PARAMANANDHAN : DUODENAL SPREAD OF GASTRIC CARCINOMA 169

THE DUODENAL SPREAD OF GASTRIC CARCINOMA BY T. L. PARAMANANDHAN

DEPARTMENT OF PATHOLOGY, UNIVERSITY OF SINGAPORE

THERE are many peculiar and unexplained facts in oncology, e.g., the enormous differences between the frequency of carcinoma of the stomach and the rarity of carcinoma of the duodenum. This is further emphasized by the extreme infrequency with which gastric carcinoma invades and replaces the surface of the duodenal mucosa, although it has no such respect for the deeper components of the duodenal wall.

In 1861 Rokitansky, in his Textbook of Pathology, made the classic statement that pyloric cancer was exactly bounded by the pyloric ring and that its growth never reached beyond into the duodenum. From then onwards, with the exception of Brinton (1865), the majority of workers agreed on the integrity of the duodenum, and this dictum has been passed down through the years in textbooks and by verbal statements in classrooms, and is accepted as a truism. There are many surgeons and pathologists who even today believe that ‘there is no love lost between the pylorus and the duodenum’, as carcinoma of the pylorus never invades or infiltrates into the duodenum. As recently as 1961 Boyd emphatically stated in a paragraph on the spread of carcinoma of the stomach, ‘The duodenum is never invaded, the tumour stopping short at the pylorus.’ Robbins (1962) fails to draw the attention of the reader to the fact that carcinoma of the stomach does invade the duodenum. Schenken and Bums (1961) drew the attention of the reader to the upward spread of cancer to involve the oesophagus, but did not mention the downward spread into the duodenum.

The idea of the so-called ‘ duodenal barrier ’ is still accepted, in spite of contrary reports of several workers, and is only slowly receiving the necessary revision, but as yet only a very small margin of the duodenum is resected, even in cases of carcinoma of the distal third of the stomach. Several theories have been advanced to explain the immunity of the duodenum. It has been attributed to the scarcity of lymphatic vessels between the two organs; to the upward flow of lymph from the duodenum towards the stomach; to the alkalinity of the duodenum; and to the obliteration of tissue spaces by the spasmodic contraction of the pyloric sphincter so as to form a mechanical obstruction to the spread of carcinoma.

Experimentally it has been proved that anatomical pathways do exist between the pylorus and the duodenum, chiefly via the lymphatics. This is testified by the natural invasion of cancer cells via the lymphatics. Whether these lymphatic plexuses communicate more freely in the submucosa or serosa is not as important as bearing in mind the fact that cancer cells are furnished with these pathways and do not hesitate to make use of them to invade the duodenum. Brinton (1865) was the first to take exception to Rokitansky’s (1861) statement. He studied 125 cases of carcinoma of the pyloric region

and found 10 cases (8 per cent) where the tumour invaded the duodenum: he also quoted Lebert’s case of Carle and Fantino (1898), discussing the pathology and treatment of gastric carcinoma, and reported 3 cases in a series of 14 (21.4 per cent) where the neoplastic infiltration had spread under Brunner’s glands for distances of 1-3 cm. It was suggested that surgical resection for gastric carcinoma should include the whole of the first part of the duodenum. Cunko in 1900, in his study of the lymphatic propa- gation of gastric carcinoma, investigated the accepted state of immunity of the duodenum and commented on the discrepancy between the macroscopic appearances and the picture seen under the micro- scope. In 8 gastrectomies he found I case of gross invasion of the duodenum and in 3 there was micro- scopic invasion. In I903 he studied 11 cases of carcinoma of the pylorus and found that macro- scopically the duodenum proper was not invaded, but that the duodenal surface of the pylorus was involved in 8 cases. Microscopic examination, however, revealed that in 3 of his cases there was involvement of 5 mm. of the duodenum and that in a fourth case there was involvement of I cm. of the duodenum. He felt that cases like the latter would cause uneasiness to the surgeon.

Cunko thought that the apparent arrest at the duodenum was due to mechanical causes. He believed that the annular muscle of the pylorus and the condensation of tissues within the submucosa formed a dividing septum between the pylorus and duodenum, constituting a barrier which, however, was not impermeable to the spread of cancer but still was the principal factor in preventing neoplastic infiltration of the duodenum. He maintained that there was a plexus of lymphatics in the stomach which communicated with a similar plexus in the duodenum.

