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[Latent autoimmune diabetes in adults: an update].

Authors: Zhi-guang, Zhou; Xia, Li;

[Latent autoimmune diabetes in adults: an update].

Abstract

Latent autoimmune diabetes in adults (LADA), presenting with a similar phenotype of type 2 diabetes at early stage, belongs to the slowly progressive subtype of autoimmune type 1 diabetes. LADA differs from classic juvenile-onset type 1 diabetes in which its autoimmune destructive process of islet beta-cells is much slower, so LADA may serve as a human model of autoimmune type 1 diabetes. Although no international standardized criteria for the diagnosis of LADA has been established, it should be noted that LADA has some specific features in clinical characteristics, susceptible genotypes, cellular and humoral immune markers, as well as islet pathology. Presence of islet autoantibodies is necessary for the diagnosis of LADA. Early insulin intervention may preserve residual islet beta-cell function in LADA. The different pathological manifestations of LADA with different autoantibody titers can help throw light on the autoimmune process, laying foundation of prevention or even cure of type 1 diabetes.

Related Organizations
Keywords

Adult, Islets of Langerhans, Diabetes Mellitus, Type 1, Humans, Insulin, Autoantibodies

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
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popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
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