PEPTIC ULCER OF THE PYLORIC REGION*

Transcription

1 VOL. 113, No. i PEPTIC ULCER OF THE PYLORIC REGION* By MORTON G. GLICKMAN, M.D.,f GEORGE SZEMES, M.D.,f PETER LOEB, M.D.4 and ALEXANDER R. MARGULIS, M.D.t SAN FRANCISCO, CALIFORNIA C ONSIDERABLE controversy exists in the literature concerning the proper classification of pyloric ulcer. From the results of histologic examination and gastric analysis, many have related pyloric ulcer to gastric ulcer.3 4 The therapeutic resuits obtained from various surgical procedures have led others to relate pyloric ulcer to duodenai ulcer Some authors have attempted to classify pyloric ulcer as an entity separate from gastric or duodenal ulcer because of a high incidence of a characteristic clinical syndrome ( syndrome pylorique, pyloric channel syndrome ) in pyloric ulcer Others have reported that this syndrome is not characteristic of pyloric ulcer and that a separate classification is not justified.4 12 The controversy results largely from lack of a consistent anatomic definition of the pyloric channel and from lack of consistent criteria that establish which ulcers are pyioric. The pyloric channel is not a well defined anatomic unit. Surgical, roentgenographic, endoscopic, and microscopic landmarks differ for localization of the pylorus. To resolve the controversy, a single definition of pyloric channel must be accepted. We believe that this definition should be a roentgenographic one. Most authors agree that the pyloric channel is most accurately localized roentgenographically.4b012 In the anesthetized patient at surgery and in the pathologic specimen after resection, the gastric antrum blends smoothly into the pylorus without anatomic demarcation of the margins of the pyloric channel.4 #{176} Histologically, no distinctive pyloric mucosa is seen. The junction of gastric and duodenal mucosa varies; usually, it underlies the pyloric sphincter, but occasionally it is as much as 2 cm. proximal to t.8 On roentgenographic examination, however, the proximal and distal limits of the pyloric channel are well defined. Distortion that results from spasm or fibrosis may present difliculty in roentgenographic localization, but the same problems also hinder surgical, endoscopic, and pathologic 12 The controversy about the existence of a characteristic syndrome in pyloric ulcer arises not only because of various definitions of pyloric channel, but also because ofvarious definitions ofpyloric ulcer. Most authors who deny the existence of a characteristic pyloric syndrome exclude some ulcers that involve the pylorus but extend beyond it. One report, for example, attempted to distinguish pyloric from pyloroduodenal ulcer.4 Another apparently excluded ulcers that extended to the pylorus from the stomach or duodenum. 2 Authors who consider pyloric ulcer a distinct clinical entity define pyloric ulcer more broadly. They include in this category all ulcers that involve the pylorus, regardless of their apparent origin or extent.9 5 This report correlates the roentgenographic, clinical, and laboratory findings in a series of patients with ulcers that involve the pylorus. We particularly emphasize the appearance and position of pyloric ulcers during healing, progression, or recurrence of disease, to determine whether a strict or broad definition of pyloric ulcer is more appropriate. MATERIAL AND METHOD Forty consecutive patients with pyloric ulcer which was diagnosed roentgenographically were studied. Criteria for inclusion into the study group were as follows: (a) an ulcer was seen in continuity with the roentgenographic pylorus; (b) the * From the Departments of Radiology,j and Medicine,t University of California School of Medicine, San Francisco, California. 47