Borrmann (1901) studied 63 cases of pyloric carcinoma and found duodenal invasion in 20 cases. In 9 of these cases the tumour was present at the line of resection of the duodenum and in 2 cases this was 2 cm. from the pylorus. Fenwick and Fenwick (1902)~ however, in a series of 87 pyloric carcinomata found only 2 cases where the neoplasm had infiltrated into the duodenum. They stated that, although malignant neoplasms of the pyloric region may project into the lumen of the duodenum, they rarely implicate the walls. In 1907 Jamieson and Dobson, in their treatise on the lymphatics of the stomach, showed by injection experiments that there was a direct continuity between the serosal plexus of the two regions. When the pyloric submucosal plexus was injected fluid travelled to the corresponding plexus in the duodenum. In addition, the fluid was carried via the lymphatics through the muscularis propria of the pylorus to appear on the serosal surface of the duodenum and pylorus. This latter was so

BRIT. J. SURG., 1967, Vol. 54, No. 3, MARCH

plentiful that any question as to the direct continuity of the two submucosal plexuses was considered to be insignificant. They concluded that the anastomosis between the lymphatics of the two regions was so abundant that the accepted state of the immunity of the duodenum was not so easily explainable. In addition, they emphasized the possibility of retro- grade lymphatic spread. Many collecting vessels

In 1927 and 1928 Horton repeated the experiments of Jamieson and Dobson (1907) and disagreed with them as he failed to demonstrate any constant con- tinuity between the submucosal plexuses of the two areas, but serosal continuity of lymphatics was demonstrated. Specimens varied with the ease with which they could be injected with a dye. The dis- continuity between the submucosal plexuses was

Table Z.-REVIEW OF LITERATURE

Author

cunco Pforringer Massachusetts General HosDital Lubarsch Castleman (1900-34)

( 1919-34) (1934) (1934)

Massachusetts General Hospital Heiberg Cain and Claisse Loewy and Bertrand Massachusetts General Hospital Ewing Coller, Kay, and McIntyre Takeoka Kajitani Aoki Marvin Fodden

Willis Lumb Zinniger and Collins McNeer, Van den Berg, Donn, and Bowden Harvey, Titherington, Stout, and St. John Berne and Freedman Eker Eker and Efskind Thomson and Robins Ishihara Sunderland, McNeer, Ortega, and Pearce Hajima and others Kato Zinniger Ohashi and others Hamaguchi and others IZirimoto Sato, Ichiba, and Takeda

Shimizu Hayashi, Ogawa, and Sato

Eker and Efskind Lewin

Fujimaki Hayashi, Ogawa, Ikeuchi, Hirose, Nakamura, and

Sato Ikeuchi, Ogawa, Hayashi, and Sat0 Present series

Year

1865 1898 1900 1901 1902 1903 1904 1926 1926 1936 1936 1936 1936 I935 1937 I939 I939 I939 I940 1941 1944 I945 1947 I947 1948

1948 I949 I949 1951 1951 1951 1951 1952 1952 1952 I953 I953 1953 1954 1957 1958 1958 1959

I959 1960

1960 1960

1960 1961

1961 1965

Frequency of Duodenal Invasion

I0/125 3/14 118

20163 2/87 4/11 610

Case report 1311857 6/65

151134 7/28

21/21 Case report Case report Case report Case report Case report Case report

14/53 Case report

1/24 38/100

7/21 9/29

2 Case reports Case report

9/36 9/92

5 i i i70 3/28 2/I70

23/80 3/28 2/16 1/41

Per Cent

8.0 21'4 12'5 31'5

2'3 36.3 66.7

0.7 9'2

11'0 25'0 I00

26.4

28.0 4'2

38.0 33'3 31'0

25'0 9.8

19.6 10.7

28.2 10.7 12'5 2.6

21'2 6.6

42.6 58.3 10.8 31.0 41'7 60.0

58.8 23.1 0.8 9 4 3

21.8 25.0

50.8 68.9

1'2

34'6

Pyloric cancer

Gastrectomies Pyloric cancer Pyloric cancer

-

- - - -

Necropsies Gastric resections Gastric resections Pyloric carcinomata -

- - - - -

Gastric resections

Gastric resections

Resections for pyloric cancer Necropsies Gastric resections

Gastric resections Necropsies-post-resection Gastric resections Necropsies-post-resection Gastric resections Pyloric carcinomata Necropsies-post-resection

