Differentiating LADA, type 1 and type 2 diabetes

It is not always easy to distinguish LADA from type 1 or type 2 diabetes. Common parameters utilized are BMI, age, family history, HLA-typing, clinical presentation, glucose variability and severity, insulin production, C-peptide levels, as well as autoantibodies against glutamic acid decarboxylase (GAD65), pancreatic islet cells (ICA) or insulin (IAA).

The article shows that other inflammatory markers could also be useful in differentiating the diagnoses. Such markers are; adiponectin, soluble tumor necrosis factor-α receptor 2 (sTNFR2), interleukin-6 (IL-6), hs-CRP, and total leukocyte number. More research is needed on how to incorporate the additional tests in clinical practice.

GT

Also see:

Other LADA related posts

Type 1 diabetes posts

General diabetes posts

Diabetes antibodies

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Diabetes Care

cross-sectional

April 2018

OBJECTIVE

To test whether differences in serum concentrations of adiposity-related low-grade inflammatory mediators could help to differentiate patients with latent autoimmune diabetes in adults (LADA), classic adult-onset type 1 diabetes, and type 2 diabetes.

Methods

This cross-sectional study involved 75 patients with LADA, 67 with classic adult-onset type 1 diabetes, and 390 with type 2 diabetes. Serum concentrations of adiponectin, soluble tumor necrosis factor-α receptor 2 (sTNFR2), interleukin-6, hs-CRP, and total leukocyte number were measured. To evaluate the differences of these markers among diabetes types, we performed logistic regression models and evaluated area under the receiver-operating characteristic curve (AUCROC) values.

RESULTS

The profile of innate immunity-related inflammatory markers correlated with metabolic syndrome components.

LADA versus classic adult-onset type 1 diabetes was independently related to sTNFR2 (odds ratio 1.9, p = 0.047) and hs-CRP levels (OR 0.7, p = 0.019)

And a higher number of total leukocytes lowered the risk of LADA compared with type 2 diabetes (OR 0.98, p = 0.036).

The logistic regression model including explanatory biomarkers explained 35% of the variation for LADA versus classic adult-onset type 1 diabetes (AUCROC 0.83, p < 0.001) and 15% of the variation for LADA versus type 2 diabetes (AUCROC 0.73, p < 0.001).

CONCLUSIONS

Inflammatory, adiposity, and immune-related markers could help to differentiate a LADA diagnosis from that of classic adult-onset type 1 diabetes, and also LADA from that of type 2 diabetes, along with islet autoantibody positivity.

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