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Development of Diffuse Fasciitis with Eosinophilia during L-Tryptophan Treatment: Demonstration of Elevated Type I Collagen Gene Expression in Affected Tissues: A Clinicopathologic Study of Four Patients

John Varga, MD; Juha Peltonen, MD, PhD; Jouni Uitto, MD, PhD; and Sergio Jimenez, MD
[+] Article, Author, and Disclosure Information

Grant Support: In part by grants AR 19101, GM 28833, and AR 35297 from the National Institutes of Health and by a grant from the Arthritis Foundation. Dr. Varga is the recipient of a Clinical Investigator Award (K08 AR 01817) from the National Institutes of Health, and Dr. Peltonen is the recipient of a Young Investigator Award from the National Neurofibromatosis Foundation.

Requests for Reprints: John Varga, MD, Thomas Jefferson University, Room M-26, Jefferson Alumni Hall, 1020 Locust Street, Philadelphia, PA 19107.

Current Author Addresses: Drs. Varga, Peltonen, Uitto, and Jimenez: Jefferson Medical College, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107.

© 1990 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1990;112(5):344-351. doi:10.7326/0003-4819-112-5-344
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We describe the cases of four women who developed a scleroderma-like syndrome during L-tryptophan treatment for insomnia or tinnitus. The illness was characterized by swelling of the extremities, skin rash, myalgia, and elevation of the peripheral blood eosinophil count, followed by rapidly progressive cutaneous and subcutaneous induration. The histopathologic examination of affected skin showed thickening of the fascia, deep dermal fibrosis, and accumulation of mononuclear cells and abundant eosinophils. The expression of the type I procollagen gene was examined by in-situ hybridizations of affected skin with a human sequence-specific complementary DNA (cDNA). Increased hybridization signals were detected in the deep dermis and fascia, indicating enhanced expression of the collagen gene. The temporal association of L-tryptophan use and the development of a scleroderma-like illness in these four patients suggests a causal relation between L-tryptophan or its metabolites and the stimulation of fibroblast collagen gene expression that results in dermal and fascial fibrosis.





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