Biomedical subjects

I Biemond

Publications and source records attributed to I Biemond.

At least 73 records · Page 4Linked to original sources

PubMed1994

Achlorhydria does not protect against benign upper gastrointestinal ulcers during NSAID use.

It is widely accepted that the absence of acid-peptic activity excludes the presence of a benign upper gastrointestinal ulcer. We assessed the frequency of a history of benign upper gastrointestinal ulcer disease in patients with and without serological evidence of achlorhydria with reference to the use of nonsteroidal antiinflammatory drugs (NSAIDs). In total 857 patients were interviewed, using a standard questionnaire with emphasis on demographic data, chronic use of NSAID, and history of upper gastrointestinal ulcers. The frequency of achlorhydria was determined by extremely low serum levels of pepsinogen A (PgA < 17 micrograms/liter). Of the total group of patients, 36 patients (4.2%; 95% CI 2.9-5.5) had a PgA lower than 17 micrograms/liter. A history of benign upper gastrointestinal ulcer was found in 57/827 (6.9%) of patients with serum PgA higher than 17 micrograms/liter and in 3/36 (8.3%) of patients with serum PgA lower than 17 micrograms/liter (NS). The three patients with upper gastrointestinal ulcer and PgA lower than 17 micrograms/liter were known to have pernicious anemia (PA) before (two patients) or simultaneously (one patient) with the diagnosis of the upper gastrointestinal ulcer and were using NSAIDs at that time. The presence of gastric acid is not obligatory for the development of ulcers during NSAID use.

Achlorhydria↗

PubMed1994

Effect of enprostil on serum gastrin and pepsinogen A and C levels in patients on long-term treatment with omeprazole.

BACKGROUND: Treatment of omeprazole induces profound inhibition of gastric acid secretion, resulting in hypergastrinaemia. In rats hypergastrinaemia induced by chronic administration of high doses of omeprazole resulted in ECL-cell hyperplasia and subsequent carcinoid formation. This finding may limit long-term therapy in man. The synthetic prostaglandin E2 analogue enprostil not only inhibits gastric acid secretion but also reduces serum gastrin in normal subjects and in peptic ulcer patients. The present study was undertaken to determine whether enprostil reduces serum gastrin in patients on long-term treatment with omeprazole. METHODS: Eight patients with reflux oesophagitis treated with 40 mg omeprazole once daily for at least 3 months received 35 micrograms enprostil t.d.s. during a 5-day treatment course. Basal and postprandial serum gastrin concentrations and pepsinogen A and C levels were measured on the day before, the first and the final day, and on the day after cessation of treatment. RESULTS: Enprostil significantly (P < 0.05) reduced basal serum gastrin from 65 +/- 15 pmol/L to 51 +/- 13 pmol/L on the first treatment day, and to 41 +/- 9 pmol/L on the final day. Enprostil also significantly (P < 0.05) reduced postprandial integrated serum gastrin from 6173 +/- 849 pmol.h/L to 4516 +/- 906 pmol.h/L and to 3532 +/- 706 pmol.h/L on the first and final treatment days, respectively. On the day after cessation of treatment basal (57 +/- 11 pmol/L) and postprandial integrated serum gastrin concentrations (5766 +/- 864 pmol.h/L) were not significantly different when compared to pretreatment values. Enprostil had no significant influence on serum pepsinogens A and C. CONCLUSION: Short-term co-administration of enprostil lowers the serum gastrin levels in patients on long-term treatment with omeprazole.

Aged↗

PubMed1994

Relation between IgG and IgA antibody titres against Helicobacter pylori in serum and severity of gastritis in asymptomatic subjects.