2 148 Glickman, Szemes, Loeb and Margulis SEPTEMBER, 1971 p vloru 5 w as de form ed roen tgenographicalls ; (c) at least 2 roentgenographic studies were obtained over a period of at least 3 weeks. Most of the patients who were excluded because of only one roentgenographic Sttl(1y or a follow-up period of less than 3 weeks required surgery for complications of their ulcer disease. Elimination of this group left a representative series of medically treated patients in whom the clinical and roentgenographic course of pyloric ulcer could be studied. The ulcers were evaluated and grouped by their size, extent, and proximity to the gastric antrum or the duodenum. History, laboratory, and endoscopic data were correlated with the roen tgenograms. PYLORIC CHANNEL SYNDROME The symptom complex of the pyloric channel syndrome consists of atypical epigastric pain, episodic nausea and vomiting, and weight loss. 4 Postprandial bloating is also often a part of the syndrome. In patients with gastric or duodenal ulcer, pain usually occurs when the stomach is empty, and is relieved by food or antacids. In the pyloric channel syndrome the pain lacks this rhythmicity. Atypical pain begins near the end of a meal. It may be relieved by vomiting or may become severe and constant. Food or antacids do not reheve the pain, but usually make it worse. Nausea and vomiting may follow meals, may occur irregularly without any temporal relation to meals, or may be experienced primarily at night. Weight loss may be marked and may lead to an erroneous diagnosis of occult malignant tumor. Atypical pain, nausea and vomiting, are infrequent symptoms in uncomplicated gastric or duodenal ulcer disease In various series in which criteria varied for location of an ulcer within the pylorus, all or part of the syndrome was reported in 25 per cent to 8o per cent of patients with pyloric ulcer.4 9 In most patients, typical findings of peptic ulcer are also present to suggest the diagnosis. Occasionally, however, the atypical symptoms so dominate the clinical state that peptic disease is not suspected. A protracted course results with symptoms gradually worsening before roen tgenographic examination is performed and the diagnosis established. 4 In our series, 26 patients (6 per cent) presented part or all of the pyloric channel syndrome. Eighteen had atypical pain and 22 had nausea and vomiting or postprandial abdominal bloating. Marked weight loss occurred in 13 patients. Roentgenograms showed signs of gastric outlet obstruction in 6 of these patients on their first examination. In i6, gastrointestinal hemorrhage was manifested by melena, guaiac-positive stools, or hematemesis. In these 16 patients and in another 4 with a past history ofpeptic disease, the diagnosis of peptic ulcer was established early. In 6 patients, however, the pyloric channel syndrome was not accompanied with typical symptoms or signs. In these, peptic ulcer was not the admitting diagnosis and was not even mentioned in the differential diagnosis on the initial work-up. Classic signs and symptoms of peptic ulcer were present in the remaining 14 patients in this series. Five had had typical pain relieved by food or antacid, and evidence ofgastrointestinal hemorrhage. In, typical pain had been present, but no hemorrhage. In another 5, there was evidence of gastrointestinal hemorrhage, but the patients were asymptomatic. CLINICAL-ROENTGENOGRAPHIC CORRELATION The ulcers were classified as large or small by the measured diameter of the ulcer crater on the initial roentgenogram. Ulcer craters less than I cm. in diameter were considered small. They were subclassified by location and extent. Ulcers that caused no deformity of the gastric antrum or duodenum were considered to be entirely within the pylorus. Those that deformed the antrum or duodenum were considered to be at the gastric or duodenal end of the pylorus. Since the normal pylorus is about i cm. long, no large ulcer