Gastrectomies

- -

- -

- - - - - -

Pyloric carcinomata Necropsies-post-resection Pyloric carcinoma Necropsies Gastric resections -

- - -

Necropsies-post-resection

Gastrectomies Necropsies

N.B. Cases described as necropsies: Post-resection are cases where a previous gastric resection was performed for primary malignant disease of the stomach, and at necropsy the duodenal stump was carefully examined for evidence of tumour.

from the pyloric subserous network run down- wards over the duodenum to reach the subpyloric or retropyloric group of lymph-nodes. As these lymph- nodes received lymphatics from the duodenum, an indirect communication also existed.

Moynihan in 1926 stressed that the duodenal immunity was more apparent than real and he advocated the removal of the whole of the first portion of the duodenum in all cases of pyloric cancer. He stated that the implication of a single lymph-node may so sufficiently disturb the direction of the lymph current that cancer cells from a primary growth may pursue an erratic course.

explained by the presence of a connective-tissue septum at the pylorus which separates the sub- mucosa of the stomach and the duodenum, and also the circular musculature of the stomach and duo- denum. This, he felt, was why carcinoma of the stomach, regardless of how extensive, practically always stops at the pylorus and rarely, if ever, invades the duodenum. When extension in that direction did occur it was along the peritoneal aspect of the duodenum. He continued by stating that it should be remembered, however, that no barrier in the human body can hold out indefinitely against the invasion of carcinoma and that, if the

PARAMANANDHAN : DUODENAL SPREAD OF GASTRIC CARCINOMA 171

patient with an extensive carcinoma of the pars pylorica should live long enough, he felt sure that the duodenum would be freely invaded.

In 1936 Castleman reviewed the material at the Massachusetts General Hospital and found 65 cases of gastric carcinoma in the Necropsy Records in the period 1900-31. All these cases had the primary carcinoma in the pyloric region. Between 1919 and 1934 in the same hospital there were 134 gastric resections for carcinoma. In many of these cases only sections of the tumour without any portion of the duodenum were available for study, yet 6 cases from the necropsy series (9.2 per cent) and 15 cases in the biopsy series showed duodenal invasion by the gastric carcinoma. In 1934 in the same hospital 28 gastric resections were performed for carcinoma and of these 7 cases (25 per cent) showed duodenal involvement. In 21 cases of prepyloric carcinoma, 6 from necropsies and 15 from surgical resections, all showed microscopic invasion of the duodenum. Castleman hence advocated the resection of the first 3 cm. of the first part of the duodenum. Follow- ing this there were individual case reports by various authors.

In 1941 Coller, Kay, and McIntyre, in a carefully conducted microscopic study of 53 resected stomachs for gastric carcinoma, found invasion of the duodenum in 14 cases (26.4 per cent). Kajitani (1945) reported an incidence of 28 per cent of cases showing duodenal involvement. Aoki (1947)~ in a series of 24 cases resected surgically, found duodenal invasion in only I case (4.2 per cent). Marvin (1947) found invasion of the duodenum in 38 cases in a series of IOO stomachs resected for malignant lesions of the pylorus. Curiously, although the overall male-to- female ratio in the IOO cases was 3'16 : I, in the 38 cases showing duodenal invasion the ratio was 1.2: I. Marvin, too, advocated the resection of 3 cm. of the duodenum to ensure a better chance of survival.

Fodden (1948) in a series of 50 cases (21 from necropsies and 29 from surgical resections) found invasion of the duodenum in 16 cases-7 from the necropsy group and 9 from the surgical resections. Lumb in 1949 reported an interesting case of lym- phatic permeation of the entire length of the intestines by a primary gastric carcinoma-the tumour had eventually invaded the perianal skin. Zinniger and Collins (1949) found invasion of the duodenum in 9 out of 36 cases of gastric carcinoma resected surgically (25 per cent).

