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Case Reports
Journal Article
Seven years of recurrent severe strongyloidiasis in an HTLV-I-infected man who developed adult T-cell leukaemia.
AIDS 1992 June
OBJECTIVE: Human T-cell leukaemia/lymphoma virus type I (HTLV-I) is endemic in Japan, the Caribbean basin and Africa, where it has been aetiologically linked to certain chronic myelopathies and adult T-cell leukamia (ATL). We sought to investigate whether strongyloidiasis, a parasitic disease common in these areas, might be a cofactor in the pathogenesis of ATL, as some reports have suggested.
PATIENTS, PARTICIPANTS: One 35-year-old HTLV-I-seropositive French West Indian man with a 7-year history of recurrent strongyloidiasis associated with episodic hyperinfestation presenting at the Centre Hospitalier Intercommunal, Villeneuve St Georges, France.
INTERVENTIONS: Treatment with various chemotherapeutic agents and symptomatic therapy for hypercalcaemia and antiviral therapy (zidovudine and interferon).
RESULTS: The patient developed ATL and died shortly after, despite chemotherapy. Immunological and virological studies performed during the last 15 months of his life showed an increase of the percentage of peripheral ATL cells, and progression from a polyclonal to a monoclonal integration of HTLV-I proviral DNA in the peripheral blood mononuclear and lymph-node cells.
CONCLUSIONS: Recurrent strongyloidiasis appears to have been a possible cofactor associated with progression from healthy carrier state to ATL in our patient.
PATIENTS, PARTICIPANTS: One 35-year-old HTLV-I-seropositive French West Indian man with a 7-year history of recurrent strongyloidiasis associated with episodic hyperinfestation presenting at the Centre Hospitalier Intercommunal, Villeneuve St Georges, France.
INTERVENTIONS: Treatment with various chemotherapeutic agents and symptomatic therapy for hypercalcaemia and antiviral therapy (zidovudine and interferon).
RESULTS: The patient developed ATL and died shortly after, despite chemotherapy. Immunological and virological studies performed during the last 15 months of his life showed an increase of the percentage of peripheral ATL cells, and progression from a polyclonal to a monoclonal integration of HTLV-I proviral DNA in the peripheral blood mononuclear and lymph-node cells.
CONCLUSIONS: Recurrent strongyloidiasis appears to have been a possible cofactor associated with progression from healthy carrier state to ATL in our patient.
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