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I Biemond

Publications and source records attributed to I Biemond.

At least 55 records · Page 3Linked to original sources

Treatment of Helicobacter pylori infection favourably affects gastric mucosal superoxide dismutases.

BACKGROUND AND AIMS: Excessive production of reactive oxygen metabolites (ROMs) by phagocytic cells is thought to contribute to the mucosal pathology of Helicobacter pylori infection. Previously, H pylori infection was shown to have a differential effect on some gastric mucosal scavenger enzymes of ROMs-namely, mitochondrial and cytoplasmic superoxide dismutases-reflected by a large increase in the cytokine inducible manganese superoxide dismutase and a marginal decrease in the constitutive copper/zinc superoxide dismutase. The present study was performed to evaluate whether these altered mucosal superoxide dismutase concentrations and activities in H pylori associated gastritis are reversed to normal by successful treatment of the infection. PATIENTS AND METHODS: In two different treatment groups-namely, omeprazole or ranitidine, in combination with clarithromycin and metronidazole (OME/AB (n = 33) and RAN/AB (n = 30))-manganese superoxide dismutase and copper/zinc superoxide dismutase concentrations were evaluated by enzyme linked immunosorbent assays in homogenates of gastric antrum and corpus biopsy specimens obtained before and eight weeks after successful treatment of H pylori infection. Superoxide dismutase activities in these homogenates were determined spectrophotometrically in eight patients of both groups before and after successful treatment. The concentrations of gastric mucosal superoxide dismutases were also determined in 12 patients with a persistent H pylori infection, with (n = 4) or without (n = 8) eradication therapy. Infection and eradication of H pylori were confirmed by a combination of culture and histology. RESULTS: Concentrations of manganese superoxide dismutase were significantly lower after than before therapy in antral (p < 0.001 in both treatment groups) and corpus (p < 0.001 in both treatment groups) mucosa. By contrast, copper/zinc superoxide dismutase concentrations were significantly higher (p < 0.001) only in antral mucosa of the OME/AB treated group. Manganese superoxide dismutase activity was significantly lower after than before treatment in antral (OME/AB p < 0.01, RAN/AB p < 0.001), but not in corpus mucosa. Copper/zinc superoxide dismutase activity was not significantly altered by therapy. In the 12 patients with a persistent H pylori infection no major changes in the gastric mucosal superoxide dismutase concentrations were found. CONCLUSIONS: The raised manganese superoxide dismutase and reduced copper/ zinc superoxide dismutase concentrations and activities in H pylori associated gastritis were reversed towards normal by successful treatment of the infection.

Adult↗

Doppler sonography evaluation of superior mesenteric artery flow to assess Crohn's disease activity: correlation with clinical evaluation, Crohn's disease activity index, and alpha 1-antitrypsin clearance in feces.

OBJECTIVE: This study was undertaken to investigate the value of Doppler flow measurements of the superior mesenteric artery (SMA) as a marker for disease activity in patients with Crohn's disease. SUBJECTS AND METHODS: Duplex Doppler sonography measurements of SMA blood flow volume were obtained in 29 consecutive patients with suspected Crohn's disease. We prospectively sought a correlation between the independent assessment of Doppler flow measurements and markers for disease activity: Crohn's disease activity index and fecal alpha 1-antitrypsin clearance and our reference standard based on clinical history, physical examination, laboratory values, endoscopy, surgery, and follow-up. RESULTS: In 27 of 29 patients, adequate measurements of SMA blood flow were obtained. In 15 patients no disease activity was judged to be present or no Crohn's disease (n = 2) was found at follow-up (group 1). In 12 patients, activity of Crohn's disease was diagnosed (group 2) on the basis of the reference standard. In group 2 the Doppler SMA blood flow values were significantly higher (p < .05) than those for group 1 (826 +/- 407 ml/min versus 323 +/- 103 ml/min). Of the other parameters investigated, only the alpha 1-antitrypsin value correlated with the reference standard but to a lesser degree than the values for SMA blood flow measurement. CONCLUSION: This prospective study shows that SMA Doppler blood flow measurements can be used to assess disease activity in patients with Crohn's disease. This approach may be of value in the diagnosis and follow-up of patients with Crohn's disease, providing directly available, quantifiable, noninvasive information on disease activity.

