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Scleroderma Esophagus: A Nonspecific Entity

HOWARD A. SCHNEIDER, M.D.; RICHARD A. YONKER, D.O.; SELDEN LONGLEY, M.D.; PAUL KATZ, M.D.; JOHN MATHIAS, M.D.; and RICHARD S. PANUSH, M.D.
[+] Article and Author Information

▸Requests for reprints should be addressed to Richard S. Panush, M.D.; Division of Clinical Immunology, Department of Medicine, Box J-277, J. Hillis Miller Health Center, University of Florida; Gainesville, FL 32610.


University of Florida and the Veterans Administration Medical Center; Gainesville, Florida.


Ann Intern Med. 1984;100(6):848-850. doi:10.7326/0003-4819-100-6-848
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Esophageal dysfunction develops in approximately 90% of patients with progressive systemic sclerosis (scleroderma) or mixed connective tissue disease (1). Abnormal esophageal motility may be one of the earliest manifestations of scleroderma because of smooth muscle involvement (2, 3). Smooth muscle is found in the lower two thirds of the esophagus and in the lower esophageal sphincter. Manometric measurements confirm the incoordination and loss of effective contractions that often progress to complete absence of esophageal contractions and reduced lower esophageal sphincter tone (4). We reviewed esophageal manometric tracings from patients with or without rheumatic disease to determine whether low-amplitude aperistalsis or

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