In December 2013, a 64-year-old African female was referred to the rheumatology clinic at our hospital with suspected RA. She reported painful hands and knees associated with early morning stiffness of two to three hours for the duration of one year. On further questioning, she reported that she had been diagnosed with pulmonary tuberculosis (TB) on the basis of positive sputum testing eight months prior to the time. The Gene Xpert test on her sputum had detected Mycobacterium tuberculosis complex, which was sensitive to rifampicin. She had subsequently been started on antituberculosis (TB) chemotherapy, which included rifampicin, isoniazid, ethambutol, and pyrazinamide. However, she had taken the treatment for only three months reportedly due to intolerance of the chemotherapy.
Rheumatological examination at that visit revealed a clinical picture suggestive of RA. She had seven swollen joints all of which were metacarpophalangeal joints and seven tender joints including the wrists, knees, and metacarpophalangeal joints. Her patient global assessment was seven, and physician global assessment was four. This indicated high disease activity with a calculated clinical disease activity index (CDAI) of 25. Her chest radiograph showed features suggestive of active tuberculosis in the right upper lobe. Periarticular osteoporosis suggestive of an early inflammatory arthritis was identified on plain radiographs of hands and feet. There were no erosions or joint space narrowing identified on the latter. Blood investigations revealed positive serological tests for RA, with a rheumatoid factor (RF) of 69 international units per millilitre (normal value < 15) and an anti-citrullinated peptide antibody (ACPA) of 53 units per millilitre (normal value < 20). Inflammatory markers were also elevated which could be either due to active arthritis or as a result of active pulmonary tuberculosis.
On the basis of chronic symmetrical polyarthritis involving predominantly small joints, plain radiographs suggestive of an early inflammatory arthritis, and supportive serological features, we diagnosed her arthritic condition as RA. Recognizing that she had not completed her anti-TB chemotherapy and she still had clinicoradiological features suggestive of active pulmonary TB, the original anti-TB chemotherapy was restarted and she was referred to the local clinic to continue the treatment for six months. As for RA, we decided not to initiate methotrexate until anti-TB chemotherapy was completed. We opted instead for a combination therapy of chloroquine and low-dose prednisone for the arthritis. In the follow-up clinic, a month later, we added sulfasalazine as her disease activity was persistently high. She subsequently defaulted the RA treatment. She however continued going to the local TB clinic to complete anti-TB chemotherapy.
When she finally returned to the rheumatology clinic after completion of six months of anti-TB therapy, we found that she had no residual symptoms and signs of RA without any specific therapy for at least 4 months. We felt that a complete resolution of arthritis would be very unlikely under anti-TB chemotherapy without adequate DMARD therapy if the patient had rheumatoid arthritis. This led to a retrospective diagnosis of PD, which is a condition known to completely resolve without joint damage on anti-TB chemotherapy.
In the subsequent 2-year follow-up without any form of pharmacological treatment, there was no relapse of the arthritis despite the serological tests for RA remaining positive, and she was discharged from the clinic. However, she presented again in January 2017 with a painful right foot, and she had been limping for a few months due to the pain. Clinical examination revealed swelling of the second and third metatarsophalangeal joints and tenderness of all of the right metatarsophalangeal joints. Repeated plain radiographs of the hands and feet revealed periarticular osteoporosis without erosions or joint space narrowing. Musculoskeletal ultrasound revealed active synovitis with increased Doppler signal in the right second and third metatarsophalangeal joints (Figure 1). No erosions were detected in the hand joints on ultrasound examination either. Serum RF was 166 international unit per millilitre, and serum ACPA was 100 units per millilitre. Serum C-reactive protein was mildly elevated at 17 milligrams per litre. She had no features to suggest reactivation of TB or reinfection with TB at this time. RA was diagnosed, and she was then started on oral methotrexate, folate, and low-dose prednisone leading to improvement of her symptoms. Written informed consent was obtained from the patient to allow publication of her clinical diagnosis and management.