Am Fam Physician. 2013;87(5):310
Error in table column headings. In the editorial “Latent Autoimmune Diabetes in Adults” (April 1, 2010, p. 843), Table 1 (p. 844) contained errors in the column headings. The rightsholder of the original table, which contained these errors, granted AFP permission to reprint the table as published. The heading over the fourth column (Diabetes) should have been “Type 1 diabetes” and appeared over the third column. The heading over the third column (Latent autoimmune type 1 diabetes) should have been “Latent autoimmune diabetes in adults” and appeared over the fourth column. The table has been corrected online and is reprinted here.
Features | Type 2 diabetes | Type 1 diabetes | Latent autoimmune diabetes in adults |
---|---|---|---|
Ketoacidosis | Usually absent | Will develop rapidly unless patient receives insulin replacement therapy | Absent at diagnosis, but may be present when patient becomes severely insulinopenic |
Cardiovascular complications | Risk 2–4 times higher than individuals who are euglycemic | Increased risk of cardiovascular morbidity and mortality related to strokes, acute coronary events, and coronary revascularizations; high incidence rates compared with euglycemic individuals, especially in women | Same risk as patients with T2DM |
Microvascular complications (retinopathy, nephropathy, neuropathy) | Increased | Increased | Increased |
Pathophysiology | Peripheral insulin resistance; reduced pancreatic beta-cell mass and function; reduced insulin secretion | Autoimmune destruction of pancreatic beta-cells | Latent autoimmune destruction of pancreatic beta-cells |
Autoantibodies | Negative |
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Insulin requirements for treatment | Usually late in the disease when the remaining beta-cell mass and function can no longer support acceptable glycemic control achieved by oral agents or incretin mimetics | Insulin is required from the time of diagnosis | Insulin should be initiated as soon as the patient develops autoantibodies |