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 patient with metastatic islet cell carcinoma of the pancreas, recurrent peptic ulcer disease, and hypergastrinemia (Zollinger-Ellison syndrome) developed symptomatic hypercalcemia and renal insufficiency; she was treated with streptozotocin after parathyroidectomy failed to control her hypercalcemia. Shortly after somewhat less than the usual recommended dose of streptozotocin was administered, the serum calcium concentration fell to near normal with complete resolution of symptoms. Seven months after therapy, mild hypocalcemia, consistent with her degree of renal impairment was noted. However, mild hypercalcemia recurred 13 months after therapy. Shortly after streptozotocin therapy, the mean serum gastrin concentration fell to near normal with radiographic disappearance of the anastomotic ulcer. At 7 and 13 months after therapy, serum gastrin levels were normal. Streptozotocin therapy was accomplished without major complications; specifically, without a detrimental effect on the creatinine clearance. Thus, although hypercalcemia in patients with pancreatic islet cell tumors is often due to associated primary hyperparathyroidism, in some patients it may be due to secretion of a hypercalcemic substance from the tumor and may respond to streptozotocin. Similarly, hypergastrinemia in patients with islet cell tumors may also respond to streptozotocin.
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PMID:Pancreatic islet cell carcinoma with hypercalcemia and hypergastrinemia: response to streptozotocin. 13 70

Twelve parathyroid chief cell adenomas from patients with primary hyperparathyroidism were incubated in a tissue culture system in the presence of different calcium concentrations and for various time periods. The endocrine response of the tissue was examined electron microscopically and radioimmunologically. After incubation in a medium of low calcium concentration the parathyroid adenomas showed ultrastructural signs of stimulation with proliferation of the hormone-synthesizing organelles. The development of the ultrastructural response could first be observed after four hours and increased up to several days. Radioimmunologically, an increase of the hormone secretion could be demonstrated. Converse results were obtained after incubation of the tumor tissue under suppressive culture conditions. To check for de-novo synthesis of the hormone released the tissue was incubated in a 75Se-methionine-containing medium. This resulted in radioactivity of the secreted parathyroid hormone, indicating de novo synthesis in our culture system. The biological potency of the released hormone was demonstrated by comparison of the PTH out of the medium with the international human MRC standard using two different radioassays.
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PMID:Correlation of electron microscopic and secretory response of human parathyroid adenomas with different calcium concentrations in organ culture. 15 Jan 11

Hypercalcemia calls first for supportive measures, eg, adequate hydration, movement or mobilization of the patient to the greatest amount tolerated, and reevaluation of drugs being taken. When immediate lowering of the serum calcium level is not clinically mandatory, oral administration of furosemide, corticosteroid, or phosphorus should be considered. In acute emergencies, saline loading and parenteral furosemide therapy should be tried first, except in a patient with renal failure and congestive heart failure, in whom peritoneal dialysis or hemodialysis should be used instead. Calcitonin can be given for the first 12 to 24 hours to lower serum calcium concentration until a definitive management plan is formulated. Corticosteroid, if not contraindicated, should be started as soon as possible. In severe primary hyperparathyroidism with hypophosphatemia, phosphorus can be given intravenously until oral phosphate therapy can be established. Surgery, of course, should be performed as soon as possible. In most cases of neoplasia, mithramycin given according to a recommended schedule is safe and frequently effective. In desperate cases, additional use of prostaglandin synthesis inhibitors probably now is justified by empirical observations. All of these therapeutic measures are used only to stabilize electrolyte balance so that the primary cause of the hypercalcemia can be treated.
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PMID:Management of hypercalcemia. 15 84

Hypercalcemia is very uncommon in small cell (oat cell) carcinoma of the lung. Two cases of this neoplasm associated with symptomatic hypercalcemia are described. Despite normal skeletal roentgenograms, metastatic bone disease was demonstrated by abnormal bone scans and bone biopsies in both patients. The combination of conventional antihypercalcemia therapy, cytotoxic cancer chemotherapy, and synthetic salmon calcitonin corrected the hypercalcemia despite progression of the small cell carcinoma. One patient with elevated serum immunoreactive parathyroid hormone (PTH) had a parathyroid adenoma at autopsy. This association emphasizes that in cases of bronchogenic small cell carcinoma with hypercalcemia, conincidental primary hyperparathyroidism should be considered.
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PMID:Hypercalcemia in small cell (oat cell) carcinoma of the lung. Coincident parathyroid adenoma in one case. 17 Oct 50

Hyperfunctioning parathyroid carcinoma is a relatively rare endocrine tumor, accounting for approximately 1% of all cases of primary hyperparathyroidism. The diagnosis is suspected when the tumor is large, parathyroid hormone (iPTH) levels are high, and a palpable tumor is present in the neck. Patients who have recurrence of hyperparathyroidism several months after surgical treatment should be suspected of having a recurrent or persistent parathyroid carcinoma. At operation, a large invasive tumor is usually found. The fibrous, inflammatory-like reaction is the most characteristic indication of malignancy. Even in tumors with minimal invasiveness, the possibility of a carcinoma should be considered if the tumor has mitotic activity and a monotonous instead of a pleomorphic cellular population. If the surgeon can recognize the possibility of parathyroid malignancy and adequately treat the patient during the initial operation, more gratifying results should be obtained.
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PMID:Cancer of the parathyroid glands. 43 61

