intrinsic-factor and Atrophy

Autoimmune atrophic gastritis (AAG) is a persistent, corpus-restricted immune-mediated destruction of the gastric corpus oxyntic mucosa with reduced gastric acid and intrinsic factor secretion, leading to iron deficiency and pernicious anemia as a consequence of iron and cobalamin malabsorption. Positivity toward parietal cell (PCA) and intrinsic factor (IFA) autoantibodies is very common. AAG may remain asymptomatic for many years, thus making its diagnosis complex and often delayed. Due to the increased risk of gastric neoplasms, a timely diagnosis of AAG is clinically important.. The gold standard for AAG diagnosis is histopathological assessment of gastric biopsies obtained during gastroscopy, but noninvasive, preendoscopic serological screening may be useful in some clinical scenarios. Serum biomarkers for AAG may be divided into 2 groups: gastric autoimmunity-related biomarkers, such as PCA and IFA, and gastric corpus atrophy/reduced gastric acid secretion-related biomarkers, such as serum gastrin and pepsinogens. The present review focuses on the clinical significance and pitfalls of serum biomarkers related to gastric autoimmunity and gastric corpus atrophy, including some discussion of analytical methods.. Serum assays for PCA, IFA, gastrin, and pepsinogen I show good diagnostic accuracy for noninvasive diagnostic work-up of AAG. Diagnostic performance may increase by combining >1 of these tests, overcoming the problem of seronegative AAG. However, appropriately designed, comparative studies with well-characterized patient cohorts are needed to better define the reliability of these biomarkers in the diagnosis of patients with AAG. Currently, positive serum tests should always be followed by the state-of-art diagnostic test, that is, histopathological assessment of gastric biopsies obtained during gastroscopy to definitively confirm or rule out AAG and eventually neoplastic complications.

Topics: Atrophy; Biomarkers; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Intrinsic Factor; Reproducibility of Results

Combined medullary sclerosis developed suddenly postoperatively in a patient with unknown Biermer's disease. The neurological lesions were undoubtedly induced by nitrogen protoxide via an inactivation of vitamin B12.

Topics: 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Abscess; Aged; Anemia, Pernicious; Anesthetics, Inhalation; Arthroplasty, Replacement, Hip; Atrophy; Autoantibodies; Autoimmune Diseases; Demyelinating Diseases; Female; Gastric Mucosa; Humans; Intestinal Absorption; Intrinsic Factor; Nitrous Oxide; Oxidation-Reduction; Paresthesia; Postoperative Complications; Proprioception; S-Adenosylmethionine; Sclerosis; Spinal Cord; Spinal Cord Diseases; Surgical Wound Infection; Vitamin B 12

Topics: Adrenal Cortex Hormones; Adult; Anemia, Pernicious; Atrophy; Autoantibodies; Autoimmune Diseases; Binding Sites, Antibody; Child; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Immunity, Cellular; Immunoglobulin A; Immunoglobulin G; Intrinsic Factor; Vitamin B 12

Topics: Anemia, Pernicious; Antibodies; Atrophy; Autoimmune Diseases; Capillaries; Chronic Disease; Dyspepsia; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Hypertrophy; Intrinsic Factor; Metaplasia; Mitosis; Pentagastrin; Pepsin A; Peptic Ulcer; Pyloric Antrum; Radiography; Stomach; Stomach Neoplasms; Thyroid Diseases; Vagotomy

Topics: Acetylcholine; Achlorhydria; Adenoma; Anemia, Pernicious; Atrophy; Duodenal Ulcer; Endocrine System Diseases; Gastrectomy; Gastric Juice; Gastric Mucins; Gastric Mucosa; Gastrins; Gastritis; Humans; Hyperplasia; Intrinsic Factor; Stomach Ulcer; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Age Factors; Anemia, Pernicious; Antibodies; Atrophy; Bethanechol Compounds; Carbachol; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Insulin; Intrinsic Factor; Methacholine Compounds; Vitamin B 12; Vitamin B 12 Deficiency

Topics: ABO Blood-Group System; Anemia; Anemia, Pernicious; Antibody Formation; Atrophy; Chemical Phenomena; Chemistry; Gastric Juice; Gastrointestinal Diseases; Gastrointestinal Neoplasms; Humans; Intrinsic Factor; Stomach

Parietal cell atrophy is considered to cause metaplasia in the stomach. We developed mice that express the diphtheria toxin receptor specifically in parietal cells to induce their death, and found this to increase proliferation in the normal stem cell zone and neck but not to cause metaplastic reprogramming of chief cells. Furthermore, the metaplasia-inducing agents tamoxifen or DMP-777 still induced metaplasia even after previous destruction of parietal cells by diphtheria toxin. Atrophy of parietal cells alone therefore is not sufficient to induce metaplasia: completion of metaplastic reprogramming of chief cells requires mechanisms beyond parietal cell injury or death.

