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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autotransplantation of the parathyroid glands is a clinically useful modality for the management of patients with certain forms of hyperparathyroidism. In conjunction with total parathyroidectomy, this procedure has been used to treat patients with primary and secondary hyperparathyroidism who have generalized parathyroid hyperplasia. Parathyroid autotransplantation is also an important adjunct to the management of patients undergoing radical thyroid or laryngeal surgery to prevent permanent hypoparathyroidism from devascularization of all in situ parathyroid tissue. The technique of parathyroid cryopreservation has been well established and provides surgeons with greater flexibility in the approach to patients undergoing reoperative parathyroid surgery in whom there is uncertainty about the functional status of the remaining parathyroid tissue. Parathyroid allotransplantation has been successfully performed in immunosuppressed patients but is rarely indicated. Parathyroid autografts can be placed heterotopically in a forearm muscle or in the sternocleidomastoid, but the former site is preferred in patients with hyperplastic or adenomatous tissue. This technique results in a low incidence of permanent hypoparathyroidism after radical parathyroidectomy, and recurrent hypercalcemia can be easily managed by local excision of a portion of the grafted tissue.
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PMID:Current status of parathyroid autotransplantation. 218 41

31 cases of primary hyperplasia and neoplasms of the parathyroid gland are reported. Among them, 23 cases were parathyroid adenoma, 6 cases parathyroid hyperplasia, one case adenoma associated with hyperplasia, and one case of parathyroid adenocarcinoma. Follow-up study demonstrated that prognosis in the adenoma group is better than that in the hyperplasia group, and one carcinoma patient died from metastasis. Regarding differential diagnosis, adenoma is usually single, with frequent presence of oppressed parathyroid tissue next to the tumor capsule; and cell atypical hyperplasia is often seen microscopically, which is usually multiple in sites, and some residual adipose tissue can be found under the microscope. Clinically, both groups manifested hypercalcemia and hypophosphatemia, especially in those cases with chief cell hyperplasia. Capsule infiltration and vascular embolism are emphasized as the differential features between benign and malignant parathyroid tumours.
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PMID:[A clinico-pathologic study of 31 cases of parathyroid hyperplasia and tumours]. 227 14

We sought an explanation for prior findings of high plasma chromogranin-A (Chr-A) in primary hyperparathyroidism. Chr-A was measured in plasma samples from 55 controls and 73 patients with primary hyperparathyroidism caused by adenoma (n = 14), sporadic or familial hyperplasia (n = 10), or familial multiple endocrine neoplasia type 1 (FMEN1; n = 49). Serum or plasma samples were also tested for calcium, PTH, gastrin, pancreatic polypeptide, CG alpha, and PRL. Plasma Chr-A was 34 +/- 10 in parathyroid adenoma, 55 +/- 33 in parathyroid hyperplasia without FMEN1, 63 +/- 88 in FMEN1, and 25 +/- 8 in controls (mean +/- SD; nanograms per ml; FMEN1 or parathyroid hyperplasia vs. control, P less than 0.05). Plasma Chr-A did not correlate with other hormonal variables in controls. Plasma Chr-A correlated with log serum gastrin (r = 0.43; P = 0.003) and plasma PTH (r = 0.52; P less than 0.05) only in FMEN1. In FMEN1, plasma Chr-A was highest in subjects with Zollinger-Ellison syndrome (ZES, 120 +/- 127; no ZES, 30 +/- 33 (P less than 0.0001). Parathyroidectomy did not decrease plasma Chr-A in patients with parathyroid adenoma or parathyroid hyperplasia. For FMEN1 patients with available pre- and postparathyroidectomy samples, Chr-A decreased postoperatively in four of five patients with ZES compared to none of six patients without ZES (P less than 0.05). Elevated plasma Chr-A is not a general feature of primary hyperparathyroidism. Elevated plasma Chr-A in primary hyperparathyroidism was restricted principally to patients who also had ZES. Primary hyperparathyroidism may influence the level of Chr-A by an effect of hypercalcemia or elevated PTH on Chr-A secretion from pancreatic islet tissue.
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PMID:Plasma chromogranin-A in primary hyperparathyroidism. 257 19