3 VOL. 113, No. Peptic Ulcer of the Pyloric Region I 49 was totally within the pylorus. Large ulcers that deformed both the antrum and the duodenum were assumed to override the pylorus. According to Shanks and Kerley,1 pyloric ulcers are usually small and shallow. Little edema surrounds them since they are situated within the muscular ring. They may appear as a small spicule or diverticulum that protrudes from the smooth pyloric channel. Occasionally the crater is not seen and only by irregularity or angulation of the channel is the location of the ulcer identified. Most of the I 8 small ulcers in this series fit this description. Those totally within the pylorus, however, and perhaps those on the antral side would be the only ones included among pyloric ulcers, if a strict definition were to be used. Small ulcers at the duodenal end and all large ulcers probably would be excluded by most authors who accept the strict definition. Table i summarizes the symptoms, location of the ulcer, type of therapy, and caliber of the pylorus in the group of small ulcers. In our series, 7 of the small ulcers were totally within the pylorus. All healed when treated medically, but I required surgery 6 nlonths later because of recurrence (Fig. I, A and B). Of the remaining ii small ulcers, 7 were on the gastric side of the pylorus and On the duodenal side. These ulcers also were Location Within pylorus Antral side Duodenal side SMAlL TABLE surrounded by little edema unless they penetrated deeply (Fig. 2, A and B). Folds in the pylorus were occasionally thickened or angulated, but in several cases were distorted only minimally. Radiating folds were seen frequently but were difficult to interpret because of the normal convergence of gastric and duodenal folds at the pylorus. Spasm was usually present, mani fested by diminished distensibility of the antrum or of the base of the duodenal bulb. In the absence of spasm, an active ulcer crater could not always be distinguished from deformity caused by a healed ulcer unless prior roentgenograms were available for comparison. Activity of an ulcer occasionally could be determined with certainty only by endoscopic examination (Fig. 3). All of the ulcers on the duodenal side of the pylorus healed without surgery. Five of the 7 ulcers on the gastric side of the pylorus responded well to medical therapy. Of the other 2, one received radiation therapy because of slow regression of the ulcer in a patient with high surgical risk. Gastric resection was performed in the other for severe hemorrhage during medical therapy. No roentgenographic evidence of gastric outlet obstruction was seen in any of tile patients with small ulcers, although ii of the 18 had pyloric channel syndrome. The caliber of the pylorus after healing was I ULCERS (crater less than i cm. in diameter) Pvloric Caliber Obstruc- ). at l ollow-up I vloric 1 herapy tion on No. of Examination (hannel Initial 1 atients Syndrome Medical Surgical Roent- Normal genogram or Wide Narrow 6 1* t * Surgery was performed for recurrence after ulcer was healed by medical therapy. t One of these patients received radiation therapy as well.

4 I 50 Glickman, Szemes, Loeb and Margulis SEPTEMBER, G. I. (A) Small ulcer (crater less than cm. in diameter) within the pylorus in a patient with pyloric channel syndrome. The superior surface of the pylorus is angulated, and the channel is widened. Thickened folds suggest that the ulcer is active. The folds do not radiate from the ulcer but, rather, from the end of the pyloric channel at the base of the bulb. (B) Same patient, 2 months later. A spot-roentgenogram in a similar obliquity shows no evidence of persistent ulcer. The pylorus has healed with widening and shortening. Clinically the patient was now asymptomatic. normal or widened in 14 patients and narrow in 4. The remaining 22 ulcers in this series were larger than cm. in diameter. All were surrounded by areas of edema approximately proportional to the size of the crater. Gastric and duodenal anatomy was often distorted markedly by spasm and edema. Several of the craters had an irregular contour that suggested malignancy (Fig. 4). The folds were usually thickened but often were not otherwise distorted. Table I, summarizes the clinical and roentgenographic data in the patients with ulcers larger than i cm. in diameter. Five of these large ulcers appeared to override the pyloric channel. These were the largest ulcers in the series, with the worst prognosis. Two required surgery because of recurrent and intractable obstruction. A third patient, who refused surgery despite recurrent obstruction, has failed to return for follow-up examination. Of the ulcers larger than i cm. in diameter, I I were situated on the gastric side of the pylorus. Eight of the I I healed without surgery. In i of the other 3 patients, medical therapy improved the ulcer, but an episode of hemorrhage 2 months later necessitated surgery. In the other 2 patients the ulcers failed to regress during medical therapy. At surgery one proved to be an adenocarcinoma and the other a reticulum cell sarcoma. These were the only 2 malignant tumors in this series. Although lymphoma not infrequently involves the pylorus, carcinoma in the pylorus is reported to be rare. The carcinoma was found at the edge of the ulcer and underlying the ulcer, but the gross pathologic appearance otherwise was that of peptic ulcer. This case may therefore be an example of an ulcercarcinoma, which presumably arises in a pre-existing peptic ulcer. In such cases a peptic ulcer may be involved in the etiology of the tumor. 3 By histologic examination it could not be determined whether the tumor arose in gastric or duodenal mucosa, since the ulcer was situated at the junction of the gastric and duodenal mucosa. In both malignant ulcers, the crater was smooth and protruded outside the contour of the stomach and pylorus. The surrounding soft-tissue mound was small and symmetric. No roentgenographic features differentiated these from benign ulcers in the same location (Fig. 5, A and B; and 6). Surgery was indicated only because of failure of the ulcer to heal with medical therapy, which emphasizes the need for

