Vitamin B12 Deficiency in type I Diabetes

Abstract

Diabetes mellitus is a group of metabolic anomalies due to defect in insulin secretion/action. In type I diabetes, there is complete absence of insulin due to destruction of pancreatic beta cells, whereas type 2 diabetes usually involves insulin resistance. A complex interaction between various environmental, genetic and immunological factors leads to development of diabetes. One major problem for treating T1DM is its difficult prognosis because it leads to many complications, including autoimmune gastritis and celiac diseases. In autoimmune gastritis auto/parietal cell antibodies are formed against the intrinsic factor leading to thegastric atrophy. While in celiac disease, intestinal villi atrophy occurs. Both these conditions have a common clinical outcome which is pernicious anemia. The patients suffering from type I diabetes have approximately threefold increased risk for developing vitamin B12 deficiency as compared to the general population. The major genetic risk factor responsible for this disease is any functional change in HLA class II alleles (HLA DQ, DR and DP). These genes are present on chromosome 6 and are involved in approximately 40% cases of type I diabetes mellitus. The production of glutamic acid decarboxylase and anti-thyroid peroxidase antibodies have also been reported to be associated with this genotype. The glutamic acid decarboxylase converts glutamic acid to gamma-amino butyric acid producing hydrochloric acid from gastric parietal cells. The antibodies against this antigen can cause achlorhydria that can ultimately lead to vitamin B12 deficiency. Hematologic and neurological disorders, as well as a variety of cardiovascular diseases, are the most commonclinical manifestations of deficiency of vitamin B12.