Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sarcoidosis is a systemic disease with predominantly pulmonary manifestations. Its frequency in Denmark is higher than previously assumed; on the basis of studies in two different areas the annual incidence was a least 10 cases/100,000 population. Because several cases remain undetected, the real incidence may be higher. The aetiology is unknown. Pathoanatomically the disease is characterized by the appearance of non-caseous epithelioid cell granulomas. The initial process in the lungs is presumably a non-granulomatous interstitial inflammation (alveolitis) with an accumulation of activated T-lymphocytes and mononuclear macrophages. Subsequent there is transition to organized granulomas and in some patients further development into fibrosis. The immunological abnormalities in peripheral blood suggest a stimulation of the humoral immunity and a inhibited cellular immunity. However, there is increasing evidence that the alveolitis may be an expression of increased cellular immunity manifesting at local sites of granuloma formation. ACE is a protein which in non-sarcoid individuals is associated with the endothelial cells, converting angiotensin I into angiotensin II and contributing to the bradykinin degradation. In sarcoidosis ACE is present in alveolar macrophages, epithelioid and giant cells. It can thus be considered as a marker for abnormal macrophage activity in the disease and has been introduced as a diagnostic tool. On examination of a widely compounded patient material we found elevated SACE in approx. 60% of sarcoidosis patients, compared with 1% in other conditions. Judged by these results, there was more than 90% probability that a patient with elevated SACE had sarcoidosis; however, a normal SACE did not preclude sarcoidosis. In newly detected sarcoidosis SACE was elevated in 50% of the patients, whereas elevated SACE was more frequent in patients with chronic active sarcoidosis (duration greater than 2 years). There was a large overlap between SACE values when the CXR stages were compared, a result which is comparable with other series. Two clinical manifestations exhibited peculiar enzyme patterns: in EN SACE was generally normal initially and subsequently increased to elevated values, and in hypercalcaemic sarcoidosis patients SACE was elevated in all. SACE was not elevated in EN of other aetiology or in non-sarcoid hypercalcaemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical and biochemical aspects of sarcoidosis. With special reference to angiotensin-converting enzyme (ACE). 609 1

Angiotensin converting enzyme was measured in the serum of 52 patients with sarcoidosis, 67 healthy control subjects and 64 patients with pulmonary and non-pulmonary diseases. The patients with sarcoidosis were classified on clinical grounds as having active or inactive disease. In 26 patients with active sarcoidosis not taking corticosteroids the mean serum ACE was significantly higher than in normal controls (P less than 0 . 001). 73% of these patients had elevated serum ACE. Only two out of 12 (17%) patients with inactive sarcoidosis not taking corticosteroids had elevated serum ACE. Serum ACE was normal in patients taking oral corticosteroids for longer than two weeks. Eighty per cent of patients with active sarcoidosis with radiological evidence of pulmonary parenchymal involvement had an elevated serum ACE compared to 25% in patients with normal chest X-rays and 60% of those with bilateral hilar lymphadenopathy. All sarcoid patients with hypercalcaemia had elevated serum ACE whereas only half of those with normal serum calcium had elevated ACE. In the patients with other thoracic and granulomatous conditions serum ACE was normal or rarely marginally elevated. Serum ACE appears to be of value in the diagnosis of active sarcoidosis.
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PMID:A clinical evaluation of serum angiotensin converting enzyme in sarcoidosis. 625 51

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

We report a case of hypercalcaemic crisis due to sarcoidosis in a 15-year-old boy. The clinical suspicion of sarcoidosis was confirmed by a liver biopsy. At admission serum calcium, 1,25(OH)2 and ACE were elevated and iPTH was suppressed. The levels of serum total and ionized calcium, iPTH, ACE, 1,25(OH)2 and 25-OH were followed and chest X-ray and pulmonary function tests were performed during systemic steroid treatment. The clinical condition improved during treatment and the paraclinical measurements normalised within 5 weeks. The mechanism whereby hypercalcaemia occurs in childhood sarcoidosis is clarified.
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PMID:Childhood sarcoidosis presenting with hypercalcaemic crisis. 780 1

