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Biomedical subjects

I M Samloff

Publications and source records attributed to I M Samloff.

At least 109 records · Page 6Linked to original sources
PubMed1979

Genetic heterogeneity of hyperpepsinogenemic I and normopepsinogenemic I duodenal ulcer disease.

In a search for a genetic marker of duodenal ulcer, we measured serum pepsinogen I levels in 168 ulcer patients and 151 of their clinically normal siblings. The ulcer patients tended to have either hyperpepsinogenemia I (pepsinogen I, greater than or equal to 100 ng/mL) or a normal level on a familial basis. Further evidence supporting this separation was the finding that the mean serum pepsinogen I level in the clinically normal siblings of the hyperpepsinogenemic patients was 91.2 ng/mL, significantly higher than the mean level (63.1 ng/mL) in the normal siblings of the normopepsinogenemic I patients. In the hyperpepsinogenemic I families the results of segregation analysis of an elevated pepsinogen I were consistent with autosomal-dominant inheritance of this trait. The genetic basis of normopepsinogenemic I duodenal ulcer was also shown by the familial aggregation of this disorder. These data provide direct evidence for genetic heterogeneity of duodenal ulcer disease.

ABO Blood-Group System↗
PubMed1978

Effect of topical acid on duodenal pepsinogen secretion in the rat.

The effect of topical acid on duodenal pepsinogen secretion was studied in the anesthetized rat. Perfusion of a 5-cm segment of the proximal duodenum with normal saline or buffered saline (pH 7.2 or 6.0) elicited no detectable pepsinogen response. Perfusion with 10, 25, and 100 mN HCl resulted in a graded increase in pepsinogen output. Acetylcholine bromide, 500 microgram/ml, in buffered saline, pH 7.2, also stimulated pepsinogen secretion. The pepsinogen response to 100 mN HCl and to acetylcholine was completely abolished by atropine. Secretin, 2 units/kg, did not alter pepsinogen output during perfusion with buffered saline or acid, while secretin, 75 units/kg, increased pepsinogen output. These observations suggest that topical acid stimulates duodenal pepsinogen secretion through a cholinergic reflex and that secretin is not a significant stimulant of duodenal pepsinogen secretion in the rat within the dose range employed (1--2 units/kg).

Acetylcholine↗
PubMed1978

Fetal pepsinogens in human amniotic fluid.

The presence of group I (Pg I) and group II (Pg II) pepsinogens was determined in 59 samples of human amniotic fluid between 11 and 40 weeks of gestation. Pg I was present in all of the samples, while Pg II was present only in samples of gestational age 32 weeks or older. No differential pattern of the fractions was present, although the first fraction of Pg I was not present in any of the samples. The sequential appearance of Pg I and Pg II suggests their fetal origin and that the synthesis of Pg I by fetal gastric mucosa may precede that of Pg II, thus serving as a potential marker of fetal maturity.

Amniotic Fluid↗
PubMed1978

Immunochemical characterization and cellular localization of pepsinogens in cat and dog.

The antigenic relationships and cellular localization of cat and dog pepsinogens were investigated by electrophoretic analysis, immunodiffusion, immunoelectrophoresis, immunoabsorption, and by immunofluorescence, respectively. Rabbit antiserum to human and hog group I (Pg I) and group II pepsinogens (Pg II) had been previously prepared. Electrophoretic analysis revealed at least eight distinct proteases in extracts of gastric and proximal duodenal mucosa, resistant to alkalinization but destroyed by sequential accidification and neutralization. Rabbit antiserum to Pg I (anti-Pg I) and Pg II (anti-Pg II) produced a single precipitin arc against each extract forming a line of nonidentity. Immunoelectrophoresis of extracts produced a single precipitin arc against anti-Pg I or anti-Pg II. The specificity of the antibodies for the group I or group II pepsinogens was confirmed by immunoabsorption. By immunofluorescnece, both Pg I and Pg II were present in mucous neck and chief cells in fundic mucosa, in the pyloric gland cells in antral mucosa, and Brunner's glands in the proximal duodenum. The results indicate that canine and feline pepsinogens are electrophoretically heterogenous, that canine and feline Pg I share antigenic determinants with each other but not with Pg II, that a similar positive relationship exists for Pg II, and that both Pg I and Pg II are localized to the peptic cell mass, consisting of four types of cells.

Animals↗
PubMed1978

Cimetidine versus intensive antacid therapy for duodenal ulcer: a multicenter trial.