AIMS: To investigate whether the absorbance index of IgG and IgA antibodies against Helicobacter pylori is related to a semiquantitative assessment of the density of H pylori colonisation in gastric biopsy specimens and to the severity of gastritis. METHODS: The grade of gastritis was scored separately for antral and fundic mucosa using three different classifications. Serum IgA and IgG antibodies against H pylori were measured by ELISA. The density of gastric H pylori colonisation was graded semiquantitatively from 0 to 3. RESULTS: Among 48 healthy volunteers studied, 17 were found to have gastritis according to Whitehead's criteria. H pylori was present in the biopsy specimens of 14 of 17 subjects with gastritis. The IgG H pylori antibody absorbance index was significantly (p < 0.05) correlated not only with the density of antral H pylori colonisation, but also with the degree of gastritis of the antrum, as assessed by the Whitehead score, activity, and the Sydney system (p < 0.05). The IgA H pylori antibody absorbance index was significantly correlated with the Whitehead score and Sydney system, but not with the activity score of the antrum or with the density of antral gastric H pylori infection. There were no significant correlations between the IgG H pylori antibody absorbance index and the gastritis scores of the fundus mucosa and the density of H pylori infection of the gastric body. The IgA H pylori antibody absorbance index was only significantly (p < 0.05) correlated with the density of H pylori colonisation and the Sydney system gastritis score of the corpus. CONCLUSIONS: The serological absorbance index of IgG antibodies against H pylori is related to the severity of antral gastritis and the density of antral H pylori colonisation. Thus a high absorbance index of IgG antibodies against H pylori points to severe antral gastritis and dense H pylori colonisation of the antrum.

Adult↗

PubMed1994

Serum pepsinogens in patients with gastric diseases or after gastric surgery.

As no comparative study is available on the categorized serum pepsinogen A and C concentrations, we have measured serum pepsinogens in patients with gastric diseases and after gastric surgery. Hyperpepsinogenemia A (> 120 micrograms/l) occurred frequently in patients with the Zollinger-Ellison syndrome (71%) and hypertrophic gastropathy (100%), whereas hypopepsinogenemia A (< 17 micrograms/l) was found mostly in patients with achlorhydria (87%) and after total gastrectomy (100%). Patients with the Zollinger-Ellison syndrome frequently (58%) had hyperpepsinogenemia C (> 40 micrograms/l), which was also the case in all patients with hypertrophic gastropathy who had in addition a low pepsinogen A:C ratio (< 1.6). Patients with achlorhydria, hypertrophic gastropathy, or after total gastrectomy fell into an aberrant category. From this study we conclude that measurement of serum pepsinogen A and C and calculation of their ratio yield information useful for differentiation of gastric abnormalities.

Aged↗

PubMed1994

Assessment of inflammatory activity in Crohn's disease.

Complaints or symptoms of Crohn's disease can be due either to intestinal inflammation or to anatomical abnormalities such as strictures, fistulas and previous intestinal resection, or to a combination of these factors. Since anti-inflammatory or immunosuppressive drugs are only effective in reducing inflammation, assessment of the presence or absence of active inflammation is of great clinical importance. Several disease activity indices have been developed, but none is able to accurately assess inflammatory activity in Crohn's disease. Furthermore, blood parameters of inflammation, such as ESR, leukocytes, thrombocytes and albumin, are not bowel-specific. In contrast, faecal inflammatory parameters are specific for intestinal inflammation. Preliminary results from our laboratory suggest that measurement of intestinal alpha 1-antitrypsin clearance is a sensitive and bowel-specific indicator of active inflammation in Crohn's disease. This inexpensive, safe and patient-friendly measurement deserves a prominent place, not only in drug trials but also in clinical management of patients with Crohn's disease.

Biomarkers↗

PubMed1993

Serum pepsinogens after interruption of long-term maintenance therapy with omeprazole in patients with reflux esophagitis.

Administration of omeprazole induces increases in serum concentrations of pepsinogens A and C. In 10 patients with reflux esophagitis who were on continuous maintenance treatment, the effect of cessation of omeprazole administration on serum pepsinogens was studied. Pepsinogens A and C were measured in serum samples on days 0, 1, 2, 4, 7, and 9 after treatment and the results were compared with the values available in eight patients at a time before omeprazole treatment. Serum pepsinogen A levels decreased gradually after cessation of omeprazole administration, and all values fell into the normal range after the seventh day of the study period, but were still higher than before therapy. Seven of 10 patients showed a decrease of pepsinogen C after nine days, but two patients had still increased levels at the end of the study period. The pepsinogen A:C ratio on the ninth day after cessation was significantly lower than on day 0 during omeprazole therapy. We conclude that long-term maintenance therapy with omeprazole induces significant increases in both serum pepsinogens. After cessation of omeprazole treatment, serum pepsinogens rapidly decrease in most patients, but continue to be higher before therapy for at least nine days.