Topics: Animals; Apoptosis; Atrophy; Azetidines; Cell Proliferation; Cellular Reprogramming; Chief Cells, Gastric; Diphtheria Toxin; Heparin-binding EGF-like Growth Factor; Intercellular Signaling Peptides and Proteins; Intrinsic Factor; Metaplasia; Mice; Parietal Cells, Gastric; Peptides; Piperazines; Plant Lectins; Stomach; Tamoxifen

Spasmolytic polypeptide (SP/TFF2)-expressing metaplasia (SPEM) is induced by oxyntic atrophy and is known as a precancerous or paracancerous lesion. We seek to determine whether the gastrin receptor or H(2) histamine receptor influence the development of SPEM. DMP-777 was administered to gastrin receptor and/or H(2) receptor-deficient mice and wild-type mice. Gastric mucosal lineage changes were analyzed. The mucosa from double knockout mice and H(2) receptor knockout mice contained elevated numbers of dual TFF2 and intrinsic factor immunoreactive cells even before DMP-777 treatment. All genotypes of mice showed SPEM after 7-day treatment. In all types of knockout mice, the number of TFF2 immunoreactive cells remained elevated after cessation of treatment. The H(2) receptor and gastrin receptor do not affect emergence of SPEM. However, it is suggested that the absence of H(2) receptor signaling causes a delay in the maturation of chief cells from mucous neck cells.

Topics: Animals; Atrophy; Azetidines; Cell Differentiation; Cell Lineage; Cell Proliferation; Gastric Mucosa; Gastrins; Intrinsic Factor; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Mucins; Muscle Proteins; Parietal Cells, Gastric; Peptides; Piperazines; Receptor, Cholecystokinin B; Receptors, Histamine H2; Trefoil Factor-2

Loss of gastric parietal cells is a critical precursor to gastric metaplasia and neoplasia. However, the origin of metaplasia remains obscure. Acute parietal cell loss in gastrin-deficient mice treated with DMP-777 leads to the rapid emergence of spasmolytic polypeptide/trefoil factor family 2 (TFF2)-expressing metaplasia (SPEM) from the bases of fundic glands. We now sought to characterize more definitively the pathway for emergence of SPEM.. Emerging SPEM lineages in gastrin-deficient mice treated with DMP-777 were examined for immunolocalization of TFF2, intrinsic factor, and Mist1, and morphologically with electron microscopy. Emerging SPEM was isolated with laser-capture microdissection and RNA was analyzed using gene microarrays. Immunohistochemistry in mouse and human samples was used to confirm up-regulated transcripts.. DMP-777-induced SPEM was immunoreactive for TFF2 and the differentiated chief cell markers, Mist1 and intrinsic factor, suggesting that SPEM derived from transdifferentiation of chief cells. Microarray analysis of microdissected SPEM lineages induced by DMP-777 showed up-regulation of transcripts associated with G1/S cell-cycle transition including minichromosome maintenance deficient proteins, as well as a number of secreted factors, including human epididymis 4 (HE4). HE4, which was absent in the normal stomach, was expressed in SPEM of human and mouse and in intestinal metaplasia and gastric cancer in human beings.. Although traditionally metaplasia was thought to originate from normal mucosal progenitor cells, these studies indicate that SPEM evolves through either transdifferentiation of chief cells or activation of a basal cryptic progenitor. In addition, induction of metaplasia elicits the expression of secreted factors, such as HE4, relevant to gastric preneoplasia.

