Gastric ulcer and gastritis. Results of short-term follow-up.
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Biomedical subjects
Publications and source records attributed to P Sipponen.
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The circulating levels of placental protein 12 (PP12), a somatomedin-binding protein, were measured by radioimmunoassay in 37 postmenopausal women with ovarian tumors. Elevated levels (above 47 micrograms/l) were observed in 16 of 25 patients (64%) with malignant and 2 of 12 patients (17%) with benign tumors. Elevated levels were more frequent and higher in patients with advanced disease. Within 1 week of surgery, the levels fell in 13 of 17 cases (77%). In addition to clinical interest, these results contribute to our knowledge of carrier proteins of growth factors in patients bearing malignant ovarian neoplasms.
Seventy-five colorectal carcinoma patients (100 separate cancers) with verified cancer family syndrome were re-examined for the evaluation of histologic characteristics in carcinomas and adenomatous polyps in this inherited syndrome in a comparison with control patients with colorectal carcinoma but no hereditary background. In the cancer family syndrome group there were significantly more mucinous carcinomas (35 to 39 percent vs. 20 percent; P less than 0.05-0.01), and also more poorly differentiated tumors (24 vs. 12 percent) than in the control group. The differences could not be explained by the site or stage of the tumors or by the age or sex of the patients. Additional adenomas occurred quite often both in cancer family syndrome patients (19 percent) and in the controls (16 percent). In the cancer family syndrome group, however, there were more adenomas with moderate or severe dysplasia (P less than 0.01) and more adenomas with villous features (P less than 0.05) than in the control group. Mucinous histologic features in colorectal carcinoma, although not fully specific, might be characteristic of cancer family syndrome, and thus serve as one sign in the identification of the syndrome. The presence of the adenoma-carcinoma sequence in cancer family syndrome also was supported, and the histologic aggressivity of the associated adenomas might signify an accelerated advancement of this phenomenon in cancer family syndrome.
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Upper gastrointestinal endoscopy revealed gastroduodenal polyps in 45 (90%) out of 50 patients with familial adenomatosis (FA), and in 11 (92%) out of 12 patients with juvenile polyposis (JP). The polyps in the fundic and corpus regions of the stomach were hamartomatous cystic body gland polyps in 28 (56%), and adenomas in 3 (6%) of the FA patients, while 6 (50%) JP patients had hyperplastic polyps in the corresponding region. The polyps in the gastric antrum and duodenum were adenomas in 6 (12%) and 25 (50%) of the FA patients, respectively, while the polyps of the corresponding regions were hyperplastic in 10 (83%) and 2 (17%) of the JP subjects. One focal adenomatous lesion in an antral hyperplastic polyp, and one duodenal adenoma were found in the JP patients. Furthermore, one duodenal adenocarcinoma was observed among the FA subjects. It is concluded that gastroduodenal polyps belong inherently both to adenomatous and to juvenile varieties of gastrointestinal polyposis, and that these two conditions have characteristic histological patterns and topography of polyps in the upper gastrointestinal tract.
The expression of the carbohydrate antigen CA 19-9 in human gastric mucosa was studied by using the monoclonal 1116 NS 19-9 antibody, immunohistochemical ABC staining technique and formalin-fixed, paraffin-embedded biopsy specimens. Among 26 gastric carcinoma (GCA) patients CA 19-9 antigen was found in 16 patients (62%). The antigen was also found in 10 (48%) out of 21 non-cancer patients who had benign gastric ulcer and in 9 (12%) out of 74 non-ulcer, non-cancer patients. In non-cancerous mucosa, the CA 19-9 antigen was localized in the surface epithelium (foveolar type of staining) and/or in goblet cells and sometimes in absorptive epithelium of metaplastic intestinal glands (goblet cell type). The foveolar type but not the goblet cell type was related to the nonsecretor status of the subject, to Le positivity and to anti-H negativity of the gastric surface epithelium. It is concluded that, although being commonly present in GCA tissue, the expression of the antigen in benign gastric tissue is too common to advocate the practical value of CA 19-9 in predicting malignant gastric lesions in immunohistochemistry.