Esophagitis, Peptic↗

PubMed1993

The frequency of extremely low serum pepsinogen, indicative of corpus gastritis with severe atrophy, in rheumatoid arthritis, other chronic rheumatic diseases and non-rheumatic diseases.

The aim of this study was to assess the frequency of corpus gastritis with severe atrophy (CGA), pernicious anaemia and combined severe atrophy of antrum and corpus by non-invasive methods (i.e. determination of low serum pepsinogen A (PgA) and serum gastrin) in outpatients with RA (n = 249), compared to outpatients with other rheumatic diseases (n = 181) and outpatients with chronic non-rheumatic diseases (n = 429). In addition we investigated whether NSAIDs could cause or prevent CGA. A low serum PgA level (< 17 micrograms/l), indicating pentagastrin-refractory achlorhydria in patients without gastric resection, was found in 13 patients (5.2%; 95% Confidence Interval (CI) 2.4-8.0) with RA, in 11 (6.1%; 95% CI 2.6-9.5) with other rheumatic diseases and in 12 patients (2.8%; 95% CI 1.2-4.4) with chronic non-rheumatic diseases (NS). Low serum PgA values were more frequent in older patients (P < 0.005) and females (P < 0.05). Pernicious anaemia occurred in RA in 1.2% (95% CI 0-2.6) of the patients while for other rheumatic diseases the frequency was 1.7% (95% CI 0-3.5) and for chronic non-rheumatic diseases 0.2% (95% CI 0-3.6) (NS). In patients with a serum PgA below 17 micrograms/l, normal serum gastrin levels (< 90 ng/l) as an indication of combined severe atrophy of antrum and corpus, were found in 1/13 patients with RA, in 3/11 with other rheumatic diseases and 2/12 with chronic non-rheumatic diseases (NS). The frequency of low serum PgA levels was no different between patients on NSAIDs 17/355 (4.8%) and those without NSAIDs 19/502 (3.8%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Diagnostic value of serum pepsinogen C in patients with raised serum concentrations of pepsinogen A.

Hypopepsinogenaemia A is often found in patients with gastric atrophy and gastric surgery. In these conditions serum pepsinogen C provides additional diagnostic information, especially when expressed as pepsinogen A:C ratio. Hyperpepsinogenaemia A has been shown in patients with duodenal ulcer disease, Zollinger-Ellison syndrome, hypertrophic gastropathy, chronic renal failure, and during omeprazole treatment. As patients with hyperpepsinogenaemia A often overlap in symptoms, endoscopical findings, and serum gastrin values, this study has evaluated whether measurement of serum pepsinogen C in subjects with hyperpepsinogenaemia A can help in differentiating clinical conditions. Serum concentrations of pepsinogen A and C were measured in serologically Helicobacter pylori negative blood transfusion donors (127) as reference population, and in patients with Zollinger-Ellison syndrome (24), duodenal ulcer (50), hypertrophic gastropathy (5), and chronic renal failure (50), and also in reflux oesophagitis patients on longterm omeprazole treatment (28). A low pepsinogen A:C ratio was found in all patients with hypertrophic gastropathy. A pepsinogen A:C ratio above the critical value of 4.7 was found in 14 (70.0%) of the Zollinger-Ellison patients, two (9.5%) of the duodenal ulcer patients, 11 (25.6%) of the patients with chronic renal failure, and in one (7.1%) of the patients receiving longterm omeprazole treatment. In fact, all but three hyperpepsinogenaemia A patients with a pepsinogen A:C ratio greater than 4.7 and normal renal function had the Zollinger-Ellison syndrome. In patients with hyperpepsinogenaemia A, a low pepsinogen A:C ratio may point to hypertrophic gastropathy, while a pepsinogen A:C ratio greater than 4.7 is suggestive for the Zollinger-Ellison syndrome.

