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 brain oedema, distribution space (DS) and brain uptake index (BUI), of L-glucose, inulin, B12 vitamin and of three polypeptidic hormones of increasing molecular weight (angiotensin-I, gastrin and insulin) were measured in the rat after sham operation, porto-caval shunt (PCS) or liver ischaemia. At an early stage following PCS or liver ischaemia brain oedema was not constant, and was only demonstrable after liver ischaemia in a large number of animals. Substances without an active transport and with a low diffusion coefficient such as L-glucose and inulin had a very low BUI, unchanged even if the 3H2O brain content or the DS were modified. B12 vitamin, DS and BUI were very high and did not change after liver ischaemia or PCS. Insulin DS and BUI were low in the three groups of animals, whereas it decreased after PCS for gastrin. A significant increase of BUI and DS (without any cerebral oedema) was demonstrated for angiotensin-I, a polypeptidic hormone of molecular weight 1300. This polypeptidic marker is in the same range of MW as the preliminary recently recognized medium-sized molecules which may be involved in the pathogenesis of encephalopathy during experimental acute liver failure. However, not only the MW, but the nature of such polypeptides may be of importance in the genesis of this limited impairment of BBB permeability.
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PMID:Early changes in blood-brain barrier permeability after porto-caval shunt and liver ischaemia. 688 42

Clinical and laboratory results are presented of 229 patients treated by highly selective vagotomy for duodenal ulcer in a non-university teaching hospital. Sixty-two per cent of the operations were performed by residents as part of their training. After 1-8 years follow-up (97 per cent complete) there were 22 recurrences (9.6 per cent). The residents had fewer recurrences than the consultants, but their patients follow-up was shorter. The usual Visick grading is presented (1, 2: 83.5 per cent; 3, 4: 16.5 per cent) as well as an additional way of grading described by Visick in 1948 which suggests that 4 per cent appear to be permanent failures. Mortality rate was 0.4 per cent, complications rate was low and side effects were in general of minor importance. Laboratory results are presented showing that the basal acid output (BAO) was reduced permanently by 65 per cent, and the PAO by 50 per cent. In patients with recurrences BAO was not reduced and the PAO was less reduced than in the non-recurrence group. Metabolic parameters did not deteriorate. Basal serum gastrin rose after operation while serum vitamin B12 remained constant with a minimal tendency to decrease.
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PMID:Results of highly selective vagotomy in a non-university teaching hospital. 712 46

Thirteen persons with normal pentagastrin-stimulated gastric H+ secretion and 17 with achlorhydria were studied with a liquid test meal after an overnight fast. Blood was drawn before and every 30 min for 180 min after start of the meal. Serum gastrin, serum PG I, and serum vitamin B12 were determined by radioassay methods. Serum PG I was significantly lower in the achlorhydric subjects than in the normal secretors. The meal induced a slight and late rise in serum PG I in the control group. In contrast, the meal caused a slight fall in the achlorhydric persons. Basal serum gastrin was significantly higher in the achlorhydric group, in whom the meal also caused a significant fall in serum gastrin, which contrasts sharply with the rise in the control group. Although serum gastrin fell significantly in the achlorhydric group, a meal-induced rise in serum gastrin was observed in some of the achlorhydric subjects with basal serum gastrin below 100 pmol/l. Serum vitamin B12 was reduced in 8 of the 17 persons with achlorhydria, and in these 8 subjects serum PG I was significantly lower than in those with achlorhydria and normal serum vitamin B12.
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PMID:The effect of a test meal on serum group I pepsinogens (PG I) and serum gastrin in persons with normal gastric H+ secretion and in persons with achlorhydria. 743 84

We have measured the serum gastrin response to feeding in 3 groups of achlorhydric patients, and have compared the results with those of 12 normal controls. An increased postprandial serum gastrin response was found in 6 of 8 patients with hypergastrinemia and pernicious anemia, in all 10 patients with hypergastrinemia and normal absorption of vitamin B12, and in 2 of 7 achlorhydric patients with normal fasting serum gastrin levels. A reduced serum gastrin response to feeding was found in 2 patients with pernicious anemia and very high basal serum gastrin levels of 3,010 and 3,800 pg/ml, and in one achlorhydric patient with normogastrinemia. The remaining 4 patients with achlorhydria and normogastrinemia had normal postprandial serum gastrin responses. It is concluded that the serum gastrin response to feeding in patients with achlorhydria is heterogeneous.
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PMID:Serum gastrin response to feeding in achlorhydric patients. 746 96