5 VOL. 113, No. i Peptic Ulcer of the Pyloric Region / / stile U r with a surrounding mound ofedema. The edema primarily involves the gastric antrum, but it extends into the pylorus and the base of the duodenal bulb. The pyloric channel is approximately normal in caliber. (B) Same patient, 5 weeks later. At this time he was asymptomatic. Although the ulcer has healed, an angulation is seen of the gastric end of the pylorus and widening of the pyioric channel. This appearance has persisted on all subsequent studies. follow-up roentgenograms of all patients with ulcer disease. Six ulcers I cm. in diameter or larger were situated on the duodenal side of the pylorus. All 6 healed with medical therapy. Many of the healing ulcers maintained the same relation to the pylorus as on the initial study. In patients, however, the healing ulcer or deformity was situated on the side of the pyloric channel opposite Location No. of Patients TABLE LARGE that seen on the initial study (Fig.7, A-C; and 8, A-C). Five of these were on the gastric side initially, but appeared to migrate toward the duodenum. The others were on the duodenal side, but appeared to migrate toward the antrum. Two small ulcers, judged initially to be within the pyloric channel because of absence of gastric or duodenal deformity, II ULCERS (crater larger than I cm. in diameter) Pyloric Channel Syndrome Therapy produced gastric deformity as they re- Obstruction on Initial Roentgenogram Pyloric Caliber at Follow-up Examination Medical Surgical Normal or Wide Overriding 5 4 3* 2 2 I 4 Antral side ii S Duodenal side It 3 3 Narrow * One patient refused surgery. t Surgery was performed for recurrence after ulcer was healed by medical therapy.

6 152 Glickman, Szemes, Loeb and NIargiilis SEPTEMBER, 1971 FIG. 3. Deformity from a healed pyloric ulcer. The pylorus is widened and angulated. Folds appear thickened and radiate from the angulation. The patient was asymptomatic and the same deformity was seen on the 3 studies over a period of 2 years. The roentgenographic appearance is indistinguishable from active ulcer however (compare with Fig. i, A and B). gressed. Table in summarizes the roentgenographic localization of the ulcers on the initial examination and at follow_up examination. Prior reports have emphasized the frequency of associated gastric or duodenal ulcers in patients with pvloric ulcer.1 6 It Small Size Small Small Large Large Large TABLE ROENIGENOGRAPHIC LOCATION OF ULCERS Initial Location Pvlorus Antrum Duodenum Overriding An trum 1)uodenu m III No. At Follow_up Examination Mid Gas- Duo- 1)y- tric denal bros Side Side I * 6 I 3 2 * Two of these ulcers appeared to be on the gastric side of the pylorus on the initial examination, on the duodenal side on the second examination, and on the duodenal side subsequently. has been suggested that most, or perhaps all, gastric ulcers result from associated or prior pyloric peptic disease that produces pyloric dysfunction. 2 Gastric stasis then predisposes to development of gastric ulcer. In our series, a second active ulcer was demonstrated roen tgenographically in 3 patients. Two of these were gastric ulcers of the lesser curvature and i was in the duodenal bulb. In another 3 patients, associated ulcers were present, but not shown Ofl the roentgenograms. Two of these were shallow ulcers, found in the stomach at gastroscopv. Another was seen at surgery in a patient with intractable obstruction of the gastric outline in whom neither roentgenographic examination had demonstrated the stomach optimally. The pvlorus was judged to be normal in r - a l IG. 4. Large ulcer (crater larger than i cm. in diameter). This patient (lid not have pyloric channel syndrome. The ulcer is considered to be on the antral side of the pyborus because the antrum is considerably deformed and the duodenal bulb is relatively spared. Folds are thickened and the pylorus is widened. The ulcer bed is irregular and the surrounding deformity is asymmetric and irregular. Gastric cytologic examinations were repeatedly normal, however, and subsequent roen tgenographic studies demonstrated complete healing.