Topics: Animals; Atrophy; Basic Helix-Loop-Helix Transcription Factors; beta-Defensins; Carrier Proteins; Cell Cycle Proteins; Cell Transformation, Neoplastic; Chief Cells, Gastric; DNA-Binding Proteins; Epididymal Secretory Proteins; Fetal Proteins; Gastric Fundus; Gastric Mucosa; Gastrins; Humans; Intercellular Signaling Peptides and Proteins; Intrinsic Factor; Metaplasia; Mice; Mice, Inbred C57BL; Mice, Knockout; Microtubule-Associated Proteins; Minichromosome Maintenance Complex Component 3; Mucins; Muscle Proteins; Nuclear Proteins; Parietal Cells, Gastric; Peptides; Precancerous Conditions; Stomach Neoplasms; Trefoil Factor-2

The loss of parietal cells from the gastric mucosa (oxyntic atrophy) is a critical step in the pathogenesis of chronic gastritis and gastric adenocarcinoma. Parietal cells are known to secrete epidermal growth factor receptor (EGFR) ligands, which are critical regulators of differentiation in the gastric mucosa. Although all of the actions of EGFR ligands are mediated through a common EGFR protein, individual ligands may produce different physiologic responses. Previous investigations have suggested that a deficit in EGFR signaling in waved-2 mice accelerates the emergence of metaplasia after induction of acute oxyntic atrophy. We sought to determine whether specific EGFR ligands regulate the metaplastic response to oxyntic atrophy.. To induce spasmolytic polypeptide-expressing metaplasia (SPEM), amphiregulin (AR) and transforming growth factor-alpha-deficient mice and their wild-type littermates were treated with DMP-777 for 0-14 days and for 14 days followed by 14 days of recovery off drug. We evaluated the gastric mucosal response to oxyntic atrophy using cell lineage-specific markers.. Although loss of transforming growth factor-alpha did not influence the induction of SPEM, loss of AR caused an acceleration and amplification in the induction of SPEM after acute oxyntic atrophy. Trefoil factor family 2/spasmolytic polypeptide and intrinsic factor dual-immunostaining cells significantly increased in the SPEM of AR-deficient mice. At the bases of glands, intrinsic factor immunoreactive cells also were costained for 5-bromo-2'-deoxyuridine, suggesting their re-entry into the cell cycle.. The absence of AR promoted the rapid emergence of SPEM in response to oxyntic atrophy.

Topics: Amphiregulin; Animals; Atrophy; Azetidines; EGF Family of Proteins; ErbB Receptors; Gastric Mucosa; Gastrins; Gene Expression Regulation; Glycoproteins; Intercellular Signaling Peptides and Proteins; Intrinsic Factor; Male; Metaplasia; Mice; Mice, Inbred C57BL; Mice, Knockout; Parietal Cells, Gastric; Peptides; Piperazines; S Phase; Somatostatin; Transforming Growth Factor alpha; Trefoil Factor-2

In addition to their role in gastric acid secretion, parietal cells secrete a number of growth factors that may influence the differentiation of other gastric lineages. Indeed, oxyntic atrophy is considered the most significant correlate with increased risk for gastric adenocarcinoma. We studied the alterations in gastric mucosal lineages elicited by acute oxyntic atrophy induced by treatment of C57BL/6 and gastrin-deficient mice with the parietal cell protonophore [S-(R*,S*)]-N-[1-(1,3-benzodioxol-5-yl)butyl]-3,3-diethyl-2-[4-[(4-methyl-1-piperazinyl)carbonyl]phenoxy]-4-oxo-1-azetidinecarboxamide (DMP-777). In both wild-type and gastrin knockout mice, DMP-777 elicited the rapid loss of parietal cells within 2 days of treatment. In wild-type mice, oxyntic atrophy was accompanied by a rapid increase in 5-bromo-2'-deoxyuridine-labeled proliferative cells and attendant increase in surface cell numbers. However, gastrin knockout mice did not demonstrate significant foveolar hyperplasia and showed a blunted proliferative response. After 7 days of treatment in wild-type mice, a second proliferative population emerged at the base of fundic glands along with the development of a mucous cell metaplasia expressing TFF2/spasmolytic polypeptide (SPEM). However, in gastrin knockout mice, SPEM expressing both TFF2 mRNA and protein developed after only 1 day of DMP-777 treatment. In wild-type mice, all changes induced by DMP-777 were reversed 14 days after cessation of treatment. In gastrin-deficient mice, significant SPEM was still present 14 days after the cessation of treatment. The results indicate that foveolar hyperplasia requires the influence of gastrin, whereas SPEM develops in response to oxyntic atrophy independent of gastrin, likely through transdifferentiation of chief cells.

