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Biomedical subjects

I M Samloff

Publications and source records attributed to I M Samloff.

At least 91 records · Page 5Linked to original sources
PubMed1982

Endoscopic and clinical findings in first-degree relative of duodenal ulcer patients and control subjects.

The first-degree relatives of duodenal ulcer patients and of control probands were evaluated clinically and by gastroduodenal endoscopy for prevalence of duodenal ulcer. The control probands were randomly selected from a control population. 199 relatives of 51 duodenal ulcer probands were interviewed, and 154 of these were endoscoped. 154 control relatives who had been endoscoped were matched with the DU relatives according to sex and age. Endoscopic evidence of present or past duodenal or pyloric ulcer was present in 20 (13.0%) of the DU relatives and in only 6 (3.9%) of the control relatives (p less than 0.01). The frequency of macroscopic duodenitis and gastric erosions was also significantly higher (p less than 0.05) in DU relatives than in controls. A history of epigastric pain was obtained in 54 (35.1%) of endoscoped DU relatives and in 24 (15.6%) of control relatives (p less than 0.01). This study has shown an increased prevalence of endoscopic evidence of duodenal ulcer in the first-degree relatives of duodenal ulcer patients. The finding that duodenitis is also more prevalent in DU relatives than in controls support the view that duodenitis is linked with duodenal ulcer.

Adolescent↗
PubMed1982

Pepsinogens I and II: purification from gastric mucosa and radioimmunoassay in serum.

Pepsinogen I and pepsinogen II were purified from gastric mucosa and used to develop a radioimmunoassay for pepsinogen II and an improved radioimmunoassay for pepsinogen I. Each immunochemically homogeneous preparation contained only its characteristic components by radioelectophoretic analysis, and migrated as a singly band in polyacrylamide gel. The mean (+/- SD) level of serum pepsinogen II in 42 healthy control subjects was 10,8 +/- 3.8 ng/ml, significantly less (p less than 0.001) than the level of pepsinogen I, which was 62.9 +/- 22.2 ng/ml. The correlation between serum pepsinogen I and pepsinogen II was highly significant (r = 0.700, p less than 0.001) in these subjects. In 20 patients with pernicious anemia the mean serum pepsinogen II level was 10.6 +/- 2.5 ng/ml, not different from normal, but significantly higher (p less than 0.001) than the level of pepsinogen I which was 5.9 +/- 4.7 ng/ml. IN 10 patients with total gastrectomy, serum pepsinogen I was 3.9 +/- 3.1 ng/ml and serum pepsinogen II was 3.2 +/- 3.1 ng/ml; both values were significantly lower (p less than 0.001) than the corresponding levels in pernicious anemia. The predominance of pepsinogen I in the serum of healthy control subjects suggests that either the gastric chief cell normally releases more pepsinogen I than pepsinogen II into the circulation or that pepsinogen I has longer metabolic clearance rate than pepsinogen II. The marked decrease in serum pepsinogen I in patients with pernicious anemia is best explained by a loss of gastric chief cells due to severe atropic gastritis of te fundic glands. The normal distribution of serum pepsinogen II levels in these patients may reflect an increased number of pyloric glands due to pyloric gland metaplasia of the proximal stomach.

Adult↗
PubMed1982

Evidence for a major dominance component in the variation of serum pepsinogen I levels.

We report here a variance component analysis of the distribution of serum pepsinogen I levels in normal individuals, using a maximum-likelihood method on entire pedigrees. The results indicate a broad heritability of 91%, with some 74% being attributed to a dominance component. This is consistent with the hypothesis that the pepsinogen I level in normals is principally determined by the action of major genes, as also seems to be the case for duodenal ulcer patients and families.

Analysis of Variance↗
PubMed1981

Selective binding of sucralfate to gastric ulcer in man.

Sucralfate is a basic aluminum salt of a sulfated disaccharide. In this study, patients with gastric ulcer were given oral multiple doses of sucralfate prior to partial gastrectomy, and binding of the drug to the ulcer lesion and to nonulcerated mucosa was estimated by chemical determination of aluminum and sulfated disaccharide. The ulcerated mucosa was found to contain, on the average, 6-7 times more sucralfate per square centimeter than the control mucosa (P less than 0.01 and less than 0.05 for aluminum and sulfated disaccharide, respectively). The high affinity of sucralfate for ulcerated mucosa, particularly the sucrose sulfate moiety, supports previous data that the beneficial effect of sucralfate in ulcer disease is due in part to complex formation between sucrose sulfate and proteins at the ulcer site.

