Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

34 subjects including 5 probands with pernicious anemia, 3 probands with severe atriphic body gastritis and 26 of their first-degree relatives were studied gastroscopically, bioptically, functionally and immunologically. In general, members of the same family revealed a trend to behave similarly with respect to the parameters studied. Signs of A-gastritis (severe atrophy of gastric body glands with a normal or almost normal antrum, achlorhydria, hypergastrinemia and parietal cell antibodies), with intrinsic factor antibodies in the gastric juice and diminished intrinsic factor secretion without anemia were found both in families of probands with atrophic gastritis and pernicious anemia. This suggests a close etiopathogenetic relation of this type of mucosal lesion to overt pernicious anemia. Determination of HCl output and serum gastrin level enabled us to distinguish two differently behaving subgroups in the series, one of them with characteristics of overt adult pernicious anemia. Very low intrinsic factor secretion was found almost exclusively in connection with the presence of intrinsic factor antibodies in the gastric juice and always with severe atrophy of gastric body glands.
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PMID:Gastric lesion and pernicious anemia: a family study. 63 45

Many alterations in metabolic and endocrine function occur in end-stage renal disease. Glucose intolerance is almost always present with uremia; it improves shortly after institution of regular hemodialysis. Hyperlipidemia (type IV) is prevalent, and atherosclerotic cardiovascular disease causes death in about 50% of patients receiving long-term hemodialysis. Although plasma levels of growth hormone usually are elevated, children with chronic renal failure show growth retardation. The occurrence of thyroid disorders is difficult to determine, since many clinical features of uremia are similar to those of hyperthyroidism and hypothyroidism. The incidence of duodenal ulcer is high, possibly due to high gastrin levels. Sex hormone disturbances are common. Anemia is a constant feature of chronic renal failure; patients usually tolerate it well.
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PMID:Metabolic and endocrine alterations in end-stage renal failure. 71 39

Several haematological findings (especially the values of serum LDH and its isoenzymes) were compared with changes in the gastrin level in pernicious anaemia. While vitamin B12 substitution therapy led to normalization of the anaemia and of the enzyme levels, gastric atrophy and, hence, the elevation in serum gastrin levels remained unchanged. Determination of serum gastrin, therefore, provides a valuable tool for the verification of the diagnosis of pernicious anaemia in treated cases.
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PMID:[LDH isoenzymes and gastrin in achlorhydri (author's transl)]. 96 Jul 4

A pathophysiological role of gastrin has been established only in the Zollinger-Ellison-Syndrome. Hypergastrinemia may be found in cases with prenicious anemia, atrophic gastritis and after all forms of vagotomy; furthermore in the excluded antrum syndrome, the short bowel syndrome, in renal insufficiency, pyloric stenoses and after oral or parenteral administration of calcium. The role of gastrin in the pathogenesis of duodenal ulcer is unknown.
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PMID:[Gastrin in internal medicine]. 96 Sep 55

Synthetic salmon calcitonin (sCT, doses of 0.7 Medical Research Council U per kg) was injected into nine normal subjects and three patients with hypergastrinemia (pemicious anemia). sCT depressed basal as well as food-stimulated serum gastrin concentrations without concomitant changes in total and ultrafiltrable concentrations of calcium in serum. Gel filtration of sera revealed that sCT reduced mainly the small components, III (gastrin-17 or "little" gastrin) and IV (gastrin-13 or "mini"-gastrin).
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PMID:Effect of calcitonin on serum gastrin concentration and component pattern in man. 117 Nov 12

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

The authors report here the results of prospective clinic study on 108 cases of the early stage of Gan-Zheng (infantile malnutrition) in children. It was proved that professor Zhan Qisun's tested recipe Sheng-Zhang-Ling(SZL) had an obvious effect in treating children with early stage of Gan-Zheng. The total effective rate was 90.2%, and the significantly effective rate was 60.79%. Various symptoms of patients using this prescription disappeared or improved. The increase of body weight, height and subcutaneous fat of these patients was faster than those of the blank control group and the group using zinc sulfate. The difference was statistically significant among those three groups. It was indicated that effects of the SZL group were not caused by children's natural growth and development. There was an obvious advantage over the zinc sulfate group with regard to clinical effects, side effects and total synthetic effects. It was concluded SZL is an effective prescription for curing patients with early stage of Gan-Zheng and stimulating children's growth and development. Hemoglobin, D-xylose in urine, serum gastrin, serum zinc ion were detected before and after the treatment. It was suggested that SZL had the effects to stimulate gastrointestinal secretion and absorption, to improve digestive function, to increase serum zinc ion and to cure anemia.
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PMID:[Early stage of gan-zheng in children treated with sheng-zhang-Ling]. 239 42

