Risk factors for hypercalcemia in patients with tuberculosis.

Background: Tuberculosis (TB) is prevalent worldwide and causes significant morbidity and mortality. TB is known to cause hypercalcemia. We aimed to assess the prevalence and risk factors for developing hypercalcemia among patients with TB. Methods: In this retrospective case-control study, patients with microbiological evidence of TB and an available serum calcium value were included between 2005 and 2016. The demographic, clinical, and laboratory details were recorded. Various risk factors were compared in TB patients with and without hypercalcemia. Results: A total of 129 patients fulfilled the inclusion criteria. Twenty percent were found to have an elevated serum calcium level, 65% of them had clinical features of hypercalcemia. In comparison, the odds of developing hypercalcemia in the presence of disseminated TB, diabetes and renal failure was 1.83, 1.60, and 7.33, respectively. Conclusion: One-fifth of patients with TB have hypercalcemia. Risk factors of the same are renal failure, diabetes, and disseminated TB.

Hypercalcaemia secondary to disseminated Mycobacterium abscessus and Mycobacterium fortuitum.

The incidence and prevalence of nontuberculous mycobacteria (NTM) infection is on the rise with many cases still going unreported. Given the vague and nonspecific clinical features of NTM infections, it is often missed or mistaken for Mycobacterium tuberculosis. The presumption that NTM infections are benign and do not contribute to morbidity no longer holds true. NTM infections need to be considered in patients with disseminated multisystem disease and in those not responding to standard M. tuberculosis treatment. As NTM infection is associated with granuloma formation, it can result in hypercalcaemia. Interestingly, there is evidence that there may be other mechanisms in play contributing to hypercalcaemia besides the increased calcitriol levels.

A case of Pneumocystis pneumonia, with a granulomatous response and vitamin D-mediated hypercalcemia, presenting 13 years after renal transplantation.

Vitamin D-mediated hypercalcemia is an uncommon complication of Pneumocystis infection. A granulomatous response resulting from Pneumocystis infection is also atypical. In this report, we describe an exceptional case of granulomatous Pneumocystis pneumonia associated with vitamin D-mediated hypercalcemia, in a patient who presented unusually late after renal transplantation. The patient's hypercalcemia resolved with treatment of the infection.

[Calcitriol induced hypercalcemia in a hunting dog with a disseminated Paecilomyces variotii infection]. / Calcitriol-bedingte Hyperkalzämie bei einem Jagdhund mit disseminierter Paecilomyces variotii-Infektion.

INTRODUCTION: A 5-year old hunting dog was presented with reduced appetite, weight loss and polyuria/polydipsia. Hematology and clinical chemistry revealed anemia, leukocytosis, increased liver enzymes, hypoalbuminemia and hypercalcemia. The cytological, pathohistological and microbiological examination identified a disseminated infection with the saprophytic mould fungus Paecilomyces variotii in the biopsies of the spleen and a lymph node. Determination of vitamin D metabolites confirmed a calcitriol induced hypercalcemia.

Fluctuating hypercalcaemia caused by cavitary Mycobacterium bovis pulmonary infection.

Hypercalcaemia occurs in many granulomatous diseases. Among them, sarcoidosis and tuberculosis are the most common causes. Other causes include berylliosis, coccidioidomycosis, histoplasmosis, Crohn's disease, silicone-induced granulomas, cat-scratch disease, Wegener's granulomatosis and Pneumocystis carinii pneumonia. Hypercalcaemia in granulomatous disease occurs as a consequence of dysregulated production of 1,25-(OH)2 D3 (calcitriol) by activated macrophages in granulomas. Hypercalcaemia in patients with Mycobacterium tuberculosis infection has been reported in 0%-28% of cases. Uncultured bronchoalveolar lavage cells from patients with M. tuberculosis produce greater amounts of calcitriol compared with controls. Although Nayar et al described hypercalcaemia in a case of sepsis associated with intravesical Bacille Calmette Guerin therapy, there are no published reports describing hypercalcaemia in patients with pulmonary M. bovis infection. We describe a patient with M. bovis cavitary pulmonary infection with sustained hypercalcaemia that fluctuated and recurred repeatedly over the course of therapy, ultimately culminating in normalisation of serum calcium when therapy had led to cure. Treatment consisted of antituberculous therapy, oral corticosteroids and intravenous bisphosphonates with a favourable outcome.