Topics: Animals; Atrophy; Azetidines; Biological Transport; Cell Lineage; Gastric Mucosa; Gastrins; Gene Expression; Intrinsic Factor; Mice; Mice, Inbred C57BL; Mice, Knockout; Mucins; Muscle Proteins; Parietal Cells, Gastric; Peptides; Piperazines; Trefoil Factor-2

Gastric morphology, function, and immunology was studied in 68 patients with pernicious anemia (PA), 183 of their first-degree relatives, and 354 control subjects. The PA relatives and controls were comparable in age and sex distribution. In both groups, mean gastric acid output decreased and mean fasting serum gastrin levels and the prevalence of atrophic gastritis increased with age. The total prevalence of chronic gastritis was similar in the two groups, but severe atrophic gastritis of the body of the stomach (AGB), achlorhydria, parietal cell antibodies, and a raised fasting serum gastrin level were significantly more common in PA relatives than in controls. Of the PA relatives 23 had severe AGB which was indistinguishable from the gastric mucosal lesion found in PA probands and was, as a rule, accompanied by several other characteristics of type A gastritis. These included a normal antrum (78%), slight or absent inflammatory cell infiltration in the gastric mucosa (70%), achlorhydria (91%), high fasting serum gastrin level (83%), parietal cell antibodies (65%), and intrinsic factor antibodies (22%). The mean age and the proportion of subjects with slight and moderate AGB of all AGB subjects was significantly lower in PA relatives than in controls. This suggests an early onset and a rapid progression from mild to severe AGB in PA relatives. Thus, the PA relatives appear to consist of two populations, one with a high and one with little or no proneness to severe AGB. This bimodal distribution suggests the participation of a single major factor, probably genetic, in the pathogenesis of severe AGB in PA relatives.

Topics: Adolescent; Adult; Age Factors; Anemia, Pernicious; Atrophy; Autoantibodies; Consanguinity; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestines; Intrinsic Factor; Male; Metaplasia; Middle Aged; Pyloric Antrum; Vitamin B 12

Topics: Achlorhydria; Aged; Anemia, Pernicious; Atrophy; Chronic Disease; Female; Gastritis; Humans; Intestine, Small; Intrinsic Factor; Malabsorption Syndromes; Pepsin A

261 subjects with a normal body mucosa or with superficial gastritis used as controls for an atrophic gastritis series have been followed up for 23--27 years. Of them, 41 died during the earlier and 63 during the present follow-up period. In all, 141 subjects were reexamined in 1976--1977 and 16 answered a questionnaire. None of the subjects had gastric carcinoma or an adenomatous polyp. One patient diagnosed and reported earlier had died of gastric carcinoma during the present period of observation. Of the subjects with normal body mucosa 58% had developed superficial and 14% atrophic gastritis. Of those with superficial body gastritis 42% had developed atrophic gastritis and 18% showed an improvement of the gastritic changes. It should be noted, however, that earlier examinations were performed with blind biopsy and the present with direct vision gastroscopic biopsy. The state of the antral and body mucosa was similar in 53%, antral changes dominated in 33% and the changes in the body in 14%. Intestinal metaplasia was found in 36%, atypical epithelium in 6%, parietal cell antibodies in 0.5% and intrinsic factor antibodies in 0.5%. The fasting serum gastrin level was above 100 ng/ml in 10%. Only 2 cases fulfilled the morphological, functional and immunological criteria of type A gastritis. The present controls differed from the atrophic gastritis series in that the topography of gastritis was different and in that the incidence of metaplasia, atypia, gastric antibodies and high serum gastrin levels was markedly lower.

Topics: Antibodies; Atrophy; Biopsy; Female; Follow-Up Studies; Gastric Mucosa; Gastritis; Gastroscopy; Humans; Intestines; Intrinsic Factor; Male; Metaplasia; Middle Aged; Pyloric Antrum; Stomach Neoplasms; Time Factors

Twenty-one patients (4 females and 17 males) were re-examined 20 years after partial gastrectomy for benign peptic ulcer. Different stages of morphological change in the gastric stump mucosa were compared with haematological parameters as well as with gastric acid and IF secretions. Biopsy specimens were taken by the direct vision technique. Haematological values including also serum vitamin B12, folate and Schilling test were determined. Gastric acid and IF secretions were lower in all patients with "selective parietal cell atrophy" in the gastric mucosa compared with those of other patients. Serum B12 and Schilling test values showed the same tendency. The present study indicates that it is possible to determine the gastric function dependent on parietal cells according to morphological criteria.