Age and close living conditions are known to be risk factors for the acquisition of Helicobacter pylori (HP) infection. It is unknown whether institutionalization of asymptomatic, elderly subjects is an additional risk factor and whether gastric function and nutritional status are affected by the HP infection. The study sample comprised 102 subjects over 65 years of age: 52 living in a nursing home and 50 at home. No subject had symptoms or previous pathology related to the upper digestive tract. In all subjects, serum levels of specific anti-HP antibodies were determined. Gastric function was evaluated by levels of pepsinogen A (PGA), pepsinogen C (PGC) and gastrin. The nutritional status of the subject was evaluated by measuring: albumin, haemoglobin, iron, ferritin, transferrin, vitamin B12, and folic acid in blood, and body mass index and mid-arm muscle area. The prevalence of anti-HP antibodies was 86.5% in institutionalized subjects (men: 100%; women:76.6%, p <0.05) and 82.0% in subjects living at home (men:86.3%; women:76.3%). No differences between the two groups were observed in levels of serum anti-HP antibodies and PGC was identified. In neither group were differences observed between serum positive (HP + ve) and negative (HP - ve) subjects with respect to the biohumoral and anthropometric indices of nutritional status. We conclude: (1) the seroprevalence of the HP infection was high (82-86%) in asymptomatic elderly patients living either at home or in an institution; (2) the presence of specific IgG anti-HP antibodies in asymptomatic elderly individuals, at home or in a nursing home, was not associated with changes in PGA levels in institutionalized subjects; (3) nutritional indices were not influenced by the presence of anti-HP antibodies.
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PMID:Helicobacter pylori infection in asymptomatic elderly subjects living at home or in a nursing home: effects on gastric function and nutritional status. 867 May 62

Cobalamin (vitamin B12) is an essential nutrient derived exclusively from bacterial sources. It is an essential cofactor for three known enzymatic reactions. Untreated deficiency, caused by either the autoimmune disease pernicious anemia or nutritional lack, results in a macrocytic anemia and/or subacute combined degeneration of the spinal cord and is eventually fatal. Cobalamin in serum is bound to two proteins, transcobalamin and haptocorrin. The former is responsible for the essential delivery of cobalamin to most tissues. Inadequate tissue availability of cobalamin results in increased concentration of methylmalonic acid and homocyst(e)ine due to inhibition of methylmalonyl-CoA mutase and methionine synthase, respectively. Strict vegetarians have long been known to be at risk of cobalamin deficiency, which develops insidiously over many years. It is now clear that a significant number of the elderly and HIV-positive individuals are also at increased risk of deficiency. Any individual with reduced ability to split cobalamin from food-protein may also become deficient even though intrinsic factor is present. Diagnosis of cobalamin deficiency has frequently relied on total serum cobalamin and the Schilling test. Newer approaches such as analysis of methylmalonic acid, homocyst(e)ine, holotranscobalamin, anti-intrinsic factor antibodies, and serum gastrin may provide more cost-effective testing, as well as identify those with a covert deficiency.
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PMID:Cobalamin. 887 26

Cobalamin (vitamin B12) deficiency is more common in the elderly than in younger patients. This is because of the increased prevalence of cobalamin malabsorption in this age group, which is mainly caused by (autoimmune) atrophic body gastritis. Cobalamin supplementation is affordable and nontoxic, and it may prevent irreversible neurological damage if started early. Elderly individuals with cobalamin deficiency may present with neuropsychiatric or metabolic deficiencies, without frank macrocytic anaemia. An investigation of symptoms and/or signs includes the diagnosis of deficiency as well as any underlying cause. Deficiency states can still exist even when serum cobalamin levels are higher than the traditional lower reference limit. Cobalamin-responsive elevations of serum methylmalonic acid (MMA) and homocysteine are helpful laboratory tools for the diagnosis. The health-related reference ranges for homocysteine and MMA appear to vary with age and gender. Atrophic body gastritis is indirectly diagnosed by measuring serum levels of gastrin and pepsinogens, and it may cause dietary cobalamin malabsorption despite a normal traditional Schilling's test. The use of gastroscopy may also be considered to diagnose dysplasia, bacterial overgrowth and intestinal villous atrophy in healthy patients with atrophic body gastritis or concomitant iron or folic acid deficiency. Elderly patients respond to cobalamin treatment as fully as younger patients, with complete haematological recovery and complete or good partial resolution of neurological deficits. Chronic dementia responds poorly but should, nevertheless, be treated if there is a metabolic deficiency (as indicated by elevated homocysteine and/or MMA levels). Patients who are at risk from cobalamin deficiency include those with a gastrointestinal predisposition (e.g. atrophic body gastritis or previous partial gastrectomy), autoimmune disorders [type 1 (insulin-dependent) diabetes mellitus and thyroid disorders], those receiving long term therapy with gastric acid inhibitors or biguanides, and those undergoing nitrous oxide anaesthesia. To date, inadequate cobalamin intake has not proven to be a major risk factor. Intervention trials of cobalamin, folic acid and pyridoxine (vitamin B6) in unselected elderly populations are currently under way.
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PMID:Age-related changes in cobalamin (vitamin B12) handling. Implications for therapy. 957 92