7 \OL. 113, No. I Peptic Ulcer of tile Pyloric Region /., rounding mass is present to suggest malignancy. The patient had pyloric channel syndrome, the characteristics of which did not differ from other patients in this series. caliber or widened on healing in 22 patients. Twelve ulcers healed with narrowing of the pylorus, but without obstruction. In 6 patients, surgery was performed before the ulcer healed. Whether the caliber of the pylorus affects the prognosis is not certain. Probably, true p\ loric narrowing resulting from fibrosis is more likely to cause obstruction eventu ally. Pvloric narrowing seen in the initial exam ination of 2 patients in this series, however, had widened at the time of healing. The pvloric channel syndrome appears to be unrelated to the caliber of the pylorus at roentgenograplvv. In the 26 patien ts with this syndrome, roen tgenograms showed gastric outlet obstruction in and pvloric narrowing in another. The pylorus was widened, however, in i6. Of the 40 ulcers studied, 33 (83 per cent) were healed by medical therapy, although 3 of these recurred later and required surgery for hemorrhage. Surgery was performed in others. One patient received radiation therapy and one refused surgery. Jndications for surgery were recurrent obstruction in 3, no roentgenographic change in 2, and hemorrhage in. In the 6 patients with gastric outlet obstruction FIG. 6. Reticulum cell sarcoma. An ulcer is present at the gastric end of the pylorus. The pyborus is wide. The antral and pyloric folds are smooth and uninterrupted. The ulcer bed is smooth, without any of the characteristics usually associated with malignant tumor. The patient had pyloric channel syndrome.

8 154 Glickman, Szemes, Loeb and Margulis SEPTEMBER, 1971 on the initial roentgenographic examination, the ulcers in 3 healed without surgery. GASTRIC ANALYSIS In most patients with pyloric ulcer, the levels of gastric acid have been reported as normal or below normal.35 In this respect, pyloric ulcers are similar to gastric ulcer. In gastric ulcer the measured gastric acid output is normal or low, whereas in most duodenal ulcers, the acid output is elevated. Since pyloric ulcer affects pyloric function, however, the measured acid level may not reflect acid secretion accurately.5 The level of measured gastric acid may be artificially low if a widened or poorly functioning pylorus permits duodenal reflux into the stomach. Conversely, it may be artificially high if the pylorus causes antral stasis. Pyloric ulcer probably produces both phenomena.2 5 In this series, gastric secretions of 2 patients were analyzed. The results showed a basal level lower than normal in i6, within the range of normal in 2, and higher than normal in 4. The technique for performing histamine stimulation was not uniform in all patients. Although the re-

9 VOL. 113, No. 1 Peptic Ulcer of the Pyloric Region 155 sults tended to follow the predicted pattern, no definite conclusions can be drawn. GASTROSCOPY Gastroscopy was performed in 12 patients. In 9 of these the ulcer was seen, but in 6 of the 9 it was reported as prepyloric. The gastroscope frequently cannot be passed into the pylorus, particularly when spasm or fibrosis is present. Thus, some pyloric ulcers may escape gastroscopic detection. By gastroscopy, however, associated gastric ulcers may be seen that are difficult to detect roentgenographically, particularly when the gastric outlet is obstructed. Furthermore, the distinction between an active ulcer and a deformity from a healed ulcer is often possible by gastroscopy. DISCUSSION Oi et al.7 have shown by histologic analysis that most or all benign gastric and duodenal bulb ulcers appear within limited mucosal areas. Gastric ulcers are found in the mucosa of the gastric antrum