Topics: Atrophy; Female; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastritis; Hemoglobins; Humans; Intrinsic Factor; Male; Postgastrectomy Syndromes; Schilling Test; Vitamin B 12

Mucosal biopsies from multiple sites in the stomachs of 21 patients with pernicious anaemia have been examined. The histological changes almost always involved the entire gastric mucosa, including that of the pyloric antrum. Metaplastic changes were almost universal and consisted of intestinal metaplasia in the body and antrum and pyloric metaplasia in the body. The severity of the pyloric metaplasia was such as to make the distinction between body and antrum on biopsy impossible. No relationship was found between serum gastrin activity and the histological appearances of the gastric antrum or body.

Topics: Adult; Aged; Anemia, Pernicious; Antibodies; Atrophy; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Hyperplasia; Intrinsic Factor; Male; Metaplasia; Middle Aged; Pyloric Antrum

Topics: Achlorhydria; Anemia, Pernicious; Atrophy; Fasting; Gastrins; Gastritis; Humans; Intrinsic Factor; Radioimmunoassay

Topics: Achlorhydria; Adult; Aged; Anemia, Pernicious; Atrophy; Autoantibodies; Autoimmune Diseases; Female; Follow-Up Studies; Gastritis; Humans; Intrinsic Factor; Malabsorption Syndromes; Male; Middle Aged; Schilling Test; Time Factors; Vitamin B 12

Topics: Adolescent; Anemia, Pernicious; Antibodies; Atrophy; Biopsy; Erythrocyte Count; Female; Gastric Mucosa; Hemoglobins; Humans; Intrinsic Factor; Reticulocytes; Vitamin B 12

Topics: Aged; Antibodies; Atrophy; Biopsy; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestinal Polyps; Intrinsic Factor; Male; Metaplasia; Middle Aged; Pyloric Antrum; Stomach; Stomach Diseases; Stomach Neoplasms

Topics: Anemia, Pernicious; Antigens; Atrophy; Cell Migration Inhibition; Gastric Mucosa; Gastritis; Humans; Intrinsic Factor; Leukocytes; Microsomes; Mitochondria; Mitochondria, Liver; Organ Specificity; Stomach

Topics: Achlorhydria; Atrophy; Autoantibodies; Biopsy; Duodenal Ulcer; Duodenum; Follow-Up Studies; Gastrectomy; Gastric Mucosa; Gastritis; Humans; Intrinsic Factor; Iron; Postoperative Complications; Stomach

Topics: Anemia, Pernicious; Antibodies; Antibody Specificity; Antigen-Antibody Reactions; Atrophy; Autoimmune Diseases; Biopsy; Chronic Disease; Complement Fixation Tests; Fluorescent Antibody Technique; Gastric Mucosa; Gastritis; Humans; Immune Tolerance; Intrinsic Factor; Stomach Ulcer

Topics: Anemia, Pernicious; Atrophy; Autoantibodies; Gastritis; Humans; Intestinal Mucosa; Intrinsic Factor; Stomach

Topics: Achlorhydria; Adult; Agammaglobulinemia; Anemia, Pernicious; Antibodies; Arthritis, Rheumatoid; Atrophy; Autoimmune Diseases; Colitis, Ulcerative; Diarrhea; Female; Fluorescent Antibody Technique; gamma-Globulins; Gastric Mucosa; Gastritis; Giardiasis; Humans; Hypersensitivity; Hypersensitivity, Delayed; Infections; Intrinsic Factor; Male; Middle Aged; Vitamin B 12

Topics: Adult; Aged; Anemia, Pernicious; Antigen-Antibody Reactions; Atrophy; Biopsy; Complement System Proteins; Female; Fluorescent Antibody Technique; Gastric Mucosa; Gastritis; Humans; Intrinsic Factor; Male; Middle Aged; Vitamin B 12

