Diabetes mellitus skin changes E10-E14 + Hauterkrankung

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 21.12.2021

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Diabetes Skin changes; Diabetogenic skin diseases; Skin and diabetes mellitus; skin changes in diabetes mellitus, dermatoses in diabetes mellitus; Skin diseases with diabetes mellitus

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Diabetes mellitus is the most common metabolic disease in humans; 5 million people in Germany suffer from this disease. About 1/3 of diabetics develop skin diseases. These occur both in manifest diabetes and in the pre-diabetic stage. However, they can also be superimposed by diabetogenically induced organ diseases (nephropathy, neuropathy, retinopathy, macro- and microangiopathy).

The diabetic skin changes are sometimes associated with a significantly increased morbidity and mortality.

4 types of diabetes are distinguished:

  • Type 1 diabetes (special form LADA diabetes)
  • Type 2 diabetes (>90%)
  • Type 3 diabetes = other specific forms of diabetes (e.g. drugs such as glucocorticoids, genetic defects in beta cell function(MODY1-14), rare immunological diseases; genetic forms)
  • Type 4 diabetes = gestational diabetes (GDM).

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  • Skin changes occur both in manifest diabetes and in the pre-diabetic stage. The percentages listed refer to several publications with larger collectives.
  • Skin changes in diabetes mellitus can be classified into 5 disease groups:
    1. Skin infections
    2. Skin diseases with overfrequent association to diabetes mellitus
    3. Skin diseases due to diabetic complications
    4. Skin diseases due to diabetogenic organ diseases and their secondary effects on the skin (e.g. effects of a diabetic nephropathy)
    5. Reactions to antidiabetic therapy (ADR).

Skin infections:

Skin diseases with hyper association to diabetes mellitus:

Skin diseases due to diabetic complications:

Skin disorders due to antidiabetic therapy:

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Prevalence of diabetes mellitus: 6% of the population. About one third of all diabetics develop skin symptoms during the course of the disease.

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It has been proven that diabetes mellitus on the one hand directly damages increased pathological glucose concentrations, on the other hand indirectly, by forming "advanced glycation end-products(AGEs)". AGEs are formed in a non-enzymatic reaction (glycation) of glucose and proteins, lipids and nucleic acid AGEs. They induce negative effects on almost all cell systems. Pathological glucose concentrations inhibit the proliferation, migration and protein biosynthesis of keratinocytes and fibroblasts. In endothelial cells they induce apoptosis and inhibit nitric oxide synthase (NOS) and thus NO synthesis. This leads to a reduced vasodilation in vivo. Pathological glucose concentrations suppress chemotaxis and phagocytosis of cell types of the innate immune defence.

AGEs interact with a number of intracellular and extracellular proteins, e.g. collagen type I, superoxide dismutase 1 or epidermal growth factor receptor and weaken their biological function. Furthermore, AGEs bind to RAGE (Receptor for AGEs). This leads to activation of the NF-κB signalling pathway with induction of proinflammatory cytokines, and both pathological glucose concentrations and AGEs lead to increased formation of intracellular oxidative stress (formation of reactive oxygen species - ROS). This is caused by a depletion of antioxidative protective enzymes such as glutathione or mitochondrial superoxide dismutase. On the other hand, ROS-generating enzymes such as nicotinamide adenine dinucleotide phosphate oxidase are induced.

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Please ask your physician for a reliable diagnosis. This website is only meant as a reference.


Last updated on: 21.12.2021