The case of a 65 year old female with myasthenia gravis and hypercalcaemia is presented. Failure of medical control of the myasthenia necessitated thymectomy at which time parathyroid exploration was also carried out. This revealed parathyroid hyperplasia and a thymoma. This association has not been previously documented in the literature.
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PMID:Parathyroid hyperplasia associated with thymoma. 260 66

Serum calcium levels were analyzed after one or more explorations for primary hyperparathyroidism in familial multiple endocrine neoplasia type I. These data covered all 85 operations (performed in many hospitals) on 61 of 62 members from 14 kindreds. After 61 initial operations, there were high rates of persistent or recurrent hypercalcemia (54 percent) and chronic hypocalcemia (10 percent). These rates contrast with lower postoperative rates of hypercalcemia (4 to 16 percent) or chronic hypocalcemia (1 to 8 percent) in large series of primary hyperparathyroidism. Persistent or recurrent hypercalcemia after initial exploration decreased only modestly in patients who underwent surgery after 1975 versus before 1975 (46 versus 63 percent). The rate for long-term remission of hypercalcemia after initial parathyroidectomy was higher after a diagnosis of parathyroid hyperplasia was made (as opposed to adenoma) (57 versus 30 percent, p less than 0.05) and after removal of three or more glands (as opposed to removal of two and a half or less) (70 versus 34 percent, p less than 0.01). Following 24 reoperations, there were also high rates of persistent or recurrent hypercalcemia (46 percent) and chronic hypocalcemia (25 percent). After surgery in unselected patients with primary hyperparathyroidism, recurrent hypercalcemia (as opposed to persistent hypercalcemia) is distinctly uncommon; however, it was frequent in familial multiple endocrine neoplasia type I, with total recurrences increasing from 21 percent at five years to 41 percent at 10 years in patients who showed a normocalcemic interval after surgery. The data indicate that the occurrence of persistent or recurrent hypercalcemia after parathyroidectomy in familial multiple endocrine neoplasia type I remains frequent. Although recurrent hypercalcemia may be characteristic of the response to any technique of parathyroidectomy in familial multiple endocrine neoplasia type I and not preventable, persistent hypercalcemia can be decreased by preoperative recognition of the specific familial cause, involvement of an experienced surgical team, and histologic confirmation of the identification of three or more parathyroid glands.
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PMID:Primary hyperparathyroidism in familial multiple endocrine neoplasia type I. Long-term follow-up of serum calcium levels after parathyroidectomy. 285 57

A syndrome of pulmonary alveolar septal calcinosis, pneumothorax, and pneumomediastinum, leading to rapidly progressive acute respiratory insufficiency and death was observed in 2 children with acute lymphoblastic leukemia (ALL). Primary clinical and radiological considerations in these patients were pulmonary edema and infection, and the diagnosis of pulmonary alveolar septal calcification was established only at autopsy. One patient, a 15-year-old girl, was found also to have parathyroid hyperplasia typical of familial hyperparathyroidism. The other, a 16-month-old girl, showed osteitis fibrosa of the bones and parathyroid hyperplasia of secondary type, suggesting that the pulmonary calcinosis resulted from hypercalcemia caused by a parathormone or prostaglandin-secreting tumor. The cause of pneumothorax and pneumomediastinum may have been rupture of calcified alveolar septa induced by high PEEP during ventilation of these patients. Other possible mechanisms contributing to hypercalcemia and pulmonary calcinosis in children with acute leukemia include bone resorption due to marrow infiltration, immobilization syndrome, renal failure, and administration of calcium, phosphate, or bicarbonate. This complication of acute leukemia in childhood is rare (2 patients in 430 autopsied over the period 1961-1982 at Childrens Hospital of Los Angeles). How often the process can be reversed if diagnosed before severe respiratory insufficiency is present is not known.
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PMID:Pulmonary alveolar septal calcinosis causing progressive respiratory failure in acute lymphoblastic leukemia in childhood. 347 56

