Ulcerative colitis developing after amoebic dysentery

Severe diarrhoea in patients with the acquired immune deficiency syndrome (AIDS) is usually a manifestation of gastrointestinal infection by a variety of organisms. We report a patient with low CD4 T celi counts who developed ulcerative colitis after amoebic dysentery. He subsequently developed acute ulcerative colitis with toxic dilatation while he was severely immunocompromised. He responded to corticosteroids and mesalazine and remains well on maintenance therapy. Diarrhoeal illness is a common occurrence in patients with the acquired immune deficiency syndrome (AIDS). This is frequently the result of infection with opportunistic organisms, although diarrhoea without infection does occur as part of chronic human immunodeficiency virus (HIV) infection. We report a heterosexual man with haemophilia who presented with toxic megacolon secondary to ulcerative colitis and responded to steroids and mesalazine. To determine the extent of his colitis an "'Indium oxine labelled leukocyte scan was performed, but in view of his neutropaenia donor leukocytes were used. To our knowledge, this is the first case of severe ulcerative colitis developing in an HIV infected patient with such severe immunosuppression. with bloody diarrhoea. He was passing up to 10 fluid motions per day, and the diarrhoea had worsened progressively over the preceding three weeks despite a course of metronidazole two weeks before admission to hospital. The bleeding responded to repeated Factor VIII cover but his diarrhoea continued unabated. He had general malaise and anorexia and had lost 6 kg in weight. He was feverish, with temperatures up to 38-5C. There was generalised colicky abdominal pain and distension, particularly in the upper part of his abdomen. He was tender to palpation in the left iliac fossa and bowel sounds were increased. Investigations at this time showed a haemoglobin concentration of 10@1 g/100 ml, a white cell count of 2 6x109 (neutrophils 21x 109/1, lymphocytes 0 4x109/l, CD4 0 17x109/l, and a CD4/CD8 ratio of 0 40). Plain abdominal x ray showed faecal loading of the right hemicolon but no gross dilatation. Repeated stool cultures and examination failed to identify any pathogens, particularly Mycobacterium tuberculosis, Cryptosporidium, Toxoplasma, Entamoeba, Microsporidium, Salmonella, and Shigella. No viruses were seen on electron microscopy nor was cytomegalovirus grown or identified using immunofluorescence from stools, urine, throat swab, or blood. Sigmoidoscopy at this time showed an acutely inflamed rectal mucosa with some contact bleeding. Biopsy specimens taken at sigmoidoscopy failed to show any evidence of Departments of Nuclear Medicine, Haemophilia, and Gastroenterology, St Thomas's Hospital, London I Sturgess S M Greenfield J Teare M J O'Doherty Correspondence to: Dr I Sturgess, Nunnery Fields Hospital, Nunnery Fields, Canterbury, Kent. Accepted for publication 29 April 1991 Case report A 44 year old heterosexual man with haemophilia who had had chronic HIV infection since 1984 presented to St Thomas's Hospital in February 1989 with diarrhoea. At that time Entamoeba histolytica was isolated and the diarrhoea responded to a course of tinidazole. There was a history of recent travel to Hong Kong, which accounted for his development of amoebic dysentery. He presented again in March 1989 with a further diarrhoeal illness and a weight loss of 3 kg. On this occasion, although no pathogens were isolated from the stool, metronidazole was given at a dose of 400 mg three times daily for 10 days. A sigmoidoscopy showed mild proctitis without ulceration and the rectal biopsy specimen showed a florid proctocolitis with crypt abscess formation Culture and immunofluorescence for cytomegalovirus were negative. At that time his CD4 counts were 0 22 x 109/l with a CD4/CD8 ratio of 0-47. In view of his diarrhoea and weight loss his disease was classified as Communicable Disease Centre stage 4a.' He was begun on zidovudine (AZT) which resulted in improvement in his symptoms, with increased weight and resolution of his diarrhoea. In late December 1989, he presented again I".Bl.:. S -..1 Figure 1: Rectal biopsy specimen showing marked acute inflammatory infiltrate ofthe lamina propria with extension into crypts andfocal crypt abscessformation. (Original magnification x400.) 408 group.bmj.com on October 21, 2017 Published by http://gut.bmj.com/ Downloaded from