Tsuneyoshi Yao

Gastric lesions in familial adenomatosis coli: Their incidence and histologic analysis

In order to detect accompanying gastric lesions, we examined 22 patients with familial adenomatosis of the colon belonging to 14 families. Various gastric lesions were confirmed in 15 patients (68.2 per cent) belonging to 13 families. The lesions were found histologically to be adenoma in nine cases, fundic gland polyposis in six, carcinoma in three, and microcarcinoid in two. Fundic gland polyposis consisting of simple hyperplasia of the fundic glands seems to be the gastric lesion specific to familial adenomatosis of the colon and rectum. Familial adenomatosis coli not only affects the colon and rectum, but is also capable of inducing tumorigenicity in other organs. The stomach is one of the organs in which extracolonic lesions occur.

Endoscopic and biopsy findings of the upper digestive tract in patients with amyloidosis

Endoscopic and biopsy findings of the esophagus, stomach, duodenum, and colorectum were studied in 37 patients with amyloidosis involving the gastrointestinal tract. Endoscopic examinations revealed fine granular appearance, polypoid protrusions, erosions, ulcerations, and mucosal friability in many cases. These findings were most marked and noticed most often in the second portion of the duodenum. The frequency of amyloid deposition in the biopsy specimens was as follows; 100% in the duodenum, 95% in the stomach, 91% in the colorectum, and 72% in the esophagus. The degree of amyloid deposition in the duodenum, which was the highest of the entire gastrointestinal tract, significantly correlated with the frequency of endoscopic findings such as fine granular appearance and polypoid protrusions. Therefore, the two endoscopic findings described above are characteristic of this disease and may reflect amyloid deposition in the mucosa or submucosa of the alimentary tract. Our results indicate that for a diagnosis of amyloidosis, it is important to examine the upper gastrointestinal tract, especially the duodenum, using endoscopy and biopsy techniques.

Natural History of Duodenal Lesions in Japanese Patients With Familial Adenomatosis Coli (Gardner's Syndrome)

The natural history of duodenal lesions was studied in 20 patients with familial adenomatosis coli/Gardners syndrome. These patients were followed for an average of 7.1 yr (range 1 yr, 7 mo to 12 yr, 2 mo) and repeatedly examined by hypotonic duodenography, duodenofiberscopy, and biopsy. Tubular adenomas of the duodenum (less than 8 mm in diameter) were present in 18 (90%). During the follow-up period, there was a slight increase or decrease in the number of duodenal adenomas in 4 patients but no distinct change in 13. In the remaining patient (aged 49 yr), a polypoid lesion (17 mm in diameter) of the duodenal bulb, which had been overlooked at the initial examination, became an advanced cancer (50 x 30 mm in size) during 22 mo. Tubular adenomatous tissue of the duodenal papilla was detected in 11 patients (55%). Follow-up study of the lesions revealed no change in endoscopic and histologic findings in all but 1 patient, in whom there was a slight enlargement of the duodenal papilla, as seen at endoscopy. These findings suggest to us that in patients with this disease, duodenal adenomas do not require prophylactic surgery. However, careful repeated follow-up examinations with endoscopic biopsy should be performed, with endoscopic removal of larger polyps when possible.

Natural history of fundic gland polyposis in patients with familial adenomatosis coli/Gardner's syndrome

In order to study the natural history of fundic gland polyposis, 23 patients with familial adenomatosis coli/Gardners syndrome were examined over a follow-up period ranging from 17 mo to 13 yr (average 6 yr). Examinations included gastric radiography and endoscopy with biopsy. Fundic gland polyps were found in 10 individuals. The size and number of polyps varied considerably. During the follow-up period, there was an increase in number or size of polyps, or both, in 5 patients (aged 8-27 yr), a decrease or disappearance in 2 patients (aged 36 and 41 yr), an initial decrease or disappearance followed by a late-occurring increase in 2 patients (aged 28 and 35 yr), In addition, malignant or adenomatous changes of fundic gland polyps were not observed in any patient. Therefore, fundic gland polyposis in patients with familial adenomatosis coli/Gardners syndrome may appear as early as 8 yr of age. In some patients there is a gradual increase in number and size of polyps, whereas in others, polyp proliferation ceases and polyps may even decrease in number and size. Our findings indicate that the fundic gland polyposis does not require prophylactic surgery and that careful periodic follow-up should suffice.

Natural history of gastric adenomas in patients with familial adenomatosis Coli/Gardner's syndrome

The natural history of gastric adenomas was studied in 26 patients with familial adenomatosis coli (FAC)/Gardners syndrome. The patients were followed for an average of 6.8 years (1 year, 5 months to 15 years 4 months) and examined repeatedly using gastric radiography, endoscopy, and biopsy. Gastric adenomas were present in 13 (50%). During the follow‐up period, there was a new appearance of gastric adenomas in six patients but no distinct change in number, size, and histologic features in the remaining seven patients. In a 51‐year‐old man, an antral adenoma that measured 13 mm in diameter and had an irregular central depression did not change in size or morphology during 4 years and 1 month, but malignant change was evident at the time of endoscopic biopsy. The findings indicate that in patients with this disease, gastric adenomas require careful repeated follow‐up examinations using endoscopic biopsy and, if feasible, endoscopic removal is recommended.

