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2-Chlorodeoxyadenosine-Induced Complete Remissions in Langerhans-Cell Histiocytosis

Alan Saven, MD; Kenneth A. Foon, MD; and Lawrence D. Piro, MD
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From Scripps Clinic and Research Foundation, La Jolla, California and the University of Kentucky, Lexington, Kentucky. Requests for Reprints: Alan Saven, MD, Scripps Clinic and Research Foundation, 10666 North Torrey Pines Road, La Jolla, CA 92037. Acknowledgments: The authors thank Mary-Helen Hader for data collection.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1994;121(6):430-432. doi:10.7326/0003-4819-121-6-199409150-00006
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Langerhans-cell histiocytosis results from the proliferation and accumulation of tissue histiocytes, clinically manifested as osteolytic lesions, hypothalamic insufficiency, and seborrheic and vesiculopustular lesions on the scalp, perineum, rectum, and vulva [1]. Treatment has been palliative and includes corticosteroids, alkylating agents, antimetabolites, vinca alkaloids, and irradiation [2]. Combination chemotherapy offers no advantage over the use of single agents and is associated with greater toxicity. 2-Chlorodeoxyadenosine (2-CdA) (cladribine, Leustatin [Ortho Biotech, Raritan, New Jersey]), a purine analog with activity in indolent lymphoproliferative disorders and myeloid leukemias [34], is potently toxic to monocytes in vitro [5]. Because tissue histiocytes are derived from the same stem cells as circulating monocytes, 2-CdA was a rational therapeutic option [6]. We therefore administered 2-CdA to three patients with Langerhans-cell histiocytosis.

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Figure 1.
Langerhans-cell histiocytosis lesions of the scalp (A), skin (B), and gingiva (C) in patient 1 before administration of 2-CdA therapy.
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Figure 2.
The scalp of patient 2 before treatment (A) and the inguinal cutaneous lesions of patient 2 before and after treatment (B and C, respectively).
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