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Biomedical subjects

I M Samloff

Publications and source records attributed to I M Samloff.

At least 73 records · Page 4Linked to original sources
PubMed1985

The histology of the stomach in symptomatic patients after gastric surgery: a model to assess selective patterns of gastric mucosal injury.

We assessed selective patterns of histological injury in the gastric mucosa of 25 patients (12 Billroth II, 8 Billroth I, 5 vagotomy and pyloroplasty) with symptoms of alkaline reflux gastritis. Each patient had 12 biopsies taken from standardised sites. Histology was scored separately for surface epithelial changes and for inflammatory cells. The traditional grading of gastritis was also done using the categories of superficial and atrophic gastritis. The main histological changes were epithelial, especially in the pits (foveolae) of Billroth II patients. Although mild to moderate atrophic gastritis was present, the inflammatory cell density was only mild. Differences between surgery types for any given histological parameter became apparent only upon the analysis of regional changes within the stomach. Conventional grading of gastritis is based mainly on degrees of gland loss and thus is mainly of value to study chronic changes. However, the type of histological evaluation used here, with standardised biopsy sites, and separate scoring of epithelial and inflammatory changes is potentially more suitable to study shorter term changes as might occur with cytoprotective or damaging agents.

Biopsy↗
PubMed1985

Pepsinogens I and II in carcinoma of the stomach: an immunohistochemical study.

Pepsinogen I is normally produced by the chief and mucus neck cells of the fundic glands, while pepsinogen II is produced by these cells and by the cardiac and pyloric glands. In this study we used antisera specific for human pepsinogen I and II to identify these antigens in tumor tissue from 64 patients with gastric carcinoma. In addition, we examined the relationship between tumor positivity and preoperative serum levels of pepsinogens I and II. Histologically, 44 of the 64 cancers were of the intestinal type (gland forming) and 20 were of the diffuse type. Of the intestinal type tumors, 16 (36.4%) contained pepsinogen II, while only 2 (4.5%) contained pepsinogen I; one tumor contained both antigens. Pepsinogen II-positive cells were found in undifferentiated and in moderately well-differentiated intestinal type tumors, but not in intestinalized gastric mucosa or in tumors arising from intestinalized glands. This suggests that tumors containing PG II arise from antral gland mucosa even when most of the antrum has undergone intestinal metaplasia. None of the 20 diffuse tumors was positive for pepsinogen I and only 3 (15%) were positive for pepsinogen II. Serum pepsinogen II levels were available in 35 patients. The mean (+/- SE) level in 6 patients with pepsinogen II-positive tumors was 29.1 +/- 3.3 micrograms/l. This was higher than the mean level of 16.0 +/- 2.1 micrograms/l in the 29 patients with pepsinogen II-negative tumors (p = 0.011). Serum pepsinogen I was elevated to 152 micrograms/l in 1 of 2 patients with a pepsinogen I-positive tumor. The results suggest that tumor pepsinogen I and II enter the circulation and contribute to their respective serum levels.

Female↗
PubMed1985

The relation of serum pepsinogen to gastric cancer and its precursors in Hawaii Japanese men: a progress report.

Prospective epidemiologic studies among Hawaii Japanese indicate that serum PG I levels below 20 micrograms/1 are highly specific for the presence of intestinal metaplasia and the intestinal type of gastric cancer; but this test shows a low level of sensitivity. Substitution of the PG I/PG II ratio for the PG I level results in a modest improvement in the level of sensitivity at the expense of some loss in specificity. Antral gastritis and intestinal metaplasia are gastric cancer precursors in this population. Abnormally low values of serum PG I or the PG I/PG II ratio predict high stage tumors in the majority of cases. It therefore does not seem likely that estimates of serum pepsinogen are likely to increase the frequency of the diagnosis of early intestinal type carcinoma of the antral portion of the stomach in this population.

Gastric Mucosa↗
PubMed1984

Low acid output in Pima Indians. A possible cause for the rarity of duodenal ulcer in this population.

