Autoimmune gastritis/ pernicious anaemia

Clinical information

Autoimmune gastritis (AIG) is a chronic inflammation of the stomach mucosa which can hinder the uptake of iron and vitamin B12 and lead to atrophic gastritis with malabsorption. The stomach mucosa is infiltrated by lymphocytes, plasma cells and granulocytes, epithelial cells become necrotic and main and parietal cells are replaced by mucoid cells. As a final stage, atrophy develops over many years. Thus, AIG inhibits production of pepsin, hydrochloride acid and intrinsic factor (IF). Due to the vitamin B12 deficiency, pernicious anaemia (PA) develops over many years. In most patients AIG proceeds asymptomatically over many years to the late stage of atrophy. Symptoms of PA are anaemia, fatigue, drowsiness and tachycardia. Moreover, the vitamin B12 deficiency inhibits the DNA synthesis, causing megaloblasts to form in the bone marrow and the gastrointestinal epithelial cells. This leads to malabsorption and diarrhoea with weight loss, anorexia, glossitis, icterus and neurological abnormalities.

Diagnostics

AIG is characterised by the occurrence of autoantibodies against parietal cell antigens (PCA) and IF. IF is a glycoprotein which is secreted by the parietal cells. It forms complexes with vitamin B12, whose absorption in the ileum is hindered by anti-intrinsic factor antibodies (IFA). Sera from AIG or PA patients contain two types of IFA (both IgG): IFA of type 1 react with the vitamin B12 binding site of the IF, those of type 2 inhibit the binding of the IF to the receptors in the ileum.  IFA are very specific for AIG. With PA, IFA occur in 40 to 80% of patients, depending on the disease duration.

Antibodies against PCA occur both in patients with AIG and PA. They are mainly of the IgG and IgA classes. The prevalence of antibodies against PCA is very high in almost all patients with chronic atrophic gastritis, amounting to nearly 100%. Antibodies against PCA also have a very high diagnostic sensitivity for PA amounting to 80 to 90% at the time of diagnosis. Over the course of disease, their prevalence decreases continuously due to the progressive destruction of the parietal cells. With respect to the specificity of the anti-PCA antibodies, it must be taken into account that they are also detected in patients with endocrinopathies and healthy blood donors.

Antibodies against PCA can be specifically detected by IIFT on tissue sections of primate stomach and by ELISA. IFA can be detected using intrinsic factor BIOCHIPs or by ELISA. Moreover, immunoblots with both antigens are available for differential diagnosis from other diseases such as coeliac disease or Crohn's disease.

Selected Products

Method
Parameter
Substrate
Species
IIFT
parietal cells
(PCA)
stomach
monkey
IIFT
Anti-Parietal cells (SM) IIFT EUROPattern
stomach
monkey
EUROLINE
Autoimmune Gastrointestinal Diseases IgG
(tissue transglutaminase (endomysium),
gliadin-analogue fusion peptide (GAF-3X),
parietal cell antigen (PCA) separately
Intrinsic factor, mannan (ASCA))
EUROLINE
EUROLINE
Autoimmune Gastrointestinal Diseases IgA
(tissue transglutaminase (endomysium), gliadin-analogue
fusion peptide (GAF-3X), mannan (ASCA))
EUROLINE
IIFT
parietal cells (PCA)
mitochondria (AMA)
stomach
kidney
(2 BIOCHIPs per field)
monkey
rat
IIFT
antibodies against parietal cells
(PCA control)
ELISA
parietal cells
(PCA)
antigen-coated
microplate wells
ELISA
ATP4B
antigen-coated
microplate wells
ELISA
intrinsic factor
antigen-coated
microplate wells
IIFT
intrinsic factor
intrinsic factor BIOCHIPs
IIFT
EUROPLUS
parietal cells (PCA)
intrinsic factor
2 BIOCHIPs per field:
stomach
intrinsic factor BIOCHIPs

monkey
IIFT
antibodies against parietal cells + intrinsic factor
(PCA + intrinsic factor ab control)
Back to top