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)

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
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PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

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

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

Primary hyperparathyroidism is a not uncommon disease in the elderly. A prevalence of 3% for women and 1% for men is reported in subjects aged 65 years and over. Routine serum calcium determination and parathyroid hormone radioimmuno-assay allow to make an early diagnosis in still asymptomatic subjects. In the elderly the clinical features of the disease are often aspecific presenting with psychiatric and/or neuromuscular and/or cardiovascular disorders. This report refers to a 75 year-old woman admitted to our Department with a suspicion of senile dementia. She was affected by loss of memory, hallucinations, nausea, loss of appetite, mild polydipsia and polyuria. The patient was dependent in one activity of daily living (Index of Independence in Activities of Daily Living, ADL) and partially dependent in instrumental activities of daily living (Instrumental Activities of Daily Living Scale, IADL). The Short Portable Mental Status Questionnaire (SPMSQ) and the Geriatric Depression Scale (GDS) showed mild mental impairment and mild depression. Routine biochemical screening revealed a significant hypercalcemia. Parathormon assay and parathyroid scintigram were performed to confirm the diagnosis of primary hyperparathyroidism. After treatment of dehydratation and hypercalcemia, parathyroidectomy was performed: a single parathyroid adenoma was found and removed. On discharge the patient was lucid and able to carry out all ADLs and IADLs.
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PMID:[Neuropsychologic symptoms of primary hyperparathyroidism in the elderly. Report of a clinical case]. 773 70

A 24 year old patient with epigastric pain, polyuria, polydipsia and hypercalcemia was admitted to the hospital. Besides the frequent causes of hypercalcemia such as primary hyperparathyroidism and malignancy-related hypercalcemia we had to consider sarcoidosis because of massive splenomegaly. The interstitial lung disease shown on x-ray films of the chest, the epithelioid granulomas in lung tissue and the increased ACE confirmed the diagnosis of sarcoidosis. Hypercalcemia is found in less than 5% of all cases with sarcoidosis. After treatment with steroids, diphosphonates and diuretics all symptoms and the hypercalcemia improved.
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PMID:[Polyuria, polydipsia]. 780 Oct 19

This article report a study of 23 cases of hypercalcemia crisis resulting from primary hyperparathyroidism (18 cases), carcinoma (4 cases) and vitamin D intoxication (1 case). In addition to the symptoms of primary diseases, the patients with hypercalcemia crisis often had anorexia, nausea, vomiting, polydipsia, polyuria, psychoneurotic symptoms, arrhthmia. The severity of the symptoms was proportional to the degree of hypercalcimia. Serum calcium concentration of patients in hypercalcemia crisis should be equal or higher than 3.75 mmol/L (15 mg/dl) or serum ionized calcium higher than 1.88 mmol/L. Treatment hypercalcemia crisis consisted of rapidly lowering the serum calcium level by various measures while actively treating the primary diseases. Our experience is to supply normal saline intravenously or orally to increase the extracellular fluid and to enhance excretion of the urine calcium by administrating furosemide. In this paper, serum calcium concentration of 5 patients with hypercalcemia crisis treated with salmen calcitonin was reduced in varying degrees. The above mentioned treatment would be beneficial to the alleviation of the crisis and the preparation for operative treatment.
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PMID:[The preliminary experiences of diagnosis and treatment for hypercalcemia crisis--clinical analysis of 23 cases]. 798 37

Primary hyperparathyroidism is a rare disease in children and is characterized by conspicuous skeletal and renal changes. A 12 year old male patient presented with symptoms of polydipsia, polyuria, general weakness, nausea, and vomiting which had begun 3 months earlier, and showed typical laboratory findings of primary hyperparathyroidism. Confirmatory diagnosis was made by elevated parathyroid hormone concentration in serum, technetium-thallium subtraction scan imaging method and histopathologic finding of chief cell hyperplasia. The laboratory findings revealed elevated levels of BUN, creatinine and decreased GFR. Kidney biopsy showed typical calcium deposits in tubules with marked tubulointerstitial infiltration. After subtotal parathyroidectomy, clinical findings improved remarkably.
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PMID:A case of primary hyperparathyroidism with hypercalcemic nephropathy in children. 799 97

Persistent hypercalcemia attributable to parathyroid gland hyperplasia was identified in 6 dogs with primary hyperparathyroidism. Clinical signs included polydipsia (n = 4), polyuria (n = 4), and signs caused by cystic calculi (n = 3). Abnormal clinical pathologic findings included hypercalcemia (mean, 13.6 mg/dl; range, 12.6 to 14.7 mg/dl; n = 6), hypophosphatemia (mean, 2.2 mg/dl; range, 1.4 to 2.9 mg/dl; n = 6), high serum alkaline phosphatase activity (mean, 222 IU/L; range, 161 to 286 IU/L; n = 3), and isosthenuria (mean, 1.012; range, 1.006 to 1.017; n = 6). Serum parathyroid hormone concentration was within the reference range or high (mean, 23 pmol/L; range, 7 to 119 pmol/L; reference range, 1.5 to 13 pmol/L) in all dogs. At surgery, the number of large parathyroid glands was variable, being limited to 1 gland in 3 dogs, 2 glands in 2 dogs, and 4 glands in 1 dog. All visibly large parathyroid glands were surgically removed from each dog. Serum calcium concentration decreased into or below the reference range within 72 hours of surgery in all dogs, confirming the diagnosis of primary parathyroid disease. Multiple nodules of adenomatous hyperplasia were identified in each dog. All 6 dogs were treated with vitamin D and calcium carbonate following surgery. The dog from which all 4 parathyroid glands were removed has remained eucalcemic for more than 1 year with vitamin D supplementation. Vitamin D and calcium administration was discontinued within 4 to 12 weeks of surgery in the remaining 5 dogs. These dogs remained eucalcemic without vitamin D supplementation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary parathyroid gland hyperplasia in dogs: six cases (1982-1991). 847 30


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