Type I Diabetes

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Type I diabetes is caused by the autoimmune destruction of insulin-producing beta cells in the islets of Langerhans, which are located in the pancreas. This leads to a need to inject insulin in order to survive. Approximately one million to 1.5 million Americans have type I diabetes, making it the second-most-common disease of childhood behind asthma. Despite improvements in care, for example, implanted insulin pumps, most people with it do not achieve the desired glycemic (blood sugar) targets, which leads to an increased risk of complications and early death. In two Scottish studies, type I diabetes led to a loss of 14.2 life-years in men, and 17.7 life-years in women when it was diagnosed before the age of 10. If diagnosed before the age of 20, the life-years lost were 11 and 13, respectively.

Type I diabetes progresses through several stages before becoming overt disease. In stage 1, autoantibodies are detected in the blood. In stage 2, dysglycemia appears. This means mildly elevated blood sugar levels during a glucose tolerance test. In stage 2, while metabolic responses to elevated glucose levels are impaired, metabolic indexes for diabetes, for example hemoglobin A1c, are normal and treatment is not necessary. In stage 3, overt disease is present requiring treatment. There have been several studies that used an antibody-containing medication to disable or kill certain white blood cells (CD8+ T lymphocytes) that were found to be the cells that attack and destroy the pancreatic insulin-producing cells. These studies tested a drug named teplizumab and found that it reduced the loss of pancreatic beta cells and delayed the onset of diabetes for up to seven years.

Recently, another study using teplizumab was published. It looked at non-diabetic relatives of patients with type I diabetes who were at least eight years of age. They had two or more diabetes-related antibodies detected in their blood and had evidence of dysglycemia on a glucose tolerance test. In other words, they were at high risk to develop type I diabetes. Although this study was a small one, at the conclusion of it they found that the median delay of onset of overt disease was two years. In addition, in the teplizumab group, 57 percent remained diabetes-free while only 28 percent remained disease free in the control group. The findings of this study and others support the notion that type I diabetes is a chronic T-cell-mediated disease and that immunomodulation, or impairing the ability of certain white blood cells (T cells) to attack the pancreas, before the development of clinical disease, can be useful. Unfortunately, the reason why a person’s own immune system attacks the pancreas remains unclear at present.

By focusing on a person’s own immune system, medical science continues to not only find ways to delay the onset of type I diabetes, but also to treat, if not one day cure, the disease using stem cells. Meanwhile, if you have a child who has close relatives with type I diabetes, get him or her to the pediatrician to be evaluated for his/her risk of getting the disease.

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