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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ostertagia ostertagi and Cooperia oncophora are widely distributed and are the most important parasites affecting young bovine livestock. Therefore, there is a substantial need for sensitive and specific parameters in support of their diagnosis, especially for sub-clinical disease correlated to production loss. In this review, the value and the application as a diagnostic tool of pepsinogen, gastrin and antibody response are discussed. An increase in pepsinogen or gastrin reflects mucosal damage caused by an Ostertagia infection. Some controversy exists about the level of pepsinogen and gastrin, which may be considered indicative for the diagnosis of clinical and sub-clinical ostertagiasis. Pepsinogen levels between 3,000 tot 4,000 mU tyrosine are regarded indicative for subclinical disease, values in excess of 5,000 mU tyrosine are considered significant for diagnosing clinical disease. For gastrin, it is suggested that based on group means, values of 400 pg/ml are indicative for subclinical parasitic disease in calves with reduced daily weight gain, while threshold levels of > or = 1000 pg/ml gastrin are representative for clinical ostertagiasis. Antibody responses to Ostertagia and Cooperia can be assessed using the enzyme immunoassay (EIA). Until now, mainly crude worm extracts have been used as antigen source in the EIA. They are not species-specific as discussed experiments provide evidence of a close relationship between the onset of parasitic disease and the evolution of the group mean parameters. However, data demonstrate serious variations between animals, which impede a reliable individual diagnosis. For longitudinal epidemiological studies especially pepsinogen and gastrin have proven their value, exhibiting fast fluctuations induced by infection or as a result of treatment. Conversely antibody levels were found to be more stable and therefore are useful in large cross-sectional studies, enabling a rough assessment of the degree of infection.
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PMID:[The serological diagnosis of gastrointestinal nematode infections in cattle]. 834 28

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.
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PMID:Inhibition of omeprazole induced hypergastrinaemia by SMS 201-995, a long acting somatostatin analogue in man. 840 51

Serum gastrin and pepsinogen concentrations were measured in 51 children infected with Helicobacter pylori, to investigate the clinical significance and influence of CagA and VacA on serum concentrations of these peptides. CagA+ was 44/51 (86%) and VacA+ was 42/51 (82%). Type I (CagA+/VacA+) included 39/51 (76%), type II (CagA-/VacA-) was 4/51 (8%), and intermediate (CagA-/VacA+, CagA+/VacA-) was 8/51 (16%). There was no significant correlation between endoscopic diagnosis and the state of CagA/VacA. Serum gastrin concentrations were not significantly correlated with the state of CagA/VacA. Serum pepsinogen I and II concentrations were significantly higher in CagA+ than in CagA-, but there was no significant difference between VacA+ and VacA-, Serum pepsinogen I/II ratio was not significantly correlated with the state of CagA/VacA. There was no significant difference between serum concentrations of gastrin, pepsinogen I and H. pylori phenotypes. However, pepsinogen II concentration was significantly higher in type I than type II. Pepsinogen I/II ratio was significantly lower in type I and intermediate than in type II. These findings suggest that CagA positively and phenotype of H. pylori could play a role in the development of upper gastrointestinal diseases in children.
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PMID:Serum gastrin and pepsinogen I, II concentrations in children with Helicobacter pylori infection: the role of CagA and VacA. 958 57

Pepsinogen A and C as well as gastrin were measured in the serum of 117 patients with rheumatic diseases. Moreover, the patients were divided up in groups by aids of a semiquantitative, rapid enzyme immunoassay for detection of Helicobacter pylori: 20 patients without H. pylori antibodies (AB) negative, 18 positive + (= weak AB-titre), 21 positive +2 (medium AB-titre), and 58 positive +3 (high AB-titre). The semiquantitative determinations of H. pylori-AB correlated with pepsinogen A, C and gastrin. Patients with H. pylori-AB positive +3 showed significantly higher values of pepsinogen C (p < or = 0.01) as well as pepsinogen A and gastrin (p < or = 0.05) than H. pylori-AB negative patients. Significantly increased levels of pepsinogen A (> 150 ng/ml) and C (> 25 ng/ml) were found to occur in 39% and 100% of patients with high H. pylori-AB titres. The measurement of serum pepsinogen C concentrations may provide additional diagnostic information of the extent of mucosal lesions in patients with positive H. pylori-AB titres treated with antirheumatic drugs. Our findings suggest that the semi-quantitative classification of positive AB-results can be useful in cases determining H. pylori infection and mucosal irritation if other investigations are not available.
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PMID:Association between serum pepsinogen A and C levels, serum gastrin concentrations and Helicobacter pylori antibodies. 1041 37

