Disseminated tuberculosis in a patient on anti-tumour necrosis factor (anti-TNF) therapy

We present a case of a young woman with Crohn's disease, treated with anti-TNF, who developed disseminated tuberculosis (TB), highlighting the risks associated with biologic therapies. This case illustrates the challenge of managing opportunistic infections in this growing patient population. A young woman with ileocolonic Crohn's disease, maintained on infliximab followed by adalimumab for a total of 3 years, presented with a 3-week history of dyspnoea, fever and abdominal pain. Initial chest X-ray revealed right basal consolidation, leading to treatment for community-acquired pneumonia (Fig 1). Her hypoxemia worsened within a few days of admission and a computerised tomography pulmonary angiogram (CTPA) excluded pulmonary embolism but demonstrated widespread nodular opacities and significant mediastinal lymphadenopathy. Despite broad-spectrum antibiotics, respiratory failure ensued, requiring intensive care unit (ITU) admission. All initial cultures, including acid-fast bacillus on sputum, were negative. A repeat QuantiFERON-TB Gold test performed during the admission returned positive, contrasting a negative result 2 years previously during her biologic therapy. Given this new result, she started anti-TB treatment. Retrospective analysis of a 6-week-old admission sputum sample ultimately identified Mycobacterium tuberculosis , and a bone marrow culture also grew the organism. The patient's 6-month hospitalisation, primarily in ICU, was complicated by prolonged ventilatory support requiring tracheostomy, acute renal failure needing intermittent renal replacement therapy, immune reconstitution syndrome (IRIS) and drug-induced pancreatitis. After extensive discussions with the regional TB specialist centre, the treatment regimen and mode of administration of the drugs were altered to achieve optimum therapeutic serum levels and steroid therapy was also started. The patient had a prolonged ventilatory weaning and was later discharged home in a stable condition on oral therapy for close outpatient monitoring. Traditional tests, such as the tuberculin skin test, have lower sensitivity in this population. Interferon-gamma release assays (IGRA) may offer improved detection rates but can still be affected by immunosuppression because of false negatives. 1,2 Isolation of the organism is still the gold standard for diagnosis, but this might take up to 4–6 weeks, causing therapeutic dilemmas. TB reactivation remains a significant concern in immunocompromised patients, with varying risks depending on the underlying condition and treatment. The risk of reactivation can increase 5–170 times compared wit the general population. Factors, such as chronic comorbidities, alcoholism, local TB burden and certain cancer treatments, contribute to this increased risk. 3,4 The management of TB reactivation in immunocompromised patients requires a multifaceted approach. This case illustrates the difficulty in achieving early diagnosis of TB reactivation and potential complications from treatments. Multidisciplinary teamwork involving different specialists is crucial to achieve an excellent clinical outcome in complex cases such as this.