Duodenal ulcer has not been observed in full-heritage Pima Indians, while gastric cancer is relatively frequent. To investigate possible underlying factors for this phenomenon, we determined gastric acid output, gastric emptying rate, and plasma levels of gastrin, pepsinogen I, and pepsinogen II in apparently healthy Pima Indians and in Caucasian controls. The Pimas had significantly lower basal and stimulated outputs of gastric acid and higher fasting and postprandial plasma gastrin concentrations than the Caucasians. Plasma pepsinogen I levels were similar in the two groups, but plasma pepsinogen II was significantly higher and the ratio of pepsinogen I to pepsinogen II was significantly lower in the Pima Indians. In addition, gastric emptying of acaloric liquid meal was significantly delayed in the Pimas. The results suggest that the absence of duodenal ulcer in Pima Indians may be related to low gastric acid production and a slow rate of gastric emptying in this population. The associated findings of hypergastrinemia, hyperpepsinogenemia II, and a low ratio of pepsinogen I to pepsinogen II suggest that the hypochlorhydria may reflect an increased prevalence of chronic gastritis in full-heritage Pima Indians. This, in turn, could represent a risk factor for the development of gastric cancer in this population.

Achlorhydria↗
PubMed1984

Gastric function and obesity: gastric emptying, gastric acid secretion, and plasma pepsinogen.

Because rapid gastric emptying and a shortened satiety period might contribute to development of obesity, this study compared gastric emptying of acaloric liquid, gastric acid production, and plasma levels of gastrin and pepsinogen I (PG I) and II (PG II) among obese and nonobese Pima Indians. Rates of fractional gastric emptying and of gastric acid secretion were similar in the two groups, basally and after an acaloric liquid meal. Basal and postprandial plasma gastrin levels did not differ significantly in obese and nonobese Pimas , but peak betazole-stimulated gastric acid output was greater in the obese group, except when normalized by body weight. The plasma PG I and PG II concentrations and PG I/PG II ratio did not differ significantly between the two groups, but the PG I/PG II ratio had a positive correlation with peak acid output. No correlation was found between fractional gastric emptying rate and degree of obesity. We conclude that an increased gastric emptying rate for liquid does not contribute to the pathogenesis of obesity in Pima Indians.

Adolescent↗
PubMed1983

Stable antibody-producing murine hybridomas.

A method is described for obtaining antibody-producing hybridomas that are preferentially retained in cultures of fused mouse spleen and myeloma cells. Hybridomas are produced by fusing mouse myeloma cells that are deficient in adenosine phosphoribosyltransferase (APRT) with mouse spleen cells containing Robertsonian 8.12 translocation chromosomes. The cell fusion mixtures are exposed to a culture medium that can be utilized only by APRT-positive cells, which results in the elimination of both unfused APRT-deficient myeloma cells and non-antibody-producing APRT-deficient hybridomas that arise by segregation of the 8.12 translocation chromosomes containing the APRT genes and the active heavy chain immunoglobulin gene.

Adenine Phosphoribosyltransferase↗
PubMed1983

Long-term follow-up of duodenal ulcer patients.

The CURE peptic ulcer clinic started in April 1974. Patients (mostly veterans) with documented ulcer disease were interviewed regularly and inpatient hospitalizations were reviewed for follow-up periods of up to 6 years. Data from 245 male ulcer patients, 190 with duodenal ulcer alone and 55 with both documented duodenal ulcer (DU) and gastric ulcer (GU), were analyzed to assess the natural history of ulcer disease and factors predicting the severity of its course. Eleven percent of clinic patients had a complication (bleeding requiring a transfusion, perforation, or obstruction) during follow-up. Complication rates were about 2.7% per year for those with no prior complication, and about 5% per year for those with a prior complication. No patient variables or ulcer markers were related to the likelihood of a complication. Patients with both DU and GU were similar to patients with DU alone on many background variables, but the combined ulcer group had a significantly higher frequency of blood group nonsecretors, increased incidence of cigarette smoking, and greater frequency of complications or ulcer hospitalization prior to entry into the study and during follow-up. These factors, together with our failure to find differences in aggressive factors (acid output and PGI), suggests that DU + GU represents a different disease entity marked by additional defects in mucosal defense.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Hypergastrinemia in obese noninsulin-dependent diabetes: a possible reflection of high prevalence of vagal dysfunction.