Adult↗

PubMed1993

Inhibition of omeprazole induced hypergastrinaemia by SMS 201-995, a long acting somatostatin analogue in man.

Whether the long acting somatostatin analogue SMS 201-995 (octreotide, Sandostatin) could inhibit the basal and meal stimulated hypergastrinaemia and hyperpepsinogenaemia induced by omeprazole was investigated. Eight healthy subjects were randomised to receive five day courses of SMS 201-995 (25 micrograms subcutaneously three times daily), omeprazole (40 mg once a day), a combination of both drugs, or placebo. Basal and meal stimulated serum gastrin and basal serum pepsinogen A and C values were measured the day before treatment, on day five of treatment, and the day after each course of treatment. Omeprazole caused significant increases in basal and meal stimulated peak and integrated serum gastrin values and pepsinogen A and C levels, which were still significantly raised the day after stopping omeprazole treatment. Giving SMS 201-995 with omeprazole significantly reduced any omeprazole induced increases in basal and meal stimulated peak and integrated serum gastrin levels; serum pepsinogen A and C values were significantly inhibited too. Serum gastrin values during combined therapy were not significantly different from those during placebo treatment, whereas pepsinogen A and C levels were still significantly raised. On the day after stopping combined therapy, basal and meal stimulated peak and integrated serum gastrin and serum pepsinogen C (but not pepsinogen A) levels were not significantly different from values obtained on the day after stopping omeprazole alone. SMS 201-995 without omeprazole significantly inhibited basal and meal stimulated peak and integrated serum gastrin levels. Pepsinogen A was also significantly inhibited by SMS 210-995, but the reduction in pepsinogen C failed to reach statistical significance. In conclusion, SMS 201-995 prevents basal and meal stimulated increases in serum gastrin during omeprazole therapy. This finding may have clinical importance in the few patients who have pronounced hypergastrinaemia because of profound long acting acid inhibition.

Adult↗

PubMed1993

Effect of short-term administration of omeprazole on serum gastrin and pepsinogens in antrectomized patients.

Omeprazole, a potent and long-acting inhibitor of gastric acid secretion, is known to increase both serum gastrin and pepsinogen A and C levels in unoperated subjects. It has been suggested that the rise in serum pepsinogens is mediated by the omeprazole-induced increase in serum gastrin. This study was undertaken to determine the role of gastrin in hyper-pepsinogenemia induced by antisecretory therapy. We have studied the effect of a 5-day course of 40 mg of omeprazole daily on fasting serum gastrin and pepsinogen A and C levels in 14 patients with an antrectomy and a Billroth I anastomosis (n = 8) or a Billroth II anastomosis (n = 6). In antrectomized patients omeprazole failed to induce any increase in basal serum gastrin. On the other hand, omeprazole increased significantly serum pepsinogen A levels in both Billroth I and II patients, while the rise in serum pepsinogen C level was significant in Billroth I, but just failed to reach statistical significance in Billroth II patients. We conclude that the stimulation of serum pepsinogens A and C by a short-term treatment with omeprazole is not mediated by increases in serum gastrin. This study further shows that omeprazole stimulates gastrin release only from the antrum and not from extra-antral sources.

Adult↗

PubMed1993

Peptic ulcer, non-ulcer dyspepsia and irritable bowel syndrome in The Netherlands and Japan.