Topics: Adolescent; Adult; Aged; Anemia, Pernicious; Atrophy; Autoantibodies; Female; Finland; Gastric Mucosa; Gastritis; Humans; Intrinsic Factor; Male; Mass Screening; Middle Aged; Rural Population; Sampling Studies

Topics: Adult; Anemia, Pernicious; Asian People; Atrophy; Autoantibodies; Female; Gastritis; Hong Kong; Humans; Hyperthyroidism; Intestinal Absorption; Intrinsic Factor; Male; Middle Aged; Stomach; Vitamin B 12

Topics: Anemia, Pernicious; Antibodies; Atrophy; Complement System Proteins; Diagnosis, Differential; Fluorescent Antibody Technique; gamma-Globulins; Gastric Mucosa; Gastritis; Humans; Intestinal Diseases; Intrinsic Factor; Metaplasia; Postgastrectomy Syndromes; Stomach Neoplasms

Topics: Achlorhydria; Aged; Anemia, Pernicious; Animals; Antigen-Antibody Reactions; Atrophy; Biopsy; Diabetes Mellitus; Female; Fluorescent Antibody Technique; Gastric Juice; Gastric Mucosa; Gastritis; Humans; Immune Sera; Intrinsic Factor; Male; Middle Aged; Prednisolone; Rats; Regeneration; Reticulocytes; Schilling Test; Stomach; Stomach Diseases; Thyroiditis, Autoimmune; Vitamin B 12

Topics: Anemia, Pernicious; Atrophy; Autoantibodies; Chronic Disease; Fluorescent Antibody Technique; Gastritis; Humans; Intrinsic Factor

Topics: Adult; Aged; Anemia, Pernicious; Antibodies, Antinuclear; Antigen-Antibody Reactions; Atrophy; Autoantibodies; Female; Gastric Juice; Gastric Mucosa; Gastritis; Humans; Intestinal Absorption; Intrinsic Factor; Male; Middle Aged; Stomach Diseases; Vitamin B 12

Topics: Aged; Antibodies; Atrophy; Biopsy; Fluorescent Antibody Technique; Gastric Juice; Gastric Mucosa; Gastritis; Histamine; Humans; Intrinsic Factor; Iron; Male; Middle Aged; Schilling Test; Vitamin B 12; Vitamin B 12 Deficiency

A method employing non-radioactive vitamin B(12) and microbiological assay is described for estimating intrinsic factor in gastric juice and for detecting antibody to intrinsic factor in serum. Satisfactory agreement was obtained between the results by this method and by a modification of the method of Ardeman and Chanarin (1963). During the first hour after gastric stimulation 11 patients with pernicious anaemia secreted between 0 and 240 units of intrinsic factor compared with between 1,600 and 39,000 units in 21 patients with other conditions. The results in three out of four patients with gastric atrophy were higher than those in pernicious anaemia but lower than in other conditions.

Topics: Anemia, Pernicious; Antibodies; Atrophy; Biological Assay; Cobalt Isotopes; Gastric Juice; Humans; Intrinsic Factor; Lactobacillus; Methods; Stomach Diseases; Vitamin B 12

Topics: Adrenal Glands; Anemia, Pernicious; Antibodies, Anti-Idiotypic; Antibody Formation; Atrophy; Gastric Mucosa; Humans; Intrinsic Factor; Thyroid Gland; Vitamin B 12

Topics: Atrophy; Gastric Acidity Determination; Gastritis; Histamine; Humans; Intrinsic Factor; Urine; Vitamin B 12

Topics: Anemia; Anemia, Pernicious; Atrophy; Cobalt Isotopes; Drug Therapy; Gastric Acidity Determination; Gastric Mucosa; Geriatrics; Hematinics; Humans; Intrinsic Factor; Pathology; Prednisolone; Regeneration; Vitamin B 12

Topics: Achlorhydria; Anemia; Anemia, Pernicious; Atrophy; Chemical Phenomena; Chemistry; Erythropoiesis; Gastric Juice; Gastric Mucosa; Gastritis; Gastrointestinal Hormones; Humans; Intrinsic Factor; Metabolism; Peptic Ulcer; Pharmacology; Physiology; Vitamin B 12

Topics: Atrophy; Duodenal Ulcer; Gastritis; Gastritis, Atrophic; Humans; Intrinsic Factor; Polyps; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer; Vitamin B 12