Following this, in the U.S.A. studies on the duodenal spread of gastric carcinoma were conducted on cases where a previous gastric resection was performed-the oral stump of the duodenum being carefully examined for evidence of residual cancer at necropsy. McNeer, Van den Berg, Donn, and Bowden (1951) reported an incidence of 9.8 per cent in a series of 92 cases. They had earlier advo- cated frozen-section examination of a circumferential section of the resected end at the time of surgery. Berne and Freedman (195 I) reported an incidence of 10.7 per cent in a series of 28 cases and Harvey, Titherington, Stout, and St. John (1951) 19.6 per cent in a series of 270 cases, whilst Thomson and Robins (1952) reported an incidence of 10.8 per cent in a series of 28 patients. In the East, Ishihara (1952)~ in

a similar series of 16 cases, reported an incidence of 12.5 per cent. He felt that, although duodenal in- vasion did occur, it did not spread very far along the long axis of the intestine and he was supported in his views by Hamaguchi and others (1958).

Eker in Norway, working on surgically resected material, reported an incidence of 1.2 per cent in a series of 170 cases, but later reported an incidence of 28.2 per cent in a series of 80 cases (Eker, 1951; Eker and Efskind, 1952,1960). Sunderland, McNeer, Ortega, and Pearce (1953) found invasion in only I case in a series of 41, whilst Zinniger (I954), in a series of IOI cases (60 surgical resections and 41 necropsies), noted duodenal invasion in 43 cases. Kato (1953) reported an incidence of 6.6 per cent in a series of 106 cases and Hajima and others (1953) 21.2 per cent in a series of 33 cases. They felt that the chances of duodenal invasion were greater in cases where the primary was of an anaplastic nature.

Studies on necropsy material in Japan gave high incidences of invasion of the duodenum. In 1959 Sato, Ichiba, and Takeda in their study showed that invasion of the duodenum occurred even in cases where the primary tumour was situated in the region of the cardia and fundus of the stomach. Hayashi, Ogawa, and Sat0 (1960) felt that there was a greater tendency to duodenal invasion in the young.

A summary of the literature is given in Table I . MATERIALS

The present study was undertaken to determine the frequency and extent to which a gastric primary carcinoma invaded the duodenum, and to determine any common denominator in those cases which showed duodenal invasion. Necropsy material was used, the patients in all cases having had no previous gastric resections. Twenty-nine cases were collected and in these the age at death varied from 17 to 82 years, the largest number being in the sixth decade. Of the 29 cases 22 were males and 7 females, giving an overall male-to-female ratio of 3.1 : I. The site of the primary gastric carcinoma in these cases was as follows:-

No. of Cases Per Cent Cardia and fundus 4 13'9 Body of stomach

Lesser curvature 8 27.6 Greater curvature I 3'5

Pyloric antrum and canal I0 345 Whole stomach 6 20.7

All 29 cases showed invasion of the serosa and all cases were Grade 3-4 (Broders's classification) adenocarcinomata. Invasion of the lymph-nodes was shown by all 29 cases. The subpyloric group of lymph-nodes was invaded in 24 cases, of which 20 cases showed invasion of the duodenum. One case showed invasion of the veins in both the stomach and the proximal portion of the duodenum.

INVASION OF THE DUODENUM In the present series of 29 cases from necropsy

material, 3 cases showed invasion of the duodenum macroscopically. In these cases the duodenal mucosa presented a peculiar wrinkled and puckered appear- ance and the sharp line of distinction between the duodenal and gastric mucosa was not recognizable (Fig. I). Microscopic examination of the sections from the duodenum, however, showed that the

172 BRIT. J. SURG., 1967, Vol. 54, No. 3, MARCH

duodenum was invaded by tumour in 20 cases serosal lymphatics and then into the duodenal wall. (68.9 per cent), and this invasion often involved the Tumour spread was more marked along the lesser mucosa and submucosa (Fig. 2). When cases where curvature than along the greater curvature. However, the primary tumour of the stomach did not involve it must be noted that in most cases the primary the distal third of the stomach were excluded, there tumour was along the line of the lesser curvature.

Pylorus

FIG. I .-Macroscopical appearances of duodenal invasion. FIG. 2.-Mucosal and submucosal spread of cancer into duodenum. ( X roo.)

