Cutaneous Complications of Diabetes Mellitus

Diabetes mellitus exerts profound effects on skin integrity, manifesting as a spectrum of complications that arise from chronic hyperglycaemia, microvascular dysfunction and impaired immune responses. Common presentations include xerosis (dry skin), pruritus, diabetic dermopathy and necrobiosis lipoidica, while more serious sequelae involve ulceration, infection and poor wound healing that may lead to limb amputation. Pathophysiological drivers include the accumulation of advanced glycation end products in the dermal extracellular matrix, reduced keratinocyte proliferation, altered fibroblast function and dysregulated inflammatory signalling. Neuropathy and microangiopathy further compromise cutaneous perfusion and sensory feedback, increasing the risk of unrecognised trauma and chronic ulceration. Clinical management spans from optimised glycaemic control and skincare regimens to targeted therapies for recalcitrant lesions. Despite improvements in metabolic regulation, skin complications remain highly prevalent and often underdiagnosed, highlighting the need for heightened awareness among clinicians and integration of dermatological assessment into routine diabetes care.

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Cutaneous Complications of Diabetes Mellitus publication trend

The graph below shows the total number of articles in cutaneous complications of diabetes mellitus across all publications each year (not limited to Nature Index journals).

Technical terms

Necrobiosis lipoidica: A chronic granulomatous skin disorder characterised by collagen degeneration and lipid deposition, often associated with diabetes.

Keratinocyte: The predominant cell type in the epidermis responsible for forming the skin’s protective barrier through proliferation and differentiation.

Advanced glycation end products (AGEs): Proteins or lipids that become non-enzymatically glycated and oxidised after exposure to sugars, contributing to tissue stiffness and inflammation.

Methylglyoxal (MGO): A reactive dicarbonyl by-product of glycolysis that modifies proteins and nucleic acids, driving cellular dysfunction in diabetes.

Janus kinase inhibitors (JAK inhibitors): Small-molecule drugs that block JAK–STAT signalling pathways to reduce inflammatory responses in cutaneous conditions.

Procollagen: The soluble precursor form of collagen synthesised by fibroblasts, essential for extracellular matrix formation and wound strength.

References

1. Skin disorders in diabetes mellitus: an epidemiology and physiopathology review. Diabetology & Metabolic Syndrome (2016).
2. A Breakthrough in the Treatment of Necrobiosis Lipoidica? Update on Treatment, Etiopathogenesis, Diagnosis, and Clinical Presentation. International Journal of Molecular Sciences (2024).
3. The Intersection of Dermatological Dilemmas and Endocrinological Complexities: Understanding Necrobiosis Lipoidica—A Comprehensive Review. Biomedicines (2024).
4. c-Myc Upregulated by High Glucose Inhibits HaCaT Differentiation by S100A6 Transcriptional Activation. Frontiers in Endocrinology (2021).
5. Evaluation of Immunomodulatory Responses and Changed Wound Healing in Type 2 Diabetes—A Study Exploiting Dermal Fibroblasts from Diabetic and Non-Diabetic Human Donors. Cells (2021).