There are a variety of common and rare skin conditions associated with diabetes mellitus (DM), including:

• diabetic dermopathy
• diabetic bullae
• necrobiosis lipoidica
• acanthosis nigricans
• eruptive xanthomas
• disseminated granuloma annulare
• scleredema

In parts 1 and 2 of this series, we’ll review factors involved in their pathogenesis and discuss current management strategies.

 

Diabetic dermopathy

Diabetic dermopathy is pathognomonic for diabetes mellitus and the commonest cutaneous manifestation. “Dermopathy” was chosen to emphasize its correlation with retinopathy, nephropathy and neuropathy. It tends to be more common in males than females, and tends to occur after age 50 years. It’s found in up to 40% of patients with DM type I and up to 50% of patients with DM type II.

Its pathogenesis is generally unknown. It tends to occur over bony prominences, and perhaps minor trauma at lesion sites may predispose to its development. Diabetic dermopathy can be induced on the legs of patients with diabetes by hot or cold insults. Microangiopathy can be a risk factor as microvascular disease may compromise blood flow resulting in slow healing, with insufficient blood flow to prevent scarring.

 

Clinical findings

• atrophic, brown macules and patches
• colour varies from erythematous to pink, dull red or brown
• shapes can be irregular, round or oval, scarlike eruptions
• may become confluent, especially on the anterior shins

 

Distribution

• bilateral with asymmetry
• most common site is on the shins
• other sites:
  • bony prominences over the lateral feet
  • anterior thighs
  • forearms

 

Asymptomatic

• patients may not recall local trauma and/or there may be a lack of sensation

The course is variable. Lesions can self-resolve in 1 to 2 years, but new “crops” of lesions may continue to appear. Recurrences are common. Resolution may leave the skin with hyper- or hypopigmentation and atrophy.

 

Diagnosis

• Given that a patient has diabetes, it’s often a clinical diagnosis. Other skin diseases associated with diabetes should also be considered.

 

Investigations

• screening for microvascular complication of diabetes (neuropathy, nephropathy, retinopathy)
• biopsy: rarely needed

 

Treatment options

• Reassure patients that the lesions themselves do not cause any increase in morbidity. They are, however, associated with serious microvascular complications of diabetes and proper screening should be done
• No treatment is effective or recommended

 

Diabetic bullae

Diabetic bullae refer to non-inflammatory, spontaneous, painless blistering that occur in patients with diabetes. They are most often acral. Aggravating or causal factors include:

• trauma
• neuropathy
• UV light
• cation imbalance

Insulin-dependent diabetics have a reduced threshold to suction-induced blistering.

On biopsy, there’s a non-inflammatory, subepidermal blister. Direct immunofluorescence studies are negative.

Patients should be reassured that the bullae heal spontaneously in 4-5 weeks, without scarring. Topical antibacterial ointments can be applied to bullae that rupture to help prevent superinfection.

 

Necrobiosis lipoidica

Necrobiosis lipoidica (NL) is a granulomatous, pretibial eruption that shows atrophy and may ulcerate. It affects less than 1% of patients with diabetes. It’s three times more common in females than males. The age of onset ranges from the 3^rd decade in patients with insulin-dependent patients and in the 5^th decade for non-insulin dependent diabetics. Necrobiosis lipoidica isn’t pathognomic for diabetes. Given a patient has NL, up to 60% may have DM, 20% have glucose intolerance or a family history of DM, and in 15%, lesions precede a diagnosis of DM by 2 years.

The pathogenesis is unknown. It may represent an immunological response to altered collagen in the dermis. Microangiopathic changes may trigger NL by causing collagen degeneration.

 

Clinical findings

• well-demarcated firm, depressed (atrophic), waxy, yellow, red-brown lesions with raised violaceous rims
• progress to round or oval scleroderma-like lesions with smooth, shiny surface
• may see some telangiectasias
• lesions may ulcerate
• be aware: squamous cell carcinomas can form in chronic ulcers

Lesions of NL are often asymptomatic. Sometimes there can be pruritus, dysesthesia and pain. There can be neurological findings within plaques such as decreased pain and light touch, decreased sweating and partial hairloss.

 

Distribution

Lesions are seldom solitary and often bilateral. Eighty-five percent occur on the legs, especially the shins. Rarely, lesions are found on the trunk, head, distal arms, palms and soles.

 

Differential diagnosis

Other granulomatous conditions should be considered:

• granuloma annulare
• sarcoidosis
• diabetic dermopathy
• stasis dermatitis
• panniculitis (e.g. erythema nodosum)
• granulomatous infections
• morphea
• necrobiotic xanthogranuloma

 

Investigations

• skin biopsy
• especially if concerned about a possible squamous cell carcinoma
• screen for diabetes
• consider leg arterial and venous studies
• severely ulcerated NL lesions require good circulation to heal

 

Treatment

The treatment of NL is challenging. There can be spontaneous resolution in up to 20% of patients after 6-12 years. Patients should be counselled to quit smoking and optimize diabetic control. Specific treatment is usually done in an attempt to prevent ulceration and reduce the risk of squamous cell carcinoma development.

Treatment options include:

• intralesional or topical corticosteroids under occlusion
• systemic corticosteroids (1-2 month course)
  • atrophy tends not to improve
  • seldom used as corticosteroids affect blood sugar control

 

Other treatment options

• topical tretinoin
  • pentoxifyllin
  • aspirin
    • goal: increase fibrinolysis, decrease platelet aggregation, decrease thromboxane A2 synthesis to decrease microangiopathy and vascular thrombosis
• niacinamide
• chloroquine
• topical PUVA
• cyclosporine
• biologicals (e.g. TNF-alpha inhibitors)
• excision and skin grafts
  • can have recurrences at edges!
  • must excise to deep fascia or periosteum to minimize chance of recurrence, split thickness skin grafting done following excision.