Clinical record

A 67-year-old man presented to the rheumatology clinic with uncontrolled rheumatoid arthritis, which was being treated with leflunomide and prednisone. He had previously not responded to gold, methotrexate and cyclosporin. His other medical history included partial gastrectomy, diabetes mellitus and chronic renal impairment.

In preparation for treatment with a tumour necrosis factor (TNF) receptor antagonist, a plain chest radiograph and tuberculin skin test were performed. The radiograph was clear, but the tuberculin skin response was strongly positive at 26 mm. The patient had received BCG vaccination more than 50 years earlier. His tuberculosis risk factors were a family history in his grandfather, and being from Eastern Europe. Given these findings, isoniazid was initiated for treatment of latent tuberculosis, with a proposed treatment plan of 6 months.

Two months later, the patient presented with fever, night sweats and a painful left hip with reduced range of movement. Ultrasound showed a large collection extending from the hip joint. The hip joint aspirate showed a mild neutrophilic infiltrate, but no organisms were detected and polymerase chain reaction (PCR) testing for Mycobacterium tuberculosis was negative.

Magnetic resonance imaging (MRI) of the hip revealed a large iliopsoas collection with femoral head signal changes and flattening (Figures). An infective cause was suspected, so arthroscopic lavage of the left hip and computed tomography (CT)-guided aspiration of the iliopsoas collection were performed. The aspirate removed 50 mL of fluid containing mildly increased neutrophils, but showed no evidence of M. tuberculosis by microscopy, culture or PCR. Nuclear technetium-99 scintigraphy showed uptake only in the femoral head, suggestive of osteonecrosis, with a differential diagnosis of osteomyelitis. A subsequent CT-guided biopsy of the psoas collection wall did not show any evidence of tuberculosis by histology, culture or PCR.

At this stage, the patient’s rheumatoid arthritis was managed with prednisone 10 mg twice daily. He was started on a full anti-tuberculous regimen comprising rifampicin, isoniazid, pyrazinamide, and ethambutol, because of the highly positive tuberculin skin test and the large psoas collection.

Two months later, a repeat CT scan showed resolution of the psoas collection, but persistence of the left hip effusion. The patient was treated with quadruple antituberculosis therapy for 2 months, but this was ceased because of diarrhoea secondary to Clostridium difficile. Over the next 4 months, several attempts to sequentially administer one to two antituberculosis medications were interrupted by recurrent episodes of pseudomembranous colitis caused by C. difficile infection, leading to total withdrawal of antituberculosis medications.

Over the ensuing months, the left hip pain continued to worsen. Tuberculosis was still considered the most likely diagnosis and an arthroscopic biopsy of the left hip synovium was performed. This showed a non-specific chronic synovitis, but no granulomas and no acid-fast bacilli on PCR testing or culture.

The patient underwent a total hip replacement 8 months after his initial presentation with left hip pain. Histology of the hip revealed osteonecrosis of the femoral head, synovial inflammation from rheumatoid arthritis and no evidence of tuberculosis. The iliopsoas collection was thought to be due to a giant iliopsoas bursa that did not recur after aspiration.