Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum pepsinogen I, serum gastrin concentration, and inflammatory scores were measured in a population of 71 children undergoing upper gastrointestinal endoscopy for investigation of upper abdominal pain. Forty four were initially colonised with Helicobacter pylori. The indices were measured before treatment (in 71 children), one month (in 41 children), and six months (in 21 children) after stopping treatment. Before treatment there was a significant correlation between serum pepsinogen concentration, total inflammatory score, and H pylori state, but no correlation between serum gastrin concentrations and H pylori state. Similarly, the total inflammatory score and serum pepsinogen concentrations were significantly correlated. There was no such correlation in children negative for H pylori. After treatment the inflammatory score improved in those patients in whom H pylori had been eradicated. There was also a significant fall in serum pepsinogen I and serum gastrin concentration in those patients in whom H pylori had been eradicated. These results were similar to those found six months after treatment had been stopped. These findings suggest that the serum pepsinogen I concentration could be considered a useful marker for gastritis and can be used as an index of severity of gastritis in H pylori positive subjects. The measurement of serum gastrin concentrations does not give useful information.
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PMID:Serum pepsinogen I and gastrin concentrations in children positive for Helicobacter pylori. 221 69

32 children (mean age 12 years, range 6-18) with non-specific abdominal pain and Campylobacter pylori positive gastritis received a six week course of daily oral amoxycillin (50 mg/kg) and tinidazole (20 mg/kg). Before treatment and one month after stopping treatment, endoscopic biopsy samples were taken from the antral mucosa and serum C pylori IgG antibody, pepsinogen I, and gastrin levels were measured in fasting blood samples. One month after treatment 30 children (94%) were cleared of C pylori and gastritis had resolved in 27 (84%) and was improved in the remaining 5. Serum IgG, pepsinogen I, and gastrin levels were significantly decreased after treatment. Of 12 children assessed at six months, 9 remained free of C pylori. Increases or decreases in IgG level indicated clearance or recurrence, respectively, of C pylori.
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PMID:Amoxycillin plus tinidazole for Campylobacter pylori gastritis in children: assessment by serum IgG antibody, pepsinogen I, and gastrin levels. 256 7

A consecutive series of 51 children (mean age 11 years) who presented with recurrent abdominal pain were investigated by upper gastrointestinal endoscopy including three antral biopsies for microscopy, culture and urease testing. Serum IgG, IgA, and IgM antibodies to Campylobacter pylori (C pylori) were measured by the ELISA technique. Serum pepsinogen I was also measured. Thirty two children showed histological evidence of gastritis. All had C pylori on microscopy and or culture. Nineteen children showed no histological gastritis nor evidence of C pylori on microscopy, culture and/or urease testing. The IgG and IgA antibody levels to C pylori were significantly higher in C pylori positive children than in the negative group (p less than 0.001). Serum pepsinogen I concentrations were also significantly higher in C pylori positive children than in negative (p less than 0.001). Measurement of IgG antibody levels, combined with serum pepsinogen I estimation, predict the presence of C pylori associated gastritis in children with a sensitivity and specificity of up to 95%. It may be used therefore to predict gastritis and even peptic ulceration in children presenting with non-specific upper abdominal pain.
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PMID:Serum pepsinogen I and IgG antibody to Campylobacter pylori in non-specific abdominal pain in childhood. 275 88

Serum pepsinogen I (PG I) levels were determined by radioimmunoassay in 23 children with peptic ulcer disease (PUD) before and after treatment with ranitidine and in 44 children who were being investigated for recurrent abdominal pain. Upper gastrointestinal endoscopy was performed in all. No lesions were detected in controls, while 18 patients showed a duodenal ulcer, 4 had an antral ulcer, and 1 had both. An 8-week course of ranitidine healed PUD in 93.5% of them, while long-term (1-5 years) endoscopic follow-up showed a 41.9% ulcer relapse rate after stopping treatment. Gastric acid secretion after pentagastrin stimulation [maximal acid output (MAO)] was tested in all controls and in 22 PUD patients: While controls had normal MAO values for their age, 65% of patients had a secretion above the normal range. No significant correlation was detected between serum PG I and MAO either in controls or in patients. Mean serum PG I concentrations were not significantly higher in the whole patient group than in controls, but PUD patients who relapsed after discontinuing ranitidine treatment had shown on admission significantly higher PG I levels when compared both with those who did not relapse and with controls. All patients who relapsed, but only 42.8% of those who did not, had a serum PG I concentration above the normal upper limit for a pediatric population (56.7 ng/ml). None of the PUD patients who had serum PG I levels under this limit relapsed. Our results suggest that pretreatment serum PG I levels in children with PUD may predict fairly accurately which will not relapse after attaining ulcer healing by a short-term ranitidine course.
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PMID:Prognostic value of serum pepsinogen I in children with peptic ulcer. 318 68