Relative risk (RR) and cumulative risk of gastric cancer (GCA) were calculated for different grades of atrophic gastritis (AG) of the antrum and body. Cross-sectional data on the occurrence of AG in a representative population sample (371 subjects), and Finnish Cancer Registry data on GCA were used in the calculations. The RR was increased significantly in severe AG of the antrum and the body (18.1 and 4.6 times, respectively), but not significantly in the less severe grades of AG. As a risk factor, severe antral and body gastritis were independent of each other. The cumulative risk, i.e., the probability of contracting GCA within the following 10 years in age groups 50-54 . . . 70-74 years was calculated to vary from 2.3% to 9.3% and from 8.7% to 31.9% in severe antral AG and from 0.9% to 4.5% and from 3.6% to 16.6% in severe body AG in males and females, respectively.
We determined the effect of postgastrectomy gastritis on serum pepsinogen I and pepsinogen II concentrations in 108 subjects with subtotal gastric resection. Eleven had normal remnant mucosa, 22 had superficial gastritis, and 75 had atrophic gastritis. In the subjects with superficial gastritis, serum pepsinogen I and II concentrations were significantly higher than in those with normal remnant mucosa, but the ratio of pepsinogen I to II did not differ from normal. In atrophic gastritis, serum pepsinogen I concentrations fell with increasing severity of mucosal damage, but pepsinogen II was persistently raised. Consequently, the ratio of pepsinogen I to II in subjects with atrophic gastritis was significantly lower than in those with superficial gastritis or normal remnant mucosa. Discriminant function analysis revealed that the ratio of pepsinogen I to II, in combination with the absolute level of pepsinogen II, had a sensitivity of 80%, a specificity of 73%, and a positive predictive value of 87% for atrophic gastritis in this population. We propose that the parallel increase in serum pepsinogen I and II concentrations in postgastrectomy superficial gastritis is because of an increased rate of endocrine release of both zymogens from the fundic glands, and that the dichotomy in pepsinogen I and II concentrations in postgastrectomy atrophic gastritis results from the loss of fundic glands, which produce both zymogens, and the appearance of metaplastic pyloric glands, which produce only pepsinogen II.
The course of chronic gastritis in the antrum and body was followed up for 7 years in 112 patients with gastric ulcer (GU). As controls served 155 subjects collected at random from the same geographical area. At the start of the study (first examination) there was a slight predominance of antrum gastritis in the series, but during the follow-up period (second examination at 4 years (61 out of 112 patients) and third examination at 7 years (39 out of 112 patients] a distinct body gastritis gradually predominated in GU patients. The healing tendency of active ulcer was accompanied by a more pronounced progression of body gastritis. The rate of body gastritis progression was very rapid and was calculated to be 11-fold as compared with that in the population at large. No immunological phenomena were associated with the body atrophy process.
To evaluate the family behaviour of acid secretion and particularly of 'hypersecretion', we have examined by pentagastrin test and direct vision gastric biopsy 342 subjects with a normal mucosa or superficial gastritis of the body mucosa, collected from a large family sample of the Finnish population. Acid output (AO) was expressed in terms of fat-free body weight (FFB), which eliminates the sex factor found by other expressions of AO. Subjects with values above 1.0 mmol/h/FFB were considered 'hypersecretors' (14 subjects, or 4% of the whole sample). They differed from the whole sample with regard to a high prevalence of signs of duodenal ulcer disease, of high serum pepsinogen, and of blood group O and lack of gastric antibodies and of high serum gastrin levels. The Fisher distribution test showed a significant family aggregation of AO values. In addition, at low AO levels there were subgroups with distinct gaps between them. This finding suggests the effect of genetic variation rather than of a common family environment. The occurrence of higher AO values in sibs but not in children of 'hypersecretors' seems to rule out the possibility of a dominant Mendelian inheritance. These present results are considered to be best compatible with a multigenetic mode of inheritance of gastric hypersecretion.