Adult↗

Low seroprevalence of Helicobacter pylori antibodies in historical sera of patients with Crohn's disease.

BACKGROUND: Our aim was to determine the seroprevalence of Helicobacter pylori antibodies in historical sera from a large group of patients with Crohn's disease and to compare the findings with those of a control group of healthy blood transfusion donors. METHODS: The historical sera from 386 patients with Crohn's disease were studied (serum age, 9.9 years; range, 0.4-21.6 years). Serum IgG and IgA H. pylori antibodies were measured with enzyme-linked immunosorbent assay. Western blots (detecting IgG only) were also used to study a subpopulation of the patients' sera and to assess the presence of cagA bands, indicating a cytotoxic variety of H. pylori. The serology of the Crohn's disease patients was compared with that of 277 age-matched controls. A longitudinal follow-up study of 14 IgG and IgA anti-H. pylori-positive and 14 IgG- and IgA-negative Crohn's disease patients was also performed (mean follow-up, 7.6 years; range, 1.7-20.5 years). RESULTS: Of the total Crohn's disease patients, 47 (12.2%) had IgG antibodies against H. pylori, 67 (17.4%) had IgA antibodies, and 31 (8.0%) had both IgG and IgA antibodies. The corresponding antibody positivities for the controls were 98 (35.4%) for IgG, 77 (27.8%) for IgA, and 64 (23.1%) for both IgG and IgA. When compared, with the control group, the seroprevalence of H. pylori in the Crohn's disease patients was significantly lower (P < or = 0.002). In addition the relative IgG response of the patients was lower than the IgA response. The opposite was true for the controls. There was no difference in the absolute levels of H. pylori antibodies between patients and controls. In the follow-up study two patients initially IgG-positive for H. pylori became negative over time; these patients had been treated for their infection. the rest, who continued to be positive, were not treated. One patient who was initially IgA-positive also became IgA-negative over time. The follow-up group, who were initially IgG- and IgA-negative, remained IgG-negative with time, and two patients became IgA-positive. Findings of anti-H. pylori IgG were confirmed with Western blots. Furthermore, these showed that of the H. pylori-positive patients (indicated by their IgG positivity), 66% were infected with a cytotoxic (cagA-positive) variety, compared to 69.4% of the controls. CONCLUSIONS: Patients with Crohn's disease have a lower prevalence of H. pylori antibodies than an age-matched control group. There is a reversal of the relative IgG and IgA responses in Crohn's disease patients compared with the controls. Of the Crohn's disease patients with H. pylori most are infected with cytotoxic varieties, similar to controls.

Adult↗

Gallbladder motility and cholecystokinin secretion during continuous enteral nutrition.

OBJECTIVES: During total parenteral nutrition, gallbladder motility is impaired, resulting in sludge and stone formation. Little is known about gallbladder motility during prolonged enteral nutrition. METHODS: We studied gallbladder motility during continuous enteral nutrition (CEN) in nine hospitalized patients with active inflammatory bowel disease. The patients received a polymeric diet (2000 kcal/24 h) by CEN through a nasogastric tube for a prolonged period. Gallbladder volumes were obtained daily by ultrasonography, starting from day 0 (before CEN) and on 7 consecutive days during CEN. At days 0, 1, 4, and 7, the gallbladder response to i.v. cholecystokinin (CCK-33; 0.5 Ivy Dog unit/kg/h) was studied. Plasma CCK levels were determined at regular intervals by radioimmunoassay. RESULTS: No significant differences were observed on day 0 between patients and a group of nine healthy control subjects in fasting gallbladder volumes (19.4 +/- 2.3 and 19.6 +/- 2.4 cm3, respectively) and gallbladder contraction during CCK infusion (56 +/- 14% and 69 +/- 7%, respectively). During CEN, from day 1 to day 7, mean gallbladder volume remained significantly (p < 0.05) reduced compared with fasting gallbladder volume, and mean plasma CCK levels remained significantly (p < 0.05) increased compared with fasting levels. Although gallbladder volume was significantly reduced during CEN, the gallbladder contractile response to CCK was not affected; at days 1, 4, and 7, gallbladder contraction was 36-57%. CONCLUSIONS: During CEN, 1) gallbladder volume is significantly reduced and plasma CCK levels are significantly increased, 2) these effects are sustained over time (7 days), and 3) the gallbladder remains responsive to exogenous CCK. These results indicate that gallbladder contractility and gallbladder responsiveness to CCK are preserved during prolonged CEN in patients with inflammatory bowel disease.

