A Case of Poncet’s Disease Masquerading Rheumatoid Arthritis

A Case of Poncet’s Disease Masquerading Rheumatoid Arthritis

Gopal Chandra Ghosh (Post Graduate Institute of Medical Education and Research & Dr. Ram Manohar Lohia Hospital, New Delhi, India)
Copyright: © 2013 |Pages: 4
DOI: 10.4018/ijudh.2013010107
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Abstract

Poncet’s disease is a rare clinical condition, occurs in in the setting of active pulmonary and extrapulmonary tuberculosis. It typically manifestated by arthritis of large joints, without direct invasion of joints by tubercle bacilli. Rarely it involves small joints thus sometimes mimic rheumatoid arthritis The author is reporting a case of a 17 year old female with evidence of active pulmonary tuberculosis presented with additive evidence of polyarthritis of large as well as small joints. On further investigation joint aspirate did not reveal any direct invasion by tubercle bacilli and patients symptoms responded completely to anti tuberculous therapy. The diagnosis of Poncet’s disease was established.
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Case Description

A 17 year old female presented to us with complaints of low grade fever and joints pain for 6 weeks. Fever was intermittent in nature, associated with loss of weight of around 5-6 kg over the diseased period, loss of apetite and cough with scanty sputum production. Joints pain was present over the small joints of right hand, bilateral knee, ankle and feet joints. Joints pain was associated with swelling of joints. There was no history of photosensitivity, malar rash, oral ulceration, back pain, rash over the body, diarrhea or burning micturition. On examination, pallor was present & there was swelling and tenderness of 2nd & 3rd proximal & distal interphalangeal joints of right hand, right 1st carpometacarpal joint, both shoulder joints, both hips, knees & ankle joints & bilateral proximal interphalangeal joints of great toe. There was no lymphadenopathy or skin rash present. Investigations revealed an ESR of 32 mm Hg per 1st hour, haemoglobin of 8 gm% & microcytic hypochromic picture on peripheral smear. Mantoux test was strongly positive (16 x 12 mm). Rheumatoid factor was positive. Anti nuclear antibody, Anti-CCP antibodies, c-ANCA and p-ANCA were negative, HIV serology was non-reactive. Urine routine examination was normal. Chest X-ray (Figure 1) revealed fibro-cavitary lesions in bilateral middle zones. Sputum Zeihl-Neelsen staining was positive for AFB (+++). CECT chest (Figure 2) revealed multiple fibro-cavitary lesions in both lung fields. X-rays of the involved joints (Figure 3) showed periarticular soft tissue swelling, there were no signs of active tuberculosis. Knee joint fluid aspiration revealed leucocyte count of 5x109 /L; there were no crystals and the cultures were sterile.

Figure 1.

Chest X-ray revealed fibro-cavitary lesions in bilateral middle zones ZONESzones

Figure 2.

CECT chest revealed multiple fibro-cavitary lesions in both lung fields

Figure 3.

X-rays of the joints showing periarticular soft tissue swelling, no signs of active joint erosion

We started the patient on tablet rifampicine 450 mg before breakfast, tablet isoniazid 600 mg, tablet ethambutol 1200 mg, tablet pyrazinamide 1500 mg thrice weekly regimen from DOTS (Directly observe Therapy-short course). On follow up after 2 weeks of treatment she became afebrile and joints pain & joints sweeling was reduced. After 6 weeks of treatment patient was completely free of joints pain.

Discussion And Conclusion

Active tuberculosis may be complicated by reactive arthritis known as Poncet’s disease (Shrivastav, 2009) where as M. tuberculosis may be isolated from the joint (Dhillon, 2012) in tuberculous septic monoarthritis. Poncet’s disease is used to indicate an aseptic polyarthritis, presumably a reactive arthritis, developing in the presence of active TB elsewhere (Kroot, 2007). Although poncet’s disease is considered a reactive arthritis, the clinical presentation of poncet’s disease differs from the pattern of reactive arthritis (Toivanen, 2004; Flores, 2003). It has been hypothesized that after infection, as a result of systemic immunisation, sensitized CD4 cells together with bacterial antigens migrate to the joints and cause arthritis (Sood,1999).

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