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From the Instituto Nacionale de Cancerologia (Dr. Fadul), Bogota, Colombia; Physicians Neurology Consultants Inc. (Dr. Lemann), St. Louis, MO; the Departments of Neurology and Biostatistics (Drs. Thaler and Posner), Memorial Sloan-Kettering Cancer Center and Cornell University Medical College, New York, NY.
Between 1980 and 1984, of 107 patients receiving 16 mg/d of dexamethasone for spinal cord compression, three (2. 8%) developed gastrointestinal (GI) perforation and two (1.9%) GI bleeding; of 226 being tapered from 100 mg/d of dexamethasone, perforation occurred in six (2.7%) and GI bleeding in eight (3. 5%). Of 125 patients with GI perforations treated between 1979 and 1986, 41 (33%) were on steroids, 24 for neurologic disease. Median duration of steroid therapy was 24 days; 20 (91%) of the neurologic patients perforated within 30 days. The steroid group had more free peritoneal involvement (p < 0. 00001), but fewer signs and symptoms of peritonitis (p < 0. 000001) than the nonsteroid group. Seventeen patients were receiving steroids for cord compression; they had significantly more rectosigmoid perforations (p < 0. 014) and associated constipation (p < 0. 000001) than the 108 remaining patients. GI perforation is a less well-recognized complication of steroid therapy in neurologic patients than is GI bleeding though it occurs as frequently, is more difficult to diagnose, and far more serious. In steroid-treated patients, prevention of constipation might avert this serious complication, while early diagnosis will improve the outcome.
Address correspondence and reprint requests to Dr. Posner, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021.
Presented in part at the thirty-ninth annual meeting of the American Academy of Neurology, New York, NY, April 1987.
Received April 8, 1987. Accepted for publication in final form June 25, 1987.
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