To study the prevalence of peptic ulcer, non-ulcer dyspepsia and irritable bowel syndrome (IBS) in the Dutch and Japanese working population, a structured history using a questionnaire on gastrointestinal symptoms during the preceding 3 months was obtained from persons undergoing a periodic medical examination. Principal components factor analysis of questionnaire responses was conducted to examine interrelationships of symptoms. In Holland, 427 men and 73 women participated (mean age 48.0 years), while in Japan 196 men and 35 women took part (mean age 48.8 years). In both the Japanese and the Dutch population, factor analysis yielded clusters of symptoms consistent with previously defined clinical syndromes: dyspepsia, diarrhoea-predominant IBS and constipation-predominant IBS. The prevalences of verified peptic ulcer history were 19% and 17% (95% confidence intervals (CI): 14-26% and 7-34%) in Japanese men and women in contrast to 5% and 0% (95% CI: 3-8% and 0-5%) in Dutch men and women respectively. The ratio of duodenal to gastric ulcer was 4.5: 1 in Holland and 1.5:1 in Japan. The 3-month period prevalence of non-ulcer dyspepsia was 13% in both the Japanese and the Dutch population and was twice as high in women as in men (p < 0.01). There was considerable overlap between dyspepsia subgroups. IBS was present in 25% of the Japanese and in 9% of the Dutch (p < 0.001) and occurred twice as often in women as in men (p < 0.01). In conclusion, factor analysis supported the existence of dyspepsia and IBS as distinct syndromes in both countries.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Influence of age and Helicobacter pylori infection on serum pepsinogens in healthy blood transfusion donors.

In a healthy population pepsinogen A and pepsinogen C increase with advancing age. As pepsinogen A and C are raised in chronic superficial gastritis which is caused by H pylori infection, we investigated whether H pylori is responsible for the age related increase of pepsinogen A and C. In H pylori positive blood transfusion donors serum pepsinogen A (mean (SD) 73 (35) micrograms/ml v 52 (19) micrograms/ml, p much less than 0.01) and C (mean (SD) 24 (13) micrograms/ml v 10 (7) micrograms/ml, p much less than 0.01) concentrations were significantly higher than in H pylori negative blood transfusion donors, while the serum pepsinogen A:C ratio mean (SD) 3.5 (1.4) v 6.2 (3.4), p much less than 0.01) was significantly decreased because of a relative greater increase in serum pepsinogen C in H pylori positive blood transfusion donors. Analysis of variance showed that pepsinogen A and C concentrations differed significantly in the different age groups (p much less than 0.01) when we considered all blood transfusion donors and H pylori positive blood transfusion donors, the mean pepsinogen levels being highest in the older age categories. In H pylori negative blood transfusion donors no such age related difference in pepsinogen A and C could be shown. In H pylori positive blood transfusion donors a weak positive but significant correlation between pepsinogen A and C and age could be shown (r = 0.30; p = 0.01 and r = 0.31; p = 0.01 respectively). In H pylori negative blood transfusion donors no correlation between serum pepsinogens and age was found. We conclude that the age related increase in serum pepsinogen A and C described in healthy control populations is caused by an increasing prevalence of H pylori infection. Serum pepsinogen A and C concentrations in patients should therefore be related to the presence or absence of H pylori infection.

Adult↗

PubMed1992

Short-term results of gastrectomy with Roux-en-Y or Billroth II anastomosis for peptic ulcer. A prospective comparative study.

Since the Roux-en-Y anastomosis prevents the sequela of postoperative enterogastric reflux after gastrectomy, this approach has been advocated as the primary procedure in patients undergoing gastrectomy for peptic ulcer. We have prospectively followed for 2 years 22 patients, in whom gastrectomy was performed with, at random, either Roux-en-Y (n = 11) or Billroth II (n = 11) anastomosis. Two of the 11 patients who had received the Roux-en-Y procedure had anastomotic ulcers, leading to reresection in one of them. These two patients were found to have the highest values for basal and pentagastrin stimulated gastric acid output. After the Billroth II procedure a single patient had a small anastomotic ulcerative lesion. Apart from differences in intragastric bile acids (p less than 0.0001) and the gastritis activity score (p less than 0.01), no significant differences were found between the patients with Roux-en-Y and Billroth II anastomosis with respect to basal and pentagastrin-stimulated gastric acid secretion, basal, postprandial and bombesin-stimulated serum gastrin secretion, serum pepsinogen A and C concentrations, the serum pepsinogen A/C ratio, postprandial glucose, and for a modified Visick grading. From this small series we conclude that, as compared with the Billroth II-anastomosis, the Roux-en-Y procedure effectively prevents enterogastric reflux, and is associated with a higher gastritis activity score, but not with differences in gastric acid, gastrin, pepsinogens, or Visick grading. Furthermore, inadequate reduction of acid secretion in some patients after the Roux-en-Y procedure may lead to recurrent peptic ulcers.

