The presence of anti-parietal cell antibodies (APCA) and/or intrinsic factor blocking antibodies (IFBA) is indicative of AAG that may develop into pernicious anemia.
The pathogenesis of the autoimmune type involves an antibody-mediated loss of parietal cells resulting in achlorhydria and an antibody-mediated loss of intrinsic factor that causes pernicious anemia.
Pernicious anemia (PA) is an autoimmune gastritis that results from the destruction of gastric parietal cells and the associated lack of an intrinsic factor to bind ingested vitamin B12.
Vitamin B12 level was less than 50pg/mL, methylmalonic acid was 0.33μmol/L, anti-parietal cell antibody was >1:640, and intrinsic factor blocking antibody was positive-confirming the diagnosis of pernicious anemia.
Pernicious anemia (PA) is an autoimmune disease of multifactorial etiologies characterized by autoimmune chronic atrophic gastritis, cobalamin deficiency (CD) due to defective absorption of dietary cobalamin from the terminal ileum, and by the presence of intrinsic factor and parietal cell antibodies.
Receiver Operating Curves (ROC) were used to compare diagnostic accuracy of gastrin and pepsinogen-I for PA in patients under chronic treatment with PPIs and in untreated patients.
For these reasons we studied the values of some markers of PA in a group of 79 first-degree relatives and we detected that the most frequent abnormalities are a decrease in serum pepsinogen I (22.7% of cases), an increase in serum gastrin (16.5% of cases) and in parietal cell antibody at a titer >or=40 (23.4% of cases).
While epidemiological evidence from patients with elevated serum gastrin levels related to pernicious anaemia does not support an increased risk for colon cancer, a recent study suggests that prolonged hypergastrinaemia is associated with an increased risk for colon cancer.
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.
The results recommend serum PG I and serum gastrin, but not parietal cell antibody, as tests for severe atrophic gastritis in relatives of patients with pernicious anemia.
TCN2 (rs9606756) GG genotype, related with lower vitamin B12 levels, was found in 3 (3.6%) autoimmune gastritis patients (2 with pernicious anaemia), but in none of controls (p = 0.02).
The patient was heterozygous for the transcobalamin (TC) II polymorphism 776C --> G. This case demonstrates the importance of functional assessment of intracellular B12 activity (e.g. serum homocysteine) in excluding B12 deficiency, the role of steroids in pernicious anaemia and a possible clinical correlation of a TCII polymorphism.
Here we describe LIPS assays for the quantification of autoantibodies to the H+, K+-ATPase A (ATP4A) and B (ATP4B) subunits, two serological markers of autoimmune atrophic gastritis and pernicious anemia.
Here we describe LIPS assays for the quantification of autoantibodies to the H+, K+-ATPase A (ATP4A) and B (ATP4B) subunits, two serological markers of autoimmune atrophic gastritis and pernicious anemia.
The rates of comorbidity in most studies were ≥1% for insulin-dependent diabetes mellitus, rheumatoid arthritis (RA), psoriasis and celiac disease (CD), ≥2% for Graves' disease, ≥3% for vitiligo, and ≥5% for pernicious anemia and Hashimoto's thyroiditis.