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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Authors show and discuss the classification proposed till now for dividing chronic atrophic gastritis into subtypes different in hystological, functional or immunological aspects. In accordance with the more recent reports, the classification into type A, type B and type AB is accepted. Genetical (factor A) and environmental agents (alcohol, smoke, drugs) as well as immunological (parietal and gastrin cell antibodies) and functional abnormalities (duodenogastric reflux), suggested to play a role in the aetiopathogenesis of chronic atrophic gastritis, are also re-examined. Finally, dynamic aspects of chronic atrophic gastritis and its association with anemia and gastric carcinoma are widely reviewed.
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PMID:[Chronic gastritis: classification, etiopathogenesis and clinical course]. 397 17

The serum values of PG I and gastrin have been established in a normal population and in several clinical diseases. The PG I is raised in duodenal, gastric, and pyloric ulcer even though the gastrin is normal. Both PG I and gastrin values are raised in renal insufficiency and the Zollinger-Ellison syndrome. The PG I is lowered in atrophic gastritis and alcoholic cirrhosis, and is at the limit of detection in Biermer anemia and total gastrectomy. Insulin and sham-feeding are stimulants for PG I release by patients with duodenal ulcer, but no correlation is observed between PG I output and PAO in the studied group. The results show that PG I is able to distinguish between associated hypergastrinemia and hypoacidity (Biermer anemia type) or a hyperacidity (Zollinger-Ellison syndrome type), and that PG I is a good indicator for gastric hypoacidity. Overlapping between normal and ulcer subjects is comparable to those obtained in acid output determinations.
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PMID:[Clinical value of determining pepsinogen I]. 651 84

Eleven adult Basenji dogs with immunoproliferative small intestinal disease (IPSID) were studied. Two items of history related to the digestive tract were characteristic: (i) chronic intractable diarrhea in most dogs, and (ii) progressive emaciation. Anorexia was intermittent in only a few dogs. In addition, skin lesions of various degrees of severity were observed, including alopecia of pinnae and ventrum, hyperpigmentation and hyperkeratosis of pinnae, and necrosis and ulcerations of margins of pinnae. The cause of the skin lesions was not determined; however, hypothyroidism did not appear to contribute to the skin changes. Standard hematologic and serum chemical values were not consistently abnormal. However, a poorly regenerative anemia, mild neutrophilia, and increased aspartate aminotransferase and alanine aminotransferase activities were generally observed in severely affected dogs. The Pelger-Huet anomaly was identified in dog 3. Maldigestion and malabsorption as determined by the N-benzoyl-L-tyrosyl-p-aminobenzoic acid and d-xylose test was documented to varying degrees in dogs with IPSID. Maldigestion was correlated with functional pancreatic exocrine insufficiency. Severe malabsorption was documented in only 3 dogs. Serum gastrin values were evaluated in these dogs because of a prior observation of parietal cell hyperplasia and gastric ulceration. Hypergastrinemia was documented in 3 dogs. Additional studies will be necessary to determine whether an acid hypersecretory state contributes to the pathogenesis of IPSID in Basenjis.
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PMID:Clinical and laboratory characterization of Basenjis with immunoproliferative small intestinal disease. 660 87

Gastric endoscopy of a 40 year old woman suffering from ill-defined epigastralgy revealed a carcinoid tumor apparently located at the mucous membrane. The tumor was neither argyrophil nor argentaffin. Immunohistochemical tests for VIP, gastrin and serotonin were negative. Biological examinations indicated hypochrome anemia and hypergastrinemia (greater than 800 pg/ml). The excision was completed by a gastrectomy of 2/3 with a Pean anastomosis. No residual tumor was detected but the fundic mucous membrane showed considerable atrophic gastritis together with a marked hyperplasia of endocrine cells giving an aspect of microcarcinoidosis. Immunohistochemical studies showed that most of the cells produced serotonin while a few cells produced gastrin or VIP. Control biopsies of the stump showed similar hyperplasia of the endocrine cells and ultrastructural studies confirmed the polymorphism of the islets. The present observation is compared to analogous cases cited in the literature. The pathogenic mechanism possibly linked to the capacity of gastrin in stimulating endocrine cells is discussed. The prognosis in these carcinoid tumors appears to be the same as in other gastric carcinoid tumors. In particular, a recent observation (Goldman et al., 1981) illustrated their aptitude to lead to metastases.
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PMID:[Chronic atrophic gastritis with carcinoid tumor and microcarcinoidosis. Report of a case with immunohistochemistry and ultrastructure study]. 662 98

