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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary hyperparathyroidism (PHPT) was the most likely diagnosis in 68 non-thiazide-treated patients with hypercalcaemia detected in a health screening. The group comprised 55 females and 13 males, with a mean age of 55.0 +/- 0.7 (S.E.M.) years. On a pair basis these patients (the observation group) were compared with a series of 68 age- and sex-matched normocalcaemic subjects (the control group) selected from the health screening register. Renal calcui and reduced creatinine clearance were encountered less frequently in the observation group than in many reports of hospitalized patients with PHPT. Compared with the control group, the observation group comprised a greater number of subjects with renal calculi (usually multiple and bilateral), constipation, mental depression and reduced creatinine clearance. The ECG Q-T interval was shorter in the observation group than in the control group. No differences were found with respect to the occurrence of gastritis and/or peptic ulcer, poly-dipsia, polyuria and general muscle weakness. On the basis of this and a previous study it was concluded that at least 3% of the 15903 subjects participating in the health screening suffered from "asymptomatic" hypercalcaemia and most probably from "asymptomatic" PHPT.
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PMID:Clinical and laboratory findings in subjects with hypercalcaemia. A study including cases with primary hyperparathyroidism detected in a health screening. 98 6

Several recent articles question whether patients with asymptomatic hyperparathyroidism and minimal hypercalcemia should be treated by parathyroidectomy. We therefore reviewed our experience in 103 consecutive patients with primary hyperparathyroidism who were treated by parathyroidectomy to determine, first, how many of these patients had asymptomatic or symptomatic hyperparathyroidism, and second, did these patients benefit from parathyroidectomy? We also analyzed the safety of parathyroidectomy in 426 consecutive patients, including 79 who required reoperation for hyperparathyroidism, specifically looking for complications and the outcome of these procedures. Our study documents the following: (1) only 2 of 103 (2%) patients referred for parathyroidectomy had "true" asymptomatic hyperparathyroidism; (2) only symptoms of fatigue, bone pain, and weight loss correlated with the degree of hypercalcemia, whereas muscular weakness, psychiatric symptoms, nocturia, polyuria, recent memory loss, constipation, and nephrolithiasis did not; (3) only 1 of 15 patients who were referred as asymptomatic were truly asymptomatic after more thorough questioning, and all 14 improved following parathyroidectomy; (4) 81% of the patients who were referred with symptoms improved following parathyroidectomy; and (5) permanent complications occurred in only 4 patients. All but 1 had reoperations for persistent or recurrent hyperparathyroidism (3 vocal cord paralyses and 1 hypoparathyroidism requiring autotransplantation of cryopreserved parathyroid tissue). There was 1 death of an 84-year-old woman with hypercalcemic crisis. Thus, most patients with hyperparathyroidism are symptomatic and benefit symptomatically and metabolically from parathyroidectomy, which is a safe operation.
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PMID:Diagnosis and management of asymptomatic hyperparathyroidism: safety, efficacy, and deficiencies in our knowledge. 176 65

Primary hyperparathyroidism was thought 30 years ago to be a rare disease, and the diagnosis was most often made in patients presenting with either bone disease or kidney stones. Today the minority of patients with hyperparathyroidism present with such symptoms, a fact accounted for by the introduction into general medical practice three decades ago of laboratory technology for efficiently determining the serum concentrations of various blood minerals, including calcium. Hypercalcemia was detected more frequently, and it was realized that most patients with hyperparathyroidism either had minor symptoms, such as constipation, polyuria, tiredness, and muscle weakness, or they were "asymptomatic" and indistinguishable from normal subjects. It was thought that primary hyperparathyroidism was a progressive disease and that sooner or later all patients would become symptomatic and require parathyroidectomy. Since this operation was curative in a high percentage of cases, it was recommended for virtually all patients once the diagnosis was established. In this contribution the long-term benefits of parathyroidectomy in patients with and without symptoms from primary hyperparathyroidism are reviewed. It is concluded that a multicenter prospective randomized trial is needed to resolve the indications for operative and nonoperative management of patients with this disease.
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PMID:Surgical therapy of patients with primary hyperparathyroidism: long-term benefits. 176 66

Shortly after diagnosis of primary hyperparathyroidism, a patient had serum hyperosmolality, polyuria, isosthenuria, profound potassium depletion, and elevated plasma antidiuretic hormone levels, all consistent with nephrogenic diabetes insipidus. After parathyroidectomy, serum calcium and serum osmolality levels fell concurrently. Profound potassium deficits did not recur. We propose that (1) hypercalcemia produced a concentrating defect and polyuria; (2) renal tubular acidosis and polyuria combined to produce severe potassium depletion; (3) hypokalemia potentiated the nephrogenic diabetes insipidus caused by hypercalcemia; and (4) postoperative disappearance of the diabetes insipidus confirmed its reversible, purely metabolic causes.
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PMID:Primary hyperparathyroidism and coexisting nephrogenic diabetes insipidus: rapid postoperative correction. 188 51