Small-intestinal involvement in famialial polyposis diagnosed by operative intestinal fiberscopy: Report of four cases

SummaryOperative intestinal fiberscopy, in which the duodenal fiberscope was introduced during laparotomy for colectomy in familial polyposis via the enterotomy opening, permitted the demonstration of small intestinal polyps in six of seven consecutive cases. Four of the six patients had adenomatous polyps in the proximal jejunum, including one patient with the concomitant presence of ileal adenomas. Polyposis due to lymphoid hyperplasia in the terminal ileum was found in three patients. Preoperative upper gastrointestinal surveys revealed adenomas in the duodenums of all seven patients, adenomas in the gastric antrum in three, and multiple hamartomas in the gastric corpus in two. Thus, in familial polyposis or Gardners syndrome, more or less the entire gastrointestinal tract seems to be involved and the term “gastrointestinal polyposis” seems to describe these conditions.

Endoscopic features of adenoma of the duodenal papilla in familial polyposis of the colon

The duodenal papillae of 24 patients with familial polyposis of the colon were examined in detail by duodenofiberscopy and endoscopic biopsy. Adenomas were detected in 12 of the 24 patients (50%). Endoscopically the duodenal papilla had a white nodular or granular surface in most of the patients in whom adenoma was detected. In two patients, however, the endoscopic picture of the adenoma at the duodenal papilla was almost normal. Based on these observations, endoscopy and biopsy of the duodenal papilla should be added to the usual examination done in patients with this disease.

Simultaneous occurrence of multiple gastric carcinomas and familial polyposis of the colon

Upper gastrointestinal survey in ten patients with familial polyposis of the colon revealed the presence of polyps and/or carcinomas of the stomach or duodenum in eight, including two cases of associated multiple gastric carcinomas with concomitant presence in one case of multiple gastroduodenal adenomatous polyps and in the other without presence of polyp. The rather frequent association of gastroduodenal polyps and cancerous lesions in familial polyposis suggests such association to be a part of the manifestation of this inherited disease and possible malignant change occurring in gastroduodenal mucosa as is generally supposed to be the case in large intestine.

Accompanying gastro-enteric lesions in familial adenomatosis coli.

An effort was made to detect accompanying gastro‐enteric lesions in 26 patients with familial adenomatosis coli (FAG) belonging to 18 pedigrees. One or more types of various gastric lesions were found in 17 (65.4%) of the 26 patients, these gastric lesions consisting of adenoma in 11 cases, fundic gland polyposis in six, carcinoma in three and microcarcinoid in two. The fundic gland polyposis composed of simple hyperplasia of the fundic glands seems to be peculiar to FAC. Duodenal lesions were present in all of the 19 patients examined and consisted of “carcinoma in adenoma” in one case and adenoma in 18 cases in which one had a microcarcinoid in addition. Out of 16 cases investigated through the entire jejunum and ileum by endoscopy and/or at autopsy, eight (50%) showed small polyps limited to the proximal jejunum. Histologic study showed adenoma in five of them. In the remaining three, polyps did seem clearly to be adenoma on endoscopy. Only four (25%) cases revealed one or a few neoplastic lesions restricted to the distal ileum. Histologic study showed malignant lymphoma in one case, and adenoma in three. The present study strongly suggests that accompanying gastroenteric lesions are higher in incidence than previously considered, and special attention should be given to the stomach and small intestine as well as to the colon and rectum. ACTA PATH. JAP. 27: 823‐839, 1977.

Long-term follow-up of 2529 patients reveals gastric ulcers rarely become malignant

To examine the relationship between peptic ulcer and gastric cancer, we investigated 2529 patients with peptic ulcer diagnosed from 1963 to 1975. During the follow-up period of 9–23 years, we found 38 in whom gastric cancer developed or who died of gastric cancer. Included were nine in whom gastric cancer was detected at the same site as the gastric ulcer initially diagnosed, and 22 in whom the gastric cancer was detected at another site. In the remaining seven, gastric cancer was given on the death certificate, but the details were unknown. When the data on gastric ulcer initially diagnosed were reevaluated, gastric cancer was suspected or could not be completely ruled out in seven of the nine in whom gastric cancer was detected at the same site. In the remaining two, a diagnosis of benign ulcer was made even when the initial data were reviewed. In these two, however, there was the possibility that the initially diagnosed gastric ulcer represents a phase of the “malignant cycle.” The number of deaths from gastric cancer in patients with gastric ulcer was significantly low, compared with that expected and computed by the age- and sex-matched general population. These results suggest that gastric ulcers rarely become malignant.