A 17-year-old woman manifested fever, abdominal pain, headache, and hypertension caused by a solitary, benign pheochromocytoma. She also had hypercalcemia and elevated plasma immunoreactive calcitonin levels. After removal of the pheochromocytoma, calcium and calcitonin levels returned to normal. Studies of peripheral and tumor venous blood showed no excess or ectopic parathyroid hormone secretion, but the tumor contained and secreted calcitonin. Sporadic pheochromocytoma may secrete calcitonin and cause hypercalcemia by non-parathyroid hormone-mediated mechanisms. The potential is clearly present for confusion with multiple endocrine neoplasia, type 2 (medullary thyroid carcinoma, pheochromocytoma, and primary hyperparathyroidism).
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PMID:Pheochromocytoma associated with hypercalcemia and ectopic secretion of calcitonin. 46 64

In order to investigate the frequency of fasting hypergastrinaemia in primary hyperparathyroidism (A) and in chronic hypercalcaemia (B), in 40 and 16 patients respectively gastrin, parathyroid hormone (PTH) and serum calcium levels were measured and compared with those of a control group (40 subjects) with similar distribution of sex and age. Moreover, possible linear relationships between these parameters were investigated. Notwithstanding significant differences in calcium and PTH levels between the three groups (A: high PTH, high Ca++; B: low PTH, high Ca++; C: normal PTH and Ca++ levels), no significant difference in gastrin levels were found. However, in the first group, a marked increase of gastrin was observed in one patient, very probably affected by a gastrin-secreting tumor (positive secretin test). While no linear relationship between PTH and gastrin values was present in all the three groups, a significant correlation between serum calcium and fasting gastrin was detectable in the group A, ruling-out the above mentioned patient. Present data suggest that PTH does not modify gastrin levels and that chronic moderate hypercalcaemia does not raise serum fasting gastrin, at least in clinical conditions. Moreover, the frequency of hypergastrinaemia in hyperparathyroidism is very low and it seems to be present only in patients with gastrin-secreting tumors.
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PMID:Fasting serum gastrin in primary hyperparathyroidism and in chronic hypercalcemia. 54 29

The incidence of fractures in primary hyperparathyroidism is highly variable. The possibility that there might be an increased susceptibility to fracture is discussed. Healing in most is without delay. Three cases of delayed or nonunion following fracture are presented. In all three, healing accelerated dramatically after excision of a parathyroid adenoma. A pathological fracture secondary to the hyperparathyroidism of parathyroid carcinoma healed after excision of the tumor allowed regression of the osseous lesions. The endocrinologic mechanisms which cause nonunion in a small percentage of cases have not been clearly elucidated.
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PMID:Delayed fracture healing in primary hyperparathyroidism. 59 80

A simple, instant, and reliable test called the Density Test, based on the difference in density between the normal and the diseased parathyroid tissue, was performed intraoperatively in 73 patients with primary hyperparathyroidism. Whereas the normal parathyroid tissue floated, the diseased tissue invariably sank in a mannitol solution with a density range between 1.049 and 1.069. With the aid of this test, a diagnosis of adenoma was made in 66 patients and of primary hyperplasia in the remaining seven. In every case the diagnosis was subsequently confirmed. Forty-two of the 66 patients with an adenoma (64%) had a unilateral exploration of the neck. The Density Test saved these patients from an unnecessary contralateral exploration by the finding of an adenoma and a normal second gland in the same side of the neck. These data show that the Density Test is useful in the intraoperative diagnosis of a diseased from a normal parathyroid tissue. Tissue that sinks within the density range of 1.049 and 1.069 is without exception diseased and should therefore be either partially or completely excised even if the gland is of average size or only of slight enlargement. If it does not sink, it is virtually certain to be normal and should be spared. The Density Test provides a valuable clue in the differentiation of primary parathyroid hyperplasia from neoplasia.
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PMID:A density test for the intraoperative differentiation of parathyroid hyperplasia from neoplasia. 61 1

Various hormones have been implicated in the genesis of hypercalcemia in patients with malignancy. Ectopic secretion of PTH by tumor has been documented in only a few patients; rather, elevated levels of circulating iPTH have been presumed to reflect tumor production of hormone in most patients. Small fragments of PTH, as well as polypeptides larger than native PTH, have been described; their biological roles are unclear. The pattern of immunoreactivity, however, has been used to differentiate patients with ectopic hyperparathyroidism from patients with concomitant primary hyperparathyroidism. Vitamin D-like sterols produced by breast cancer seldom reach plasma levels necessary for physiological effects. Members of the prostaglandin family have been proposed to induce hypercalcemia through osteoclast activation or alteration of the immune system and also to affect the frequency of bone metastases. At present, no direct evidence is available to prove a direct role for these effects and prostaglandins are most useful as possible indicators of disease activity.
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PMID:Mechanisms of hypercalcemia in malignancy. 65 92


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