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)

The expression of inducible nitric oxide synthase (iNOS) expression and release of nitric oxide (NO) from macrophages are markedly increased in granulomatous infections. Activation of macrophages 1alpha-hydroxylase results in an increase of 1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)]. However, the significance of this increased production is not completely understood. In this study, we analyzed 1,25(OH)(2)D(3) and NO production in patients with tuberculosis infection and hypercalcemia and used lipopolysaccharide (LPS) to stimulate RAW 264.7 cells in an attempt to assess iNOS expression and gaseous NO production regulated by 1,25(OH)(2)D(3). Peroxynitrite (OONO(-)) production and lactate dehydrogenase activity were also examined. Without additional stimulation, peripheral-blood mononuclear cells (PBMCs) from patients with tuberculosis converted more 25-hydroxyvitamin D(3) to 1,25(OH)(2)D(3) than did those from normal controls. These PBMCs released less NO than did those from control subjects, at baseline and in the stimulated state. We found that 1,25(OH)(2)D(3) dose-dependently inhibited iNOS messenger RNA expression of the LPS-stimulated RAW 264.7 cells and also significantly reduced the gaseous NO release and OONO(-) production. Paralleling the 1,25(OH)(2)D(3)-induced inhibition of NO release were reductions in OONO(-) and LDH production. In conclusion, 1,25(OH)(2)D(3) inhibited iNOS expression and reduced NO production by LPS-stimulated macrophages in the range of physiological doses. Inhibition of the NO surge was coupled with a reduction in OONO(-) and LDH production. Increased 1,25(OH)(2)D(3) production and decreased release of NO from the PBMCs of patients with tuberculosis and hypercalcemia were also noted. We propose that 1,25(OH)(2)D(3) production by macrophages may protect themselves against oxidative injuries caused by the NO burst. In the case of tuberculosis infection, increased 1,25(OH)(2)D(3) synthesis may further contribute to the development of an unwanted phenomenon-hypercalcemia.
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PMID:1-alpha,25-Dihydroxyvitamin D3 regulates inducible nitric oxide synthase messenger RNA expression and nitric oxide release in macrophage-like RAW 264.7 cells. 1474 81

Soft tissue calcification is a frequent complication in end-stage renal disease (ESRD) patients with a high serum calcium-phosphate product, but systemic involvement of both the visceral organs and skin is rarely seen. We report on a newly diagnosed ESRD patient with gouty nephropathy who had initial presentations of extensive intradermal tophi, diffuse calcinosis, and hypercalcemia. He received maintenance hemodialysis (HD) with low-calcium dialysate (1.25 mEq/l) for 11 months. Although the above complications diminished, serum calcium remained elevated. Thereafter, unexpected cervical lymphadenitis from a Mycobacterium tuberculosis (TB) infection with high extra-renal production of calcitriol was found. Serum calcium levels normalized only after anti-TB treatment for 2 months. We thought that this patient might have had occult TB infection before the start of HD, which resulted in calcitriol production and hypercalcemia. In addition, concomitant hyperphosphatemia in chronic renal failure contributed to severe diffuse calcinosis. After the initiation of HD therapy, both the elevated serum calcitriol levels and accelerated resolution and mobilization of diffuse calcinosis from low-calcium HD contributed to persistent hypercalcemia.
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PMID:Diffuse calcinosis and intradermal tophi in a uremic pateint: effect of low-calcium hemodialysis and mechanism of hypercalcemia. 1504 22

Eleven cases of tuberculous peritonitis (TBP) in hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) patients at the Kaohsiung Veterans General Hospital in Kaohsiung, Taiwan between 1991 and 2000 were studied retrospectively (six cases in the HD group and five cases in the CAPD group) The diagnosis of TBP was established by either positive ascite tuberculosis (TB) culture or biopsy-proven chronic granulomatous inflammation. Fever and abdominal pain were the most common symptoms, while leukocytosis and unexplained hypercalcemia were the most common laboratory findings. Ascite analysis showed a lymphocyte predominance in all HD patients, but in only 40% of the CAPD patients. The mean duration of a diagnosis by ascite TB cultures was six weeks, while a diagnosis confirmed by laparascopic biopsy took one week. All four fatal cases were diagnosed by TB cultures. Laparoscopic biopsy provided a rapid diagnosis and resulted in low morbidity and mortality in our patients. Based on our review of all possible abstracts found in a Medline search from 1966 to 2002 using the keywords tuberculosis, peritonitis, uremia, and dialysis, this may be the first study of TBP in different dialysis patients.
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PMID:Tuberculous peritonitis in different dialysis patients in Southern Taiwan. 1515 86

Tuberculosis remains an important cause of infection in chronic haemodialysis patients. Frequent extrapulmonary involvement, non-specific presentation and limited diagnostic tools usually make early diagnosis difficult. Herein, we report on an 83-year-old female patient who had been on regular heamodialysis therapy for 15 years, who presented with asymptomatic hypercalcaemia and pancytopenia. Haemophagocytic syndrome was documented during the admission period. Mycobacterium tuberculosis was cultured from bone marrow 1 month after her demise. This case report highlights the non-specific manifestations of extrapulmonary tuberculosis in dialysis patients and the limited value of conventional diagnostic methods. We would like to recommend aggressive intervention and early tissue aspiration from possible infectious sites when tuberculosis cannot be completely ruled out. Disseminated tuberculosis should be considered as an indication of hypercalcaemia where haemophagocytic syndrome occurs simultaneously.
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PMID:Hypercalcaemia and haemophagocytic syndrome: rare concurrent presentations of disseminated tuberculosis in a dialysis patient. 1531 32

