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Chapter 38 (page 194)
Most cases of prolapse of gastric mucosa into the duodenum occurred de novo, in the
absence of other lesions of the upper gastrointestinal tract. However, in a considerable
number of cases other lesions were also encountered during the radiological, surgical or
post mortem examinations. The most frequent associated conditions were the following:
Not infrequently active duodenal ulceration was encountered (Pendergrass 1930; Scott
1946; Manning and Gunter 1950; Zimmer 1950; Keet 1952). Cases associated with
healed duodenal ulceration were also described (Eliason et al. 1926; Archer and Cooper
1939; Fermin 1950).
Melamed and Hiller (1943) described a case in which a large gastric ulcer was situated on
the prolapsed mucosa. In other cases active gastric ulceration was located elsewhere in
the stomach, i.e. away from the prolapsing mucosa (Hawley et al. 1949; Keet 1952).
Changes in the Pyloric Musculature.
Changes of a hypertrophic or fibrotic nature in the pyloric musculature with consequent
narrowing of the pyloric aperture were reported by various authors. Meyer and Singer
(1931), Archer and Cooper (1939) and Zacho (1948) noted a perceptible thickening in the
pyloric musculature in some of their cases. In a verified case of Ferguson (1948) the
pyloric muscle was greatly hypertrophied. In his 3 cases Rees (1937) found the pyloric
muscle to be constricted, having the appearance of a white fibrous ring in one case.
Manning and Gunter (1950) noted thickening of the pyloric muscular ring in 4 of their 6
cases. Zimmer (1950) described a case with a duodenal ulcer and acute inflammatory
changes in the pyloric mucosa and musculature. From these descriptions no clear picture
emerged as to the nature and extent of the pyloric hypertrophy.
Cases with an abnormally wide pyloric aperture have also been described. Eliason et al.
(1926) noted this feature in one case which came to operation. In the cases described by
Nygaard and Lewitan (1968) and by Köhler (1950), the radiographs showed the
pyloric aperture to be widely dilated.
Differences of opinion regarding the histology, pathogenesis and classification of gastritis
have been referred to previously (Chap. 28). In the present context it is to be expected
that different authors may have used different criteria in diagnosing gastritis. A number
of cases of transpyloric prolapse of gastric mucosa have been described in which
"gastritis" was mentioned as an associated lesion.
Bohrer and Copleman (1938) described one case in which there was associated acute and
subacute gastritis. In two verified cases of Norgore and Shuler (1945) the pyloric region
showed evidence of chronic gastritis. Histological examination of the resected mucosa in
5 operated patients described by Scott (1946), showed a slight increase in lymphocytes,
plasma cells and eosinophils throughout the mucosa and submucosa; however, this was
not considered sufficient to warrant a diagnosis of gastritis. Judd and Moe (1947)
described a case in which erosive gastritis and infiltration by plasma cells were present.
A verified case described by Nygaard and Lewitan (1948) had chronic gastritis and
healed erosions. One of the 3 verified cases of Hawley et al (1949) showed a moderate
infiltration of the gastric mucosa with plasma cells and lymphocytes. The second case
showed no gross evidence of gastritis, and the third, in which 2 gastric ulcers were also
present, had acute on chronic inflammatory reaction in the pyloric area. Two cases of
verified circular prolapse studied by Manning and Gunter (1950) both showed chronic
gastritis with heavy infiltration of lymphocytes and plasma cells in the prolapsed mucosa,
submucosa and muscularis mucosae. In his verified case Teng (1962) found the
submucosa to be thickened and oedematous; there was mild inflammatory reaction
without ulceration. White et al. (1966) found the prepyloric mucosal folds to be
hyperaemic and oedematous with a granular, inflammatory appearance.
Ulceration and Haemorrhage.
Cases with superficial ulceration of the prolapsed mucosa and consequent slow oozing of
blood from the ulcerated surfaces were described by a number of authors (Pendergrass
and Andrews 1935; Bohrer and Copleman 1938; Archer and Cooper 1939; MacKenzie
et al 1946; Scott 1946; White et al. 1966). In some cases massive gastro-intestinal
haemorrhage occurred (Ferguson 1948; Moon and Speed 1949; Fredel 1960). The
above authors usually regarded ulceration and haemorrhage as a true complication of the
Obstruction of the Pyloric Aperture by Redundant Gastric Mucosal Folds.
Gastric mucosa prolapsing into the duodenum may, at times, pile up in the form of large,
redundant prepyloric folds causing obstruction at the gastric outlet (Schmiedin 1911;
Eliason et al 1926; Scott 1946; Judd and Moe 1947; Zacho 1948; Fredell 1960). (In
the 2 cases of Zacho there was associated pyloric muscular hypertrophy). It seems that
redundant prepyloric mucosal folds, causing obstruction, may also be regarded as a true
Malignancy does not appear to be a complication of gastric mucosal prolapse. The
presence of benign papillomata on prolapsed mucosa was reported by Pendergrass and
Andrews (1935). In one of the polyps a small plaque of malignant tissue was
encountered; it was considered to be an incidental finding not directly related to the
prolapse. One other case associated with malignancy was described, namely that of Rubin
(1942), in which the malignant polypoid process involved the entire gastric mucosa. This
appeared to be a case of general gastric polyposis with malignant degeneration, not
confined to the prolapsed mucosa. According to Nygaard and Lewitan (1948) no
instance of malignant change in a true case of transpyloric mucosal prolapse had been
reported up to that time. This statement still appears to be valid at the present time.
However, a primary gastric carcinoma may prolapse into the duodenum, causing a
rounded, intraluminal filling defect in the bulb, as described by Joffe et al. (1977).
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