10 I 56 Glickman, Szemes, Loeb and Margulis SEPTEMBER, 1971 within 2 cm. of its junction with the mucosa of the body of the stomach. Occasionally the body-antrum mucosal junction lies farther distally than usual, near the pyloric muscle.7 In these cases a gastric ulcer might easily involve the pylorus. Duodenal ulcers develop in duodenal mucosa within 2 cm. of the antrum-duodenal mucosal j u8 Although the antrumduodenal junction usually underlies the pylorus, occasionally it was located as much as 2 cm. proximal from t.8 In these cases pyloric ulcers ma be entirely within duodenal mucosa. Duodenal and pyloric carcinoma (origi- Ilating at the gastroduodenal mucosal junction) are rare, whereas carcinoma arises commonly in gastric mucosa. If the mucosa of origin of an ulcer at the pylorus could be determined by roentgenography, the distinction between antropyloric, pyloric, and pyloroduodenal ulcers (a strict definition) would be useful. Thus pyloric ulcers could be classified on the basis of malignant potential. Because of the vanable location of the gastroduodenal mucosal junction, however, definition of pvloric ulcer in clinical or radiologic terms is justified. Clinical characteristics of ulcers in the p) loric region are governed primarily by their influence on pvloric muscular mechanism. Extension of the ulcer to the duodenum or to the antrum apparently does not change the clinical features, the state of the pvloric sphincter, or the response of the ulcer to therapy. The pyloric channel syndrome was manifested frequently in patients with ulcers totally within the pyloric channel. Similar symptoms were also evoked in patients with ulcers on the antral and duodenal sides of the pylorus. Response to medical thenap also was similar, regardless of extension to the stomach or duodenum. In each of these locations, however, large ulcers produced more severe symptoms and required surgery more frequently than did ulcers smaller than i cm. in diameter. The apparent migration ofmany of these ulcers across the pylorus also suggests that roentgenographic differentiation of pyloric ulcers from pyloroduoden al or an tropylonic ulcers is unnecessary. That an ulcer actually migrates is unlikely, but probably changes in degree and location of anatomic distortion produce the appearance of migration. Whether roentgenographic localization is inaccurate because of distortion, or whether the ulcer actually moves, is unimportant, however. The location of the ulcer within the pylorus does not influence clinical presentation, therapeutic choices, or prognosis. All ulcers in the region of the pylorus should therefore be considered as part of a spectrum of a single disease (a broad definition of pyloric ulcer). Pylonic ulcer, then, is related to gastric and duodenal peptic disease, but may cause a characteristic, atypical clinical syndrome. The actual frequency of pylonic channel syndrome in pylonic ulcer remains unresolved. It may be higher than that seen in this series because those with highgrade obstruction that required immediate surgery were excluded. Not all patients with the pvloric channel syndrome present a diagnostic problem. In many, melena or hematemesis suggests peptic disease and leads to the proper diagnostic and therapeutic course. Nevertheless, a number of patients remain whose symptoms are not typical of peptic disease. In 6 patients in this series who were sufficiently ill to be admitted to the hospital, the diagnosis of peptic ulcer was not mentioned on the initial work-up after admission. Undoubtedly a number of others with less severe symptoms were treated as outpatients without definitive diagnosis. Even in those in whom the diagnosis is suspected, weight loss and atypical symptoms may lead to unnecessary surgery because of clinical suspicion of malignant tumor. More than half the patients in this group had pylonic channel syndrome.