Anastomosis, Roux-en-Y↗

PubMed1991

Comparative evaluation of carcinoembryonic antigen, secretory component, and mucins in index and metachronous adenomas of the colorectum.

Of 124 patients who underwent endoscopic polypectomy, 70 were colonoscopically reevaluated during a mean period of 10 years. On the basis of the clinical outcome, the patients were divided into three groups: group 1, 31 patients who had a colon still with no adenomas or cancer; group 2, 35 patients in whom one or more metachronous adenomatous polyps developed; and group 3, 4 patients in whom a carcinoma of the colon subsequently developed. In addition to the clinical and pathological features, the pattern of the immunohistologic staining for carcinoembryonic antigen and secretory component was studied. Moreover, the mucin histochemical staining intensity of neutral mucins, sulfomucins, and sialomucins was evaluated. The features of the 40 index adenomas obtained from patients in group 1 were compared with the features of the 51 index adenomas from patients in group 2. Furthermore, these characteristics of the index adenomas were compared with those in the 69 metachronous adenomas of the group 2 patients. It was found that male sex (P less than 0.005) and a history of colorectal neoplasia (P less than 0.02) are main factors for the development of new adenomas. The neutral mucins were less abundant in the group 2 index adenomas (r = -0.21; P less than 0.05). The expression of the other evaluated markers was not significantly different between both groups, although the group 2 index adenomas were significantly smaller (r = -0.22; P less than 0.05) and showed a trend toward a more pronounced cytoplasmic expression of carcinoembryonic antigen than the index adenomas from group 1 (22% vs. 12.5%). Moreover, it was found that in comparison with the index adenomas, metachronous adenomas were significantly smaller (r = -0.24; P less than 0.01) and more sessile (r = 0.20; P less than 0.002). Significant negative correlations, i.e., decrease, were also found in the expression of carcinoembryonic antigen (surface P less than 0.001; cytoplasmic P less than 0.05) and neutral mucins (P less than 0.005) between the index adenomas and the metachronous adenomas, whereas positive correlations were found for secretory component (P = 0.0001) and sulfomucins (P less than 0.05). These findings suggest that a limited production of neutral mucins in the goblet cells of a small index adenoma from a male patient with a history of colorectal neoplasia is indicative of an increased risk for the development of new colorectal adenomas. Furthermore, the clinical, mucin histochemical, and immunohistochemical findings of the metachronous adenomas show less malignancy-associated features than those of the index adenomas.

Adenocarcinoma↗

PubMed1991

Weekend treatment with 20 and 40 mg omeprazole: effect on intragastric pH, fasting and postprandial serum gastrin, and serum pepsinogens.

Weekend treatment with 20 mg omeprazole reduces ulcer relapse rates but the results may improve with a higher dose regimen. We have evaluated three day weekend treatment with 20 and 40 mg doses of omeprazole in eight healthy subjects in a double blind crossover study. Twenty four hour ambulatory intragastric pH and basal and meal stimulated serum gastrin and serum pepsinogens A and C values were studied. The investigations began on the Friday before the third weekend course of omeprazole and were repeated on alternate days, except Sundays, for two weeks. When compared with values before the study, median 24 hour intragastric pH and basal and meal stimulated gastrin concentrations were significantly (p less than 0.01-0.05), but transiently, raised with both doses of omeprazole. Basal pepsinogen A and C values were significantly (p less than 0.01) increased on all study days, but did not return to their pre-study values before the next weekend dose, except for pepsinogen C in subjects treated with 20 mg omeprazole. A dose dependent effect was found for all parameters studied (p less than 0.05). In conclusion, weekend treatment with 20 and 40 mg omeprazole produces pronounced and dose dependent increases in intragastric pH, basal and meal stimulated serum gastrin, and basal serum pepsinogen A and C without inducing prolonged hypoacidity or hypergastrinaemia. Weekend treatment with 40 mg omeprazole merits further study in the prevention of peptic ulcer relapse.