Although primary hyperparathyroidism and malignant diseases account for approximately 90% of the causes of hypercalcemia, they could occur in association with granulomatous diseases such as tuberculosis or sarcoidosis, especially in developing countries. Hepatic tuberculosis is difficult to diagnosis without suspicion in cases with normal findings on chest radiographs. We report a 70-year-old woman who presented with hypercalcemia due to hepatic tuberculosis. The diagnosis was made by a computed tomography scan and laparoscopic evaluation. After treatment with anti-tuberculosis medication, her hypercalcemia resolved. Increased vitamin D synthesis by activated macrophages in the granuloma tissue is the major mechanism of hypercalcemia in tuberculosis.
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PMID:Hypercalcemia in hepatic tuberculosis: a case report in Korea. 1582 71

An HIV positive man being treated for disseminated tuberculosis developed hypercalcaemia 17 days after starting highly active antiretroviral therapy (HAART). Hypercalcaemia resolved with stopping HAART and was thought to be due to immune reconstitution inflammatory syndrome.
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PMID:Hypercalcaemia complicating immune reconstitution in an HIV-infected patient with disseminated tuberculosis. 1664 87

A 69-year-old man with a 10-year history of diabetes mellitus and 1-year history of steroid treatment for nonspecific interstitial pneumonia presented with a nightly fever of over 39 degrees C after surgery for a false abdominal aortic aneurysm. Hypercalcemia was detected, despite acute renal dysfunction. There was no laboratory evidence of collagen disease or infection including tuberculosis. Polymerase chain reaction (PCR)-based amplification of DNA from a bone marrow biopsy specimen revealed Mycobacterium tuberculosis. Antituberculous chemotherapy was initiated. Early bone marrow biopsy and the use of new techniques such as PCR can avoid delay in initiating the proper treatment for compromised patients.
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PMID:Miliary tuberculosis with hypercalcemia, and a false abdominal aortic aneurysm, but no pulmonary findings. 1717 May 4

In a retrospective review of 241 patients with active pulmonary tuberculosis, hypercalcemia was found in 62 (26%). It was detected on presentation in 48 patients and developed in 14 patients 4 to 6 weeks aftr the start of antituberculous therapy. The mean (+/- SD) serum calcium level in those cases was 2.78 (+/- 0.137) mmol/L. The majority of cases (67.6%) had a mild rise in the calcium level that remained below 2.8 mmol/L but 35% had a level that ranged between 2.8 and 3.0 mmol/L. Only 2.4% had serum level higher than 3.0 mmol/L, which could explain the predominant absence of hypercalcemia-related symptoms. Hypercalcemia was more common in patients older than 50 years (P<0.05), but this did not correlate with the extent of the tuberculosis shown on radiological evaluation. Spontaneous return to normocalcemia occurred in all 42 patients who underwent serial assessments of their serum calcium concentration, 6 to 8 weeks after the start of chemotherapy. Saudi Arabia is known to have a high prevalence of vitamin D deficiency, but none of our patients were immobilized or had received vitamin D supplements or multivitamins. This supports the view that vitamin D intake does not play a major role in inducing hypercalcemia in cases of active pulmonary tuberculosis, as has been suspected.
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PMID:Hypercalcemia in active pulmonary tuberculosis. 1758 5

A 36-year-old Nigerian woman on thrice-weekly dialysis presented with symptoms and signs of hypercalcaemia. Laboratory findings were consistent with tertiary hyperparathyroidism. Parathyroid hormone levels remained elevated and she underwent elective parathyroidectomy. Intra-operatively all 4 parathyroid glands and local lymph nodes showed necrotising granulomas with occasional acid-fast bacilli, pathognomonic of tuberculosis (TB). Post-operatively she completed a full course of anti-TB therapy and at 9 months she experienced complete resolution in her plasma biochemistry and was essentially symptom-free. This is a rare yet fascinating cause of hypercalcaemia in a dialysis patient and is the first recorded case of tubercular involvement of parathyroid tissue in a case of tertiary hyperparathyroidism. This report demonstrates the coexistence of 2 diseases that simultaneously worsened hypercalcaemia and thus emphasises the importance of the differential diagnosis and of careful histological examination post-operation.
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PMID:Tuberculosis complicating tertiary hyperparathyroidism in a patient with end-stage renal disease: a case report. 1858 34

This retrospective review presented the prevalence and manifestations of tuberculosis among renal transplant recipients in our center between 1987 and mid 2007. The prevalence of tuberculosis was 5/151 (3.3%) recipients with a median age of 49 years (range = 38-55). The median time of diagnosis after transplantation was 23 months (range = 1-47). All five patients had pulmonary tuberculosis. None developed extrapulmonary infection. Presenting symptoms were fever (60%), productive cough (80%), weight loss (40%), and hemoptysis (20%). One patient had non-parathyroid-related hypercalcemia. Cyclosporine dosage needed to be increased in all patients. Two subjects who experienced side effects of hepatitis and/or jaundice from rifampicin were switched to second-line drugs. Infection with Mycobacterial tuberculosis is a not uncommon problem in renal transplant recipients especially in endemic areas. Tuberculosis must be excluded for immunosuppressed patients with clinical or radiological suspicion.
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PMID:Prevalence and manifestations of tuberculosis in renal transplant recipients: a single-center experience in Thailand. 1879 Feb 40


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