11 VOL. 113, No. Peptic Ulcer of the Pylonic Region 57 Awareness that this syndrome is commonly present in patients with pyloric ulcer may lead to earlier and more accurate diagnosis. Since most patients who do not require immediate surgery respond well to medical management, earlier diagnosis results in significant benefit. Because many of these ulcers probably arise in the gastric mucosa, the possibility of malignancy must always be considered. Some roentgenographic characteristics common to malignant ulcers were seen in many of the benign ulcers larger than i cm. in diameter. The carcinoma and the lymphosarcoma in this group were roentgenographically indistinguishable from each other and from benign ulcers. Followup roentgenographic examination until healing is important in pylonic ulcers, just as in gastric ulcers, to exclude the possibility of malignancy. Cytologic examination of gastric secretions, if not a routine procedure, should be performed in suspicious cases. Although some of the patients in this series were followed for as long as 7 years, most were observed for only a relatively short time. Therefore, a long-term prognosis cannot be assessed from this study. The number of ulcers that healed under medical management is encouraging. Some authors state that pylonic ulcers are resistant to medical therapy and that most require surgery.6 The prognosis of overriding ulcers does appear to be poor. A trial of intensive medical therapy, however, and strict adherence to dietary precautions after healing may result in avoidance of surgery in most pylonic ulcers. Even some patients with gastric outlet obstruction may be relieved and the ulcer healed on medical management. SUMMARY Of 4o patients with pyloric ulcers, 26 (6 per cent) presented a characteristic clinical syndrome consisting of atypical pain, nausea and vomiting, and weight loss. No difference was noted in clinical presentation, course, or prognosis between ulcers limited to the pviorus and ulcers on the gastric or duodenal side of the pvlonus. Furthermore, ulcers frequently appeared to migrate across the pylorus on follow-up studies. Therefore, we believe that all ulcers that involve the pylorus should be considered pyloric ulcers, regardless of extent. Two malignant ulcers were found; one was an adenocarcinoma and the other a lymphoma. Neither could be differentiated on roentgenographic or gross pathologic examinations from benign ulcer. Morton G. Glickman, M.D. Department of Radiology University of California San Francisco San Francisco, California REFERENCES I. BURGE, H., GILL, A. M., and LEWIS, R. H. Pyloric-channel syndrome and gastric ulceration. Lancet, 1963, I, BURGE, H. W. Vagotomy. E. Arnold, London, BUTSCH, W. L. Ulcers ofpyloric ring. Proc. Staff Meet. Mayo Clin., 935, 10, loulk, W. T., COMFORT, M. W., Burr, H. R., DOCKERTY, M. B., and WEBER, H. M. Peptic ulcer near pylorus. Gastroenterology, 1957, 32, I-IARKINS, H. N., and NYHUS, L. M. Surgery of the Stomach and Duodenum. Second edition. Little, Brown & Company, Boston, MURRAY, G. F., BALLINGER, W. F., II, and STAFFORD, E. Ulcers ofpyboric channel. Am. 7. Surg., 1967, 113, Or, M., OSHIDA, K., and SUGIMURA, S. Location of gastric ulcer. Gastroenterology, 1959, 36, Oi, M., and SAKURAI, Y. Location of duodenal ulcer. Gastroenterology, 1959, 36, RUFFIN, J. M., JOHNSTON, D. H., CARTER, D. D., and BAYLIN, G. J. Clinical picture of pyboric channel ulcer: analysis of one hundred consecutive cases. 7.A.M.A., 1955, 159, RUSSELL, W. A., WEINTRAUB, S., and TEMPLE, H. L. Analysis of x-ray findings in 405 cases of benign gastric and pyloric ulcer. Radiology, 1948,51, II. SHANKS, S. C., and KERLEY, P. A Text-book of X-Ray Diagnosis. Third edition. Volume III: Abdomen. W. B. Saunders Company, Philadelphia, 1958.

12 Glickman, Szemes, Loeb and Margulis SEPTEMBER, SOMMER, A. W., DYSART, D. N., and HAINES, R. D. Pyboric channel ulcer, radiologic aspects. 7.A.M.A., 1960, 174, SPJUT, H. J. Pathology-relation to roentgenologic diagnosis. In: Alimentary Tract Roentgenology. Volume I. Edited by A. R. Margulis, and H. J. Burhenne. C. V. Mosby Company, St. Louis, 1967, pp TEXTER, E. C., JR., BAYLIN, G. J., RUFFIN, J. M., and LEGERTON, C. W., JR. Pyloric channel ulcer. Gastroenterology, 1953, 24, TEXTER, E. C., JR., SMITH, H. W., BUNDESEN, W. E., and BARBORKA, C. J. Syndrome pylorique: clinical and physiologic observations. Gastroenterology, 1959, 36,

13 This article has been cited by: 1. Marc S. LevinePeptic Ulcers [CrossRef]