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Chapter 29 (page 139)
In their description of 6 cases of AHPS, Skoryna et al. (l959) included one case in which
pyloric muscular hypertrophy was associated with a lesser curvature gastric ulcer situated
6.0 cm orally to the pylorus (Chap. 24). The muscular hypertrophy involved the canalis
egestorius as described by Torgersen (l942). It was surmized that the pyloric hypertrophy
was probably the primary lesion.
Knight (l961) described a case of a 37 year old male in which a benign gastric ulcer, 6.0
cm proximal to the pylorus, was associated with AHPS (Chap. 24). The area of muscular
hypertrophy was 2.5 cm in length and the walls measured 1.5 cm in thickness, i.e. it
appeared to be a typical case of AHPS limited to the pyloric sphincteric cylinder.
Whether there was a causal relationship between the gastric ulcer and the pyloric
hypertrophy was not clear. (Two other cases of AHPS described by Knight were not
associated with gastric ulceration). According to him it was likely that the gastric ulcer
was the result rather than the cause of the AHPS. This was consistent with the
experimental findings of Dragstedt et al. (l954), who had previously produced gastric
ulceration in dogs by occluding the pylorus.
Burge et al. (l963) described 2 adult cases in each of which a benign gastric ulcer situated
high on the lesser curvature was associated with what they called the "pyloric channel
syndrome". In one case radiography showed a narrowed pyloric “antrum” suggesting
malignancy, while operation revealed severe benign organic stenosis of the pyloric area
with a tiny eccentric aperture. In the second case, in which radiography showed tapering
of the prepyloric stomach and deformity of the duodenal cap (in addition to the high
gastric ulcer), microscopic examination of the resection specimen revealed unilateral
pyloric muscle hypertrophy with small round-cell infiltration and fibrosis. It was thought
that the pyloric channel syndrome, with associated gastric stasis, was the probable cause
of the gastric ulceration in these cases.
During histological examination of resection specimens in 37 cases of chronic gastric
ulceration, Du Plessis (l963) found associated atrophic gastritis of the whole of the
pyloric gland area in 62 percent of cases, and of half the pyloric gland area in 92 percent.
(Comment: In cases of gastric ulceration the pyloric glandular zone may be
more extensive than in normal controls as described in Chapter 5).
Garret et al. (l966) studied antral contraction waves by means of small water-filled
balloons placed in the "distal antrum" in normal controls and 13 patients with benign
gastric ulceration. In 10 of the patients the ulcer was situated at or below the incisura
angularis but orally to the pyloric region. The amplitude and duration of Type II waves
were similar in health and gastric ulcer patients, but there was a significant reduction in
the number of these waves in the ulcer group. Normal motility patterns were obtained
after the ulcer had healed. It was concluded that the gastric ulcer had a secondary effect
on motility; there could be an interruption between action potentials and the contractile
mechanism of antral smooth muscle.
Schrager et al. (l967) performed histological studies of the "antrum" in 40 resection
specimens obtained from cases of gastric ulceration. In 31 cases the ulcer was situated at
a distance of 5.0 cm to 10.0 cm proximal to the pylorus; in 5 cases it was at a distance of
2.5 cm to 5.0 cm, and in 4 cases at a distance of 0 cm to 2.5 cm from the pylorus. While
a zone of gastritis surrounded the ulcer in all instances, the main inflammatory changes
were found in the "antrum". These consisted of widespread destruction of pyloric glands,
intestinalization, and in a few cases complete mucosal atrophy, usually associated with
marked fibrosis in the submucosa. In 7 stomachs (it is not clear what the exact situation
of the ulcer was in these cases) the changes had been severe enough to produce stenosis
of the "antrum". Schrager et al. (l967) quoted a number of previous authors who had
found that the inflammatory changes of gastritis in cases of gastric ulceration were
confined to the "antrum". These changes were much more intense in cases of gastric
ulceration than in duodenal ulceration; while intestinal metaplasia was uncommon in
duodenal ulceration, it was frequently encountered in cases of gastric ulcer. Most
previous authors held the view that the inflammatory changes preceded the ulceration,
and that the inflammation of the antrum was the more fundamental change.
Kwong et al. (l970) studied the electrical activity in the distal 6.0 cm of the "antrum" in
patients with gastric ulceration by means of serosal electrodes implanted at operation and
mucosal electrodes introduced via nasogastric tubes. Recordings in 12 control subjects
showed a wave frequency of 3 cycles per minute; there was a significantly higher
frequency in 8 patients with gastric ulceration. The amplitude of the waves, the shape of
the wave forms and the conduction time of the electrical impulses were the same in the
two groups.
Gear et al. (l97l) pointed out that gastric ulcer was frequently associated with chronic
gastritis, but that the relationship between the two was controversial. Some previous
studies had suggested that gastritis was the primary change, with the gastric ulcer
supervening; other studies had indicated that the ulcer was the primary lesion with
gastritis an accompanying zonal change. Features of the gastritis associated with chronic
benign gastric ulcer in 35 untreated cases were studied by means of fibreoptic
gastroscopy and biopsy; there were 14 prepyloric ulcers and 21 in the body of the
stomach. Biopsies were taken in the prepyloric area, from the middle of the lesser
curvature, from the high lesser curvature and the middle of the greater curvature. A
marked difference in the distribution and severity of the gastritis in the two subgroups
was found, the changes being more severe and more extensive in ulcers of the body of the
stomach. In general, there was a tendency for the more severe atrophic changes to be
found distally in the "antrum" and on the lesser curvature, while the greater curvature was
least affected. Another group of 28 patients with gastric ulceration had a gastroscopy
before and after medical treatment. In most cases biopsy specimens from the second
examination showed a similar, or worse, grade of gastritis than those from the first. In a
third group of patients, in whom the gastric ulceration had been treated by vagotomy and
pyloroplasty, the atrophic gastritis and intestinal metaplasia commonly became worse
after surgery.
Gear et al. (l97l) concluded that the gastritis associated with chronic gastric ulcer was
regional, with the distal part of the stomach and midpart of the lesser curvature the most
severely affected. Ulcers of the body of the stomach were associated with more
extensive and more severe gastritis than ulcers of the prepyloric region. It was felt that
gastritis was the basic disease process with gastric ulceration a secondary phenomenon.
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