Lymphadenopathy is common in human immunodeficiency virus (HIV) infection, and may be the presenting feature. This article describes f ive patients who underwent biopsy for unexplained lymphadenopathy. Their biopsies showed reactive hyperplasia and four of the patients were discharged without a firm diagnosis; within 5 years, all were subsequently diagnosed HIV positive. In contrast, lymphadenopathy in the fifth case prompted a rapid diagnosis of HIV infection.
A 61-year-old man presented to the rheumatology clinic with a 2-year history of rightsided low back pain without radiation. There were no systemic features such as weight loss, pyrexia or sweats. He had been recently admitted with epididymo-orchitis. However, a chest X-ray was normal and acid and alcohol-fast bacilli (AAFB) were not demonstrated on microscopy of pus from a scrotal sinus. Clinical examination was unremarkable. Initial investigations revealed a mild microcytic anaemia (haemoglobin 11.1g/dl and mean cell volume 79.9 fl) and normal inflammatory parameters (C-reactive protein 6 mg/litre and erythrocyte sedimentation rate (ESR) 20 mm/hr). A white cell count was 9.8 x109/litre and rheumatoid factor was negative. Total globulin was elevated at 36 g/litre but immunoglobulins and prostate specific antigen were normal. A repeat chest X-ray was normal. Lumbar spine X-rays showed obliteration of the right sacroiliac joint with adjacent sclerosis and suspicion of erosive change. Magnetic resonance scan of the area demonstrated destructive change in the right sacroiliac joint and a possible soft tissue mass anteriorly, suggestive of either a low-grade tumour of cartilage or an infective process (Figure 1). Subsequent computed tomography-guided biopsy of the soft tissue mass was unsuccessful. The patient continued to experience increasing pain in the right lumbar area and underwent a right sacroiliac joint biopsy under image intensification at another centre. Histology of the biopsy specimen was consistent with low-grade active chronic osteomyelitis but no organism was isolated. Empirical treatment with flucloxacillin was started. Brucella serology was subsequently negative. A repeat magnetic resonance scan showed worsening of the right sacroiliac joint destruction with bone oedema and ring-enhancing lesions post-gadolinium. An open biopsy of the right sacroiliac joint was performed and histological examination of this specimen demonstrated AAFB on microscopy. Mycobacterium tuberculosis was eventually found on culture. Histology of the de-calcified specimen showed non-caseating granulomata and a Ziehl–Nielsen stain was negative. He was treated with antituberculous treatment for a total of 12 months. Repeat investigations on discontinuing therapy showed sclerosis of the affected joint on plain films with a normal haemoglobin level (15.0 g/dl) and ESR (8 mm/hr).
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