PubMed · 11269039
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K Tamayose, K Oshimi. 2000. [Pernicious anemia].. https://pubmed.ncbi.nlm.nih.gov/11269039/
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Human autoimmune gastritis is an organ-specific autoimmune disease of the stomach. It is characterized by the development of disease-specific autoantibodies and a pathology that specifically targets specialized cells within the gastric environment. The autoantigens associated with this disease have been defined as the gastric H+/K+ ATPase and intrinsic factor. The development of experimental disease models has been pivotal in our contemporary understanding of autoimmunity. Here we review mouse models of autoimmune gastritis and their relevance to human autoimmune gastritis associated with pernicious anemia. We appraise some historical as well as recent studies of experimental autoimmune gastritis (EAG), highlighting key findings that have formed the basis of our current understanding of the etiology and mechanism(s) associated with autoimmune gastritis. A precise understanding of the pathogenesis of autoimmune gastritis will permit the design of innovative and rational therapeutic strategies to prevent, arrest, ameliorate or reverse the disease.
Pernicious anaemia is an autoimmune atrophic gastritis inducing vitamin B12 deficiency by malabsorption. This disease may be diagnosed in the absence of any anaemia, on a neuropathy or when one or several autoimmune disorders co-exist. Typically, pernicious anaemia is revealed by macrocytic megaloblastic anaemia. Diagnosis is done on low serum vitamin B12, raised serum homocysteine, parietal cell and, intrinsic factor antibodies. Pernicious anaemia should be treated indefinitely by monthly intramuscular hydroxocobalamin. Because of an increased incidence of gastric carcinoma, endoscopy should be evenly performed.
An 11-year-old black male presenting with severe subacute sensory ataxia, unusual skin hyperpigmentation, megaloblastic anemia, low serum B12 levels, and an abnormal part I Schilling test was diagnosed with pernicious anemia in the context of a polyglandular syndrome. Intrinsic factor and thyroid microsomal antibodies were positive, and thyroid-stimulating hormone levels were undetectable. There was a strong familial aggregation because the mother, a maternal aunt, the maternal grandfather, and the maternal great-grandmother had been diagnosed with pernicious anemia, albeit of unspecified etiology. Spinal magnetic resonance imaging (MRI) demonstrated extensive demyelination of the posterior columns along the entire length of the cord, as well as areas of contrast enhancement. Treatment with cobalamin produced complete remission of the neurologic deficits and normalization of the MRI findings in the short space of 2 months. Although rare, childhood pernicious anemia is a treatable disease that should be included in the differential diagnosis of the sensory ataxias in children. In this article, we review the causes of pernicious anemia in children and discuss the MRI findings.