Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric mucosal lesions are common in patients with cirrhosis. Among them, snake skin pattern gastropathy (SSPG) is the most distinguishing one. A prospective study was conducted to investigate the incidence of SSPG in cirrhotic patients, the relationship between the degree of portal pressure and SSPG, and the possible association of SSPG with serum levels of gastrin and pepsinogen I. SSPG was found to be significantly more common in 100 cirrhotic patients than in 100 age- and sex-matched healthy controls (41% vs 0%, P less than 0.0001). Hepatic venous pressure gradient and serum gastrin and pepsinogen I levels were measured in 21 cirrhotic patients with SSPG and 25 cirrhotics without SSPG. There was no significant difference in hepatic venous pressure gradient (16.1 +/- 4.4 mmHg vs 16.1 +/- 4.9 mmHg, P greater than 0.05), serum gastrin level (78.0 +/- 26.7 pg/mL vs 80.1 +/- 32.5 pg/mL, P greater than 0.05) and serum pepsinogen I level (69.5 +/- 26.6 ng/mL vs 65.2 +/- 26.1 ng/mL, P greater than 0.05) in cirrhotic patients with or without SSPG. In conclusion, SSPG is common in cirrhotic patients. Portal pressure per se may not be the only factor causing SSPG--other aggressive factors may be needed together to cause the gastropathy. There is no evidence of correlation between serum gastrin or pepsinogen I level and SSPG.
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PMID:Snake skin pattern gastropathy in cirrhotic patients. 191 21

To investigate whether hypergastrinemia and low serum levels of pepsinogen I are associated with gastric hypoacidity in cirrhosis with capillary ectasia of gastric mucosa and whether this alteration is secondary to the presence of atrophic gastritis, two groups of patients were studied: 1) 12 cirrhotic patients with diffuse gastric red spots at the endoscopic examination, and 2) 12 cirrhotic patients with endoscopically normal mucosa. Vascular ectasia of the gastric mucosa was histologically confirmed in all patients with gastric red spots. The study of base-line and stimulated acid gastric secretion showed that 9 of 12 (75%) cirrhotics with gastric vascular ectasia had achlorhydria and that 8 of these 9 patients had high base-line gastrin serum levels (greater than 130 pg/ml) and low base-line pepsinogen I serum levels (less than 20 ng/ml). Base-line gastrin and pepsinogen I serum levels were significantly greater and lower, respectively, in patients with gastric vascular ectasias than in cirrhotics without these lesions. None of the patients of either group had complete atrophy in the corpus of the stomach, and only 4 of the 9 cirrhotics with gastric vascular ectasia and achlorhydria had moderate atrophy. These results show that achlorhydria is frequently associated with hypergastrinemia and low pepsinogen I serum levels in patients with cirrhosis and gastric vascular ectasias and suggest that this disturbance is not secondary to a morphologic abnormality of the gastric mucosa.
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PMID:Gastric vascular ectasias in cirrhosis: association with hypoacidity not related to gastric atrophy. 259 68

The present review concentrates on environmental factors which influence the outcome of peptic ulcer disease by acting from the outside. Endogenous risk factors, such as acid output, pepsin secretion and serum pepsinogen, gastritis and mucosal defense, blood group, and secretor status, are only dealt with when they help to explain the mechanism by which exogenous risk factors affect the upper gastrointestinal mucosa. After outlining the wax and wane of peptic ulcer, it is concluded that these changes resulted from similar temporal patterns of occupational workload in the general population. Cross sectional studies also support the contention of occupational workload being a risk factor in peptic ulcer, explaining several characteristic features of peptic ulcer, such as its sex, race, and social class distribution, increased incidence in immigrant workers, seasonal variation, healing by bed rest, and urban versus rural distribution. Susceptible subjects may react to a rise in occupational workload and acute exposure to stressful life events by increased gastric secretion which, in turn, leads to ulceration and symptoms. Cigarette smoking, intake of aspirin and related drugs, dietary salt, and alcohol abuse represent additional environmental risk factors, which form the etiologic link of the association of peptic ulcer with chronic lung disease, rheumatoid arthritis, hypertensive disease, and liver cirrhosis, respectively.
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PMID:Factors which influence the incidence and course of peptic ulcer. 307 62