Three hundred and seventy-seven subjects with different conditions of the gastric body mucosa have been followed up for 30-34 years, first by the 'blind' suction biopsy method and since 1973-1976 by the direct-vision endoscopic method. Body gastritis revealed a distinct worsening trend during the whole follow-up period. However, during the last follow-up period some slowing down of the process was also discernible. In the antrum there was a distinct healing trend during that period. Thus all cases of distinct atrophic gastritis limited to the antrum and found at the re-examination in 1973-1976 had disappeared during the last follow-up period owing to regression of the antral or continuation of the body process. On the other hand, a considerable proportion of cases of diffuse antrofundal atrophic gastritis found in 1973-1976 appeared in 1983-1984 in the 'pure' body atrophic gastritis group, obviously due to regression of the antral process. This indicates the existence of an alternative pathway via diffuse antrofundal atrophic gastritis for the development of atrophic gastritis limited to the body area. The occurrence of parietal cell antibodies was on the whole a poor indicator of the progression of atrophic gastritis. However, the development of the end-stage (severe) atrophic gastritis was significantly associated with their presence. Atrophic changes of the body mucosa were not found in 1983-1984 in any cases of duodenal ulcer disease, whereas in patients with gastric polyps atrophic gastritis affecting only the body was, as a rule, present. No case of gastric carcinoma was detected during the last follow-up examination.
A simple method for grading gastritis is to assess the severity of round cell infiltration and the loss of normal glands, and this may be applied to both antral and body changes. However, there is, as yet, no satisfactory classification of gastritis. In population samples, gastritis shows a linear increase in age-specific prevalence so that the annual increase in the body atrophic gastritis pool up to geriatric age is constant (1.5%). In the elderly, there appears to be a retardation of the process, particularly in the antral mucosa, where some healing trend is demonstrable. This dynamic behaviour is qualitatively similar in all population samples collected in Finland and Estonia. On the other hand, the dynamic behaviour of gastritis in different subpopulations differs markedly from that in the population at large. In pernicious anemia patients and their first-degree relatives, the progression of body atrophic gastritis in its final stages is about 20 times more rapid than in a general population, while, simultaneously, antral gastritis displays a distinct healing tendency. A behaviour opposite to that in pernicious anemia is seen in patients with active or healed duodenal ulcer disease and in duodenitis: antral gastritis behaves, on the whole, similarly to that in the general population, but in the body mucosa there occurs virtually no progression with age, and the mucosa generally remains normal or at the stage of superficial gastritis. However, after antrectomy body gastritis progresses rapidly in the remnant at first, but it slows down later and then closely resembles that in the general population.(ABSTRACT TRUNCATED AT 250 WORDS)
Upper gastrointestinal endoscopy with biopsies from the antrum, body and duodenum, as well as tests for acid secretion were performed on 43 uraemic patients, 17 women and 26 men, (mean age 49.7 years) and on 46 patients with well-functioning renal transplant received 10 months earlier (12 women and 34 men, mean age 40.6 years) in order to study the background of peptic lesions in uraemic patients. Eighty-nine age- and sex-matched subjects selected from a random population sample consisting of 434 persons served as a control group. All groups of renal patients were similar with respect to the prevalence and severity of antral or body chronic gastritis. Compared with control subjects their antrum had significantly less advanced chronic gastritis, which was due to the lack of atrophic changes. Furthermore, the gastric body tended to show fewer alterations than that of the controls. The acid secretion capacity in the renal patients decreased with the increasing severity of atrophic changes in the body mucosa. However, definite hypoacidity was found in some of the renal patients with normal body mucosa. Thus, a true "state of hypoacidity" seems to occur in chronic uraemia.
