Endocrine Abstracts

Introduction: A potential cause of panhypopituitarism could be cerebral tubercular lesions, that are often misdiagnosed. Hormonal effects could be related directly to primary tubercular lesions, or after starting antitubercular therapy. Paradoxical reaction (PR) in tuberculosis is defined as clinical or radiological worsening of pre-existing tuberculous lesions or development of new lesions after beginning an appropriate antitubercular therapy (ATT). It has been suggested that the mechanism underlying a PR is an excessive immune response.

Case Report: A 26-year-old man presented to the Emergency Department with a two-week history of fever, headache, visual impairment and fatigue. He was known to have a Mycobacterium tuberculosis axillary adenopathy treated with ATT consisting of rifampicin, isoniazid, ethambutol and pyrazinamide, shifted to a maintenance therapy with Isoniazide and Rifampicine three months before. The patient was taking his medication regularly. On examination all clinical parameters were normal; general physical evaluation was unremarkable except for visual loss. Initial laboratory investigations revealed anterior hypopituitarism, (secondary adrenal, gonadal and thyroid failure) without central diabetes insipidus. Cerebrospinal fluid analysis did not show abnormal findings (in particular acid fast bacilli stains on liquor, cultures, PCR for M. tuberculosis and cryptococcal antigens were negative). A chest x-ray was negative. An MRI of the brain with gadolinium enhancement showed a polylobate cystic suprasellar lesion with thickening of pituitary peduncle. The lesion showed ring enhancement with gadolinium, compatible with a flogistic lesion. Visual perimetry examination showed bilateral temporal deficit. Due to the clinical worsening while on ATT and the absence of secondary infection, a paradoxical reaction to ATT was suspected and the patients was managed with high dose dexamethasone (8 mg daily) added to standard therapy for hypopituitarism showing gradual response to the treatment. There was a complete regression of visual deficit and a partial reduction of the intracranial lesion (an MRI was repeated). The patient was discharged after ten days in good general conditions, with the indication to continue corticosteroids for two months.

Conclusions: Our patient’s neurological finding after the beginning of ATT may have been a new development or a progression of intracranial tuberculoma. A paradoxical reaction to ATT should be suspected in any patient in ATT who present with neurological findings and hypopituitarism. Paradoxical tuberculomas are observed in approximately 1% of all active tuberculosis cases. Corticosteroids are the only anti-inflammatory drug that can be used in the management of PR.