Adult↗

Gastric mucosal plasminogen activators in Helicobacter pylori infection.

Long-term H. pylori associated gastritis is recognized as a pathogenic factor in gastric carcinogenesis. In gastric carcinomas the amount and activity of the tissue-type plasminogen activator (t-PA) have been reported to be decreased, whereas those of the urokinase-type plasminogen activator (u-PA) were increased, contributing to the neoplastic and invasive process. The present study was performed to determine t-PA and u-PA levels and activity in gastric mucosa from 102 patients and to investigate whether these levels are influenced by H. pylori infection. The antigen concentration and activity of t-PA and u-PA in corpus mucosa were low (P < 0.001) compared with those in antral mucosa, although for the u-PA activity this did not reach statistical significance. In H. pylori-associated antral gastritis the mucosal t-PA antigen concentration and activity were found to be decreased (P < 0.001) compared with normal mucosa, whereas in H. pylori-associated pangastritis the corpus t-PA levels were not affected. The antigen concentration and activity of u-PA were found to be significantly (P < 0.005) increased, both in H. pylori-associated gastritis of antrum and corpus mucosa. Levels of u-PA in histologically normal corpus mucosa of patients with an H. pylori-associated antral gastritis were also found to be increased (P < 0.05). In conclusion, the alterations in the plasminogen activator profile found in H. pylori-associated gastritis, ie, a decrease in t-PA and an increase in u-PA, show a similar tendency as the previously found alterations in gastric carcinomas, which provides additional support for the possible involvement of H. pylori-associated gastritis in the pathogenesis of gastric carcinoma.

Adolescent↗

Cholecystokinin receptors in human pancreas and gallbladder muscle: a comparative study.

BACKGROUND & AIMS: Cholecystokinin (CCK) receptors mediate pancreatic secretion and gallbladder contraction. Hitherto, little information on characteristics of CCK receptors in the human pancreas was available. This study identifies CCK receptors in the human pancreas and compares their characteristics with the CCK receptors in the human gallbladder. METHODS: Visualization and quantification of 125I-Bolton-Hunter sulfated CCK octapeptide (125I-BH-CCK-8) binding to tissue sections of the human pancreas and gallbladder were performed by storage phosphor autoradiography. RESULTS: Specific bindings for CCK were visualized in pancreatic tissue and the smooth muscle layer of the gallbladder. Binding of 125I-BH-CCK-8 to the pancreas was inhibited by agonists with the affinities (dissociation constant) of CCK (0.11 nmol/L) approximately gastrin (0.15 nmol/L) and by antagonists with the affinities of CCK-B receptor antagonist (L365,260, 0.18 nmol/L) > CCK-A receptor antagonist (lorglumide, 8.1 nmol/L). In contrast to the pancreas, binding of 125I-BH-CCK-8 to the gallbladder muscle was inhibited with high affinity by CCK-8 and lorglumide but was replaced to a small degree by gastrin and L365,260. CONCLUSIONS: The sub-types of receptors for CCK in the human pancreas and gallbladder are different. The human pancreas predominantly expresses CCK-B receptors, whereas only CCK-A receptors were localized in the human gallbladder muscle.

