eds. How University
do we need?
2. Iglehart JK. Health policy report. The future supply of physicians. N Engl J Med 1986;314:860-4. 3. Report of the Graduate Medical Education National Advisory Committee. Department of Health and Human Services, 1980. 4. Cox MW, Aday LA, Levey GS, Andersen RM. National study on internal medicine manpower 10. Internal medicine residency and fellowship training: 1985 update. Ann Intern Med 1986;104:241-5. 5. Report of the National Commission on Digestive Diseases. Volume 4. Part 3. Reports on the Workgroups on Health Care Delivery. U.S. Department of Health, Education, and Welfare, 1978. 6. McGill DB. President’s commentary. AGA News 1986;20(4):13. 7. Greenberger NJ. Changes in gastroenterology 1960-1985: lessons from the past and implications for the future. Gastroenterology 1985;89:933-8.
Address requests for reprints to: Sydney Cohen, MD., Temple University School of Medicine, 3400 North Broad Street, Philadelphia, Pennsylvania 19140. The Training and Education Committee of the American Gastroenterological Association consists of Sidney Cohen (Chairman], Philip Toskes, John Walsh, Steven Werlin, Walter Rubin, William Snape, Jr., Seymour Sabesin, David Sachar, Michael Sorrell, Atilla Ertan, William Lee, William Duane, Donald Murphy (ad hoc), Thomas Browning (Patient Care Committee), and Glenn Lehman (American Society for Gastrointestinal Endoscopy representative). This position paper has been reviewed and approved unanimously by the Governing Board of the American Gastroenterological Association.
Duodenal Diaphragmatic Lesions and Nonsteroidal Antiinflammatory Drugs Dear Sir: The interesting paper by Bjarnason et al. (1) stimulated us to communicate a similar experience and some findings of the literature. A 65-yr-old woman was examined in July 1987 because of episodes of postprandial vomiting, colicky abdominal pain with diarrhea, and significant weight loss for the past 3 yr. The patient had no previous history of serious illness except for rheumatoid arthritis. For her arthritic disease she had received gold injections, salicylates (for 20 yr), and nonsteroidal antiinflammatory drugs in the last 7 yr. The main laboratory findings were anemia of chronic disease and hypoalbuminemia. An upper gastrointestinal series showed a moderate enlargement of the duodenal bulb followed by two thin and symmetrical narrowing areas (jejunum and ileum were normal). Endoscopy demonstrated a duodenal membrane 3 cm past the pylorus, a second duodenal membrane was seen 5 cm past the first stricture, and a third duodenal membrane was encountered 4 cm past the second septum [all of them covered with normal mucosa). The septa had a single centrally located opening that just admitted the passage of the endoscope (9 mm). A longitudinal duodenotomy was carried out and the diaphragmatic lesions were excised. After 1 yr, the patient remains asymptomatic with normal laboratory and radiologic findings. Histologically, those lesions consisted of duodenal mucosa and submucosa. Signs of mild fibrosis were seen in the submucosa. It is interesting to note that a review of the literature showed
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that some adult patients with duodenal diaphragms were carriers of ankylosing espondylitis and severe osteoarthritis (2,3]. In other cases, the association was with rheumatoid arthritis and these patients also received, among other drugs, salicylates and naproxen (4,5). In adult patients, the etiology of duodenal diaphragmatic lesions is usually assumed to be congenital. It is, however, possible to cite an exception. “In the present case, congenital diaphragm as a cause appears remote. The late presentation might be the result of an unrecognized inflammatory episode occurring in adult life ” (2). A similar presumption has been previously reported (6). The findings in our patient clearly remind us of those features communicated by Bjarnason et al. Perhaps the main difference between these cases is the location of the gastrointestinal tract where the diaphragmatic lesions were found. As first documented in patients with small bowel strictures (l), we believe that the duodenal diaphragmatic lesions in our patient are etiologically related to the action of nonsteroidal antiinflammatory drugs. CLALJDIO R. BlLDER, M.D. PEDRO E. MORGANTE, M.D. JOSE L. FERNANDEZ,
Servicio de Gastroenterologia Sanatorio Giiemes-Hospital Buenos Aires, Argentina
1. Bjarnason I, Price AB, Zanelli G, et al. Clinicopathological features of nonsteroidal antiinflammatory drug-induced small intestinal strictures. Gastroenterology 1988;94:1070-4. 2. Ross JA, Isaac AR, Lyon DS. Duodenal diaphragm presenting in late adult life. Br J Surg 1964;51:632-3. 3. Dorken P, Evans DW. Congenital duodenal stenosis in a patient aged 78 years. Gut 1967;8:313-4. 4. Economides NG, Fortner TM, Dunavant WD. Duodenal diaphragm associated with superior mesenteric artery syndrome. Am J Surg 1981:141:274-6. 5. Jex RK, Hughes RW. Endoscopic management of duodenal diaphragm in the adult. Gastrointest Endosc 1986;32:416-9. 6. Hudson CN. Congenital diaphragm of the duodenum causing intestinal obstruction in an adult. Br J Surg 1961;49:234-6.
Storage of Breath H, in Vacutainer Gaseous Contamination
Dear Sir: We have read with interest the article by Ellis et al. (1) describing a simple technique of storage of breath samples for H, analysis. The results of their studies provided a convenient manipulation involving the use of mineral oil or water at the end of the syringe barrel. The manipulation reduced the leakage of H, and other gases to negligible levels (~3%) over the 2-wk period when compared with using unmodified standard glass syringes. Also mentioned by the authors was another technique in regard to vacutainer storage of breath gas samples, which was reported by Niu et al. in 1979 (2). Our concern, at this moment, is the potentially serious gaseous contamination created by the vacutainer tubes when used for this purpose. The vacutainer tubes are certainly a convenient and dependable means of storage of breath samples for H, analysis, but from our previous investigations (3) (see Table 11, they pose a serious problem, i.e., hydrogen and methane could be detected in various vacutainer tubes as the result of the sterilization process from either the silicone tube coating or the organic additives such as heparin, citrate, oxalate, ethylenediaminetetraacetic acid, or polyanetholesulfonate.