Corrections



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Am Fam Physician. 2013 Mar 1;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.

Table 1.

Clinical Features of Type 2 Diabetes, Type 1 Diabetes, and Latent Autoimmune Diabetes of Adulthood

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

  • GAD-65 autoantibodies

  • Islet-cell antigen-2

  • Insulin autoantibodies

  • note: Unlike LADA, T1DM patients typically are positive for all three autoantibodies

  • GAD-65 autoantibody is typically the only one detected

  • Islet-cell antibodies

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


T2DM indicates type 2 diabetes mellitus; GAD-65 indicates glutamic acid decarboxylase; LADA indicates latent autoimmune diabetes in adults; T1DM indicates type 1 diabetes mellitus.

Reprinted with permission from Unger J. Diagnosing and managing latent autoimmune diabetes in adults. Practical Diabetology. 2008;21(1):33.

Table 1.   Clinical Features of Type 2 Diabetes, Type 1 Diabetes, and Latent Autoimmune Diabetes of Adulthood

View Table

Table 1.

Clinical Features of Type 2 Diabetes, Type 1 Diabetes, and Latent Autoimmune Diabetes of Adulthood

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

  • GAD-65 autoantibodies

  • Islet-cell antigen-2

  • Insulin autoantibodies

  • note: Unlike LADA, T1DM patients typically are positive for all three autoantibodies

  • GAD-65 autoantibody is typically the only one detected

  • Islet-cell antibodies

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


T2DM indicates type 2 diabetes mellitus; GAD-65 indicates glutamic acid decarboxylase; LADA indicates latent autoimmune diabetes in adults; T1DM indicates type 1 diabetes mellitus.

Reprinted with permission from Unger J. Diagnosing and managing latent autoimmune diabetes in adults. Practical Diabetology. 2008;21(1):33.


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