To elucidate the relation of noninsulin-dependent (type II) diabetes mellitus to plasma levels of gastrin, pepsinogen I, and pepsinogen II, gastric acid secretion, and gastric emptying, we studied diabetic and nondiabetic obese Pima Indian subjects. Fasting and postprandial plasma gastrin concentrations were significantly higher (P less than 0.02) in diabetic than in nondiabetic subjects, but gastric acid outputs basally, after an acaloric liquid meal, and in response to betazole were similar in the two groups. Plasma pepsinogen I and pepsinogen II levels were also similar in both groups. A significant negative relation (r = -0.84; P less than 0.01) was found between basal gastrin levels and gastric acid production in nondiabetic Indians, but not in diabetic Pimas. The fractional gastric emptying rate of an acaloric liquid meal was significantly decreased in diabetic Pimas (P less than 0.01); and at least one test showing abnormal vagal function, as estimated by the Valsalva maneuver, heart rate changes between deep expiration and inspiration, and postural hypotension, was found in every diabetic subject. These findings suggest that hypergastrinemia in type II diabetes is not related to hypochlorhydria, but, instead, results from autonomic dysfunction with slow gastric emptying.

Adult↗
PubMed1983

Inhibition of peptic aggression by sucralfate. The view from the ulcer crater.

Acid and pepsin have been designated the "aggressive factors" in peptic ulcer because they are essential for ulcer formation and because a reduction in their luminal concentrations is usually followed by ulcer healing. Acid enables peptic aggression by converting pepsinogen to pepsin, by providing the highly acidic pH required for pepsin activity, and by denaturing proteins, thereby increasing their susceptibility to the action of pepsin. Pepsin causes peptic aggression by hydrolyzing peptide linkages which bind together the constituent amino acids of proteins. The first step in this reaction is the formation of a complex between the active site of pepsin and the protein substrate. Sucralfate, which is the basic aluminum salt of sucrose octasulfate, inhibits this step by forming an electrostatic complex with proteins. As such, sucralfate inhibits peptic aggression without decreasing acid-pepsinogen secretion or raising intragastric pH. Because of its affinity for proteins and its insolubility and inherent viscosity in acid, sucralfate forms a physical coating over the ulcer crater. This coating further inhibits peptic aggression by producing a barrier to the diffusion of acid and pepsin. Additionally, the basic aluminum moieties of sucralfate may serve to buffer hydrogen ions as they attempt to permeate the viscous layer. The sum of these effects appears to explain the ability of sucralfate to accelerate the rate of healing of peptic ulcer.

Aluminum↗
PubMed1983

Pathological acid secretion not due to gastrinoma.

There are few detailed studies of patients with pathological hypergastrinaemia of antral origin. We have identified four patients with severe acid hypersecretion associated with peptic ulcer disease and in whom no evidence for gastrinoma or isolated retained antrum could be found. Three of these patients also had hypergastrinaemia. In two patients, one with gastric ulcers and one with duodenal ulcer disease, the hypergastrinaemia appeared to be due to antral gastrin cell hyperfunction and there was also evidence for mild antral gastrin cell hyperplasia. In the other hypergastrinaemic patient, a primary intestinal gastrin cell hyperfunction syndrome was suspected, but a hidden gastrinoma could not be excluded. The remaining patient had nearly fatal hypersecretory ulcer disease and cimetidine failed to control the hypersecretory state. In this patient the hypersecretion responded to a more potent H2 antagonist with resolution of a metabolic encephalopathy. No general pathophysiological mechanism could be identified in these patients or in larger groups of patients with gastric or duodenal ulcer disease.