Sarcoidosis is a multisystemic disorder of unknown etiology that most commonly affects adults between 20 and 40 years of age. Patients with sarcoidosis frequently present with bilateral hilar lymphadenopathy and pulmonary infiltration, and often with ocular and skin lesions. The diagnosis is established when clinical and radiographic findings are supported by histologic evidence of non-caseating epithelioid cell granulomas found on tissue biopsy. Diagnosis of sarcoidosis requires exclusion of other causes of granuloma formation. Sarcoidosis is also characterized by distinctive laboratory abnormalities, including hyperglobulinemia, an elevated serum angiotensin converting enzyme level, evidence of depressed cellular immunity manifested by cutaneous anergy and, occasionally, hypercalcemia and hypercalciuria. Glucocorticoids remain the mainstay of therapy when treatment is required, although other anti-inflammatory agents are being used increasingly often.
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PMID:Sarcoidosis: a primary care review. 1049 6

A 65-year-old man was admitted to our hospital because of thirstyness and left lower abdominal pain. On admission, he was found to have urolithiasis, renal insufficiency (BUN: 73 mg/dl, Crt: 4.4 mg/dl), and hypercalcemia (13.2 mg/dl). Chest X-ray films and computed tomograms showed enlargement and calcification of the hilar lymph nodes, and thickened interlobar fissures in both lungs. Levels of angiotensin converting enzyme (30.2 IU/l) and 1.25 (OH)2VitD3 (66.4 pg/ml) were elevated. Histologic examination of the specimen obtained from transbronchial lung biopsy showed non-caseous epithelioid cell granulomas. Because the level of parathyroid hormone was normal and no malignancies were detected, a diagnosis of sarcoidosis was made. Treatment with extracorporeal shock wave lithotripsy, transurethral lithotomy, saline infusion, and prednisolone (30 mg/day) alleviated the urolithiasis, renal insufficiency, and hypercalcemia. After discharge, the patient was followed up and given prednisolone therapy. About 1 month after the prednisolone dose had been tapered to 15 mg/day, the patient experienced dyspnea and facial and pedal edema. Because congestive heart failure was diagnosed, he was re-admitted to our hospital for a second time. Although he was then placed on intensive therapy, he died of ventricular tachycardia associated with sarcoidosis of the heart.
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PMID:[Sarcoidosis with hypercalcemia, urolithiasis, renal insufficiency, and heart failure]. 1048 65

Sarcoidosis is a multisystem granulomatous disease of unknown origin. No single biological marker allows definitive diagnosis of sarcoidosis or may accurately predict the disease prognosis. However, some biological markers are helpful tools as diagnostic aids and disease activity markers. At the blood level, lymphopenia with CD4 depletion, elevated levels of serum-angiotensin converting enzyme, lyzozyme, beta 2 microglobulin and disturbed calcium metabolism resulting in hypercalcemia and hypercalciuria can help guide diagnosis. Lymphocytic alveolitis with a high CD4/CD8 ratio in bronchoalveolar lavage fluid is highly suggestive of the disease. A wide range of new biological markers are proposed but their pronostic significance is still controversial. In clinical practice, biological markers may help in monitoring treated patients with sarcoidisis.
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PMID:[Biological manifestations of sarcoidosis]. 1124 Apr 24

A 31-year-old man presented with a widespread papular eruption and systemic symptoms including renal colic and decreased exercise tolerance. The combination of clinical features and laboratory investigations that revealed an elevated angiotensin converting enzyme level and hypercalcaemia enabled a diagnosis of sarcoidosis to be made. Multiple skin biopsies showed prominent Touton-like giant cells which delayed the diagnosis. Giant cells are frequently seen in sarcoidal granulomas but in some cases their prominence and Touton-like appearance may suggest alternative diagnoses such as xanthogranulomas.
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PMID:Sarcoidosis with prominent giant cells. 1190 66