Adult↗

Expression of receptors for gut peptides in pancreata of BOP-treated and control hamsters.

The growth of pancreatic cancers may be influenced by certain gut peptides. However, the alteration of gut peptide receptors in the progress of pancreatic carcinogenesis is largely unknown. With storage phosphor autoradiography, this study visualized and characterized receptors for cholecystokinin (CCK), somatostatin (SST), bombesin (BBS), secretin and vasoactive intestinal peptide (VIP) in pancreata of control hamsters (n = 7) and pancreatic preneoplastic lesions (n = 10) or adenocarcinomas (n = 10) of N-nitrosobis(2-oxopropyl)amine (BOP)-treated hamsters. The specific CCK-A and secretin receptors expressed in normal pancreata were markedly reduced in pancreatic preneoplastic lesions and absent in adenocarcinomas. In the development of pancreatic tumours, the subgroup of SST receptors did not change, but both the affinity and binding capacity declined. In comparison with the binding of VIP to normal pancreata, specific VIP binding was significantly lower in preneoplastic lesions and almost absent in pancreatic adenocarcinomas. No specific binding for BBS was detected in normal pancreas or (pre)neoplastic lesions of hamster pancreas. The reduction or absence of receptors for CCK, secretin, SST and VIP in hamster pancreas with the progress of carcinogenesis suggests that in BOP-treated hamsters, pancreatic adenocarcinomas have, to a large extent, lost the hormone-dependent characteristics of the original tissue.

Adenocarcinoma↗

Visualization and characterization of CCK receptors in exocrine pancreas of rat with storage phosphor autoradiography.

Studies on cholecystokinin (CCK) receptors in rat pancreas are usually performed on homogenates. Using storage phosphor autoradiography, a new imaging technique with a high sensitivity and large linear dynamic range, we visualized and characterized CCK receptors in tissue sections of normal rat pancreas. The density of CCK receptors in pancreatic tissue sections from 10 normal rats appeared to be unevenly distributed and variable in serial sections. The binding of labeled CCK-8 was markedly inhibited by CCK-8 and CCK-A receptor antagonists, but it was only weakly affected by gastrin and CCK-B receptor antagonists. At room temperature the CCK-8 dose-inhibition curve was fitted by a two-site model: one with a high-affinity but low-capacity site and another with a low-affinity but high-capacity site. The CCK-8 dose-inhibition curve showed that the inhibition of the variable high-density receptors took place at a low concentration of CCK-8, while the diffuse low-density receptors were inhibited at the high concentration of 1 microM CCK-8. Binding of labeled CCK-8 at 37 degrees C was homogeneous with a low affinity and comprised only 4% of that found at room temperature. In summary, an uneven density of CCK receptors in the rat exocrine pancreas was observed and attributed to the variable expression of high-affinity CCK receptors in pancreatic acini.

Animals↗

Seroepidemiology of gastritis in Japanese and Dutch male employees with and without ulcer disease.