The serum levels of CA 19-9 and carcinoembryonic antigen (CEA) were determined in 37 patients with benign colorectal diseases and in 111 patients with newly discovered colorectal carcinomas or clinically verified relapses. In cancer patients, the CA 19-9 level ranged from normal (0-37 U ml-1) to 77,500 U ml-1 whereas all samples but one from patients with benign colorectal diseases had a normal value. CA 19-9 was increased in 46% and 45% of patients with an advanced (Dukes C or D) carcinoma or a verified recidive, respectively. Only one out of 26 patients (4%) with a localized (Dukes A or B) carcinoma displayed an elevated CA 19-9 level (greater than 37 U ml-1). No clear correlation was found between the CA 19-9 and CEA levels. The sensitivity of the CA 19-9 test (36%) was poorer than that of the CEA assay (69%), but the new test was markedly more specific (97% vs 70%) than the CEA assay.
Age-related trends of gastritis and intestinal metaplasia (IM) were studied in 476 endoscopically examined and bioptically proved cases of gastric carcinoma (GC), 263 of which were of intestinal (IGC) and 213 of diffuse (DGC) types. Endoscopic biopsy specimens from the area around the tumour were available in all cases, and from the antrum and/or body distant from the tumour area in 238 cases. A representative sample of an endoscopically and bioptically examined Finnish population consisting of 431 subjects was used as control material. In patients with IGC the prevalence of atrophic gastritis in the gastric area affected by the tumour was higher and that of superficial gastritis lower than expected, and the age-group scores of gastritis and IM were situated above the age-dependent line of gastritis scores of controls in all age groups studied. This was seen to indicate a more rapid progression of gastritis in IGC patients than in the population at large. In the opposite area of the stomach, i.e. in the tumour-free area, the progression of gastritis and IM was virtually similar to that in controls. No such differences were seen with regard to DGC. It is concluded that IGC is dynamically closely linked to gastritis and IM, while in DGC no such relationship is demonstrable.
We counted the number of granulated mast cells with high iron diamine staining, and the number of eosinophils with hematoxyline-eosin staining, in the lamina propria of the jejunum in 12 untreated patients with intestinal cow's milk allergy (CMA), 47 with celiac disease (CD), and 14 controls. A decreased number of mast cells and an increased number of eosinophils were found in 58% of patients with CMA, and in 60% of those with CD. The number of mast cells showed a significant positive correlation with the villous height, and the number of eosinophils a negative correlation with both the villous height, and the number of mast cells. Appropriate dietary treatment resulted in a rise in the number of granulated mast cells and a decrease in the number of eosinophils in both patient groups.
Serum CA 19-9 antigen concentrations were measured in 246 patients with benign and histologically confirmed malignant gastrointestinal diseases. The CA 19-9 concentration was above the upper limit of the normal range (0-37 U/ml) in 76% of patients with pancreatic carcinoma, 73% of patients with cholangiocarcinoma, 42% of patients with gastric carcinoma, and 22% of patients with hepatoma. High CA 19-9 concentrations were found mainly in patients with a metastasised cancer, whereas 71% of patients with a localised carcinoma had normal CA 19-9 concentrations. All of the patients with benign gastric diseases had normal CA 19-9 values. Moderately increased concentrations were found in 15-36% of the patients with benign pancreatic, liver, and biliary tract diseases. alpha-fetoprotein was a better marker for hepatomas than CA 19-9. CA 19-9 was better than carcinoembryonic antigen in differentiating malignant from benign diseases. The results indicate that the CA 19-9 assay is not completely specific for cancer but serves as a valuable adjunct, especially in the diagnosis of pancreatic carcinoma.
Serum concentrations of the placental protein 12 (PP12), measured by radioimmunoassay, were found to be elevated in 15 out of 16 (94%) patients with primary liver cancer, 10 out of 68 (15%) patients with other gastrointestinal malignancies, 5 out of 10 (50%) patients with cirrhosis; and 1 out of 33 (3%) patients with benign gastrointestinal disease. No correlation was observed between the serum levels of alphafetoprotein (AFP) and PP12 in patients with primary liver cancer. Using immunoperoxidase staining, PP12 was localised in malignant hepatocytes and hyperactive nodules of cirrhosis, but rarely in malignant cells of other gastrointestinal cancers. Fetal liver was PP12 positive, while adult normal liver was negative. These results indicate that PP12 has certain oncodevelopmental characteristics.