Human gastric mucosa contains aspartic proteinases that can be separated electrophoretically on the basis of their physical properties into two major groups: Pepsinogen I (PGA, PGI); and Pepsinogen II (PGC, PGII). Pepsinogens consist of a single polypeptide chain with molecular weight of approximately 42,000 Da. Pepsinogens are mainly synthesized and secreted by the gastric chief cells of the human stomach before being converted into the proteolytic enzyme pepsin, which is crucial for the digestive processes in the stomach. Pepsinogen synthesis and secretion are regulated by positive and negative feed-back mechanisms. In the resting state pepsinogens are stored in granules, which inhibit further synthesis. After appropriate physiological or external chemical stimuli, pepsinogens are secreted in the stomach lumen where hydrochloric acid, secreted by the parietal cells, converts them into the corresponding active enzyme pepsins. The stimulus-secreting coupling mechanisms of pepsinogens appear to include at least two major pathways: one involving cAMP as a mediator, the other involving modification of intracellular Ca(2+)concentration. Physiological or external chemical stimuli acting through the intracellular metabolic adenyl cyclase are more effective in inducing ' de novo ' pepsinogen synthesis than those acting through intracellular Ca(2+). The activation of protein kinase C (PK-C) would appear to be involved in regulatory processes. The measurement of pepsinogens A and C in the serum is considered to be one of the non-invasive biochemical markers for monitoring peptic secretion and obtaining information on the gastric mucosa status of healthy subjects. Recently, pepsinogen measurements have been used as an effective biochemical method for evaluating and monitoring patients with gastrointestinal diseases and for checking the effects of drug treatment. The level of PGA in the serum is always high in normal gastritis, while in atrophic gastritis it is always low. In both cases the PGC level in the serum is high. In most gastrointestinal pathologies the ratio between the PGA/PGC decreases. Various reports concerning hormone and/or enzyme modification as well as gastrointestinal distress in the case of long distance exercise have been reported. It has been suggested that the origin of the gastrointestinal distress experienced by long distance runners is a transient ischaemia of the gastric mucosa; it is also suggested that a hypobaric-hypoxic environment could contribute to induce gastric mucosa necrosis. Interrelation between gastrointestinal distress, hypobaric-hypoxic environment and modifications of PGA and PGC, gastrin and cortisol was evaluated in 13 athletes after a marathon performed at 4300 m. Gastrointestinal symptoms occurred in approximately 40% of the athletes. After the race the athletes showed a significant increase of gastrin and cortisol, while the ratio between PGA/PGC decreased. No relationship was observed between gastrointestinal symptoms and hormonal changes after the race. A control group of five subjects, who had been exposed to the same environmental conditions, showed no gastrointestinal or hormonal alteration. Conversely, control subjects presented a significant decrease of cortisol related to the circadian rhythm. The same incidence of gastrointestinal symptoms at high altitude and at sea level and the absence of pathological alteration of PGA and PGC in the serum of the athletes indicates that running a marathon and living for 6 days at 4300 m does not induce gastric mucosa necrosis. Cortisol and gastrin alteration observed in the athletes at this altitude would seem to be related to an activation of the mesopontine and forebrain structures involved in the behavioural and metabolic integration of the autonomic control and arousal and psychophysical-exercise stress. 2000 Academic Press@p$hr
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PMID:Pepsinogens: physiology, pharmacology pathophysiology and exercise. 1067 78

In this paper the different options for the diagnosis of gastrointestinal nematode infections are discussed. Diagnostic tests have a role in confirming the clinical diagnosis of parasitic gastroenteritis, but are more important for herd health monitoring of nematode infections, in particular for cattle. Therefore, emphasis is placed on discussing the available diagnostic parameters on their usefulness for that purpose. For clinical diagnosis the clinical signs, combined with the history of the animals is usually sufficient and a laboratory confirmation is not required. Faecal egg counts are, with two exceptions, not suitable for confirmation of the clinical diagnosis, because correlation between faecal egg counts and infection levels is usually low. These exceptions are the diagnosis of haemonchosis in small ruminants and the detection of anthelmintic resistance. This also limits the value of DNA-based tests of faecal material; even quantitative tests of nematode species specific DNA will have little value for diagnosis and monitoring. Pasture larval counts and worm counts are useful parameters for basic epidemiological studies on nematode infections. However, they are too laborious to be used for either routine diagnosis or monitoring. Blood parameters, such as gastrin and pepsinogen and serology are valuable tools for diagnosis. Pepsinogen and ELISAs based on recombinant proteins show most promise as parameters for herd health monitoring. However, extensive epidemiological studies are still needed before these parameters can be implemented in routine herd health monitoring schemes for parasitic gastroenteritis.
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PMID:Value of present diagnostic methods for gastrointestinal nematode infections in ruminants. 1087 14