OBJECTIVE: To explore the state of the gastric mucosa in individuals with and without peptic ulcer disease from populations with contrasting peptic ulcer risks. DESIGN: Pepsinogen A, pepsinogen C, gastrin and Helicobacter pylori antibodies are serological markers of gastritis. A decreasing pepsinogen A-C ratio and pepsinogen A level are known to reflect an increasing severity of corpus atrophy, whereas gastrin levels decrease with an increasing severity of antral atrophy when corpus atrophy is present. Helicobacter pylori-positive men, with and without a peptic ulcer history, were the focus of the study. METHODS: In 190 Japanese and 425 Dutch male employees, of similar age (mean age 49 years) and level of occupation, fasting serum samples were analysed in the same laboratory for IgG antibodies to H. pylori, pepsinogen A, pepsinogen C and gastrin. Any history of ulcer disease was verified through case notes. RESULTS: The H. pylori seropositivity rate was higher in the Japanese men (72%) than in the Dutch (33%). There were 23 (12%) Japanese and 18 (4%) Dutch men with a verified duodenal ulcer history, and 14 (7%) Japanese and two (0.5%) Dutch men with a verified gastric ulcer history. H. pylori-positive men with a duodenal ulcer history differed from the H. pylori-positive men without an ulcer history in that they had a significantly higher mean pepsinogen A level (64 and 51 micrograms/l in Japanese men and 71 and 57 micrograms/l in Dutch men) and also a higher mean pepsinogen A-C ratio, whereas pepsinogen C and gastrin levels did not differ. In H. pylori-positive gastric ulcer patients the mean gastrin level was significantly lower than in H. pylori-positive men without ulcer disease (17 and 37 pmol/l in Japanese men), whereas pepsinogen levels were similar. CONCLUSION: This study suggests that in H. pylori-positive duodenal ulcer patients there is less mucosal atrophy of the corpus and in H. pylori-positive gastric ulcer patients more atrophy of the antrum than in H. pylori-positive individuals without peptic ulcer disease.

Adrenergic beta-Antagonists↗

Risk factors of peptic ulcer disease: different impact of Helicobacter pylori in Dutch and Japanese populations?

Helicobacter pylori, non-steroidal anti-inflammatory drugs, family history, blood group O, hyperpepsinogenaemia A, alcohol and smoking have been reported to be risk factors for peptic ulcer disease. The strength of causal risk factors may differ in different populations. In 215 Japanese and 493 Dutch employees of similar age, gender and type of occupation, a structured history was obtained using a questionnaire and fasting serum samples were analysed for IgG antibodies to H. pylori and pepsinogen A all in the same laboratory. A past ulcer history was verified through case notes. We found that H. pylori seropositivity, a high serum pepsinogen A and a family history of ulcer disease were significant and independent risk factors for peptic ulcer disease. For H. pylori seropositivity there was a 20-fold increased risk among the Dutch and an eight-fold increased risk among the Japanese. The seroprevalence of H. pylori was 90% in 20 Dutch subjects with a verified ulcer history and 95% in 41 Japanese ulcer subjects; it was 29% in Dutch non-ulcer subjects and 70% in Japanese non-ulcer subjects. The cumulative difference in risk to develop peptic ulcer disease at the age of 48 years between H. pylori-infected and -uninfected subjects was 24.5-3.0 = 21.5% for the Japanese and 11.8-0.5 = 11.3% for the Dutch. Duodenal ulcer disease was associated with a high coffee consumption only among the Japanese population, where this habit was much less prevalent than among the Dutch. In conclusion, the characterization of peptic ulcer risk factors as weak or strong has no universal basis: the present study shows that from a diagnostic point of view H. pylori appears to be a weaker risk factor for peptic ulcer disease in a society with a higher seroprevalence. However, from an aetiological point of view, H. pylori has an even greater impact on ulcer morbidity in the Japanese than in the Dutch population.

Adult↗

Gastric mucosal superoxide dismutases in Helicobacter pylori infection.

BACKGROUND: The mucosal pathology of Helicobacter pylori infection may in part be due to excessive production of reactive oxygen metabolites (ROMs) by phagocytes. The influence of H pylori infection on mucosal superoxide dismutases, some major scavenger enzymes of ROM was investigated. In humans superoxidase dismutase is present in at least two forms-that is, mitochondrial manganese (Mn)-superoxide dismutase and cytoplasmic copper-zinc (CuZn)-superoxide dismutase. METHODS: The amount and activity of both superoxide dismutases were measured, respectively by enzyme linked immunosorbent assay (ELISA) and spectrophotometrical enzyme activity assay, in gastric biopsy homogenates of patients with normal mucosa (n = 39) and in patients with H pylori related gastritis (n = 71). Infection and gastritis were confirmed by a combination of culture, serology, and histology. RESULTS: The amount (p < 0.001) and activity (p < or = 0.05) of Mn-superoxide dismutase were increased by about twofold to three-fold, whereas the amount and activity of CuZn-superoxide dismutase showed a slight decrease in gastric mucosa of patients with H pylori gastritis, in both antrum and corpus, compared with normal mucosa of patients without H pylori infection. Mn-superoxide dismutase concentrations in biopsy specimens of histologically normal corpus from patients with an inflamed antrum were significantly higher (p < 0.01) than that of patients with a histologically normal antrum. CONCLUSION: H pylori infection has a differential effect on mitochondrial and cytoplasmic superoxide dismutase in the gastric mucosa, reflected by a pronounced increase in the cytokine inducible Mn-superoxide dismutase and a marginal decrease in the constitutive CuZn-superoxide dismutase.

