TRP (r = -0.663, p less than 0.001). On the other hand, there were negative correlations between plasma 24, 25-(OH)2D and serum Ca (r = -0.457, p less than 0.01) or urinary cAMP (r = -0.562, p less than 0.005) or nephrogenous cAMp (r = -0.561, p less than 0.005), and a positive correlation was seen between plasma 24, 25-(OH)2D and %TRP (r = 0.519, p less than 0.005). After parathyroidectomy, a distinct depression of plasma 1, 25-(OH)2D and reciprocal elevation of plasma 24, 25-(OH)2D were observed in 1 degree HPT. Furthermore, there was a clear elevation of plasma 24, 25-(OH)2D as well as plasma 1, 25-(OH)2D after treatment with maintenance doses of 1 alpha-OH-D3 or 1 alpha, 25-(OH)2D3 in HP and PHP. It is concluded that plasma vitamin D metabolites are very useful as the indicators of parathyroid function.
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PMID:[Plasma vitamin D metabolites in parathyroid diseases (author's transl)]. 698 Jan 45

Oral administration of prednisone (30 mg/day for 9 days) to six normal individuals induced a significant rise in the concentration of serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] within 2 days. In four patients with primary hyperparathyroidism a larger increase of 1,25-(OH)-2D was observed within 3 days. In these patients the 1,25-(OH)-2D concentration remained elevated during the whole period of prednisone administration (10 days) whereas in the control group it had returned to basal levels or below after 9 days of prednisone administration. This response appeared dependent upon parathyroid hormone (PTH) as we found no change in the (basally low) 1,25-(OH)2D concentrations in five patients with hypoparathyroidism during 3-4 days of prednisone administration (30 mg/day). In these patients vitamin D medication had been interrupted 3-5 days before the administration of prednisone, whereafter serum calcium was kept between 2.10 and 2.30 mmol/1 by means of calcium infusion. The response of 1,25-(OH)2D to prednisone is best explained by a stimulatory action of glucocorticoids upon PTH secretion or by the induction of increased PTH sensitivity.
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PMID:Short-term effect of prednisone on serum 1,25-dihydroxyvitamin D in normal individuals and in hyper- and hypoparathyroidism. 698 68

Early reports of patients with metabolic bone diseases such as nutritional osteomalacia, Fanconi syndrome, indicated an association with aminoaciduria. This association has since been described in osteomalacia of G. I. or hepatic origin, secondary to anticonvulsant therapy, tumors, and chronic renal failure. Aminoaciduria also occurs in primary hyperparathyroidism. In nutritional osteomalacia, vitamin D deficiency was thought to be responsible for the renal tubular abnormality, since it responded to treatment with vitamin D. However, since the description of aminoaciduria in hyperparathyroidism, the literature has been divided concerning the etiology of aminoacidura in conditions associated with abnormal vitamin D metabolism because secondary hyperparathyroidism often occurs in these conditions. Recently, some cases of Fanconi syndrome and a case of tumor-associated osteomalacia have been described with low or absent plasma 1,25-dihydroxycholecalciferol levels, normal serum PTH, and aminoaciduria. In one of these cases, and more recently in patients with chronic renal failure, it has been demonstrated that treatment with 1,25(OH)2D3 can improve amino acid transport independently from changes in serum PTH levels. 1,25(OH)2D3 therefore normally opposes the aminoaciduric effect of PTH. This is an agreement with observations which demonstrate that 1,25(OH)2D3 also opposes the phosphaturic action of parathyroid hormone.
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PMID:Aminoaciduria--its relationship to vitamin D and parathyroid hormone. 699 53

As a general principle in the treatment of primary hyperparathyroidism due to single adenoma, unilateral parathyroidectomy was applied to 50 patients and compared with another group of 50 conventionally explored patients. Twenty-five patients were explored only on the "adenoma" side. The other 25 patients were explored on both sides, avoiding biopsies at the first. In the conventionally explored patients, the adenoma was removed and one to three normal glands were biopsied. Oil-red-O technique was used in the intraoperative microscopical examination. The patients in whom the operation could be limited to the "adenoma" side had a statistically more favorable situation concerning early postoperative hypocalcemia, length of operation time, and need for calcium and vitamin D substitution. The principle of unilateral parathyroidectomy in conjunction with intraoperative oil-red-O staining technique is advocated in hyperparathyroidism due to single adenoma because it offers more reliable peroperative distinction between uni- and multi-glandular involvement, reduced operation time, decreased risk for complication, reduced early hypocalcemia, and more favorable technical conditions for reoperation.
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PMID:Unilateral parathyroidectomy in hyperparathyroidism due to single adenoma. 705 36

Of 2,058 patients who had surgically proven primary hyperparathyroidism at the Mayo Clinic from 1965 through 1979, 51 or 2.5 percent had associated nonmedullary thyroid carcinoma. A history of radiation exposure to the head and neck was obtained in 14 of 43 patients questioned. Thyroid disease consisted of grade 1 papillary adenocarcinoma in 48 cases and pure follicular adenocarcinoma in 3 cases. The parathyroid disease included 41 single adenomas and 5 cases of parathyroid hyperplasia; 5 patients had 2 adenomas. At follow-up, none of the patients had evidence of metastatic thyroid carcinoma. Ten patients were receiving calcium or vitamin D supplementation for protracted hypocalcemia presumably due to the increased insult to the parathyroids from combined bilateral thyroidectomy and parathyroidectomy. More consecutive thyroidectomy, along with parathyroid autotransplantation when indicated, will provide definitive treatment of the thyroid cancer and at the same time minimize the risk of postoperative hypoparathyroidism.
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PMID:Primary hyperparathyroidism and nonmedullary thyroid cancer. 706 49

Tumoral calcinosis is an uncommon and seemingly unrecognised disease of obscure aetiology. A case in a young Caucasian boy aged 14 is reported. The characteristic clinical features, radiological and pathological findings are described. The condition must be differentiated from other varieties of pathological calcification such as chronic vitamin D intoxication, the milk-alkali syndrome, chronic nephritis, primary hyperparathyroidism, calcinosis universalis, calcinosis circumscripta and dystrophic calcification.
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PMID:Tumoral calcinosis: a case report and review of the literature. 708 93


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