FIG. 3.-Villi with dilated lymphatics filled with tumour. ( x 100.)

was a spread into the duodenum in 19 of 25 cases (76 per cent). In all cases of pyloric carcinoma, regardless of whether there was invasion by car- cinoma, there was some degree of lymphocytic infiltration in the duodenum, which could be inter- preted as representing stasis produced by proximal permeation of malignant cells.

MODE OF SPREAD In 17 cases invasion of the duodenum was chiefly

via lymphatics. In the other 3 cases invasion ap- peared to be predominantly by direct infiltration of sheets of anaplastic cells. In cases where there was extensive involvement of the mucosa, tumour cells were seen distending the villi (Fig. 3), but the surface epithelium was intact. In the few cases where this was destroyed, it appeared to be more likely to be due to post-mortem autolysis and not due to invasion and ulceration. Brunner’s glands, too, appeared to be particularly resistant-they were often compressed by enormously dilated lymphatics con- taining tumour cells, but the tumour cells were con- fined by the endothelium of the lymphatics (Fig. 4). It was difficult to decide whether the invasion occurred via the submucosal lymphatics or via the

FIG. 4.-Tumour in lymphatics, amidst Brunner’s glands. ( X 30.)

In the few cases where the tumour was only along the greater curvature there was no invasion of the duodenum.

LAYERS OF DUODENUM INVOLVED The submucosal layer was most frequently affected,

being followed by the serosa. The frequency with which the different layers were involved is as follows :

No. of Cases Submucosa only 2 Muscularis only I Serosa only 2 Mucosa and submucosa 2 Mucosa, submucosa, and muscularis I Submucosa and serosa 8 Muscularis and serosa I AU layers 3

When the serosa was involved, however, the invasion was frequently extensive.

EXTENT OF SPREAD The extent of spread varied from 0.5 to 22.6 cm.

in I case, and this was the lower line of resection. In 55 per cent of the cases showing duodenal invasion there was no tumour beyond the first 3 cm. of the duodenum. The portion of the pyloric ring covered

PARAMANANDHAN : DUODENAL SPREAD OF GASTRIC CARCINOMA I73

by duodenal mucosa was taken as the commencement of the duodenum in this study. All measurements were made on formalin-fixed tissue.

DISCUSSION The frequency of spread appears to be very high,

but it must be borne in mind that the materials used in this study were from cases where there had been no previous surgery for carcinoma of the stomach. Considering that Marvin (1947) found it in 38 per cent of cases which were considered resectable, the present value is not high. Castleman (1936) found it in IOO per cent of his series of pyloric carcinomata. In spite of the present series being confined to necropsy material, the tumour had not extended beyond the first 3 cm. of the duodenum in 55 per cent of cases showing duodenal invasion.

The above findings and those of other workers in this field who have devoted time to this particular problem should refute all the statements that carci- noma of the stomach, regardless of how extensive, practically always stops short at the pylorus. No layer of the duodenum is immune to the spread of cancer. The layer of predilection in the duodenal wall was the submucosal layer, confirming the findings of Marvin and Castleman. In the present series, although the overall male-to-female ratio was 3.1 : I, this ratio in cases showing duodenal invasion was 2.3 : I.

All cases showing duodenal invasion showed involvement of the subpyloric group of lymph-nodes and in all cases of pyloric carcinoma there was lymphocytic infiltration of the duodenum. Trans- duodenal spread of carcinoma may hence represent a retrograde spread which takes place as a direct result of a block occurring following invasion of the lymph- nodes, and the cancer cells take the pathway of least resistance, downwards in this instance, over the same pathway which usually carries lymph upwards. Since malignant gastric lesions do invade the duo- denum, the traditional total gastrectomy where a cuff of I cm. of the duodenum only is resected certainly needs revision, especially in cases where the primary tumour extends to within 5 cm. of the pyloric ring.

SUMMARY This study was undertaken to determine the

frequency and extent of spread of gastric carcinoma into the duodenum, and to find any common factors in those cases showing this spread. The literature is reviewed. It must be emphatically stated that gastric lesions do invade the duodenum, especially if the gastric lesion abuts the pyloric ring. The mode of spread may be either by lymphatic permea- tion or by direct spread, or a combination of the two. The extent of invasion may be extensive, but even at necropsy 55 per cent of cases showing invasion of the duodenum were within 3 cm. of the commencement of the duodenum. There appears to be a slightly greater frequency of invasion in females as compared to males, but it must be remembered that the series is small and hence no conclusion can be drawn.