Adolescent↗

Nonulcer dyspepsia in a Dutch working population and Helicobacter pylori. Ulcer history as an explanation of an apparent association.

BACKGROUND: There is considerable debate about whether Helicobacter pylori infection is important in causing nonulcer dyspepsia. Many studies assessing this relationship have been performed in selected patient populations and included patients with a history of peptic ulcer. General population-based data with attention to ulcer history are needed to clarify this relationship. METHODS: A questionnaire on ulcer history and dyspeptic symptoms during the preceding 3-month period was obtained from apparently healthy employees who underwent a periodic medical examination in the Netherlands. In addition, serum samples were analyzed for anti-H pylori IgG antibodies. RESULTS: A total of 427 men and 73 women, aged 22 to 69 years, participated in the study. None of the women but 27 men (6%) had a previous diagnosis of peptic ulcer. Among 19 unoperated-on men with verified duodenal (17 subjects) and gastric (two subjects) ulcer, 89% were H pylori positive, while 74% had frequent dyspeptic symptoms in the 3 months before the study. Among the 400 men and 73 women without an ulcer history, the 3-month period prevalence of frequent dyspepsia was 13% and 21%, respectively. The rate of H pylori positivity was 25% in subjects with nonulcer dyspepsia and 29% in all others. The H pylori infection rate increased with age and with a lower occupational level but was independent of gender. In the male population, various differences in symptoms between H pylori-positive and H pylori-negative subjects could be detected when the 27 subjects with a history of ulcer were included, whereas these differences disappeared when these subjects were excluded. CONCLUSIONS: In the Dutch working population, nonulcer dyspepsia is not related to H pylori infection, whereas for duodenal ulcer the relationship is clear. The apparent association between dyspeptic symptoms and H pylori infection is entirely accounted for by subjects with an ulcer history.

Adult↗

Serological parameters in assessment of degree of gastritis in healthy volunteers.

This study was undertaken in healthy volunteers to determine the relation between serum levels of pepsinogen A, pepsinogen C, pepsinogen A:C ratio, and gastrin on the one hand and histology of the gastric mucosa on the other. The grade of gastritis was scored separately for antral and fundic mucosa by three different classifications: Whitehead, activity, and the Sydney score. Among 48 healthy volunteers studied, 17 were found to have gastritis according to the criteria of Whitehead. Fourteen of these 17 subjects with gastritis had H. pylori in gastric biopsies. In all 48 subjects serum pepsinogen A (r = 0.298-0.506; P < 0.01-P < 0.05), pepsinogen A:C ratio (r between -0.377 and -0.495; P < 0.001-P < 0.05) and gastrin (r = 0.38-0.695; P = 0.007-P < 0.01) were significantly correlated to the severity of both antral and body gastritis as assessed by all three classifications. In contrast, there was no significant correlation between serum pepsinogen C and any of the gastritis scores. When the 17 subjects with gastritis were analyzed separately, there were no correlations between the parameters studied and gastritis of the antrum. Regarding the corpus mucosa, serum PgA correlated significantly with the activity score (r = 0.520; P = 0.03), weakly with the Sydney score (r = 0.465; P = 0.06), but not with the Whitehead score. Serum PgC correlated with the Whitehead (r = 0.555; P = 0.02) and Sydney score (r = 0.523; P = 0.03), but only weakly with the activity score (r = 0.441; P = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Gut peptide receptors in pancreata of azaserine-treated and normal control rats.