Adult↗
PubMed1981

Family studies of hypergastrinemic, hyperpepsinogenemic I duodenal ulcer.

Antral G-cell hyperfunction is a rare cause of hypergastrinemia, hyperchlorhydria, and duodenal ulcer disease. We found evidence for a familial basis for this disorder. The probands were two young men with aggressive duodenal ulcer who had basal and postprandial hypergastrinemia, hyperpepsinogenemia I, and basal and pentagastrin-stimulated hyperchlorhydria. All characteristics returned to normal after antrectomy and vagotomy. Antral gastrin concentrations and quantitative G-cell counts were normal, indicating hyperfunction of G-cells rather than hyperplasia. Four of 10 first-degree relatives of the two patients shared with them the combination of postprandial hypergastrinemia and hyperpepsinogenemia I. The aggregation of these abnormalities in tow families, each identified by a proband with hypergastrinemic, hyperpepsinogenemic l duodenal ulcer, suggests that antral G-cell hyperfunction may have a genetic basis.

Adolescent↗
PubMed1981

Pepsins, peptic activity, and peptic inhibitors.

Our information about gastric pepsinogen secretion and peptic activity is incomplete because of the heterogeneity of pepsinogen and pepsin, and the lack of assays specific for the different pepsins in gastric juice. In general, the peptic activity of gastric juice parallels acid output, and the limited clinical information obtained from tests of gastric acid secretion is not enhanced by the determination of the peptic activity of gastric juice. Nevertheless, the inhibition of this activity is of prime importance in the pharmacotherapy of peptic ulcer disease. This can be accomplished by inhibiting the secretion of acid and pepsinogens, raising the pH of gastric juice, inhibiting the binding of pepsin to its substrate, adsorbing pepsin, or inhibiting the active site of pepsin. The first three strategies have been shown to be effective in accelerating the rate of healing of peptic ulcer.

Antacids↗
PubMed1980

Serum pepsinogen I and gastrin in relation to extent and location of intestinal metaplasia in the surgically resected stomach.

A study of 177 patients undergoing distal subtotal gastrectomy indicates that a preoperative serum pepsinogen I (PGI) level below 20 ng/ml predicts the presence of gastic carcinoma and the degree of intestinal metaplasia of the gastric antrum. The serum gastrin level was not predictive of carcinoma or of the degree of intestinal metaplasia. Of the 15 patients with a low serum PG level, 13 had carcinoma and 2 had atypical polyps. The PG I level in a stored serum sample from 4 of 30 patients fell from normal to abnormal over a period of 8-9 years. Each of these converters had invasive carcinoma of the stomach. This suggests that persons showing a fall in serum PG I to abnormal levels during serial analyses should be evaluated for the possibility of gastric carcinoma.

Adult↗
PubMed1980

Serum pepsinogen I as a predictor of stomach cancer.

Among 7498 Japanese men who were examined from 1967 to 1970, 48 were subsequently diagnosed with stomach cancer and had premorbid stored sera available for serum pepsinogen I analysis. The median interval between serum collection and diagnosis of cancer was 44.5 months (range, 3 to 103 months). A low pepsinogen I level was found in 15 of the 48 patients with stomach cancer and in only six (6.3%) of 96 matched control subjects (p < 0.001). All 15 patients with low pepsinogen I levels belonged to the subgroup of 38 who had the intestinal-mixed-other histologic types of gastric cancer. This finding indicates that a low serum pepsinogen I level is a subclinical marker of increased risk for these histologic types of gastric cancer.

Aged↗
PubMed1979

Duodenal-ulcer disease associated with elevated serum pepsinogen I: an inherited autosomal dominant disorder.