Billroth II resection was carried out in 1000 duodenal ulcer patients in the period 1948-1956. Twenty-two to thirty years later, gastroscopy and biopsy was performed in 196 of 423 survivors. Chronic atrophic gastritis appeared in 93 per cent of the cases, 47 per cent showed slight and 46 per cent severe changes. Seven per cent had normal mucosa. The microscopic grade of gastritis proved to be independent of age, alcohol and tobacco consumption and serum gastrin. No correlation between clinical status, such as dumping, diarrhoea, vomiting and pain, haematological parameters and the microscopic grade of gastritis, could be found. It is suggested that gastritis might be caused by reflux of bile, pancreatic and intestinal juices, and that postgastrectomy symptoms and anaemia do not depend on the microscopic grade of gastritis.
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PMID:Causes and clinical significance of gastritis following Billroth II resection for duodenal ulcer. 686 Sep 6

The clinical features, the results of gastric secretory function tests, and the duodenojejunal morphology of six infants (aged 0.42-1.23 years) with anemia and melena considered to be due to latent cow's milk intolerance (LCMI) were compared with the findings in nine infants (aged 0.19-0.87 years) with cow's milk-induced malabsorption (CMI). The infants with LCMI had a short period of breast feeding, normal weight gain without symptoms of malabsorption, and no atopic history. The maximal acid secretion was decreased (p < 0.01) and the concentration of fasting serum gastrin raised (p < 0.01) compared with the controls. Gastric biopsy revealed epithelial degeneration in three and erosion in one out of four samples. The duodenojejunal biopsy revealed slight changes in two samples, the others being normal. The number of eosinophils was increased in four out of six biopsies. Although the number of intraepithelial lymphocytes was increased in LCMI the rise was not as significant as in children with CMI (p < 0.05). We conclude from our results that LCMI seems to be a seperate clinical entity. The determination of fasting serum gastrin, maximal gastric acid secretion and intraepithelial lymphocytes on duodenojejunal biopsy appear to be helpful in making the diagnosis.
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PMID:Cow's milk intolerance with melena. 744 1

Cobalamin deficiency must be suspected in all patients with unexplained neuropsychiatric symptoms or unexplained anemia. Special attention should be paid to patients at risk of developing cobalamin deficiency such as elderly people, vegetarians, HIV-infected patients, patients with gastrointestinal diseases and patients with autoimmunity or a family history of pernicious anemia. The assays aimed to answer the question: does this patient suffer from cobalamin deficiency, include analysis of P--cobalamins and analyses of the metabolites that accumulate upon cellular cobalamin deficiency, P--methylmalonate and P--homocysteine. P--cobalamins or especially a fraction of P--cobalamins, P--TC cobalamins are markers for latent cobalamin deficiency. An increased concentration of P--methylmalonate that decreases upon injection of cobalamin indicates overt metabolic cobalamin deficiency. The same holds for P--homocysteine but this analysis is less specific than P--methylmalonate. We suggest that either assay of P--cobalamins or P--methylmalonate is employed as screening test for cobalamin deficiency, and that further tests are performed only if the initial test in combination with the clinical picture gives an unclear answer. Once cobalamin deficiency has been diagnosed, the cause for the deficiency should be sought and the patient should be treated for life. Cobalamin absorption tests such as the Schilling test are considered of limited use. Gastric atrophy is likely to be present in patients with increased P--gastrin or decreased P--pepsinogen A. However, this condition can be diagnosed also by upper gastrointestinal endoscopy.
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PMID:How to diagnose cobalamin deficiency. 770 Dec 43

