Specifically, prolonged hyperglycemia and secondary chronic inflammation set the stage for protein glycation, with formation of advanced glycation end products (AGEs). It is thought that these AGEs in cutaneous and connective tissues stiffen collagen, leading to scleroderma-like skin changes.2
These microvascular and fibroproliferative changes are also considered important contributors in the etiology of DC and trigger finger, ultimately leading to increased collagen deposition and fascial thickening.4,5 In addition, increased activation of the polyol pathway may occur secondary to hyperglycemia, resulting in increased intracellular water and cellular edema.5
The differential is comprisedof components of systemic disease
The differential diagnosis includes tropical diabetic hand, autoimmune-related scleroderma (also called systemic sclerosis), complex regional pain syndrome, and diabetic scleredema.
Tropical diabetic hand, a potentially dangerous infection, is generally found only in tropical regions and in the setting of injury.5,6
Autoimmune-related scleroderma may be diagnosed alongside other signs and symptoms of CREST: calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. In the absence of other signs and symptoms, and in the presence of uncontrolled diabetes, biopsy would be needed to definitively diagnose it. Clinically, diabetic hand can be distinguished with concurrent involvement of the upper back.
Continue to: Complex regional pain syndrome