Acknowledgements.-I wish to thank the Ministry of Health, Singapore, for permission to use the material. My thanks are due to Mrs. Mary

Low and associates for the histological sections, to MI-. L. S. Chia for the photographs, and to Miss Lim Siew Peck for secretarial assistance. I would also like to thank my colleagues in the medical profession who helped in obtaining reprints, chiefly Dr. K. Sugai of Japan, presently of Singapore, who in addition provided translations.

REFERENCES AOKI, K. (1947), quoted by SHIMIZU, H. (1959). BERNE, C. J., and FREEDMAN, M. A. ( I~s I ) , Am. 3. Surg.,

BORRMANN, R. ( I~oI) , quoted by CASTLEMAN, B. (1936). BOYD, W. (1961), Textbook of Pathology, 7th ed. London:

Kimpton. BRINTON, W. (1865)~ Lectures on Diseases of the Stomach,

2nd ed. London. CAIN, A., and CLAISSE, R. (1939), Archs Mal. Appar.

dig., 29, 834. CARLE, A., and FANTINO, G. (1898), Arch. klin. Chir., 56,

248. CASTLEMAN, B. (1936)~ Ann. Surg., 103, 348. COLLER, F. A., KAY, E. B., and MCINTYRE, R. S . (1941),

A.M.A. Archs Surg., Chicago, 43, 748. CUNI~O, B. (I~oo), quoted by CASTLEMAN, B. (1936). -- (1903), quoted by FODDEN, J. H. (1948). EKER, R. (1951), Acta chir. scand., 101, 112. -- and EFSKIND, J. (1952), Acta path. microbiol.

stand., 30, 371. ---- (1960), Acta chir. scand., suppl. 264. EWING, J. (1940), Neoplastic Diseases. A Treatise on

Turnours, 4th ed. Philadelphia: Saunders. FENWICK, S., and FENWICK, W. S . (1902), Cancer and

Other Tumours of the Stomach. London. FODDEN, J. H. (1948), Br. 3. Cancer, 2, 239. FUJIMAKI, M. (1960), Acta med. biol., Niigata, 8, 83. HAJIMA, M., and others (1953), quoted by SHIMIZU, H.

HAMAGUCHI, E., and others (1958), quoted by HAYASHI, K., and others (1961).

HARVEY, H. D., TITHERINGTON, J. B., STOUT, A. P., and ST. JOHN, F. B. ( I~s I ) , Cancer, N . Y . , 4, 717.

HAYASHI, K., OGAWA, S., IKEUCHI, H., HIROSE, S., NAKAMURA, Y., and SATO, H. (1961), Nagoya med. 3., --- - and SATO, H. (1960), Ibid., 6, 101. HEIBERG, B. (1937), Hospitalstidende, 80, 881. HORTON, B. T. (1927) Proc. Staff Meet. Mayo Clin., 2,

312. -- (1928), Am. 3. Anat., 41, 197. IKEUCHI, H., OGAWA, S., HAYASHI, K., and SATO, H.

(1961), Nagoya med. J., 7, 99. ISHIHARA, H. (1952),J. Jap. surg. SOC., 53, 98. JAMIESON, J. K., and DOBSON, J. F. (1907), Lancet, I,

1061. KAJITANI, T. (1945), quoted by SHIMIZU, H. (1959). KATO, S . (1953),J. Kumamoto med. SOC., 27, 552. KIRIMOTO, K. (1958), Osaka Daig. Igaku Zasshi (Med. 3. LEWIN, E. (1960), Acta chir. scand., suppl. 262. LOEWY, G., and BERTRAND, 1. (I939), Archs Mal. Appar.

LUBARSCH, 0. (1926), quoted bv IKEUCHI, H., and others

82, 5.

( 1959).

7, 90.

Osaka Univ.), 10, 1223.

dig., 29, 407. . . _ .. - . .

(1961).

and BOWDEN, L. A. ( I~sI ) , Ann. Surg., 134, 2.