A 57-year-old female was admitted to our hospital with general lassitude, loss of appetite, nausea, upper abdominal pain, thirst, polydipsia and polyuria. On admission, she had an asymmetrical pear-shaped tumor in the right supraclavicular region and severe hypercalcemia. Plasma C-PTH was elevated to 22.72ng/ml. Plasma calcitonin was also elevated to 336 pg/ml. She died of respiratory and cardiac failure of two weeks after admission without any positive response to the treatment, including hemodialysis. Pathohistologically, the tumor was a parathyroid adenoma. The concentrations of C-PTH, intact PTH and calcitonin in the tumor tissue were markedly high: 4.56 micrograms/g wet, 13.9 ng/g wet and 50.7 ng/g wet, respectively. Immunohistologically, the tumor cells and the fibrous stroma were stained strongly positive to rabbit anti-human calcitonin antibody and rabbit anti-human N-PTH antibody by indirect immunoperoxidase staining. Calcitonin-producing tumors, except for medullary thyroid carcinoma are rarely reported. To our knowledge, this is the first report of such a calcitonin-producing parathyroid adenoma associated with primary hyperparathyroidism.
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PMID:A case of calcitonin-producing parathyroid adenoma with primary hyperparathyroidism. 258 94

An adult Keeshond had clinical signs associated with hypercalcemia, including inappetence, polyuria, polydipsia, and vomiting. Blood biochemical findings and urinary clearance studies were consistent with a diagnosis of primary hyperparathyroidism. Histomorphometric analysis of trabecular bone in an iliac crest biopsy indicated increased bone remodeling activity. Surgical exploration of the neck revealed an oval mass, which was removed by blunt dissection. Histologic diagnosis was parathyroid gland adenoma. The dog died because of renal failure on the eighth postoperative day. This report defines primary hyperparathyroidism in the dog, thus facilitating diagnosis for the veterinary clinician.
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PMID:Primary hyperparathyroidism in a dog: biochemical, bone histomorphometric, and pathologic findings. 380 43

Acute primary hyperparathyroidism is an unusual form of primary hyperparathyroidism characterized by life-threatening hypercalcemia. Forty-three cases reported in the literature since 1974 are reviewed, along with five new cases. The average age of the patients was 55 (27 to 82), with an even distribution between men and women. Marked hypercalcemia (17.5 +/- 2.1 mg/dl) was accompanied by parathyroid hormone levels 20 times normal. Virtually all patients had symptoms. Hyperparathyroid bone disease occurred in 53 percent of patients; even more (69 percent) had nephrolithiasis or nephrocalcinosis. Combined renal and skeletal involvement was seen in 50 percent. Only three deaths were recorded. The pathophysiology of the acute hyperparathyroid state is unknown but appears to consist of uncontrolled parathyroid hormone secretion followed by cycles of hypercalcemia, polyuria, dehydration, reduced renal function, and worsening hypercalcemia. These features of acute primary hyperparathyroidism are compared with the features reported in the literature antedating multichannel screening, and with the features of the common form of primary hyperparathyroidism. Clinical guidelines by which the diagnosis may be suspected are also reviewed.
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PMID:Acute primary hyperparathyroidism. 381 20

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

A 13-year-old girl presenting with abdominal pain, polyuria, polydipsia, and radiologically confirmed renal calculi was diagnosed as having primary hyperparathyroidism. Laboratory data revealed markedly elevated serum calcium, low phosphorus, and elevated parathyroid hormone. Other parathyroid function tests also confirmed the diagnosis of primary hyperparathyroidism. Ultrasound examination showed a small echogenic nodule in the parathyroid gland. Following a single gland resection, the extremely high serum calcium level promptly decreased to normal range, and it has remained normal.
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PMID:Primary hyperparathyroidism. Case report and management. 399 65

Primary hyperparathyroidism was diagnosed in two German shepherd pups from a litter of four females. Clinical signs were apparent by two weeks of age and included stunted growth, muscular weakness, and polydipsia/polyuria. Radiography revealed diffuse reduction in bone density. Both pups had marked hypercalcemia, hypophosphatemia, increased plasma immunoreactive parathyroid hormone concentrations and increased fractional clearance of inorganic phosphate in the urine. Intravenous infusion of one affected pup with calcium gluconate failed to suppress the plasma concentration of immunoreactive parathyroid hormone, suggesting autonomous secretion of parathyroid hormone. Necropsy of the other pup at eight weeks of age revealed diffuse hyperplasia of parathyroid chief cells, nodular hyperplasia of thyroid C-cells, skeletal alterations consistent with fibrous osteodystrophy, hypercalcemic nephropathy, and extensive mineralization of the lungs and gastric mucosa. The dam and sire were half sibs. One male pup from a previous litter of six had developed similar clinical signs and radiographic lesions, suggesting autosomal recessive inheritance. This is the first report of hereditary primary hyperparathyroidism in domestic animals, a disease which may be analogous to hereditary neonatal primary hyperparathyroidism in children.
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PMID:Primary hyperparathyroidism in German shepherd dogs: a disorder of probable genetic origin. 646 98


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