Hypercalcaemia caused by active pulmonary tuberculosis in an elderly person without fever or pulmonary symptoms.

Many diseases can cause hypercalcaemia, including primary hyperparathyroidism, cancer, drugs and granulomatous diseases. A nursing home resident aged 81 years was admitted because of altered mental status. The patient did not have fever, cough, sputum or night sweat. Hypercalcaemia was identified as a cause of the consciousness disturbance. Chest radiograph showed no acute process. Laboratory workups revealed elevated serum levels of 1,25-(OH)2 vitamin D3 and positive T-spot test. Microscopic examination of the suctioned sputum identified acid-fast bacilli, which was confirmed as Mycobactrium tuberculsosis Tuberculosis should be considered as the important cause of hypercalcaemia since early diagnosis and treatment is recommended for preventing its outbreak among people with close contacts with patients.

Mycobacterium avium-intracellulare and the unpredictable course of hypercalcemia in an AIDS patient

Abstract A 37-year-old man with AIDS presented with altered mental status four weeks after stopping his medications for Mycobacterium avium-intracellulare (MAI). He had low CD4 cell count and severe hypercalcemia. Bone marrow biopsy revealed bone marrow infiltration by granulomas positive for acid-fast bacilli and cultures grew MAI. His hypercalcemia continued to worsen with the initiation of MAI therapy but we were able to treat it successfully with pamidronate and calcitonin.

Mycobacterium avium-intracellulare and the unpredictable course of hypercalcemia in an AIDS patient.

A 37-year-old man with AIDS presented with altered mental status four weeks after stopping his medications for Mycobacterium avium-intracellulare (MAI). He had low CD4 cell count and severe hypercalcemia. Bone marrow biopsy revealed bone marrow infiltration by granulomas positive for acid-fast bacilli and cultures grew MAI. His hypercalcemia continued to worsen with the initiation of MAI therapy but we were able to treat it successfully with pamidronate and calcitonin.

Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses.

The authors present a puzzling case of nephrolithiasis, hypercalcaemia, amenorrhoea, short stature and gross skeletal deformities in a 30-year-old female. Multiple pituitary hormone deficiency and metabolic bone disease were initially considered but were eventually excluded. The final diagnosis is genitourinary tuberculosis (TB) which caused the hypercalcaemia, nephrolithiasis and amenorrhoea, and also found to have the syndrome of multiple exostoses which explained the gross skeletal deformities and the short stature. After treatment with anti-TB therapy, there was resolution of hypercalcaemia and return of regular menstruation. The short stature and gross skeletal deformities remain as part of the congenital syndrome.

Mycobacterium microti infection associated with spindle cell pseudotumour and hypercalcaemia: a possible link with an infected alpaca.

A 44-year-old woman who had recently been on immunosuppressive therapy presented with malaise, cough, fever, weight loss, lymphadenopathy, severe hypercalcaemia and a paratracheal mass on imaging. The initial impression was of disseminated malignancy, and lymphoma was suspected. A mediastinal biopsy showed a mycobacterial spindle cell pseudotumour containing acid and alcohol fast bacilli (AAFB). Sputum microscopy demonstrated AAFBs, confirmed as Mycobacterium tuberculosis complex by PCR. Prolonged culture grew Mycobacterium microti, an organism often associated with disease in small rodents and llamas. M microti isolates from postmortem samples of an alpaca at a nearby farm were genetically indistinguishable. Although the patient had not visited the farm, concurrent illness in her adopted stray cat suggested a possible zoonotic connection. The patient responded to antituberculous therapy, and rehydration and pamidronate for hypercalcaemia. We believe the hypercalcaemia was caused by a similar mechanism to raised calcium levels sometimes seen in tuberculosis.

Diffuse calcinosis and intradermal tophi in a uremic pateint: effect of low-calcium hemodialysis and mechanism of hypercalcemia.

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.