Gut peptides are involved in the growth and carcinogenesis of the exocrine pancreas of rats after treatment with azaserine. However, little is known about the influence of azaserine on expression of gut peptide receptors in the pancreas of the rat. Cholecystokinin, bombesin, somatostatin, secretin, and vasoactive intestinal peptide receptors were therefore visualized and quantified by storage phosphor autoradiography in pancreata of either saline control or azaserine-treated rats. As expected, putative preneoplastic lesions were formed in the pancreata of the azaserine-treated but not in the control animals. The pancreata of control rats contained receptors for cholecystokinin, bombesin, somatostatin, secretin, and vasoactive intestinal peptide. Cholecystokinin receptors were of the A-type and showed, in contrast to the other receptors, a heterogeneous expression due to variability of the high-affinity receptors. In the pancreata of azaserine-treated animals a significantly increased binding capacity of high-affinity receptors fro cholecystokinin was found not only in atypical acinar cell nodules but also in non-nodular pancreas when compared to pancreas of control rats (P < 0.05). Neither atypical acinar cell nodules nor non-nodular pancreas of rats treated by azaserine were shown to possess receptors for the other four types of gut peptide receptors. The spectrum of peptide receptors in pancreas of control and azaserine-treated rats in this study may help to understand the mechanism whereby gut hormones may modulate pancreatic carcinogenesis.

Animals↗

Seroepidemiology of gastritis in Japanese and Dutch working populations: evidence for the development of atrophic gastritis that is not related to Helicobacter pylori.

Serological markers of gastritis, like pepsinogen A, pepsinogen C, gastrin, and Helicobacter pylori antibodies, can be used to explore the state of the gastric mucosa in populations with contrasting cancer risks. A decreasing pepsinogen A:C ratio and an increasing serum gastrin are known to reflect an increasing severity of atrophic corpus gastritis, which is a precursor of gastric cancer. In 723 subjects (without gastroduodenal surgery) from Japanese (n = 225) and Dutch (n = 498) working populations, which had a similar composition of age (mean 48 years), sex (male to female ratio 6:1), and type of occupation, fasting serum samples were analysed for IgG antibodies to H pylori, pepsinogen A, pepsinogen C, and gastrin in the same laboratory. H pylori infection was significantly more prevalent in the Japanese than in the Dutch (74.7% and 31.3%); as was a very low pepsinogen A, indicative of severe mucosal atrophy (4.4% and 1.6%). Among subjects with and without severe mucosal atrophy the H pylori seropositivity rate was similar. Between the Japanese and the Dutch there were significant differences in mean gastrin (31.8 and 13.4 pmol/l) and pepsinogen A:C ratio (1.7 and 2.9). These intercountry differences were as great for H pylori negative subjects (gastrin: 23.7 and 10.3 pmol/l, pepsinogen A:C ratio: 2.4 and 3.2) as for H pylori positive subjects (gastrin: 34.6 and 20.1 pmol/l, pepsinogen A:C ratio: 1.5 and 2.5). The intercountry difference in gastrin nearly disappeared after stratification into categories of pepsinogen A:C ratio. In conclusion, the intercountry differences in pepsinogen A:C ratio and gastrin reflect a higher prevalence of mild and severe mucosal atrophy of the corpus in the Japanese than in the Dutch, both among H pylori positive and negative subjects. Thus, these findings suggest that in the Japanese the development of atrophic gastritis is in part unrelated to H pylori.

Adult↗

Serum gastrin and mucosal somatostatin in Helicobacter pylori-associated gastritis.

