Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of the osmolarity of intragastric instillates on pepsin secretion was studied in rats anaesthetised with urethane. Irrigation of the stomach with solutions of sucrose and NaCl, resp. caused a concentration-dependent increase in pepsin output. A stimulation was observed already by hypotonic solutions and the maximal effect was obtained by 300 m-osmole/l of sucrose and by 600 m-osmole/l of NaCl (13- and 10-fold stimulation resp.). A similar time course in the increase of pepsin output was produced by hyperosmotic solutions (600 m-osmole/l) of sucrose, urea, NaCl and choline chloride. Pepsin output was stimulated maximally within 30 min and decreased thereafter, but remained at about 4--6-fold higher levels than during the previous irrigation with distilled water. Replacement of hyperosmotic instillates by distilled water reduced pepsin secretion to the initial level. Hypertonic ethanol (600 m-osmole/l) increased pepsin output only slightly. Vagotomy, pretreatment with atropine (1 mg/kg i.v.) or cimetidine (5 mg/kg i.v.), local anesthesia of the gastric mucosa with 4% lidocaine or intravenous infusion of PGE2 (2 microgram/kg X min) did not antagonise the stimulation of pepsin output induced by hyperosmotic NaCl (600 m-osmole/l). The results indicate that the increase of the osmolarity of intragastric instillates stimulates pepsin secretion in the rat without involvement of neural (vagal or local cholinergic reflexes) or hormonal mechanisms (release of gastrin) which are known to stimulate gastric secretion in the gastric phase.
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PMID:Osmotic stimulation of pepsin secretion in the rat. 35 99

Hyperglucagonaemia and hypergastrinaemia were observed in some severely burnt patients during their illness. Hyperglucagonaemia seemed to be related to the severity of illness rather than to the burn itself, and the close correlation of glucagon concentrations with glucose and urea and its inverse correlation with bicarbonate concentrations suggest that glucagon might contribute to the hypercatabolic state. One patient developed high levels of gastrin and massive bleeding from a stress ulcer of the duodenum. Possibly gastrin hypersecretion may have a role in the pathogenesis of Curling's ulcer.
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PMID:Hypersecretion of glucagon and gastrin in severely burnt patients. 112 28

During the last years interest has focused on the trophic effect of gastrin in colorectal carcinomas. Some reports indicated an increased serum level of gastrin in patients with colorectal adenomas or carcinomas. In a prospective study in 261 patients submitted to colonoscopy fasting serum gastrin concentrations were determined. 91 patients served as control, 89 patients had one or more adenomas, 55 patients suffered from a colorectal carcinoma, 17 had a benign, postoperative stenosis of the colon, and 9 had a chronic inflammatory bowel disease. All patients fulfilled the following criteria: No regular drug intake, no previous gastric or small bowel operation, no known ulcer disease, no abnormalities in serum calcium, creatinine, triglycerides, cholesterol and blood urea. Mean gastrin level was 86.63 +/- 23.8 pg/ml in the control, 84.57 +/- 25.1 pg/ml in the adenoma group and 84.6 +/- 24.4 pg/ml in the carcinoma group. No difference of serum gastrin levels were observed regarding sex, age, tumor stage and localisation.
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PMID:[Serum gastrin level in patients with colorectal adenoma or carcinoma]. 141 56

Although Helicobacter pylori is now accepted as the major aetiological factor in chronic gastritis in man, many of the factors which determine its pathogenicity are unknown. The organism has adapted to survive in the low-pH environment of the stomach, partly through its ability to buffer hydrogen ion by the hydrolysis of urea and by the presence of lectins on its surface, which bind to gastric mucosa and epithelial cells. After attachment, harmful toxins and enzymes have access to the gastric cells and cellular damage and an immune response ensues. In patients with duodenal ulceration, Helicobacter pylori-related gastritis predominantly affects the gastric antrum and has a high prevalence. Excessive gastrin production has been suggested as a potential aetiological factor linking infection with duodenal ulcer development. Perhaps more important is the association between gastric metaplasia of the duodenal epithelium, which is correlated with acid load and is more extreme in H. pylori positive patients with duodenitis. Organisms may subsequently spread from the gastric antrum into areas of gastric metaplasia in the duodenal bulb, leading to areas of chronic duodenitis and ultimately frank ulceration. It should not be overlooked, however, that other factors such as genetic predisposition, blood group, stress, drugs and smoking all have a role to play in the outcome, given the comparatively small number of patients in the general population infected with H. pylori who develop ulcer disease.
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PMID:Role of Helicobacter pylori in gastritis and duodenitis in man. 144 34