A 54 year old man presented with frontal headaches for one year. A CT scan of the head revealed a pituitary mass. He denied a change in vision or galactorrhea, but did have decreased frequency of erections and a recent episode of renal stones. On physical exam, the cranial nerves were normal. Visual field exam revealed mild bilateral temporal defects. The genitalia were normal and the testes were soft. Laboratory evaluation revealed: Na, 134 mM/l; K, 6.7 mM/l; Cl, 104 mM/l; HCO3, 22 mM/l; BUN, 47 mg/dl; Cr, 8.3 mg/dl; Ca, 12.5 mg/dl; Phos, 5.5 mg/dl; prolactin, 32.0 ng/ml; T4, 4.46 microg/dl; TSH, 2.07 microU/ml; LH, 18.1 mIU/ml; FSH 3.2 mIU/ml; alpha subunit 1.6 ng/ml; testosterone 255 ng/dl; cortisol, 20.3 microg/dl; cortisol after 250 microg cortrosyn, 38.5 microg/dl (time 60 minutes); growth hormone, 1.4 ng/ml; IGF-1, 47 ng/ml; PTH, <1 pg/ml; 25-hydroxyvitamin D, 14 ng/ml; 1,25-dihydroxyvitamin D, 69 pg/ml. These results were felt to be consistent with a non-PTH-mediated hypercalcemia, such as humoral hypercalcemia of malignancy, or a vitamin D-mediated hypercalcemia, such as lymphoma, sarcoidosis or tuberculosis. Head MRI demonstrated a 3.5 x 3.5 x 2.5 cm heterogeneous mass enlarging the sella, deforming the clivus and compressing the cavernous sinus, basilar artery and left side of the optic chiasm. There was a small focus of high signal in the superior part of the mass on the T1-weighted image from either a proteinaceous cyst with early calcium deposition or sub-acute blood. These radiographic findings were felt to be consistent with a pituitary adenoma. The patient was treated with intravenous hydration and thyroxine 50 microg daily and underwent a transsphenoidal resection of the pituitary lesion. Pathologic examination revealed a pituitary adenoma with multiple granulomas and crystalline material; this was consistent with sarcoid within the adenoma. Post-operatively, the serum LH fell to 5.5 mIU/ml. A subsequent transbronchial biopsy revealed multiple non-caseating granulomas. A serum ACE level was elevated at 132.6 U/l. He received oral prednisone 60 mg daily with resolution of the hypercalcemia. Neurosarcoidosis occurs in 5 to 15% of patients with sarcoidosis and can involve the hypothalamus and pituitary gland. This is the first reported case of sarcoidosis occurring within a pituitary adenoma.
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PMID:Sarcoidosis within a pituitary adenoma. 1213 93

We report sarcoidosis-related hypercalcemia in a patient undergoing hemodialysis, The patient, a 54-year-old woman, had been undergoing maintenance hemodialysis since 1989. The cause of end-stage renal disease was membranoproliferative glomerulonephritis. The patient was admitted to our hospital in January 2002 for the treatment of hypercalcemia(13.5 mg/dl), which was diagnosed in December 2001. Chest X-ray showed bilateral hilar lymphadenopathy, chest CT scan showed mediastinal lymph node swelling, and Ga-scintigraphy showed abnormal accumulation of gallium in the mediastinum. The patient's intact-PTH was 80-100 pg/ml. ACE(31.4 IU/l) and 1.25(OH)2D3(85 pg/ml) were elevated, and the bronchial lavage fluid CD4/CD8 ratio was slightly elevated. Epitheloid granulomatous tissue was obtained from a subclavian lymph node biopsy. Thus, the patient was diagnosed with sarcoidosis. The hypercalcemia and bilateral hilar lymphadenopathy improved with corticosteroid therapy.
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PMID:[Sarcoidosis and hypercalcemia in a patient undergoing hemodialysis]. 1270 5


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