Intestinal-type gastric adenocarcinomas usually are preceded by chronic atrophic gastritis. Studies of gastric cancer prevention often rely on identification of this condition. In a clinical trial, we sought to determine the best serological screening method for chronic atrophic gastritis and compared our findings to the published literature. Test characteristics of potential screening tests (antibodies to Helicobacter pyloni or CagA, elevated gastrin, low pepsinogen, increased age) alone or in combination were examined among consecutive subjects enrolled in a study of H. pylori and preneoplastic gastric lesions in Chiapas, Mexico; 70% had chronic atrophic gastritis. English-language articles concerning screening for chronic atrophic gastritis were also reviewed. Sensitivity for chronic atrophic gastritis was highest for antibodies to H. pylori (92%) or CagA, or gastrin levels >25 ng/l (both 83%). Specificity, however, was low for these tests (18, 41, and 22%, respectively). Pepsinogen levels were highly specific but insensitive markers of chronic atrophic gastritis (for pepsinogen I <25 microg/l, sensitivity was 6% and specificity was 100%; for pepsinogen I:pepsinogen II ratio <2.5, sensitivity was 14% and specificity was 96%). Combinations of markers did not improve test characteristics. Screening test characteristics from the literature varied widely and did not consistently identify a good screening strategy. In this study, CagA antibodies alone had the best combination of test characteristics for chronic atrophic gastritis screening. However, no screening test was both highly sensitive and highly specific for chronic atrophic gastritis.
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PMID:Screening markers for chronic atrophic gastritis in Chiapas, Mexico. 1121 66

Pernicious anemia is a macrocytic anemia due to cobalamin deficiency, which is the result of intrinsic factor deficiency. Pernicious anemia is associated with atrophic body gastritis, whose diagnostic criteria are based on the histologic evidence of gastric body atrophy associated with hypochlorhydria. Serological markers suggesting the presence of oxyntic mucosa damage are increased levels of fasting gastrin and decreased levels of Pepsinogen I. Without the now obsolete Schilling's test, intrinsic factor deficiency may not be proven, and gastric intrinsic factor output after pentagastric stimulation has been proposed. Intrinsic factor autoantibodies are useful surrogate markers of pernicious anemia. The management of patients with pernicious anemia should focus on the life-long replacement treatment with cobalamin and the monitoring to early diagnose an eventual onset of iron deficiency. Moreover, these patients should be advised about possible gastrointestinal long-term consequences, such as gastric cancer and carcinoids.
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PMID:Diagnosis and management of pernicious anemia. 2194 76

Dyspepsia is a functional GI disorder consisting in a wide range of symptoms. The main diagnostic challenge has been whether to perform an EGD or an abdominal US in order not to miss organic lesions, but to avoid unnecessary and sometimes invasive tests. Pepsinogen serology has been proposed as an useful non-invasive test to explore the status of the gastric mucosa, suggesting this strategy as an adequate approach in management of dyspepsia. In a primary care setting, 266 dyspeptic patients were investigated to establish the proper diagnosis. The workup included upper GI endoscopy with biopsies, a structured questionnaire including type and severity of symptoms, serological determination of serum pepsinogens, gastrin 17 and IgG against Hp. Inclusion criteria were dyspeptic symptoms (epigastric pain, nausea and/or vomiting, post prandial fullness, early satiation) lasting more than 1 year and the association between symptoms and food ingestion.. Helicobacter pylori infection was present in 114 subjects, characterized by high levels of pepsinogen II and IgG against Hp. Twenty subjects were classified according with the diagnosis of chronic body atrophic gastritis. Nausea and post prandial fullness were the most frequent symptoms (48% and 41%, respectively) in the studied population, followed by epigastric pain and early satiation (37% and 26% respectively). A diagnosis of normality by serological diagnosis was found in half of patients experiencing epigastric pain and in about 60% of subjects with the three other symptoms (nausea, post prandial fullness, and early satiation). In conclusion, this experience confirms the clinical usefulness of serology in dyspepsia, contributing to correctly diagnosing CAG and H.p. infection in such patients and providing a good correlation with the clinical picture.
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PMID:Functional Dyspesia. 3292 64


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