<p>Latent Autoimmune Diabetes in Adults (LADA) is a type of diabetes that can phenotypically resemble type 2 diabetes upon initial presentation but expresses the autoimmune component of type 1 diabetes. While technically classed as type 1 diabetes, LADA is distinct from type 1 and 2 diabetes because of its intermediate progression that may or may not lead to complete insulin dependence. Differentiation is made with the presence or absence of autoantibodies and C-peptide. This is demonstrated in the following case. A 29-year-old Black female with a history of gestational diabetes and two-year history of prediabetes was ultimately diagnosed with type 2 diabetes with an A1c of 6.6% and was treated with metformin 500&#xa0;mg twice daily. Her blood glucose suddenly rose to &gt; 400&#xa0;mg/dL and A1c to 8.6% after 8 months of therapy. Her BMI was 22.45&#xa0;kg/m<sup>2</sup>. Her provider ordered a C-peptide which measured 1.3 ng/mL (normal 0.8–5.2 ng/mL). Since this was technically normal, the provider continued with the type 2 diabetes diagnosis. Recognizing the C-peptide was low-normal, the clinical pharmacist ordered autoantibody tests, discovering a positive glutamic acid decarboxylase antibody (GADA) &gt; 250 IU/mL (normal &lt; 0.0–5.0 IU/mL) and confirming the diagnosis of LADA. The pharmacist discontinued metformin and initiated a basal/bolus insulin regimen with titration. Autoantibody testing is crucial to determine the proper diagnosis when the C-peptide is low-normal and should be prioritized. Recognition of the signs of LADA and proper diagnostic testing can lead to earlier optimal treatment and prevention of diabetes complications.</p>

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Proper diagnosis of latent autoimmune diabetes in adults prompts appropriate pharmacotherapy; C-peptide is just one component

  • Jenna C. Record,
  • A. Cole Eichelberger,
  • Brianna L. Johns,
  • Gage T. Bouziden,
  • Jeremy L. Johnson

摘要

Latent Autoimmune Diabetes in Adults (LADA) is a type of diabetes that can phenotypically resemble type 2 diabetes upon initial presentation but expresses the autoimmune component of type 1 diabetes. While technically classed as type 1 diabetes, LADA is distinct from type 1 and 2 diabetes because of its intermediate progression that may or may not lead to complete insulin dependence. Differentiation is made with the presence or absence of autoantibodies and C-peptide. This is demonstrated in the following case. A 29-year-old Black female with a history of gestational diabetes and two-year history of prediabetes was ultimately diagnosed with type 2 diabetes with an A1c of 6.6% and was treated with metformin 500 mg twice daily. Her blood glucose suddenly rose to > 400 mg/dL and A1c to 8.6% after 8 months of therapy. Her BMI was 22.45 kg/m2. Her provider ordered a C-peptide which measured 1.3 ng/mL (normal 0.8–5.2 ng/mL). Since this was technically normal, the provider continued with the type 2 diabetes diagnosis. Recognizing the C-peptide was low-normal, the clinical pharmacist ordered autoantibody tests, discovering a positive glutamic acid decarboxylase antibody (GADA) > 250 IU/mL (normal < 0.0–5.0 IU/mL) and confirming the diagnosis of LADA. The pharmacist discontinued metformin and initiated a basal/bolus insulin regimen with titration. Autoantibody testing is crucial to determine the proper diagnosis when the C-peptide is low-normal and should be prioritized. Recognition of the signs of LADA and proper diagnostic testing can lead to earlier optimal treatment and prevention of diabetes complications.