Although the commonest familial form of primary hyperparathyroidism is parathyroid hyperplasia, a few families have manifested parathyroid adenomas. We describe a family in which four members developed cystic parathyroid adenomas. Although calcium levels returned to normal after resection of the adenoma, a second adenoma would often develop several years later (we have termed this temporal sequence adenomatosis). Each adenoma had a cystic histologic appearance, and three of four normal-sized parathyroid glands also contained many cysts. No other endocrine tumors have appeared, but in three patients the hyperparathyroidism was complicated by fibrous maxillary or mandibular tumors that resembled ossifying fibromas rather than the brown tumors generally found in patients with hyperparathyroidism. Each patient with an adenoma was hypercalciuric, but two were obligate carriers of hypocalciuric hypercalcemia. This familial occurrence of the rare cystic parathyroid adenoma suggests the presence of a distinct hereditary syndrome. The genetic basis may be the simultaneous inheritance of familial hypocalciuric hypercalcemia and another trait that may increase the urinary excretion of calcium.
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PMID:Familial cystic parathyroid adenomatosis. 359 49

A unique case of familial hyperparathyroidism associated with carcinoma of the colon is presented. Two brothers presented initially with colonic carcinoma and years later both were found to have primary hyperparathyroidism on the basis of parathyroid hyperplasia. This raises the issue of associated malignancies in patients with hyperparathyroidism, especially if they are found to be familial. One member of the family developed severe, recurrent hypercalcemia with bone disease, and thus the need for continued follow-up is emphasized.
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PMID:Familial hyperparathyroidism in association with colonic carcinoma. 359 82

Parathyroidectomy is usually followed by a decrease in serum calcium, a lessening of symptoms, and a normocalcemic state that continues for years. Evaluation of parathyroid gland function after parathyroidectomy over a protracted period showed a continued hypersecretory state in many normocalcemic patients and is reported here for the first time. Patients identified with parathyroid hyperplasia (more than one gland excised) and patients who later developed mild renal failure were excluded. Seventy-seven patients undergoing parathyroidectomy with only one enlarged gland removed and the other normal-sized glands viewed or examined by biopsy were followed up from 5 to 16 years. Two patients developed recurrent hypercalcemia at 4 and 9 years after surgery. Seventy-five patients are considered "cured" and have normal serum calcium values. However, 28 (37%) of these normocalcemic patients have persistent elevations of parathyroid hormone. This increased parathyroid gland function suggests a continuing stimulation of the remaining glands. The rarity of clinical recurrence may be related to effective adaptations that prevent overt hypercalcemia. Many parathyroid adenomas appear to represent nonneoplastic disease.
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PMID:Parathyroid metabolism after operative treatment of hypercalcemic (primary) hyperparathyroidism. 368 52

We have studied 46 members of a large kindred with familial hypocalciuric hypercalcaemia (FHH) after a neck exploration failed to cure hypercalcaemia in an asymptomatic patient. Serum calcium, serum phosphate, plasma parathormone and vitamin D metabolites do not distinguish affected members from patients with hyperparathyroidism. Because of the continuing debate as to whether or not FHH is a variant of, or distinct from, hyperparathyroidism, we have carried out a review of surgical experience with subtotal parathyroidectomy in hyperparathyroidism secondary to parathyroid hyperplasia and in FHH. Whereas the procedure is successful in 90 per cent of the former cases only one case of FHH has been cured by it. This provides evidence for the two conditions being aetiologically distinct. Before patients with asymptomatic hypercalcaemia are referred for parathyroid surgery the calcium:creatinine clearance ratio should be measured using a 2 h urine sample collected after an overnight fast and a fasting blood sample. If this ratio is less than 0.01 then screening of first degree relations should be undertaken before any parathyroid surgery is performed. Unnecessary surgery can therefore be avoided.
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PMID:Familial hypocalciuric hypercalcaemia as a differential diagnosis of hyperparathyroidism: studies in a large kindred and a review of surgical experience in the condition. 394 16


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