Endocrine Abstracts

Introduction: Primary adrenal insufficiency (PAI) is a potentially life – threatening condition. About 75–80% of cases of PAI are caused by autoimmune destruction, while TB accounts for 7–20% of cases; however, adrenal tuberculosis is still the primary cause of PAI in developing countries. Adrenal tuberculosis is difficult to diagnose because symptoms are non-specific. Moreover, if the patient had no prior contact with TB patients, no past history of pulmonary TB and no active pulmonary lesions at presentation, the diagnosis is more difficult. The diagnosis is therefore often delayed and patients may first present with a life-threatening crisis.

Case report: An 63-year-old male patient was admitted in surgical department for important weight loss (30 kg in 12 months), weakness, nausea, fatigue and loss of appetite, mental confusion and dizziness. A chest and abdominal CT-scan with intravenous contrast revealed multiple mediastinal adenopathies and bilaterally enlarged adrenal glands with unomogenous nodular lesions (on the right – 16/13/22 mm, on the left – 50/38/47 mm) with diffuse calcifications and heterogeneous peripheral enhancement, highly suggestive for malignant tumors. He was directed to our clinic for specific investigations. At admission he was semiconscious and had low blood pressure – 90/60 mmHg and heart rate – 90/min. On physical examination slightly hyperpigmentation of the skin and buccal mucosa was observed. Blood results revealed hyponatremia, hyperpotassemia, hypochloremia and hypoglycemia. Serum cortisol level was <1 μg/dl and serum ACTH was >1250 pg/ml, confirming primary adrenal insufficiency and high dose intravenous hydrocortisone therapy was initiated rapidly. The patient general symptoms greatly improved under iv Hydrocortisone and he was redirected for surgical intervention, undergoing left suprarenalectomy. Histopathological examination revealed typical granulomatous inflammation with Langhans giant cells and caseous necrosis, the tissue PCR test confirming the presence of Mycobacterium tuberculosis. The patient was transferred to a tuberculosis hospital for specific treatment, a combination of four drugs was administered in addition to oral Hydrocortisone and Fludrocortisone. Over the next few weeks the patient’s status markedly improved.

Conclusions: Computed tomography play vital role in the diagnosis of the PAI etiology, yet CT findings cannot always differentiate TB from other adrenal pathologies such as fungal infections, hemorrhage or malignancy. In our case, malignancy could not be excluded without first obtaining tissue for pathological examination. Adrenal TB is rare but an important disease entity that must be identified early, requiring prompt treatment with antituberculosis drugs and appropriate steroid therapy.