Simultaneous 24-hour intragastric acidity and plasma gastrin concentrations were measured in 12 duodenal ulcer patients before and on the twenty-eighth day of treatment with either ranitidine 150 mg b.d. or omeprazole 20 mg o.m. Median integrated 24-hour intragastric acidity was decreased significantly from 1148 to 490 and 36 mmol.hour litre-1 during treatment with ranitidine and omeprazole, respectively, whilst median intragastric 24-hour plasma gastrin was raised significantly from 328 to 799 and 1519 pmol.hour litre-1 respectively. When the results of all 48 experiments were considered together, there was a significant inverse correlation between the 24-hour integrated values for intragastric acidity and plasma gastrin concentration. Both drugs caused a significant elevation of plasma gastrin throughout the 24 hours, although ranitidine had no effect on intragastric acidity from 1900 to 2200 hours. When compared with similar profiles of acidity and gastrin in pernicious-anaemia patients, the modest elevations of plasma gastrin observed in this study suggest that neither drug will be associated with clinically relevant enterochromaffin-like cell proliferation in duodenal ulcer patients.
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PMID:Twenty-four-hour intragastric acidity and plasma gastrin concentration before and during treatment with either ranitidine or omeprazole. 297 26

Zollinger-Ellison syndrome and myelofibrosis were diagnosed concurrently in a 10-year-old neutered female Brittany Spaniel. Documentation of gastric ulceration, hypergastrinemia, and gastrin-secreting islet cell tumor with splenic metastases facilitated the diagnosis of Zollinger-Ellison syndrome. Patchy long-bone medullary sclerosis, nonregenerative anemia and thrombocytopenia, multiple acellular bone marrow aspirates, marked splenic extramedullary hematopoiesis, and acellular core bone marrow biopsy with areas of necrosis and fibrosis supported the diagnosis of myelofibrosis. Despite the medical and surgical management attempted, the dog was euthanatized because of signs of severe intractable bone pain. Myelofibrosis has been documented in association with canine and human neoplastic disease. A direct causal relationship between gastrinoma and myelofibrosis was not clearly established in this instance.
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PMID:Zollinger-Ellison syndrome and myelofibrosis in a dog. 339 36

The ratio of pepsinogen I to pepsinogen II in the circulation decreases progressively with increasing severity of atrophic gastritis of the fundic gland mucosa. Fasting blood was obtained from 359 free-living and institutionalized elderly people (age range, 60 to 99 years). A pepsinogen I/pepsinogen II ratio less than 2.9, indicating atrophic gastritis, was found in 113 (31.5%) subjects. The prevalence of atrophic gastritis increased significantly with advancing age (P less than .05). Within the atrophic gastritis group, 84 had a pepsinogen I level greater than or equal to 20 micrograms/L, indicating mild to moderate atrophic gastritis, and 29 had a pepsinogen I level less than 20 micrograms/L, indicating severe atrophic gastritis or gastric atrophy. A significant increase in the prevalences of elevated serum gastrin levels (P less than .005), low serum vitamin B12 levels (P less than .005), circulating intrinsic factor antibody (P less than .005), and anemia (P less than .025) was observed with stepwise increases in severity of atrophic gastritis. Subjects with atrophic gastritis exhibited a lower mean serum vitamin B12 level (P less than .05) and a higher mean folate level (P less than .05), but no difference was detected in mean hemoglobin levels or serum levels of iron, ferritin, retinol or alpha-tocopherol. It is concluded that serum pepsinogen I and pepsinogen II levels can be used to determine the prevalence and severity of atrophic gastritis, that atrophic gastritis is common in an elderly population, and that atrophic gastritis is associated with vitamin B12 deficiency and anemia. Further, higher folate levels in atrophic gastritis may be related to an accumulation of 5-methyl tetrahydrofolate in serum due to vitamin B12 deficiency and/or greater folate synthesis by the intestinal flora resulting from bacterial overgrowth secondary to hypo- or achlorhydria.
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PMID:Fundic atrophic gastritis in an elderly population. Effect on hemoglobin and several serum nutritional indicators. 377 80


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