Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalcemia after renal transplantation (post-T hypercalcemia) has been detected in 29 (16.7%) of 174 long-term survivors. The mean time of onset of hypercalcemia was 69 days after renal transplantation (range 3-210). In 18 patients the hypercalcemia was mild and resolved spontaneously (transient) from 2-65 months (mean 19) after onset. In 4 patients serum calcium normalized concurrently with rejection episodes. In 7 patients the hypercalcemia was more pronounced (permanent), being terminated by subtotal parathyroidectomy in 5 and persisting in 2 recipients. The hypercalcemia was asymptomatic except in one patient, who developed calculi in the graft and a fall in graft function, all of which disappeared after parathyroidectomy. At operation the parathyroid glands showed hyperplasia, except in one case with an adenoma in one of the hyperplastic glands. Serum phosphorus was markedly decreased, to the same extent in transiently and permanently hypercalcemic recipients. Serum parathyroid hormone (S-PTH) was increased in all of 5 patients with permanent and in 3 of 8 with transient post-T hypercalcemia. In normocalcemic and in transiently hypercalcemic recipients the mean S-PTH was identical, but significantly lower than in the permanently hypercalcemic recipients. S-PTH was suppressed to the same extent during an i.v. calcium infusion in patients with post-T hypercalcemia and with primary hyperparathyroidism.
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PMID:Hypercalcemia and parathyroid function after renal transplantation. 31 22

The overproduction of parathyroid hormone as caused by a simple hyperplasia or an adenoma leads to pathological changes in various organs which are termed primary hyperparathyroidism. The blood phosphates increase in case of long-standing disturbances of the metabolism, e.g. chronic renal insufficiency. In this way and due to other causes, the production of parathyroid hormone is increased. The resultant clinical picture is termed secondary hyperparathyroidism. Both forms are associated with osseous changes also in the maxillofacial skeleton. Tertiary hyperparathyroidism may develop from secondary hyperparathyroidism if the metabolic disorder in the renal form cannot be eliminated by kidney transplantation and if the process in the parathyroid becomes independent (autonomous hyperparathyroidism). Besides these three forms, there are two others, quaternary hyperparathyroidism and quinary hyperparathyroidism, which are described.
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PMID:[Hyperparathyroidism]. 36 8

The pathogenesis of the association of medullary sponge kidney and hyperparathyroidism from parathyroid adenoma remains obscure. This unusual case of medullary sponge kidney and secondary hyperparathyroidism due to renal-leak hypercalciuria gives insight into a possible mechanism for the occurrence of medullary sponge kidney with parathyroid adenoma. Suppressible hyperparathyroidism due to renal calcium wasting could represent an intermediate stage in the development of unsuppressible parathyroid hormone secretion. Thus, parathyroid adenoma occurring with medullary sponge kidney may represent a consequence of disordered renal calcium excretion rather than a primary abnormality.
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PMID:Medullary sponge kidney and renal-leak hypercalciuria. A link to the development of parathyroid adenoma? 43 Jun 89

Parathyroid morphology and blood chemistry were studied in five patients with primary hyperparathyroidism treated with 1,25-dihydroxycholecalciferol (1,25-DHCC) for 2 to 11 days before planned operation. Before the institution of treatment all patients were hypercalcemic, whereas the serum immunoreactive parathyroid hormone (iPTH) concentration either was elevated or normal. During the treatment the urinary phosphate excretion was significantly increased, whereas the calcium excretion and the serum concentrations of calcium and phosphate were unaffected or only slightly changed. Serum iPTH decreased during the first days of treatment, but returned then to increased levels close to the pretreatment ones. The treatment was tolerated well by the patients. Light and electron microscopy of the removed parathyroid glands disclosed one adenoma in each of the five patients, the other glands exhibiting either a slight hyperplasia or a normal appearance. Both the adenomatous and the non-adenomatous parathyroid tissue showed a predominance of dark chief cells and three of the adenomas exhibited a varying number of atrophic and oxyphil cells. The non-adenomatous glands were composed of atrophic and dark chief cells. Signs of low functional activity were ultrastructurally observed in the parathyroid parenchymal cells. It is suggested that 1,25-DHCC treatment of patients with primary hyperparathyroidism inhibits parathyroid hormone secretion.
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PMID:Influence of 1,25-dihydroxycholecalciferol on parathyroid activity in patients with primary hyperparathyroidism. 43 14

A rare case of a large cervicomediastinal parathyroid cyst associated with hypercalcemia and an elevation of serum parathyroid hormone is presented. The pathogenesis of such a large cyst is discussed, hemorrhage into an adenoma being the most likely cause. Clinical investigations which should be carried out for any cystic mass at the root of the neck should include a serum calcium, and if this is found to be elevated, the possibility of the cyst being of parathyroid origin should be considered. In view of the high concentration of parathyroid hormone found within the cyst, aspiration of the cyst contents for parathyroid hormone estimation might well prove a valuable test to confirm the diagnosis.
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PMID:Giant functioning cervicomediastinal parathyroid cyst. 47 54