LUMB, G. (1949)~ Br .J . Surg., 37, 41. MCNEER, G., VAN DEN BERG, HENRY, jun., DONN, F. Y.,

MARVIN. C. P. (1w7L Thesis. Graduate School of . < ..,- Medicine, University of Minnesota.

Boston med. surg. J., 195, 383. MASSACHUSETTS GENERAL HOSPITAL CASE REPORTS (1926),

----- (1935), New Engl. 3. Med., 216, 212. ---- - (1939), Ibid., 221, 832.

I74 BRIT. J. SURG., 1967, Vol. 54, No. 3, MARCH

MOYNIHAN, B. G. A. (1926)~ Abdominal Operations. SCHENKEN, J. R., and BURNS, E. L. (1961), in Pathology London. (ed. ANDERSON, W. A. D.), 4th ed. St. Louis: Mosby.

OHASHI, S., and others (1957), quoted by HAYASHI, K., SHIMIZU, H. (I959), Arch. jap. Chir., 28, 1334. and others (1961). SUNDERLAND, D. A., MCNEER, G., ORTEGA, L. G., and

PFORRINGER, S. (1904)~ quoted by SHIMIZU, H. (1959). PEARCE, L. S. (I953), Cancer, N.Y., 6, 987. ROBBINS, S. L. (1962), Textbook of Pathology, 2nd ed. TAKEOKA, H. (1944), quoted by SHIMIZU, H. (1959).

Philadelphia : Saunders. THOMSON, F. B., and ROBINS, R. E. (1952)~ Surgery ROKITANSKY, C. VON (1861)~ quoted by CASTLEMAN, B. Gynec. Obstet., 95, 341.

(1 936). WILLIS, R. A. (1948)~ quoted by FODDEN, J. H. (1948). SATO, H., ICHIBA, K., and TAKEDA, Y. (1959), Gann, 50, ZINNIGER, M. M. (1954), Am. Surg., 20, 920.

409. - -_ and COLLINS, W. T. (1949), Ann. Surg., 130, 557.

THE ASSOCIATION OF GASTRIC CARCINOMA WITH DUODENAL ULCER

BY G. I?. BURNS AND J. TAUBMAN DEPARTMENTS OF SURGERY AND DIAGNOSTIC RADIOLOGY, POSTGRADUATE MEDICAL SCHOOL

AND HAMMERSMITH HOSPITAL

CARCINOMA of the stomach developing after gastric 1950; Magovern, Friedman, and Freund, 1953; surgery for duodenal ulcer is well recognized and the Pouplier, 1954; Ryan and Beal, 1957; Bernardo, incidence has been found to be almost identical to Soderberg, and Migliaccio, 1958; Shnirel’man, 1959; the expected frequency for the intact stomach in Alcala-Santaella, Fernandez Criado, Padron, and the general population. If the previous operation Villarreal, 1960; Nahodil, 1961 ; Sawyer, Sawyer, and has been carried out for gastric ulcer, however, the Spencer, 1962). Two further cases are described here.

CASE REPORTS Case I.-A 51-year-old waitress had suffered from

recurrent epigastric pain and vomiting for 40 years. She had slight relief from alkalis and food. She was first seen at Hammersmith Hospital in 1957, when a barium-meal examination showed deformity of the duodenal bulb, as a

A B FIG. case I. Barium-meal radiograph in 1959. A, Erect view showing gastric ulcer.

6, Localized view of the ulcer.

risk of subsequent gastric carcinoma is increased result of healed ulceration, and no evidence of ulceration (Helsingen and Hillestad, 1956). Coexisting duodenal Of the stomach. Simple dietary treatment was advised. ulcer and gastric carcinoma in the absence of previous In I959 she attended again with epigastric pain and a ulcer surgery is much less common. we have been barium-meal examination (Fig. I) then showed a moderate-

sized gastric ulcer on the posterior wall of the lesser curve, able to find only 78 definite in the literature with a markedly deformed duodenal bulb, and normal (McCrea, I935 ; Fischer, Clagett, and McDonald, gastric emptying. Gastroscopy revealed a shallow gastric 1947; Lampert, Waugh, and Dockerty, 1950; ulcer at the angulus and a hypertrophic gastric mucosa. Epstein and Mendell, 1950; Romcke and Sponland, Diets and antacids were prescribed.