To delineate genetic factors involved in the pathogenesis of duodenal ulcer, serum pepsinogen I levels were determined by radioimmunoassay in two large kindreds with multiple members affected with duodenal ulcer. An elevated serum immunoreactive pepsinogen I concentration (greater than 100 ng per milliliter) segregated as an autosomal dominant trait in these families. Furthermore, 10 of 11 patients with clinical ulcer disease in these families had hyperpepsinogenemia. An elevated serum pepsinogen I concentration appears to be a subclinical marker of the ulcer diathesis in families with this autosomal dominant form of peptic-ulcer disease.

Duodenal Ulcer↗
PubMed1979

An appraisal of tests for severe atrophic gastritis in relatives of patients with pernicious anemia.

The sensitivities, specificities, and predictive values of parietal cell antibody, serum gastrin, and serum pepsinogen I (PG I) for severe atrophic gastritis of the oxyntic gland mucosa have been determined in 171 first-degree relatives of 62 patients with pernicious anemia. Parietal cell antibody had the lowest sensitivity (65%), specificity (87%), and predictive value (44%). A low serum PG I and a high serum gastrin had identical specificities (97%), and similar predictive values (84 vs 83%), but the sensitivity of a low serum PG I was greater than that of a high serum gastrin (91 vs 83%). Parietal cell antibody was found in 19 of 148 relatives without severe atrophic gastritis and occurred as an isolated finding in 17. In contrast, 14 of the 15 relatives with severe atrophic gastritis who had parietal cell antibody also had a high serum gastrin and a low serum PG I. A high serum gastrin together with a low serum PG I had a specificity of 100%. The results recommend serum PG I and serum gastrin, but not parietal cell antibody, as tests for severe atrophic gastritis in relatives of patients with pernicious anemia.

Anemia, Pernicious↗
PubMed1979

Actions of histamine, secretin, and PGE2 on cyclic AMP production by isolated canine fundic mucosal cells.

Cyclic AMP production was studied in isolated canine fundic gastric mucosal cells. Histamine, prostaglandin E2 (PGE2), and secretin increased cyclic AMP production by unenriched mucosal cells. In separated cell fractions, histamine stimulation of cyclic AMP production correlated with the parietal cell content of the fractions. Secretin in concentrations above 1 nM stimulated cyclic AMP production, and this effect correlated with the pepsinogen content of the separated cell fractions. At concentrations above 1 microM, PGE2 stimulated cyclic AMP production; this effect was found in all separated cell fractions and was not associated with any of the available cell markers. PGE2 stimulation of cyclic AMP production was, however, negatively correlated with the parietal cell content. Thus, histamine stimulated cyclic AMP production by parietal cells and secretin stimulated production of cyclic AMP by chief cells. PGE2 stimulation of cyclic AMP production could not be localized to a single cell type but occurred primarily in nonparietal cells.

Animals↗
PubMed1979

Gastric morphology, function, and immunology in first-degree relatives of probands with pernicious anemia and controls.

Gastric morphology, function, and immunology was studied in 68 patients with pernicious anemia (PA), 183 of their first-degree relatives, and 354 control subjects. The PA relatives and controls were comparable in age and sex distribution. In both groups, mean gastric acid output decreased and mean fasting serum gastrin levels and the prevalence of atrophic gastritis increased with age. The total prevalence of chronic gastritis was similar in the two groups, but severe atrophic gastritis of the body of the stomach (AGB), achlorhydria, parietal cell antibodies, and a raised fasting serum gastrin level were significantly more common in PA relatives than in controls. Of the PA relatives 23 had severe AGB which was indistinguishable from the gastric mucosal lesion found in PA probands and was, as a rule, accompanied by several other characteristics of type A gastritis. These included a normal antrum (78%), slight or absent inflammatory cell infiltration in the gastric mucosa (70%), achlorhydria (91%), high fasting serum gastrin level (83%), parietal cell antibodies (65%), and intrinsic factor antibodies (22%). The mean age and the proportion of subjects with slight and moderate AGB of all AGB subjects was significantly lower in PA relatives than in controls. This suggests an early onset and a rapid progression from mild to severe AGB in PA relatives. Thus, the PA relatives appear to consist of two populations, one with a high and one with little or no proneness to severe AGB. This bimodal distribution suggests the participation of a single major factor, probably genetic, in the pathogenesis of severe AGB in PA relatives.

Adolescent↗