A 73 year old woman was hospitalized for recurrent occult gastrointestinal bleeding. She had been treated with iron replacement for a microcytic anemia at the age of 67 years remaining on iron and was well until 1989, when she again was hospitalized with symptomatic anemia (hemoglobin 5.4 9um/dl). Urea, electrolytes, liver function, serum vitamin B12 and red cell folate tests were normal. The gastrointestinal blood loss continued, and she became dependent on transfusions, receiving 60 unites of blood over the course of a year. Investigation confirmed iron deficiency with occult blood loss, and showed antibodies to gastric parietal cells, with a title of 1:160. At gastroscopy a series of longitudinally arrayed red streaks were seen radiating to the pylorus, the typical appearances of antral vascular ectasia or watermelon stomach. The diagnosis was confirmed histologically. Prednisolone therapy, initially at a dose of 30 mg, successfully stopped the bleeding and other drugs were withdrawn except from carbimazole and tolbutamide. Prednisolone also restored the gastric acid secretion to normal (basal acid output 2.7 mEq/hour, peak acid output 14 mEq/hour) with a corresponding fall in gastrin to 70 pg/ml. However, prednisolone caused hyperglycemia even at a reduced dose of 10 mg/day. It was replaced by a standard estrogen-progesterone pill (loestrin 30) containing 30 mcg of ethinyl estradiol and 1.5 mg of norethisterone taken daily for 3 weeks each month. After an endoscopic antral biopsy she received 4 units of blood, but otherwise maintained her hemoglobin concentration on iron alone over this period with a considerable reduction in gastrointestinal bleeding.
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PMID:Gastric antral vascular ectasia: maintenance treatment with oestrogen-progesterone. 161 93

Eradication of Helicobacter pylori is associated with a fall in serum gastrin but the way in which the infection raises the serum gastrin concentration is not clear. It may be related to the ammonia produced by the bacterium's urease stimulating gastrin release by the antral G cells. Alternatively, the antral gastritis induced by the infection may modify the regulation of gastrin release. We have examined serum gastrin in 10 patients before and 24 hours after starting triple anti-H pylori treatment consisting of tripotassium dicitrato bismuthate 120 mg four times daily, metronidazole 400 mg three times daily, and amoxycillin 500 mg three times daily. The urease activity, assessed by the 20 minute value of the 14C-urea breath test, fell from a median of 176 (range 116-504) kg% dose/mmol CO2 x 100 pretreatment to 5 (2-15) at 24 hours (p less than 0.005). The median antral gastritis score was 6 (4-6) pretreatment and fell to 3 (2-5) at 24 hours (p less than 0.02), and this was due to resolution of the polymorphonuclear component. Despite this complete suppression of bacterial urease activity and partial resolution of antral gastritis the median basal gastrin concentration remained unchanged, being 57 ng/l (45-77) pretreatment and 59 ng/l (45-80) at 24 hours and the median integrated gastrin response to a standardised meal was also unaltered, being 4265 ng/l/min (range 1975-8350) and 4272 ng/l/min (range 2075-6495) respectively. These findings do not support a causal association between H pylori urease activity and hypergastrinaemia and show rapid improvement of antral gastritis after starting anti-H pylori treatment.
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PMID:Is Helicobacter pylori associated hypergastrinaemia due to the bacterium's urease activity or the antral gastritis? 175 56

The mechanism of the hypergastrinaemia associated with Helicobacter pylori infection is unknown. It may be an effect of the ammonia produced by the bacterium near the antral epithelial surface. We have examined the effect on serum gastrin of inhibiting H pylori urease activity with acetohydroxamic acid in six duodenal ulcer patients. On day 1 the fasted patients received placebo tablets at 8 am, a peptide meal at 10 am, and a 14C urea breath test at 11.30 am. The next day 750 mg acetohydroxamic acid was administered orally in place of the placebo. The median (range) 30 minute breath test value (dose/mmol CO2 X kg body wt X 100) was 152 (111-335) on day 1, but only 22 (14-95) the next day (p less than 0.03). Further studies performed in one subject confirmed that acetohydroxamic acid lowered the ammonium concentration and raised the urea concentration in gastric juice. The inhibition of urease activity and ammonia production did not result in a fall in the basal gastrin concentration or in the median integrated gastrin response to the peptide meal, which was 78 ng/1.h (range 21-222) on day 1 and 79 ng/1.h (33-207) the next day. Ten days after acetohydroxamic acid, the urea breath test values were similar to those before treatment. This study shows that the raised gastrin concentration in patients with H pylori infection is not directly related to the organism's urease activity. It also shows that temporary suppression of H pylori urease activity does not clear the infection.
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PMID:Effect of inhibition of Helicobacter pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer subjects. 188 67

