Initial laboratory investigations showed an ESR of 96 mm (normal: 0–20), alkaline phosphatase of 147 IU/l (normal: 28–124) and a γ-glutamyl transferase of 162 IU/l (normal: 3–50). The serum angiotensin converting enzyme level was normal. The tuberculin skin test was <5 mm. Chest radiograph showed bilateral hilar and right paratracheal adenopathy and right upper lung zone fibrocavitary infiltrate. CT of the chest confirmed the adenopathy and alveolar pulmonary infiltration. A transbronchial lung biopsy revealed chronic non-caseating granulomatous inflammation (). Special stains for fungi and acid fast bacilli (AFB) were negative. Baseline spirometry revealed moderate restriction (forced vital capacity 2.15 litres, 53.6% predicted). A diagnosis of pulmonary sarcoidosis was made and the patient was commenced on oral prednisolone 1 mg/kg/day. Anti-tuberculous therapy was discontinued after AFB cultures were negative at 6 weeks.
Transbronchial lung biopsy revealing chronic non-caseating granulomatous inflammation.
On a follow-up visit at 8 weeks, the patient reported progressive resolution of symptoms along with radiological and spirometric improvement. Oral steroids were gradually reduced to 30 mg/day over an 8-week period. Soon thereafter, he started to complain of numbness in both lower limbs. This was initially thought to be isoniazid-induced neuropathy. However, neurological examination revealed atrophy of the muscles of the lower extremities with more proximal than distal weakness. Proximal strength was graded as 3/5 compared to distal which was 4/5 according to the Medical Research Council scale. Upper extremities did not show any atrophy or weakness. The deep tendon reflexes were symmetrically decreased in all extremities. The sensory examination was unremarkable. Electro-diagnostic studies revealed bilateral denervation of muscles supplied by L2, L3 and L4 roots without any involvement of sensory nerves, consistent with the diagnosis of a polyradiculopathy. There was no evidence of neuropathy or myopathy. MRI of the spine showed disseminated bony involvement with multiple contrast enhancing areas of abnormal signal intensity involving the whole lumbar vertebral column, that is, L1–5, along with evidence of minimal paravertebral and epidural collection (). Sarcoidosis involving the spine was suspected, and a biopsy of L3 vertebra showed non-caseating chronic granulomatous inflammation ().
Figure 2 (A) Sagittal T1 weighted image of the lumbar spine showing abnormal hypo-intense signals in L1, L2, L3 and L5. (B) Sagittal T2 weighted image of the lumbar spine showing abnormal heterogeneous high signals in L1, L2, L3 and L5. (C) Postcontrast sagittal (more ...)
Biopsy of L3 vertebra showing non-caseating chronic granulomatous inflammation.