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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 multisystemic disorder of unknown cause characterized by the formation of immune granulomas in involved organs. It is an ubiquitous disease with incidence (varying according to age, sex, race and geographic origin) estimated at around 16.5/100,000 in men and 19/100,000 in women. The lung and the lymphatic system are predominantly affected but virtually every organ may be involved. Other severe manifestations result from cardiac, neurological, ocular, kidney or laryngeal localizations. In most cases, sarcoidosis is revealed by persistent dry cough, eye or skin manifestations, peripheral lymph nodes, fatigue, weight loss, fever or night sweats, and erythema nodosum. Abnormal metabolism of vitamin D3 within granulomatous lesions and hypercalcemia are possible. Chest radiography is abnormal in about 90% of cases and shows lymphadenopathy and/or pulmonary infiltrates (without or with fibrosis), defining sarcoidosis stages from I to IV. The etiology remains unknown but the prevailing hypothesis is that various unidentified, likely poorly degradable antigens of either infectious or environmental origin could trigger an exaggerated immune reaction in genetically susceptible hosts. Diagnosis relies on compatible clinical and radiographic manifestations, evidence of non-caseating granulomas obtained by biopsy through tracheobronchial endoscopy or at other sites, and exclusion of all other granulomatous diseases. The evolution and severity of sarcoidosis are highly variable. Mortality is estimated at between 0.5-5%. In most benign cases (spontaneous resolution within 24-36 months), no treatment is required but a regular follow-up until recovery is necessary. In more serious cases, a medical treatment has to be prescribed either initially or at some point during follow-up according to clinical manifestations and their evolution. Systemic corticosteroids are the mainstay of treatment of sarcoidosis. The minimal duration of treatment is 12 months. Some patients experience repeated relapses and may require long-term low-dose corticosteroid therapy during years. Other treatments (immunosuppressive drugs and aminoquinolins) may be useful in case of unsatisfactory response to corticosteroids, poor tolerance and as sparing agents when high doses of corticosteroids are needed for a long time. In some strictly selected cases refractory to standard therapy, specific antiTNF-alpha agents may offer precious improvement. Some patients benefit from topical corticosteroids.
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PMID:Sarcoidosis. 1802 32

A 49 y.o. man was admitted for investigation of an intense fatigue associated with nausea, vomiting, weight loss and headache. Examination and work-up reveals a moderate hypercalcaemia and a panhypopituitarism attributed to a craniopharyngioma. Extensive work-up has excluded the most frequent causes of hypercalcaemia and we finally attributed this anomaly to the adrenal failure. In this article, we discuss the diagnostic approach, the etiology and physiopathology of this hypercalcemia and his association with endocrinological anomalies such as adrenal failure.
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PMID:[Adrenal insufficiency and hypercalcemia--an unusual presentation]. 1805 Jun 1

Neurologic sequelae after cardiopulmonary bypass have a multi-factorial etiology. Although it is typically thought that a neurologic dysfunction means a focal lesion, symptoms of a brain disorder can be initiated by metabolic disruption such as from hyper- or hypoglycemia, hypercalcemia, renal and hepatic injury, fatigue, and anesthesia. However, one of the most important causes of acute neurologic dysfunction is edema. Brain swelling is associated with the systemic inflammatory response and the passage of deformable microemboli. The larger question is whether acute symptoms associated with brain swelling because of a breakdown of the blood-brain barrier contributes to a long-term negative outcome caused by cell loss.
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PMID:Deformable emboli and inflammation: temporary or permanent damage? 1829 22

A 75-year-old woman was admitted to our hospital because of general fatigue. She had suffered from sarcoidosis during her 40s with remission, but subsequently she experienced progression of hypercalcemia and renal dysfunction for 7 years. On admission, she showed marked hypercalcemia (up to 15.5 mg/dl) and renal failure (serum creatinine 2.5 mg/dl). Plasma intact PTH level was elevated (up to 190 pg/ml), and thyroid ultrasonography and (99m) Tc-MIBI scintigraphy detected a parathyroid mass, which was surgically removed and histologically confirmed to be a parathyroid adenoma. However, even after surgery her serum calcium remained elevated, but subsequent administration of glucocorticoid for sarcoidosis completely normalized her hypercalcemia. The simultaneous occurrence of primary hyperparathyroidism and sarcoidosis is rare, and our data suggest that high plasma PTH and 1,25(OH)D exerted an additive effect on the occurrence of severe hypercalcemia.
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PMID:Coexisting primary hyperparathyroidism and sarcoidosis in a patient with severe hypercalcemia. 1838 29

A 24-year-old man was admitted to the hospital for pancytopenia. Peripheral blood test and bone marrow aspiration demonstrated an increase in hypogranular promyelocytes. Karyotype analysis and RT-PCR showed 47, XY, t(15;17)(q22;q12), +12, and PML-RARA, respectively. The patient was diagnosed as having acute promyelocytic leukemia microgranular type (M3v) and was therefore administered all-trans retinoic acid (ATRA). Idarubicin and Ara-C were later added to the treatment regimen because of an increased number of leukemic cells. Nausea, vomiting and general fatigue associated with hypercalcemia developed on day 30. There were no findings indicating infection. The administration of ATRA was thus suspected to have induced hypercalcemia. ATRA was therefore discontinued and prednisolone and elcatonin were administered instead. Five days after this change, the serum calcium level normalized. Complete remission was thereafter confirmed on day 45. Hypercalcemia associated with ATRA therapy for APL is rare, and to date, there have been no case reports describing hypercalcemia associated with M3v in the literature. Interaction of fosfluconazole was suspected of causing hypercalcemia when used concomitantly with ATRA.
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PMID:[Hypercalcemia associated with all-trans retinoic acid therapy for microgranular type acute promyelocytic leukemia]. 1864 8