In a prospective study, eight young healthy subjects (five with an active H. pylori infection in the antral mucosa) were treated with a course of tripotassium dicitrato bismuthate, amoxycillin and metronidazole. The triple therapy eradicated infection when assessed 20-24 weeks later by antral biopsy (urease, histology, and 13C urea breath test [4 out of 5 subjects]). Twenty-four hour intragastric acidity and plasma gastrin concentration were measured before treatment, and 4-6 weeks and 20-24 weeks post-treatment. Treatment did not affect acidity in either the H. pylori-positive or H. pylori-negative groups, nor did it affect the plasma gastrin profile in the H. pylori-negative group. Eradication of H. pylori infection in five subjects caused a drop of the median integrated 24-hour plasma gastrin concentration from 558 pmol.h/L before treatment to 307 and 289 pmol.h/L at 4-6 and 20-24 weeks post-treatment, respectively. It is concluded that H. pylori infection is associated with 24-hour hypergastrinaemia, and that in apparently healthy subjects normal gastric physiology can be restored by eradication of the infection.
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PMID:Eradication of Helicobacter pylori abolishes 24-hour hypergastrinaemia: a prospective study in healthy subjects. 188 27

Continuous haemofiltration (CHF) mimics physiological glomerular filtration. Blood flows through a haemofilter, which is permeable to water and to all those substances not bound to plasma proteins, of up to about 6,000 d molecular weight. Ten to twenty liters of ultrafiltrate (UF) can be filtered daily. Solute concentration in this UF is very similar to that in plasma water. Because of the large volumes involved, the UF must be replaced continuously with an electrolyte solution. Electrolyte and acid-base disturbances can thus be easily and rapidly corrected. There are different techniques of CHF. Continuous arteriovenous haemofiltration (CAVH) avoids the use of an external blood pump, as the patient's own arterial pressure is used to drive the blood through the filter via a large-bore arterial catheter. On the other hand, continuous venovenous haemofiltration (CVVH) requires the use of a blood pump with a pressure alarm and an air bubble detector. Supplementary diffusive transport [CAVH(D),CVVH(D)] can improve the clearance of low molecular weight toxins, such as urea. In these techniques, there is a continuous flow of dialysate in the UF compartment of the haemofilter. One of the major problems with CHF is the anticoagulation of patients who are at risk of developing haemorrhagic complications. Unfractionated heparin is used most often, but other drugs have been used: low molecular weight heparin, prostacyclin, nafamostat, or sodium citrate. The neutralization of heparin has also been suggested. Because the fluid balance can be easily managed by CHF, patients in acute renal failure can be given standard intravenous feeding. Many small endogenous molecules, such as gastrin, are probably removed by CHF. However, most drugs have a molecular weight less than 6,000 d, and are not totally protein-bound. They are therefore likely to be ultrafiltered, and so, become inefficient. As a result, the drugs used should be adapted to the haemofilter, and vice versa. More than any extracorporeal circulation, CHF increases the incidence of bacterial blood contamination, because of its continuous use. Routine blood cultures should be carried out. Moreover, blood is cooled during its passage in the extracorporeal circuit, leading to hypothermia. There are some devices which prevent this. Renal function can be completely replaced with the production of 12 to 15 l UF a day. CHF must be started early on in the course of the renal failure. When the concentration of blood urea is greater than 40 mmol.l-1 diffuse transport must also be used.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Continuous hemofiltration: an extrarenal filtration method used in intensive care]. 192 60

We studied histologically antral biopsies from 89 consecutive patients with chronic renal failure for Helicobacter pylori (previously Campylobacter pylori). A dose-response gastric secretion test was also performed. The frequency of Helicobacter-positive subjects was low (15/89, 17%), corresponding to figures reported in the literature for young symptomless volunteers. Helicobacter-positive patients had significantly more frequently upper gastrointestinal symptoms than Helicobacter-negative individuals (P less than 0.05). Antral gastritis was more common in the Helicobacter-positive than in the Helicobacter-negative renal patients (P less than 0.01), but the incidence of body gastritis did not differ between them. The Helicobacter-positive patients had lower serum urea levels (P less than 0.01) and higher acid outputs (P less than 0.001) than Helicobacter-negative subjects. All patients had raised fasting serum gastrin levels, which possibly obscured the difference between Helicobacter-positive (283 pg/ml) and -negative (331 pg/ml) patients. We conclude that in chronic renal failure gastric colonization of Helicobacter pylori is not more frequent than usual. It correlates positively with antral gastritis, gastric acid output and upper gastrointestinal symptoms, but negatively with serum urea levels.
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PMID:Gastric Helicobacter and upper gastrointestinal symptoms in chronic renal failure. 193 Sep 36


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