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)

We report results for adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood from 183 patients with disorders of calcium metabolism (primary hyperparathyroidism, secondary hyperparathyroidism of malabsorption, primary hypoparathyroidism, Paget's disease, acromegaly, hypercalcemia of malignancy, osteoporosis, sarcoidosis, idiopathic hypercalciuria, and familial hypocalciuric hypercalcemia). The correlation and the equation for the linear regression between adjusted ionized calcium (y) and actual ionized calcium (x) were y = 1.011x + 0.005 mmol/L, r = 0.992, Sy,x = 0.021 mmol/L. Results were similar within each diagnostic group. Consistent agreement between adjusted and ionized calcium was observed in 96.7% of patients representing a variety of the most frequently encountered disorders of calcium metabolism. Thus we find adjusted ionized calcium to be as useful as actual ionized calcium for evaluation of patients with such disorders. Adjusted ionized calcium may therefore also be a logical choice for establishing agreement between laboratories for reference intervals in healthy adults.
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PMID:Adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood compared for clinical evaluation of patients with disorders of calcium metabolism. 231 Dec 30

Eighty nine cases with hypercalcaemia were seen during the period 1975-87. Malignancy of nonparathyroid tissue was responsible in 72 cases (80.9%). The other causes were primary hyperparathyroidism (11 cases), hypervitaminosis D (5) and sarcoidosis (1). Every patient with hypercalcaemia needs careful evaluation to establish the aetiological basis so that specific treatment may be instituted.
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PMID:Evaluation and aetiopathogenesis of hypercalcaemia. A study of 89 patients. 238 15

In normal individuals, 1,25-dihydroxyvitamin D (1,25-D) levels regulate calcium (Ca) absorption according to Ca intake; its synthesis is stimulated by low Ca intake, probably via increased parathyroid hormone (PTH) secretion, to increase Ca absorption, and suppressed during high intake to reduce Ca absorption. The body also adapts Ca absorption in response to renal Ca excretion, and phosphate absorption in response to phosphate intake. These adaptations may fail or be impaired in certain diseases. In disorders of overadaptation, the intestinal tract absorbs excessive amounts of Ca due to overproduction of 1,25-D, as in absorptive hypercalciuria, sarcoidosis, primary hyperparathyroidism, and tumoral calcinosis. Intestinal hyperabsorption and hypercalciuria may occur on both low- and high-Ca diets. Primary hyperparathyroidism and hypoparathyroidism are bihormonal, related to over- and underproduction, respectively, of both 1,25-D and PTH. Underadaptation disorders are typically related to low 1,25-D synthesis or resistance to this metabolite; examples include postmenopausal osteoporosis, chronic renal failure, and osteomalacia. Many of these adaptational disorders can be relieved or improved by manipulating Ca, phosphate, sodium, or protein intake or by administering exogenous 1,25-D. Overabsorption of Ca and other substances, such as oxalate, may be responsible for Ca nephrolithiasis. Hypocitraturia (which may be a complication of certain diseases or the result of unbalanced diet or excessive exercise), diets high in readily metabolizable sugars and purine-rich proteins (meat, poultry, and fish), and low fluid intake can all contribute to stone formation. Various regimens may reduce the risk of Ca nephrolithiasis.
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PMID:Calcium metabolism. 268 27

Hypercalcaemia is a frequent situation in clinical practice. An earlier detection is facilitated by routine analysis of serum calcium. The clinical manifestations depend on severity and the rate of onset of hypercalcaemia. Paucisymptomatic and asymptomatic presentations are the most frequent. Causes of hypercalcaemia are numerous and the mechanisms are various. PTH and vit. D play a preponderant part. In first of all iatrogenic cause are eliminated (all vit D preparations, thiazide diuretics, milk-alkali syndrome). Among non neoplastic hypercalcaemia primary hyperparathyroidism is the first diagnosis. Nephrolithiasis and asymptomatic forms are the most frequent presentations actually. The biochemical profile is not always typical. Generally the association of echography and tomodensitometry lead to the topographic diagnosis. Parathyroid surgical exploration is often necessary in difficult cases. Secondary, the other rare causes of hypercalcaemia are studied: sarcoidosis and granulomatosis disease, thyrotoxicosis and dome endocrinopathies, immobilisation hypercalcaemia, familial hypocalciuric, hypercalcaemia. All of this causes of hypercalcaemia are potentially reversible.
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PMID:[Non-neoplastic hypercalcemia]. 271 64

Patients presenting with hypercalcaemia caused by the co-existence of sarcoidosis and primary hyperparathyroidism may present a diagnostic problem. Tests for sarcoid activity, together with the cortisone suppression test and an estimation of the immunoreactive parathyroid hormone level are all necessary to differentiate between those conditions.
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PMID:Hypercalcaemia in sarcoidosis co-existing with primary hyperparathyroidism. A case report. 272 21

We recently encountered two patients with coexistent hyperparathyrodism and sarcoidosis presenting with hypercalcaemia. The association between hypercalcaemic primary hyperparathyroidism and sarcoidosis is reviewed.
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PMID:Co-existing hyperparathyroidism and sarcoidosis presenting with hypercalcaemia--a diagnostic challenge. 279 75