Parathyroid lipoadenomas and lipohyperplasias are rare histologic variants with both an increase in stromal fat and parenchyma. We report the most comprehensive single institution series of lipoadenomas and lipohyperplasias to date and review the literature. Eight lipoadenomas and 3 lipohyperplasias (27 y period) were reviewed. The mean age was 60.3 years (range: 50 to 77 y) with a female predilection (1.75:1). The most common symptoms on presentation were fatigue (55.6%) and bone/joint pain (44.4%). Only 1 patient was euparathyroid. Ultrasound localized lipoadenomas in 50% of tested cases whereas sestamibi was successful in 71.4%. Despite increased stromal fat (median: 50%), the weight and the appearance of large, occasionally nodular expansions of parathyroid parenchyma within the fatty stroma distinguished lipoadenomas and lipohyperplasias from normal parathyroid tissue; none of the cases were misclassified as normal on frozen section. Mean weight for lipoadenomas was 1553 mg (range: 173 to 4587 mg), whereas the mean weight for lipohyperplasia glands was 389.1 mg. Variant morphologies included follicular patterned, oxyphil predominant, and thymic elements (thymolipoadenoma). In 1 lipohyperplasia case, not all glands were involved. Oil Red O stains showed decreased intracytoplasmic lipid in most cases. Median follow-up was 9.2 months (range: <1 to 51 mo). Only 1 lipohyperplasia patient had persistent hypercalcemia, but was asymptomatic. Lipoadenomas and lipohyperplasias are clinically similar and as histologically diverse as their conventional counterparts. Lipoadenomas are more difficult to localize preoperatively by imaging. Despite the potential difficulty at frozen section, accurate weight documentation and recognition of key histologic features diminish this challenge.
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PMID:Parathyroid lipoadenomas and lipohyperplasias: clinicopathologic correlations. 1881 23

A 58-year-old previously healthy man presented with diplopia of rapid onset over a few days. Examination demonstrated bilateral sixth and right fourth cranial nerve palsy. MR imaging showed a large sellar mass with significant destruction of the pituitary fossa. Laboratory tests revealed very high serum prolactin (2,483 ng/dl, reference range 3-13 ng/dl). Dopamine agonist therapy was initiated with significant decline in PRL levels; however, nausea, fatigue, and anorexia developed. Within a few weeks the patient developed renal failure and hypercalcemia. Urine protein electrophoresis revealed large free monoclonal kappa peaks while extensive plasmocytosis was evident in bone marrow aspirates. On bone scan numerous lytic lesions were present. A transsphenoidal excisional biopsy was performed which demonstrated two distinct populations of cells, corresponding to a plasma cell tumor and a lactotroph adenoma. Treatment for multiple myeloma was initiated along with radiotherapy for the sellar tumor. Only a few cases of solitary plasmocytomas of the pituitary region have been reported. Few cases of prolactinomas coexisting with other sellar tumors has been described. We discuss in this report possible pathogenic and functional connections between these two tumors. We suggest that in the presence of extensive cranial nerve involvement, atypical imaging findings for a pituitary adenoma and severe hyperprolactinemia, the possibility of a collision tumor should lead the physician to consider excisional tumor biopsy or surgery in addition to dopamine agonist therapy.
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PMID:An unusual collision tumor comprising a prolactinoma and a plasmocytoma originating from the sellar region. 1884 27

A 10-year old girl presented with fatigue, hypercalcemia, and subperiosteal phalangeal osteolytic lesions. Ultrasonography and MIBI scintigraphy showed a structure near the lower pole of thyroid gland. The structure macroscopically appeared as adenoma, histologically it was thymic tissue. Bilateral neck exploration together with exploration of cervical thymic extensions was performed; adenoma was not found. During next two years, the level of calcium and parathormone raised, bone mineral density decreased. Ultrasonography, MRI, CT and PET/CT were negative. Adenoma was located by MIBI-SPECT/CT near the left border of jugulum. It was found dorsolateral to left common carotid artery and removed.
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PMID:Ectopic parathyroid adenoma in child. 1954 2

A 47-year-old man presented with multiple lung metastases from parathyroid carcinoma that caused hyperparathyroidism and refractory hypercalcemia. Lung radiofrequency (RF) ablation was repeated to decrease the serum calcium and parathyroid hormone levels and improve general fatigue. Pulmonary resection was combined for lung hilum metastases. The patient is still alive 4 years after the initial RF session. He has received 20 RF sessions for 50 lung metastases during this period.
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PMID:A case report of 20 lung radiofrequency ablation sessions for 50 lung metastases from parathyroid carcinoma causing hyperparathyroidism. 1988 31

Most common causes of hypercalcemia are hyperparathyroidism, malignancy, vitamin D-mediated conditions such as sarcoidosis, and vitamin D toxicity. Less commonly, hypercalcemia can be caused by drugs such as thiazide diuretics and lithium. Mild hypercalcemia is usually asymptomatic but severe hypercalcemia is associated with nausea, vomiting, abdominal pain, excessive thirst, muscle weakness, lethargy, confusion, and fatigue. We are reporting a case of abdominal pain and altered mental status caused by thiazide-induced severe hypercalcemia of 19.8 mg/dL. This is the most severe case of thiazide-induced hypercalcemia that we have seen reported. Patients on thiazide diuretics should have their electrolytes frequently checked, especially patients on calcium supplements. Management usually includes hydration and discontinuation of drugs causing hypercalcemia.
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PMID:Thiazide-induced severe hypercalcemia: a case report and review of literature. 2006 44


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