Title: Hypercalcemia revealing of a granulomatose tuberculosis: a case report

Biography:

Dr Youcef Chafik Belgaid: practitionner nephrology assistant, Nephrology department dialysis and kidney transplantation, UHS of Batna, Algeria.

 

Abstract

Introduction:

Hypercalcemia is defined by total calcemia greater than 2.6mol/1, the etiologies are dominated by parathyroid adenoma and cancers. Hypercalcemia can be seen during most granulomatosis, sarcoidosis being the most common cause, but can also occur during tuberculosis, HODGKIN disease, non-Hodgkin's lymphoma.

The diagnosis of granulomatosis as the cause of hypercalcemia is often difficult.

Patients and methods:

This is an observational case control study performed in a patient with appropriate severe PTHi hypercalcemia.

This is the 67-year-old  man, electrician by profession, with lymph node tuberculosis in 1989 treated and declared cured, presenting with stage 3 chronic kidney disease on interstitial tubulo nephropathy who consults for impairment of the general condition.

He presents a global dehydration with a polyuropolydipsic syndrome, vomiting with obstinate constipation, dorso lumbar rachialgies with functional impotence of the two lower limbs.

At ECG: diffuse shortening of the QT space.

Results:

Biology: Urea :1,8g/l, creatinine: 21mg/l, Cl à 24 ml /min/1, 73m2

Hemoglobin:5, 9g/dl, Blood smear: without anomalies, EEP: hypo albuminemia, hyper alpha1, alpha2 and beta globulin .

Corrected calcemia :3,6mmol/l, albuminemia: 22g/l

Phosphoremia: 1mmol/l    PTHi :8, 7pg/l

25(OH)vitD: 9 ,7micromol/l     1,25 (OH)2vitD: 47ng/l

CPK: 100 UI               LDH: 240 UI

the intradermal reaction (IDR) to  the tuberculin: Phlyctenular reaction

Morphology:

Standard chest X-ray: paravertebral spindle D8 –D10.

CT scan of the dorso lumbar spine: dorso lumbar spondylodiscitis evoking a specific infectious disease such as tuberculosis with necrotized cervico-mediastinal lymphadenopathy.

Abdominal pelvic ultrasound: renal micro lithiasis with splenic macro calcifications. Left foot X-ray: vascular calcifications.

Pathological anatomy:

Bone marrow biopsy puncture: discret granulocytosis.

Lymph node biopsy: granuloma epithelio giganto cell with caseous necrosis.

Discussion:

Urea – creatinine dissociation and acute worsening on a chronic background are secondary to dehydration induced by vomiting and polyuropolydipsic syndrome due to this hypercalcemia.

It is severe hypercalcemia(3.6mmol/l) with appropriate PTHi.The low value of vitamin D signs a deficient state and eliminates the intoxication with vitamin D .The renal production of 1 alpha hydroxylase has collapsed and the calcitriolemia is supposed to be low  by deficiency in its precursor (25(OH) vitamin D).A normal value of calcitriol suggests the extra renal production of 1 alpha hydroxylase .Lymphadenopathy with fistulization, tuberculin IDR, POTT sickness suggests a tuberculous origin which is confirmed by the anatomopathological study. Hypercalcemia is secondary to tuberculous granulomatosis. It is chronic (renal lithiasis, vascular and splenic calcifications): well tolerated at some point, aggravated and maintained by prolonged bed rest.

Conclusion:

The diagnosis of hypercalcemia secondary to granulomatosis would be easy to evoke in a patient known for granulomatosis or has suggestive symptoms with appropriate PTH hypercalcemia, without hypophosphatemia and hypercalcitriolemia.

In front of any tuberculosis or other granulomatosis, screening for hypercalcemia (asymptomatic in most cases) is systematic.