Hypercalcemia is a common biochemical abnormality. It is usually possible to make a presumptive diagnosis of its cause by relatively simple means. In a large majority of cases this involves differentiating between primary hyperparathyroidism and malignancy-associated hypercalcemia. Clinical evaluation and parathyroid hormone assay are particularly useful. Since the management of hypercalcemia in the short term generally involves non-specific measures such as rehydration, the inability to make an immediate accurate diagnosis presents less of a problem than might otherwise be the case. The definitive diagnosis of hyperparathyroidism, malignancy and sarcoidosis requires histological confirmation.
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PMID:Clinching the diagnosis: an approach to the investigation of hypercalcemia. 302 Apr 90

Primary hyperparathyroidism has been increasingly diagnosed among whites since the advent of the biochemical autoanalyzer. However, the condition remains uncommon among Orientals. Our experience with 31 patients at the Queen Mary Hospital, University of Hong Kong, in the periods before and after we began to use the biochemical autoanalyzer was reviewed. The prevalence of primary hyperparathyroidism rose slightly from 3.1 to 3.7 per 100,000 hospital population. In both periods skeletal manifestation was the major clinical presentation, followed by hypercalcemic symptoms and urologic disease. Asymptomatic hypercalcemia occurred in three of 31 patients despite the use of the biochemical autoanalyzer. Preoperative localization was carried out in 27 patients and was helpful in nine (33.3%) of them. The surgeon explored all four parathyroids, removed the diseased gland(s), and examined a biopsy specimen of one normal-appearing gland. There were 27 adenomas, two carcinomas, one four-gland hyperplasia, and one sarcoidosis. Twenty-eight patients had transient hypocalcemia after parathyroidectomy and required calcium supplements for variable periods. Before and after we began to use the biochemical autoanalyzer, there was minimal change in the prevalence and clinical pattern of primary hyperparathyroidism seen in our hospital. In our experience, successful parathyroidectomy depends more on the surgeon's operative technique than on preoperative localization.
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PMID:Primary hyperparathyroidism: its clinical pattern and results of surgical treatment in Hong Kong Chinese. 336 91

From October 1981 to the end of 1984, 13 patients with primary hyperparathyroidism (PHPT) and 17 with secondary hyperparathyroidism (SHPT) received fresh autografts of diseased parathyroid tissue into their subcutaneous abdominal adipose tissue. Because of previous surgery to treat hyperparathyroidism (HPT) (23%), concomitant thyroid surgery (26%), and a high proportion of multiglandular disease (73%), the patients were at high risk for HPT. During the follow-up period, hypercalcemia was diagnosed in five patients and successfully treated in four: by graft excision in two patients, by excision of a fourth gland from the neck in one patient, and with prednisolone in a patient with sarcoidosis. At follow-up (an average of 30 months after grafting), one patient had HPT and 29 others were euparathyroid. Parathyroid tissue can survive and function in adipose tissue, as was demonstrated by normocalcemia in 14 patients (whose only probable remaining parathyroid tissue had been transplanted into fat), by the demonstration that graft-dependent hypercalcemia could be eliminated by excision of the transplant, and by the demonstration of viable parathyroid tissue by microscopic examination of excised grafts. Autotransplantation of diseased parathyroid tissue into fat is simple and reliable. In cases of recurrent HPT, all or a portion of the graft can be removed while the patient is under local anaesthesia. If infiltrating growth occurs, broad excisions can be performed without sacrificing vital structures.
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PMID:Autotransplantation of diseased parathyroid glands into subcutaneous abdominal adipose tissue. 357 47

This is a first report of primary hyperparathyroidism (HPT) masquerading as a destructive fibrous sphenoid sinus "Brown tumor" associated with progressive blindness and hypercalcemia. Diagnosis of a Brown tumor was delayed despite serial computerized tomography of the head and repeated transnasal and transethmoid sphenoid biopsies demonstrating diffuse fibrosis. Only detection and medical evaluation of hypercalcemia, demonstrating elevation of both serum calcium and C-terminal parathyroid hormone with an elevated chloride/phosphate ratio, prompted neck exploration, thus confirming a solitary left superior parathyroid adenoma. Postoperative normocalcemia occurred synchronously with the return of light perception and the arrest of sphenoid sinus and parasellar erosion. Although maxillary Brown tumors of secondary HPT have been reported, this is the first report of osteitis fibrosa of the sphenoid sinus. Differential diagnosis of an erosive sphenoid lesion with cranial nerve dysfunction, exclusive of inflammatory or vascular disease, should include sarcoidosis, primary and metastatic sphenoid carcinoma, fibrous dysplasia, giant cell reparative granuloma, midline lethal granuloma, chordoma, and chondrosarcoma. Furthermore, the bony destructive lesions with concomitant hypercalcemia of sarcoidosis and HPT are distinguishable by radiographic and laboratory analyses and by the Dent corticosteroid suppression test. Hypercalcemia of primary HPT is associated with elevated serum C-terminal parathormone, osteitis fibrosa, a negative Dent test, and a chloride/phosphate ratio greater than 33 in 94% of primary HPT patients. Hypercalcemia of sarcoidosis is associated with a normal or decreased C-terminal parathormone assay and a positive Dent test, as well as elevated serum immunoglobulins and erythrocyte sedimentation rate, and a positive angiotensin-converting enzyme assay.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sphenoid sinus brown tumor, hypercalcemia, and blindness: an unusual presentation of primary hyperparathyroidism. 379 83


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