In a randomized double blind multicenter trial, patients treated with cimetidine (800 or 1200 mg daily) or an intensive regimen of Al-Mg antacid (210 ml daily) had similar rates of duodenal ulcer healing and pain relief. After 4 weeks of treatment, the proportion of patients with ulcer healing by endoscopy were: cimetidine (1200 mg), 21 of 33 (64 percent); cimetidine (800 mg), 19 of 32 (59 percent); and antacids, 15 of 29 (52 percent). These proportions did not differ significantly. Eighty per cent of cimetidine-treated patients became asymptomatic by week 4, as did 63 percent of antacid-treated patients (P greater than 0.1). No untoward effects were observed during cimetidine treatment. Twenty-seven per cent of antacid-treated patients reported diarrhea.

Adult↗
PubMed1978

Effect of one-month treatment with cimetidine on gastric secretion and serum gastrin and pepsinogen levels.

The inhibitory effects of cimetidine on gastric acid and pepsin secretion were studied before and after 1 month of treatment with 300 mg of cimetidine four times a day in 15 male duodenal ulcer patients. Cimetidine inhibited both pentagastrin- and peptone meal-stimulated acid secretion significantly better before, than after, 1 month of treatment. Similarly cimetidine inhibited pentagastrin-stimulated pepsin secretion significantly better before treatment. Meal-stimulated serum gastrin concentrations were significantly higher after treatment. The mechanism(s) of these effects was not apparent.

Cimetidine↗
PubMed1977

Predisposition to spina bifida: Search for a relation to maternal gastric acid secretion.

The peak acid output of the stomach in a group of 71 mothers of spina bifida children and in 71 matched controls was estimated indirectly by the serum level of group I pepsinogens. The mean levels did not differ significantly, suggesting that the conjectured teratogen is not specially acid-labile. The variance was significantly higher in index subjects than in controls, but the interpretation of this finding is not clear.

Female↗
PubMed1977

Effect of betazole on serum group I pepsinogen levels: relationship to gastric acid output in unoperated and postoperative patients.

A significant association has previously been found between a betazole-induced decrease in serum group I pepsinogen (PG I) levels and a low peak acid output (PAO) in symptomatic patients with vagotomy and gastric resection or a drainage procedure. This study compares the effect of betazole on serum PG I levels and gastric acid output in 245 unoperated patients (115 duodenal ulcer, 25 prepyloric ulcer, 32 gastric ulcer, 73 nonulcer) and in 73 symptomatic postoperative patients (15 subtotal gastric resection, 28 vagotomy and gastric resection, 30 vagotomy and drainage). A negative serum PGI response (2-hr serum PG I level less than 92% of basal) occurred in 10 (4.1% of the unoperated patients and in 31 (42.5%) of the postoperative patients. Seven (70%) of the former and 29 (93.5%) of the latter patients had a PAO of less than 10 mEq per hr, indicating that a negative serum PG I response is associated with a low PAO in both unoperated and postoperative patients. The PAO was greater than 10 mEq per hr in 93.1% of the 277 patients with a 2-hr serum PG I level of more than 92% of basal. Additional studies revealed that neither aspiration of gastric juice nor perfusion of the stomach with acid altered the serum PG I response. This suggests that topical acid does not modulate the effect of betazole on serum PG I levels. Finally, a negative serum PG I response has been shown to be paradoxical, in that gastric pepsin levels have been found to increase over basal concurrently with the decrease in serum PG I levels.

Betazole↗
PubMed1976

Serum group I pepsinogen levels and their relation to gastric acid secretion in patients with and without recurrent ulcer.

Serum group I pepsinogen (PG I) levels have been determined by radioimmunoassay in 15 patients without, recurrent ulcer after vagotomy and either a gastric resection or a drainage procedure. The mean (+/-SE) levels were 151.8 +/- 16.9 ng per ml in the patients with recurrent ulcer and 79.7 +/- 9.8 ng per ml in those without recurrence (P less than 0.001). A recurrent ulcer was present in 6 of 7 patients with an elevated serum PGI (greater than 175 ng per ml) but not in any of 10 patients with a low serum PGI (less than 50 ng per ml). The correlation between serum PG I and peak acid output (PAO) was statistically significant in patients with recurrent ulcer (pi=0.815, P less than 0.001) and in those without recurrence (r= 0.540, P less than 0.025). In patients with recurrent ulcer, a serum PG I level within the normal range (50 to 175 ng per ml) was uniformly associated with a PAO of more than 10 mEq per hr. In contrast, of 10 patients without recurrent ulcer and a normal serum PG I, eight had a PAO of less than 10 mEq per hr. The reason for the discordant results in the two groups of patients is not certain.

Adult↗
PubMed1976

The effect of betazole on serum group I pepsinogen levels: studies in symptomatic patients with and without recurrent ulcer after vagotomy and gastric resection or drainage.