AIMS: The aims were to study gastrin concentrations and gastric mucosal somatostatin and gastrin concentrations in relation to the extent of gastritis in Helicobacter infection. METHODS: We measured basal serum gastrin concentrations in antral mucosal biopsy specimens and somatostatin concentrations in corpus biopsy specimens in 88 consecutive dyspeptic subjects undergoing endoscopy. These subjects were divided into three categories on the basis of histology, serology, and culture: H. pylori-positive pangastritis, H. pylori positive antral gastritis with normal body histology, and H. pylori-negative controls. Statistical evaluation was done with the Wilcoxon rank sum test. RESULTS: Basal serum gastrin concentrations were significantly increased only in subjects with pangastritis and not in those with antral gastritis only, as compared with controls (mean +/- SEM: 72 +/- 7, 46 +/- 10, and 42 +/- 7 ng/l, respectively). Subjects with pangastritis or antral gastritis had significantly lower antral somatostatin concentrations than controls (mean +/- SEM: 0.80 +/- 0.07, 1.03 +/- 0.15, and 2.40 +/- 0.31 micrograms/g(protein), respectively). We also found significantly lower antral gastritis only as compared with controls (mean +/- SEM: 62 +/- 13, 78 +/- 16, and 165 +/- 25 micrograms/g(protein), respectively). In subjects with pangastritis a significantly lower concentration of somatostatin was found in the corpus biopsy specimens than in those with antral gastritis only and controls. CONCLUSIONS: These results suggest that hypergastrinemia in H. pylori gastritis is not caused by antral gastritis and antral somatostatin deficiency alone but that corpus inflammation plays a key role in the origin of hypergastrinemia. Furthermore, in patients with pangastritis a corpus mucosal somatostatin deficiency was found.

Adolescent↗

Serum values of pepsinogens and antibodies to Helicobacter pylori in relation to a history of peptic ulcer disease and NSAID use.

The present study was undertaken to investigate whether patients with a history of peptic ulcer disease (PUD) have serological features indicative of the presence of more severe gastritis, compared to patients without a history of PUD. In addition we investigated whether current chronic use of non steroidal anti-inflammatory drugs (NSAIDs) was associated with serological features indicative of a chemical (type C) gastritis. In total 850 consecutive outclinic patients were interviewed by a standard questionnaire with emphasis on demographic data, diagnosis, chronic use of NSAID, and history of PUD. Serum pepsinogen A (PgA) and pepsinogen C (PgC), the PgA:PgC ratio, and IgA and IgG antibodies to H. pylori were measured in all patients. After controlling for age, sex, H. pylori seropositivity, and presence of RA, a correlation was found between a decreased pepsinogen A:C ratio and the use of NSAID. Patients with a history of PUD have serological features indicative of a persistently more severe gastritis. Secondly we found serological evidence for the existence of a chemical (type C) gastritis in NSAID users.

Adolescent↗

Localization and quantification of cholecystokinin receptors in rat brain with storage phosphor autoradiography.

The present study evaluated a new imaging technique that demonstrated the application of storage phosphor autoradiography in the localization and quantification of cholecystokinin receptors in rat brains and compared the results with film autoradiography. Cryostat sections were incubated with [125I]Bolton-Hunter-labeled sulfated cholecystokinin octapeptide followed by exposure to a storage phosphor-imaging screen and suitable autoradiography film. To obtain satisfactory images, it took 6 days with film autoradiography vs. 15 hours with the storage phosphor technique. Both film and storage phosphor autoradiograms showed the same cholecystokinin receptor distribution in brain sections; however, the film imaged more details. To reach the lowest possible response ratio between low and high receptor density regions in rat brains, storage phosphor autoradiography was about 240-fold faster than film. In addition, the new technique presented a considerably larger exposure time range for maintaining that ratio. The binding per area showed a linear relationship with the thickness of sections between 5 and 14 microns. In the linear response range, the quantitative results of both methods are comparable. In conclusion, storage phosphor autoradiography is a faster technique for localizing and quantifying peptide receptors in tissue sections but slightly compromised in resolution when compared with film autoradiography.

Animals↗