Hypercalcemia associated with infection by Cryptococcus neoformans and Coccidioides immitis.

BACKGROUND: Of the 13 reported cases of hypercalcemia associated with fungal infection, 1 was caused by Cryptococcus neoformans and probably mediated by increased levels of 1,25-dihydroxyvitamin D [1,25(OH)2D]. Eight others were associated with Coccidioides immitis, of which only 2 had measured 1,25(OH)2D levels; in both, they were diminished. We report a patient with human immunodeficiency virus infection and simultaneous C. immitis and C. neoformans pneumonia and C. immitis fungemia associated with hypercalcemia. METHODS: Consecutive measurements of serum total and ionized calcium, phosphorous, blood urea nitrogen, creatinine, 25(OH)D, 1,25(OH)2D, parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrp) and albumin were performed over a period of 46 months. RESULTS: While the patient was hypercalcemic, intact serum PTH and PTHrp were undetectable, serum 25(OH)D levels were normal, and serum 1,25(OH)2D levels were in the high normal range. Successful treatment of the C. immitis and C. neoformans infections resulted in resolution of the hypercalcemia and increase of PTH and PTHrp to the normal range. CONCLUSION: In some patients with HIV infection, coincident hypercalcemia, and severe fungal infection, the responsible factor may be 1,25(OH)2D. Although total serum levels of this compound may not be frankly elevated, they are inappropriately high for the circumstances. Free 1,25(OH)2D levels should be determined in this situation.

Disseminated coccidioidomycosis associated with hypercalcemia.

This article describes a patient in whom disseminated infection with coccidioidomycosis was associated with hypercalcemia. The patient had a low level of 1,25-dihydroxyvitamin D and a suppressed parathyroid hormone value, an indication that the hypercalcemia was not mediated by vitamin D or parathyroid hormone. The episode resolved readily with administration of pamidronate, an outcome suggesting that this is effective treatment of hypercalcemia of this origin. On follow-up of the patient while he was receiving antifungal therapy for Coccidioides immitis, calcium values remained normal.

Hypercalcaemic crisis as the presenting manifestation of abdominal tuberculosis: a case report.

This report deals with a young man having prolonged fever presenting with hypercalcaemic crisis. Subsequent investigations confirmed tuberculosis (TB) peritonitis in the absence of pulmonary involvement as the cause of his symptoms. His hypercalcaemia and fever resolved with anti-TB therapy. Abdominal TB needs to be included in the differential diagnosis of otherwise unexplained hypercalcaemia especially in our region where TB is an endemic problem and is treatable.

Hypercalcemia in a patient with hypoparathyroidism and Nocardia asteroides infection: a novel observation.

Hypercalcemia is associated with numerous chronic granulomatous processes and chronic infections. Increased production of 1,25-dihydroxyvitamin D by activated macrophages has been shown to be the cause in most cases. In this article, we describe a case of hypercalcemia related to infection with Nocardia asteroides. In a 34-year-old woman who previously had hypocalcemia, acute hypercalcemia developed coincident with Nocardia pericarditis. The hypercalcemia resolved after treatment of N. asteroides with sulfisoxazole. Parathyroid hormone and phosphorus levels were within normal limits, and total 25-hydroxyvitamin D levels were only mildly increased. After successful treatment of the Nocardia infection, the patient required supplemental calcium and vitamin D. Her hypercalcemia was temporally related to the duration of the N. asteroides infection. We believe this is the first reported case of hypercalcemia associated with N. asteroides infection.

Hypercalcemia associated with Aeromonas hydrophila gastro-enteritis.

We describe a 4 year old girl with acute Aeromonas hydrophila gastro-enteritis who presented with a combination of hypercalcemia, metabolic alkalosis, and renal impairment. Serum parathyroid hormone was not elevated. Both milk-alkali syndrome and intoxication of vitamins A and D were ruled out. The hypercalcemia, metabolic alkalosis, and renal impairment were improved by fluid infusion and intravenous administration of furosemide. Gastro-enteritis also improved with oral administration of the antibiotic norfloxacin. The association of A. hydrophila gastro-enteritis with hypercalcemia has not been described previously.