Serum group I pepsinogen (PG I) levels have been determined before and at intervals after the administration of betazole hydrochloride (Histalog) in 50 symptomatic postoperative patients, 20 with and 30 without recurrent ulcer, after either a vagotomy and gastric resection or a drainage procedure. In patients with recurrent ulcer, mean serum PG I levels increased after betazole and reached a maximum of 116.5 +/- 2.2% (SE) of basal at 2 hr; range 98.9 to 135.7%. In contrast, mean serum PG I levels decreased in patients without recurrent ulcer and reached a nadir of 75.0 +/- 4.3% of basal at 2 hr; range 46.9 to 142.4%. All 20 patients with recurrent ulcer and 5 patients without recurrence had a 2-hr serum PG I level of more than 98% of basal, while each of the remaining 25 patients without recurrent ulcer had a 2-hr level of less than 92% of basal. A 2-hr serum PG I level of more than 98% of basal was also correlated with a vagotomy and drainage, a peak acid output of more than 11 mEq per hr, and a positive insulin test, while a level of less than 92% of basal was correlated with a vagotomy and gastric resection, a peak acid output of less than 11 mEq per hr, and a negative insulin test. In addition, basal serum PG I and serum gastrin levels were significantly higher (P less than 0.001) in patients with the former type of PG I response than in those with the latter type of response. The cause of each type of response is not certain, but the data suggest that one of the determinants may be the completeness of vagotomy.

Adult↗
PubMed1976

Immunofluorescence studies of gastric heterotopia of the small intestine in Crohn's disease.

A patient with long-standing Crohn's disease of the large and small intestine was found to have extensive gastric metaplasia of the ileum. Most metaplastic glands were of the pyloric type, but numerous oxyntic glands with parietal and chief cells were also seen. By immunofluorescence the chief cells contained both the group I and group II pepsinogens, while the pyloric gland cells contained only the group II pepsinogens. Gastric-containing or other endocrine cells were not detected in the metaplastic pyloric and oxyntic glands. The latter findings are consistent with the concept expressed by Pearse that the endocrine and exocrine cells of the gastrointestinal mucosa may originate from different precursor elements during embryogenesis.

Choristoma↗
PubMed1975

Serum group I pepsinogens by radioimmunoassay in control subjects and patients with peptic ulcer.

Serum group I pepsinogen (PG I) levels have been determined by radioimmunoassay in 924 subjects. The mean levels in 300 healthy control subjects and in 389 hospitalized controls were 110.6 and 100.0 ng per ml, respectively. The "normal" range is estimated to be between 50 and 175 ng per ml. The mean level of serum PG I in 7 patients with Zollinger-Ellison syndrome was 503.9 ng per ml; values ranged between 315 and 921 ng per ml. The 77 patients with duodenal ulcer had a mean serum PG I level of 221.3 ng per ml; 49 (63.6%) had values greater than 175 ng per ml. The distribution of serum PG I values was bimodal in the patients with duodenal ulcer whereas it was unimodal in both groups of control subjects. Mean serum PG I levels in 13 patients with both duodenal and gastric ulcer and in 18 patients with prepyloric ulcer were, respectively, 177.2 and 179.4 ng per ml. Approximately one-half of these patients had high values. The 28 patients with gastric ulcer had a mean serum PG I level of 116.6 ng per ml; 6 (21.4%) had high values. With the exception of 3 patients with gastric ulcer, none of the 136 patients with peptic ulcer had a low (less than 50 ng per ml) level of serum PG I. In 37 patients with chronic alcoholism the mean level of serum PG I was 73.4 ng per ml. The observed gradient in the mean level of serum PG I among the groups of patients studied is similar to that which has been reported for maximally stimulated gastric acid output. This finding suggests that the secretory potential of the fundic gland mucosa of the stomach may be reflected by the level of PG I in serum.

Adolescent↗
PubMed1975

A study of the relationship between serum group I pepsinogen levels and gastric acid secretion.

Serum group I pepsinogen (PG I) levels, basal acid output, and peak acid output (PAO) have been determined in 120 patients, 54 with duodenal ulcer, 14 with prepyloric ulcer, 12 with gastric ulcer, and 40 without ulcer. The correlation between serum PG I and PAO was statistically significant (r = 0.736, P less than 0.001) up to a serum PG I level of 250 ng per ml. Serum PG I levels above 250 ng per ml were associated with a plateau in the PAO. Each of 8 patients with a serum PG I of less than 40 ng per ml had a PAO of less than 10 mEq per hr. Of 34 patients with a serum PG I over 200 ng per ml, 29 (85.3%) had a PAO of greater than 40 mEq per hr and all had a PAO above 34 mEq per hr. Of 51 patients with a serum PG I between 60 and 150 ng per ml, 47 (92.2%) had a PAO of between 10 and 40 mEq per hr. The results indicate that a significant relationship exists between the concentration of PG I in serum and the acid secretory capacity of the gastric mucosa.

Duodenal Ulcer↗