Adult↗

PubMed1991

Repeated intravenous bolus injections of omeprazole: effects on 24-hour intragastric pH, serum gastrin, and serum pepsinogen A and C.

We determined the effect of four times daily dosing with intravenous omeprazole on 24-h intragastric acidity, serum gastrin, and serum pepsinogen A and C in 10 fasting subjects (median age, 23.5 years). Two dose regimens (80-20-20-20 mg and 80-40-40-40 mg) were compared in a randomized placebo-controlled crossover study. Intragastric pH was continuously monitored during 24 h, using combined glass electrodes, and blood samples were taken every 6 h. Repeated boluses of omeprazole every 6 h significantly increased (p less than 0.01) the median 24-h intragastric pH compared with placebo (median pH, 3.7 (140 mg/day), 4.3 (200 mg/day), and 1.4 (placebo)) but failed to continuously raise pH levels above 4.0 in 8 (140 mg/day) or 9 (200 mg/day) of 10 subjects. No advantage of the 200-mg dose over the 140-mg dose was demonstrated. A cumulative effect of intravenous omeprazole was shown after repeated boluses but also a marked interindividual variation in response, which was correlated with the omeprazole area under the plasma concentration time curve. A significant elevation of serum gastrin coincided with the increased pH levels, which was followed after 12-18 h by a significant increase of both serum pepsinogens.

Adult↗

PubMed1991

Assessment of plasma fibronectin in Crohn's disease.

Plasma fibronectin concentrations were measured by an ELISA method in two groups of patients with Crohn's disease. In the first study the value of fibronectin as acute phase protein was determined in 48 patients. There was a poor but significant correlation (r = 0.294, p = 0.043) between disease activity and fibronectin concentration in these patients. However, fibronectin was found to show the best correlation with the disease activity of eight acute phase parameters tested. In the second study, the relation between development or presence of fibrosis/stenosis in the intestine of 91 patients with Crohn's disease was related to the plasma fibronectin concentration. The incidence of this type of lesion was found to increase with the level of fibronectin in the plasma together with the disease history of these patients, in particular when intestinal resection had to be performed. These observations reveal that assessment of fibronectin in plasma of patients with Crohn's disease is of limited value for the determination of disease activity, but that its concentration is related to the biological behavior, i.e. formation of fibrosis/stenosis, of the inflammatory lesion.

Adult↗

PubMed1990

Effect of long-term treatment with omeprazole on serum gastrin and serum group A and C pepsinogens in patients with reflux esophagitis.

Twenty-nine nongastrectomized and three partially gastrectomized patients with chronic reflux esophagitis resistant to 12 weeks' treatment with histamine H2-receptor antagonists were treated with a daily oral dose of 20-40 mg of omeprazole for 12-30 months. Basal serum gastrin, serum pepsinogen A, and serum pepsinogen C concentrations were monitored at regular intervals. Serum gastrin levels significantly (P less than 0.01) increased threefold to fourfold during the first 1-2 months of the study when all patients ingested 40 mg of omeprazole daily. Dose reduction to 20 mg did not significantly decrease gastrin levels. Serum gastrin levels showed a trend to further increase after the first 3 months of treatment, reaching statistically significant differences for values from the 3-12-month period (P less than 0.05) and from the 3-24-month period (P less than 0.005). Women and patients with high basal serum gastrin levels before omeprazole treatment were more likely to achieve higher serum gastrin levels during omeprazole treatment. Serum pepsinogen A and C levels were significantly (P less than 0.01) increased at all time intervals during long-term treatment with omeprazole. No significant tendency toward higher serum pepsinogen C levels in time was observed. However, serum pepsinogen A levels and the ratio of pepsinogen A to pepsinogen C further increased significantly (P less than or equal to 0.05) during the initial 3-12-month period. However, this trend was not observed anymore afterward. Antrectomized patients did not show increases in serum gastrin and serum pepsinogen A and C levels, suggesting that hypergastrinemia may be involved in the observed hyperpepsinogenemia.

Aged↗