Chronic atrophic corpus gastritis, termed as autoimmune corpus gastritis or type A gastritis, and primary biliary cirrhosis (PBC) are characterized by a common immunological process against the exocrine glandular structures of both the stomach and bile duct. However, there has been controversy over whether atrophic corpus gastritis is associated with PBC. Recently, it has been suggested that Helicobacter pylori plays an important role in the early stage of atrophic corpus gastritis due to the induction of autoantibodies that are reactive with a protein in the gastric parietal cells. One hypothesis is that molecular mimicry, possibly resulting from H. pylori infection, might be responsible for initiating an autoimmune response in a predisposed host due to cross-reactivity among gastric mucosal, bile ductular, and bacterial antigens. The aim of this study is to assess whether atrophic changes of the gastric corpus could affect patients with PBC, and to determine the correlation with H. pylori infection. Sixteen patients with PBC were enrolled in this study. All patients were examined by serological studies of anti-pyruvate dehydrogenase (PDH) antibody, anti-H. pylori antibody, gastrin and vitamin B12. Gastroscopy was performed on all patients in order to verify the histological findings and to microscopically identify H. pylori. Atrophic corpus gastritis was found in 2 of 16 patients with PBC (12.5%), one of whom was confirmed to have pernicious anemia, a developed stage of atrophic corpus gastritis. H. pylori infection in the gastric corpus and the anti-H. pylori antibody were found in 7 (43.8%) and 11 (68.8%) of 16 patients, respectively. Anti-H. pylori antibody was confirmed to be positive in both of the patients with atrophic corpus gastritis, although H. pylori was absent in the gastric biopsy specimen. There was a positive correlation between anti-PDH antibodies and anti-H. pylori antibodies in sera from patients with PBC. Atrophic corpus gastritis is not frequently involved in PBC. However, H. pylori is a possible pathogenic factor in atrophic corpus gastritis in PBC patients because of the presence of anti-H. pylori antibody. A positive correlation between the titer of anti-PDH antibodies and the titer of anti-H. pylori antibodies was confirmed. Consequently, H. pylori infection could induce autoimmune responses in the development of both PBC and atrophic corpus gastritis. H. pylori infection associated with PBC requires further study.
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PMID:Atrophic corpus gastritis and Helicobacter pylori infection in primary biliary cirrhosis. 1183 19

The classic workup of a patient for possible PA is revisited in light of the vanishing Schilling test. The vagaries of testing for B12 and blocking antibodies are reexamined. The advantages and disadvantages of newer tests such as MMA and serum gastrin levels are catalogued. At this juncture in the evolution of new test strategies, there is a considerable controversy regarding the significance of high MMA levels in the face of normal B12 levels, particularly in the elderly. Hopefully, this controversy will soon be resolved and the newer crop of tests will be proven and accepted in the workplace. Still, the words of Alexander Pope spring to mind: "Be not the first by whom the new are tried, Nor yet the last to lay the old aside."
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PMID:Modern approaches to the investigation of vitamin B12 deficiency. 1213 70

Glucagonoma of the pancreas is a rare tumor with distinct clinical manifestations, such as necrolytic migratory erythema,weight loss, anemia, diabetes mellitus, and hypoamino-acidemia. We report the case of a 68-year-old Japanese man who underwent curative resection for malignant glucagonoma of the pancreas diagnosed through anemia and diabetes mellitus. The patient had had diabetes mellitus for 20 years. Anemia was diagnosed in 1998. On admission, the hemoglobin level was 8.3g/dl, but the levels of serum iron, vitamin B12, and erythropoietin and, the number of reticulocytes were within normal limits. The levels of carcinoembryonic antigen (CEA), carbohydrate antigen (CA)19-9, and DUPAN-2 were also within normal limits, and exocrine function of the pancreas (PFD, 75%) was normal. Ultrasonography (US) revealed a hypoechoic tumor in the distal pancreas. Computed tomography (CT) demonstrated a high-density area 4 cm in diameter with calcification. The serum glucagon level was very high (2360 pg/ml), but the levels of other hormones such as somatostatin or gastrin were within normal limits, while insulin was low. Glucagonoma of the pancreas was diagnosed, and distal pancreatectomy with splenectomy was performed. Histological examination revealed a malignant endocrine tumor,which was immunohistochemically positive for chromogranin A and glucagon. Two months after the operation, the serum glucagon level had decreased to within normal limits and the hemoglobin level had increased to 10.4 g/dl. The case of glucagonoma reported here was found through diagnostic examinations of anemia and treated by surgical resection, by which the patient's anemia was largely alleviated. Therefore, we recommend checking patients who have diabetes mellitus and anemia in order to diagnose and treat glucagonoma in its early stage.
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PMID:Malignant glucagonoma of the pancreas diagnoses through anemia and diabetes mellitus. 1291 65


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