A study is presented of 14 patients with hyperparathyroid crisis treated at the Massachusetts General Hospital between 1964 and 1978. These patients showed diverse clinical manifestations that were indistinguishable from those in patients with pseudohyperparathyroidism. Their symptoms varied from progressive fatigue, malaise, and weakness to those related to the gastrointestinal and urinary tracts. The one biochemical alteration commonly found among these patients was the rapid increase in the serum calcium. There was a concomitant rise in the BUN in 50% of the patients and in the creatinine in 80%. The diagnosis was established by an elevated immunoreactive parathyroid hormone (PTH) level in all eight patients (100%) who had the radioimmunoassay; by the presence of subperiosteal resorption of the phalanges in six of the eight patients (75%); and in three of four patients (75%) by the loss of the lamina dura of the teeth. The 12 patients who had surgery all survived; the two who did not died. Thirteen patients (93%) had a neoplasm--an adenoma in 12 and a carcinoma in one. One patient had hyperplasia (7%). Nine patients (64%) received hypocalcemic drug therapy. The serum calcium temporarily fell to 12 mg/100 ml in five patients (56%) but failed to budge in four (44%). Simultaneous treatment with saline infusion, furosemide and with hypocalcemic drugs over a prolonged period compounded the difficulty at operation by increasing interstitial edema. Our findings from this study show prompt surgical intervention as the ideal treatment for hyperparathyroid crisis, preferably, within 72 hours of the acute onset of symptoms.
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PMID:Hyperparathyroid crisis: clinical and pathologic studies of 14 patients. 51 79

In a patient with hyperparathyroidism (HPT) two neck explorations with identification of three normal parathyroid glands were carried out. Cervical and mediastinal vein catheterization with blood sampling for determination of parathyroid hormone (PTH) confirmed drainage of large amounts of PTH to a mediastinal vein. Two thoracic explorations were negative anterior and posterior mediastinum). The operations were performed during 1971 and 1978 and extensive, progrediating decalcification with brown tumour formation was radiologically demonstrated during that time. Diminished renal function, skeleton pain and mental depression necessitated a last exploration, at which a 2 cm large parathyroid adenoma was found in the left carotid sheath just below the left mastoid process. The adenoma was drained into mediastinal veins through long anastomotic branches.
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PMID:Hyperparathyroidism--a life-threatening disease in 1978. A case report. 53 42

The disappearance rate of immunoreactive plasma parathyroid hormone (iPTH) was studied, employing two different antisera, following removal of parathyroid adenoma in patients with primary hyperparathyroidism. One antisera contained antibodies against both the NH2 region and the COOH terminal of the molecule (antiserum 211/32, Wellcome Laboratories), the other contained antibodies against antigenic sites of the terminal COOH portion (Immuno Nuclear Corporation antiserum). The iPTH plasma level dropped in all patients following removal of the adenoma. The half-life was longer than that of the native hormone and shorter than that of the terminal fragment with both antisera, being 38.8 min for the 211/32 and 32.9 min for the I.N.C. antiserum. Whilst this finding might be expected for the 211/32 antiserum, on account of its characteristics, it is difficult to offer an explanation for the observed half-life of the I.N.C. anti serum which is specific for the terminal COOH region. These results appear to suggest that the terminal COOH fragment may be further metabolized and that its longer half-life, observed by other authors, is due to the antisera used recognizing the antigenic sites in a fragment smaller than the terminal COOH portion of the molecule, rather than to the effective half-life of the entire fragment.
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PMID:[Studies of the half-life of plasma parathyroid hormone: rate of disappearance of immunoreactive fragments of the hormone after surgical removal of the parathyroid adenoma in primary hyperparathyroidism]. 55 Aug 91

The effect of 1,25-dihydroxycholecalciferol (1,25-(OH)2-D3) on parathyroid hormone secretion by porcine parathyroid glands and human parathyroid adenoma tissue was investigated by in vitro incubation. The addition of 100 nmoles 1,25-(OH)2-D3 to the medium inhibited significantly the release of immunoreactive parathyroid hormone by 63--65%. This suppression was reversible when 1,25-(OH)2-D3 was removed again. The inhibition of parathyroid hormone release observed in human parathyroid adenoma tissue was similar to that in normal porcine parathyroid glands. This indicates that adenoma tissue is sensitive to regulatory influences. As well as calcium, 1,25-(OH)2-D3 may act as another feedback inhibitor of parathyroid hormone secretion.
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PMID:The effect of 1,25-dihydroxycholecalciferol on the parathyroid hormone secretion of porcine parathyroid glands and human parathyroid adenomas in vitro. 57 21

A case is presented of a 52-year-old man with a swelling in the neck and dysphagia resulting from an intrathyroid cystic parathyroid adenoma. Hypercalcaemia and unusually high parathyroid hormone levels were detected preoperatively. The adenoma was removed by partial hemithyroidectomy. The literature is reviewed.
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PMID:Intrathyroid cystic parathyroid adenoma: a rare case of hyperparathyroidism. 58 75


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