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Immune reconstitution eosinophilia due to schistosomiasis
  1. R Fernando1,
  2. R Miller2
  1. 1Department of GU Medicine, New Cross Hospital, Wolverhampton WV10 0RP, UK
  2. 2Department of Sexually Transmitted Diseases, Royal Free and University College Medical School, Mortimer Market Centre, Mortimer Market, Off Capper Street, London WC1E 6AU, UK
  1. Correspondence to:
 Dr Miller;
 rmiller{at}gum.ucl.ac.uk

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A 21 year old black African heterosexual woman, formerly resident in south east Africa, presented in early October 2000 on arrival in the United Kingdom. Examination revealed hepatosplenomegaly. Investigation showed Hb = 10.2 g/dl, WBC = 2.9 × 109/l (neutrophils = 1.5, lymphocytes = 0.8, and eosinophils = 0.3 × 109/l). Blood urea and electrolytes were normal. Liver function tests showed alkaline phosphatase = 1704 (normal = 45–122) U/l, and alanine transaminase = 65 (normal = 7–63) U/l. Hepatitis A and C serology was negative; hepatitis B serology showed sAg negative and cAb positive. Serum α fetoprotein was negative. An HIV-1 antibody test was positive, plasma HIV-1 RNA level >75 000 copies/ml, CD4 count = 170 cells × 106/l. An abdominal ultrasound confirmed hepatosplenomegaly; there was no intra-abdominal lymphadenopathy and no ascites. A chest radiograph showed micronodular shadowing throughout both lungs. In order to rule out the possibility of tuberculosis, bronchoscopy was performed. Staining and culture of bronchoalveolar lavage fluid was negative for bacteria, mycobacteria, fungi, and parasites. A bone marrow biopsy showed only non-specific reactive changes; culture was negative. A liver biopsy showed portal fibrosis with a moderate chronic inflammatory infiltrate, but no cirrhosis; a schistosomal egg was seen. Schistosomal antibodies were detected by ELISA, positive at level 4 (optical density = 0.767). A diagnosis of schistosomiasis was made.

The patient began highly active antiretroviral therapy (HAART) with stavudine, lamivudine, and efavirenz on 1 December 2000. Four weeks after starting HAART the HIV RNA level had fallen to 25 000 copies/ml, CD4 count remained at 170 cells × 106/l but the eosinophil count had risen to 0.8 × 109/l (normal = 0.04–0.44 × 109/l). After 4 months of HAART the HIV level was below the limits of detection, the CD4 count had risen to 230 cells × 106/l, and the eosinophil count had further risen to 1.5 × 109/l. At this time the patient agreed to treatment of schistosomiasis with praziquantel (40 mg/kg in two divided doses in 1 day). Following praziquantel the eosinophil count fell to 0.5 × 109/l.

The development of eosinophilia in this HIV infected patient with schistosomiasis occurred in the context of a falling HIV RNA level and an increase of CD4 count, indicating partial immune reconstitution.

Partial restoration of cell mediated immunity induced by antiretroviral therapy, as demonstrated by recovery of partial CD4+ T lymphocyte reactivation to memory antigens,1,2 may cause development of an inflammatory response, in this case eosinophilia, in patients latently affected with opportunistic and non-opportunistic pathogens. Reactivation mycobacterial lymphadenitis,3 cryptococcal meningitis,4 and cytomegalovirus retinitis5 and pneumonitis6 have been described. The case described here suggests that development of an eosinophilia to schistosomiasis should be added to the list of immune reconstitution phenomena.

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