Thirty-nine subjects have been studied: 14 with hepatic cirrhosis who had not been subjected to surgery, 13 cirrhotic patients in whom portacaval shunt had been performed, and 12 normal controls. In all of them, we performed serum determinations of pepsinogen I, both basal and after pentagastrin stimulation, and of basal gastrin levels, as well as analyses of basal and stimulated gastric acid secretion (basal acid output and maximal acid output). The values for pepsinogen I, basal or post-stimulation, were higher (p less than 0.001) in patients with cirrhosis who had not undergone surgical shunt than in those in the control group. However, there were no statistically significant differences when these two groups were compared with the patients who had been subjected to portacaval shunt. In this last group of patients, seven had levels similar to those of the controls, and six presented higher values. Likewise, the values for gastric acid secretion were similar in the three groups of patients, and the basal gastrin level was lower (p less than 0.001) among patients with liver cirrhosis, whether or not they had undergone surgery, than among the control population. In conclusion, the functional alterations of the gastric mucosa in patients with hepatic cirrhosis are not significantly different from those found in cirrhotic patients with portacaval shunt.
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PMID:Study of the secretion of pepsinogen I in cirrhotic humans with and without portacaval shunt. 333 58

To characterize bleeding from gastric red spots in patients with cirrhosis, three groups of patients were studied: (a) 11 cirrhotic patients bleeding from gastric red spots, (b) 18 nonbleeding cirrhotic patients without gastric red spots, and (c) 13 noncirrhotic patients with endoscopic normal mucosa (controls). Histologic examination of antral biopsy specimens revealed a diffuse capillary ectasia without inflammation in 8 of the 11 cirrhotic patients with gastric lesions. Morphometric analysis disclosed a significantly greater mean mucosal capillary cross-sectional area in cirrhotic patients with gastric lesions (mean +/- SE, 1371 +/- 320 microns2) than in those without gastric lesions (541 +/- 61 microns2) (p less than 0.005) or controls (353 +/- 20 microns2) (p less than 0.001). Hypergastrinemia was detected in 8 of the 11 cirrhotic patients with lesions, in 2 of the 18 cirrhotic patients without gastric lesions, and in none of the controls (p less than 0.001). Gastrin serum levels correlated significantly (r = 0.80) with mean mucosal capillary cross-sectional area in patients with cirrhosis. Pepsinogen I serum levels below 20 ng/ml were observed in 7 of the 11 cirrhotic patients with lesions, in 1 of the 18 cirrhotic patients without lesions, and in none of the controls. These data indicate that bleeding from gastric red spots in patients with cirrhosis is a distinct entity characterized by vascular ectasia of the gastric mucosa. This condition seems to be associated with hypergastrinemia and low serum levels of pepsinogen I.
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PMID:Gastric mucosal vascular ectasias causing bleeding in cirrhosis. A distinct entity associated with hypergastrinemia and low serum levels of pepsinogen I. 349 59

The gastric mucosal lesions represent a frequent cause of hemorrhage in the portal hypertension (PHG) and in the hepatic cirrhosis. This study was undertaken to assess the structural and ultra structural modifications in the intimal lamina of the stomach in this pathology. The cells of mucosa show graded alterative transformations. In the gastric mucosa, some of the chief (enzymatic) cells present a quasi-normal histological organization; others increased alterations such as irregular and heterochromatic nuclei, fewer cytoplasm organelles, numerous clear vesicles and heterogeneous lysosomes. The parietal (oxyntic) cells show in their apical cytoplasm wide dilatations of the intracellular canalicles, vesicles, a reduced number of organelles and irregular nuclei. The enteroendocrine cells (APUD) present an increased number of granules and organelles in the cytoplasm. The connective inter-glandular tissue contains active fibroblasts, micro inflammatory zones, blood vessels with hypertrophied endothelium, irregular and dilated lumen. Subsequent to these alterations in the structures of the gastric mucosa in portal hypertension, the function of synthesis/excretion of the pepsinogen, lipase, hydrochloric acid, intrinsic factor, serotonin, etc. are affected.
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PMID:The gastric mucosa in portal hypertension: structural and ultrastructural observations. 2049 42