The etiology, prognosis, and optimal management of primary gastric carcinoids remain controversial. Records of 36 consecutive patients with gastric carcinoid (15 men) were reviewed retrospectively between 1975 and 1990. Follow-up was complete in 97% of cases. Mean age at diagnosis was 58.4 years (range 24-82 years). The clinical presentations included anemia (72%), pain (69%), and carcinoid syndrome (11%). Associated autoimmune and endocrine abnormalities were common and included atrophic gastritis (67%), pernicious anemia (58%), hypothyroidism (39%), diabetes (19%), Addison's disease (6%), and hyperparathyroidism (6%). Lesions were nonantral in 78%, involving only the corpus in 42%, the fundus in 28%, and only the antrum in 8%; 42% were multiple. Urinary 5-hydroxyindoleacetic acid (5-HIAA) and serum gastrin levels were elevated in 17% and 50% of those tested, respectively. Histologic examination revealed that 28% of lesions were > or = 2 cm, and 33% had liver metastases on presentation or developed them during follow-up. Eight patients (22%) died of tumor with a median survival of 39 months. The presence of metastases, atypical histology, serosal involvement, and size > 2 cm were adverse prognostic factors. In patients without hypergastrinemia (n = 6), 66% developed metastases, 60% had elevated 5-HIAA, and 50% died of carcinoid tumor. In sharp contrast, those patients with hypergastrinemia and "typical" gastric carcinoids (n = 15), metastases and death did not occur (p < 0.003 and p < 0.005, respectively, compared with eugastrinemic patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diverse clinical and pathologic features of gastric carcinoid and the relevance of hypergastrinemia. 772 31

As already reported short-term rHuEpo treatment influences plasma insulin, glucagon, pancreatic polypeptide (PP), and gastrin secretion in haemodialysed patients. The present study aimed to assess the influence of long-term rHuEpo treatment on secretion of above mentioned hormones. A total of 27 haemodialysed patients and nine healthy subjects were examined. Nine patients with uraemic anaemia were treated with rHuEpo for 12 months (Epo group) while another nine patients did not receive rHuEpo (non-Epo group), but were monitored biochemically and clinically as patients of the Epo group. The third group (HD) comprised nine haemodialysed patients with a haematocrit value of > or = 30% without rHuEpo therapy. In all subjects plasma levels of insulin, glucagon, gastrin, and PP were estimated before and after administration of a test meal. Patients of the Epo group were examined before and after 6 and 12 months of rHuEpo treatment (patients of the Epo group) or clinical monitoring (patients of the non-Epo group) respectively, while only one test was performed in patients of the HD group and healthy subjects. Six months of rHuEpo treatment was followed by an increase of fasting insulinaemia and a decrease of basal plasma level of glucagon and PP. At that time point rHuEpo therapy also increased the response of insulin, glucagon, and gastrin to the test meal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of long-term erythropoietin treatment on insulin, glucagon, pancreatic polypeptide, and gastrin secretion in haemodialysed patients. 807 22

The study aimed to assess the influence of long-term rhu-EPO treatment on secretion of pancreatic polypeptide (PP) and gastrin. A total of 27 haemodialysed patients and nine healthy subjects were examined. Nine patients with uraemic anaemia were treated with rhu-EPO for 12 months (EPO group), while another nine patients did not receive rhu-EPO (non-EPO group), but were monitored biochemically and clinically as patients of the EPO group. The third group (HD) comparised nine haemodialysed patients with a haematocrit value > or = 30% without rhu-EPO therapy. In all subjects plasma levels of PP and gastrin were estimated before and after administration of a test meal. Patients of the EPO and non-EPO group were examined before and after 6 and 12 months of rhu-EPO therapy (EPO group) or clinical monitoring (non-EPO group) respectively, while only one test was performed in patients of the HD group and healthy subjects. Six months rhu-EPO therapy was followed by an decrease of basal plasma level of PP and increased response of gastrin to the test meal. After 12 months of rhu-EPO therapy basal plasma level of PP was still lower, the response of PP secretion to a test meal was higher, while that of gastrin secretion lower that the pretreatment ones. Our results suggest, that rhu-EPO treatment exerts effect on secretion of PP and gastrin. These alterations seem not to be related to improvement of the haematological status.
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PMID:[Influence of long-term human recombinant erythropoietin treatment on secretion of pancreatic polypeptide and gastrin in hemodialysed patients with chronic renal failure]. 883 57


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