Pathophysiology and laboratory diagnosis of pernicious anemia

Ban-Hock Toh1

  • 1Department of Medicine, Southern Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, and Australian Clinicalabs, Clayton, VIC, Australia. ban-hock.toh@monash.edu.

Immunologic Research
|August 20, 2016
PubMed

Insights

Pernicious anemia results from autoimmune gastritis damaging stomach parietal cells, leading to intrinsic factor and acid loss. Diagnosis involves antibodies, anemia, and elevated gastrin.

Area of Science:

  • Gastroenterology
  • Immunology
  • Hematology

Background:

  • Pernicious anemia is a hematologic condition stemming from chronic atrophic gastritis affecting stomach parietal cells.
  • Autoimmune gastritis, characterized by Th1 CD4 T cell activation against gastric H/K ATPase, precedes corpus atrophy by 10-20 years.

Purpose of the Study:

  • To detail the pathogenesis, clinical presentation, and diagnostic criteria of pernicious anemia and its precursor, autoimmune gastritis.
  • To highlight the association of autoimmune gastritis with other autoimmune conditions.

Main Methods:

  • Review of the pathophysiology of autoimmune gastritis and pernicious anemia.
  • Description of diagnostic laboratory findings, including antibodies and blood counts.
  • Discussion of the clinical associations of autoimmune gastritis.

Main Results:

  • Autoimmune gastritis involves parietal cell antibodies targeting gastric H/K ATPase, leading to loss of intrinsic factor and HCl acid.
  • Intrinsic factor loss causes cobalamin deficiency, while acid loss results in iron deficiency anemia.
  • Laboratory diagnosis relies on specific antibodies, megaloblastic anemia, and elevated serum gastrin.

Conclusions:

  • Pernicious anemia is a complex condition with a long preclinical phase of autoimmune gastritis.
  • Accurate diagnosis requires a combination of serological markers, hematologic evaluation, and assessment of acid secretion.
  • Autoimmune gastritis is linked to other autoimmune disorders, suggesting a shared underlying immune dysregulation.

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