We evaluated in children with abdominal complaints the prevalence of Helicobacter pylori gastric and duodenal colonization and the histological features of gastric and duodenal mucosae. Fifty patients, aged 1-17 years, underwent upper endoscopy for recurrent abdominal pain, vomiting and/or gastrointestinal bleeding. With serological, bacteriological and/or histological methods twenty-eight children were demonstrated to be Helicobacter pylori-positive. No statistically significant differences were observed with regard to age, sex and indication to perform endoscopy. Eighty-two percent of Helicobacter pylori-positive patients had gastritis and/or duodenitis. The Helicobacter pylori-positive children had higher Helicobacter pylori specific IgG levels than the Helicobacter pylori-negative ones (p < 0.001). No statistically significant differences were found between Helicobacter pylori-positive and Helicobacter pylori-negative subjects, for gastrin and pepsinogen I. Since the frequency of Helicobacter pylori infection in children with gastrointestinal complaints is high, in patients undergoing upper endoscopy, the sistematical examination of bioptic samples for bacteriological and histologic procedures is of great importance.
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PMID:[High incidence of Helicobacter pylori infections in an endoscopic pediatric patient series]. 780 63

We report on a case of chronic atrophic gastritis in which the serological markers of gastric diseases were strictly monitored for 2 years after successful Helicobacter pylori (H. pylori) eradication. A 31-year-old man with upper abdominal pain was diagnosed as having H. pylori infection. Laboratory examination revealed low serum levels of pepsinogen (PG) I, low PG I/II ratio, and low plasma levels of ghrelin. Upper gastrointestinal endoscopy revealed severe corpus-dominant atrophic gastritis. H. pylori eradication therapy was performed. Successful eradication was confirmed three months later by the 13C urea breath test. Decreased serum PG II levels and an increased serum PG I/II ratio were detected a week after completion of the eradication therapy. The serum anti-H. pylori IgG titer decreased to less than 75% of the baseline level by 24 weeks after completion of the eradication therapy. On the other hand, the plasma levels of total and active ghrelin showed no marked changes after successful eradication therapy. This is the first report of long-term follow-up of changes of the plasma ghrelin levels after H. pylori eradication therapy, the observations suggesting that reduction of plasma ghrelin levels cannot be achieved merely by H. pylori eradication, without resolution of the gastric atrophy.
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PMID:Long-term strict monitoring of plasma ghrelin and other serological markers of gastric diseases after Helicobacter pylori eradication. 1578 80

We report a case of multifocal gastric cancer with a variety of macroscopic and histological findings. A 65-year-old woman was admitted with upper abdominal pain. Her familial history was remarkable in that her mother had died of gastric cancer. The hematological and blood biochemical values were normal, but the serum was positive for Helicobacter pylori immunoglobulin G, and the serum pepsinogen test was also positive. Gastrointestinal fiberscopy showed many granulomatous lesions coexisting with pedunculated polypoid lesions and marked atrophic gastritis throughout the stomach. We performed total gastrectomy with regional lymph node dissection. There were four separate cancers and three hyperplastic polyps with entire intestinal metaplasia. The pathological findings of these multifocal gastric cancers varied, with coexisting differentiated and undifferentiated types, and early and advanced types. One of the pedunculated polypoid lesions was accompanied by papillary adenocarcinoma. Although multifocal gastric cancer is not uncommon, the present case is considered an extremely unusual example of gastric cancer.
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PMID:Multifocal gastric cancer with a variety of histological findings coexisting with hyperplastic polyps: report of a case. 2177 1