LAUSR

To the Editor:An 8-y-old girl presented with palpable purpura in the lower limbs, knee arthritis, and abdominal pain of 2 d duration. There was no history of bloody diarrhea, failure to thrive, eye complaints, or oral ulcers. Investigations revealed a normal hemogram (Hb 11.2 g/ dL, WBC 12,600/mm, platelet 340,000/mm) and raised acute phase reactants [Erythrocyte sedimentation rate (ESR) 24 mm/h; C-reactive protein (CRP) 46 mg/L]. Renal and liver function, urine routine, ultrasonography (abdomen) and stool for occult blood were normal. Antinuclear antibody, anti-double stranded DNA, antineu t roph i l cy top lasm ant ibod ies , C3 , C4 , and antiphospholipid antibodies were negative. The diagnosis of Henoch–Schönlein purpura (HSP) was considered and he received prednisolone (1 mg/kg/d) with progressive dose reduction with significant improvement. However, 10 d later while on tapering dose of corticosteroid, she had a new flare of abdominal pain, arthritis, palpable purpura with additional symptoms of bloody diarrhea with erythema nodosum of lower limbs. Suspecting inflammatory bowel disease, upper gastrointestinal endoscopy was done which was normal . Colonoscopy revealed pancolonic mucosal inflammation and contiguous superficial ulcerations. Colonic biopsy revealed diffuse active colitis with neutrophilic infiltrates with crypt distortion, cryptitis, and crypt abscesses and no evidence of vasculitis. Skin biopsy revealed leukocytoclastic vasculitis (LV) with negative immunofluorescence staining for immunoglobulin A (IgA) in the capillaries. Therefore, our diagnosis was revised to LV associated with ulcerative colitis (UC). She was treated with oral prednisolone and sulphasalazine with improvement of all the intestinal, cutaneous, and articular symptoms with gradual reduction in her acute phase reactants and fecal calprotectin (246 to 62 μg/mL) within 4 mo. Extraintestinal manifestations are commonly seen in UC involving skeletal system (arthritis in our case), eyes, liver, and skin. Cutaneous lesions include erythema nodosum (present in our case) , pyoderma gangrenosum, vitiligo, and vasculitis (present in our case) [1]. Our case fulfilled both HSP and UC criteria [1, 2], indicating a possible co-existence, but positive colonic biopsy with no vessel involvement and skin biopsy of LV with negative IgA deposits confirmed the UC diagnosis. There are limited data regarding LV associated with UC [3]. LV is not related to the extent of colonic involvement, has a relapsing course, and is due to deposition of immune complexes in the vessels [4]. To our knowledge, this is the first case from India demonstrating cutaneous LV associated with UC mimicking HSP.