Adult↗
PubMed1983

Morphology and dynamics of the gastric mucosa in duodenal ulcer patients and their first-degree relatives.

The prevalence of antral and body gastritis was determined in 30 duodenal ulcer patients and in 143 of their first-degree relatives, and compared by conventional mathematical and stochastic analyses with data on gastritis in a representative Finnish population sample. For conventional analysis, the controls for the duodenal ulcer patients and for the duodenal ulcer relatives, were matched for age and sex. For stochastic analysis, the duodenal ulcer patients and their 99 siblings were compared with the total control population of 434 subjects. The prevalence of gastritis affecting mainly the antral mucosa, and both antral and body mucosa to a similar extent was significantly higher in duodenal ulcer patients than in both controls and in relatives. The prevalence of antral and body gastritis in DU relatives and their controls was similar. However, the prevalence of subjects with normal antral and body mucosa was significantly lower. Stochastic analysis revealed more rapid progression of antral gastritis with age in the duodenal ulcer patients than in their siblings or controls and less rapid progression of body gastritis. The overall progression of antral and body gastritis was similar in DU siblings and their controls, but a dichotomy in the mean antral gastritis score of DU sibships was found, indicating high and low antral gastritis liability subgroups. The mean score of DU sibships having a mean age of less than 50 years behaved dynamically like DU patients, while the mean scores of sibships with a higher mean age had a low liability to develop antral gastritis. Most duodenal ulcer siblings who themselves had a duodenal ulcer, ulcer scar or duodenitis were found in the "high antral gastritis liability" subgroup.

Adult↗
PubMed1983

Pachydermoperiostosis, hypertrophic gastropathy, and peptic ulcer.

Two brothers with pachydermoperiostosis, an autosomal dominant syndrome characterized by digital clubbing, periosteal new bone formation, coarse facial features with thick, furrowed, and oily skin, presented in their twenties with severe complicated duodenal ulcer disease requiring multiple operations. Their father and one paternal uncle also had pachydermoperiostosis and a past history of ulcer dyspepsia. The mother, one sister, two maternal aunts, and one other paternal uncle were healthy. Both brothers had giant hypertrophic gastritis (Ménétrier's disease). Their pentagastrin-stimulated acid output and fasting and meal-stimulated serum gastrin levels were normal, but their serum pepsinogen I and II levels were markedly elevated. The father had hypochlorhydria and a low serum pepsinogen I/II ratio, suggesting atrophic gastritis. This family study raises the possibility that pachydermoperiostosis, hypertrophic gastropathy, and peptic ulcer may be genetically related.

Adult↗
PubMed1982

Age- and sex-related behaviour of gastric acid secretion at the population level.

Pentagastrin-stimulated gastric acid output and the histology of the antral and body mucosa were examined in 72 computer-selected probands and their 365 relatives, altogether 437 cases. The frequencies of upper abdominal complaints, peptic ulcer and hiatal hernia, and blood group distribution were comparable with those of the population at large. Acid output, expressed as mmol/h, mmol/h/kg of total body weight (TBW), mmol/h/kg of lean body mass (LBM), and mmol/h/kg of fat-free body weight (FFB), correlated with the changes in the body mucosa but not with those in the antrum. Acid output was lower in females than in males when expressed as mmol/h or mmol/h TBW but not when expressed in terms of FFB, which better than LBM accounts for the variation in the gastric surface area and, in this manner, for that of the parietal cell mass. This suggests that the lower acid output in females is due to a smaller gastric surface area and correspondingly smaller parietal cell mass rather than to a lower reactivity of the cells to stimulation. Acid output decreased with increasing age in both sexes, and this was due to a concomitant increase in the incidence and severity of atrophic changes in the body mucosa. An age-related decrease in acid output was not seen in males with a normal body mucosa. In females with a normal body mucosa, however, output expressed in terms of FFB showed a significant increase with age. The reason for this increase is not clear. In males and females with superficial gastritis of the body mucosa acid output decreased with increasing age regardless of the formulation used.

Adolescent↗