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Research Article Free access | 10.1172/JCI105531
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. John S. Fordtran, Dept. of Internal Medicine, The University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, Texas 75235.
*Submitted for publication June 30, 1966; accepted November 3, 1966.
Supported by research grant AM-06506 and training grants T1-AM-5395 and T1-AM-5490 from National Institutes of Health.
Find articles by Fordtran, J. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. John S. Fordtran, Dept. of Internal Medicine, The University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, Texas 75235.
*Submitted for publication June 30, 1966; accepted November 3, 1966.
Supported by research grant AM-06506 and training grants T1-AM-5395 and T1-AM-5490 from National Institutes of Health.
Find articles by Rector, F. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. John S. Fordtran, Dept. of Internal Medicine, The University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, Texas 75235.
*Submitted for publication June 30, 1966; accepted November 3, 1966.
Supported by research grant AM-06506 and training grants T1-AM-5395 and T1-AM-5490 from National Institutes of Health.
Find articles by Locklear, T. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas
†Address requests for reprints to Dr. John S. Fordtran, Dept. of Internal Medicine, The University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, Texas 75235.
*Submitted for publication June 30, 1966; accepted November 3, 1966.
Supported by research grant AM-06506 and training grants T1-AM-5395 and T1-AM-5490 from National Institutes of Health.
Find articles by Ewton, M. in: JCI | PubMed | Google Scholar
Published March 1, 1967 - More info
Water and electrolyte movement in the jejunum of normal subjects and patients with sprue was measured during perfusion with isotonic electrolyte solutions. Normal subjects absorbed water, sodium, and potassium. By contrast, in patients with sprue (seven with adult celiac sprue and one with tropical sprue) who had diarrhea and steatorrhea, these substances were secreted into the intestinal lumen. This indicates that the jejunal mucosa of these patients was in a secretory state with respect to water and electrolytes.
A method is presented for detecting abnormalities in the effective pore size in disease states. The method is based on the principle of restrictive diffusion and involves measuring the simultaneous diffusion rates of solutes of different molecular size. Since the method does not depend on measurement of water flow in response to osmotic pressure gradients, it can be used in disease states in which absorption and secretory processes involving water may be abnormal.
The ratio of urea to tritiated water diffusion in the jejunum of normal subjects averaged 0.8, compared to 0.2 in patients with sprue. This indicates a marked decrease in the effective pore size of the jejunal mucosa in sprue. This conclusion was strengthened by the finding that erythritol and L-xylose, which are somewhat larger solutes than urea, are essentially non-absorbable in small bowel involved with sprue.