Diabetes Mellitus and the Skin: Recognition and Management of Cutaneous Manifestations

William B. Horton, MD; Patrick L. Boler, MD, PharmD; Angela R. Subauste, MD


South Med J. 2016;109(10):636-646. 

In This Article

Dermatologic Conditions Associated With Both T1DM and T2DM

Diabetic Dermopathy

Diabetic dermopathy (DD), also known as shin spots, is considered to be the most common cutaneous marker of DM.[52] One study demonstrated that 40% of patients with DM in an Israeli hospital had DD, which was statistically significant in patients older than 50 years.[52] Population studies from Sweden show that DD affects 33% of patients with T1DM, 39% of patients with T2DM, and 2% of control subjects.[4,53] DD also appears to serve as a possible clinical indicator of the presence of more serious DM complications, including retinopathy, nephropathy, and neuropathy.[52]

DD presents clinically as small (<1 cm), well-demarcated, round-to-oval atrophic hyperpigmented lesions on the pretibial areas of the lower extremities (Fig. 4B).[4,54] The lesions usually are bilateral with an asymmetrical distribution. Histologically, lesions show edema of the papillary dermis, thickened superficial blood vessels, extravasation of erythrocytes, and a mild lymphocytic infiltrate.[55–57] The extravasated erythrocytes leave hemosiderin deposits, which provide the brownish hyperpigmentation.[56]

The diagnosis of DD usually is made by clinical appearance, although biopsy can be used for confirmation in unclear cases. No treatment is necessary for DD, which is asymptomatic and does not lead to morbidity.[10] Lesions tend to resolve spontaneously on their own within 1 to 2 years, leaving atrophic hypopigmentation at the site of origin.[4,10,58]


Xerosis, or xeroderma, refers to dry skin. It is the second most common DM skin manifestation.[4] One prospective study has identified xerosis in 26.4% of patients with DM.[3] Patients with DM often have autonomic neuropathy, a complication that increases the risk for xerosis.[58,59] The presence of xerosis increases the risk of complications, including infection and ulceration.

The manifestations of xerosis occur along a spectrum, becoming more serious as the condition persists and/or worsens. When skin is overly dry, it initially reddens and develops cracks.[60] If dryness continues, the skin also may begin to scale or flake. Winter is a peak time for dry skin because of the low humidity in ambient air and heating units that force hot, dry air into the home or workplace.[61] Air conditioning also may induce xerosis because it removes much of the moisture from the air.[61,62]

The diagnosis of xerosis is made based on clinical appearance and presentation. Referral to a dermatologist is not necessary.[4] PCPs should educate patients about the importance of skin hygiene, including applying fragrance-free creams or lotions within 3 minutes of finishing bathing to enhance moisturization of the skin.[4]


Psoriasis is a chronic, immune-mediated inflammatory skin disorder, and both genetic and environmental factors contribute to its development.[4,63] The appearance of psoriasis typically is characterized by erythematous scaly papules and plaques occurring most commonly in areas of skin friction, such as the scalp, elbows, knees, hands, feet, trunk, and nails.[4] Approximately 9% of patients with either T1DM or T2DM have psoriasis.[64] One study has demonstrated that psoriasis is associated with increased incidence rates of new-onset DM.[65]

Psoriasis usually can be diagnosed based on physical examination.[66] Laboratory and histopathologic confirmation rarely is needed; however, if the clinical diagnosis is unclear, then skin biopsy may be used for confirmation.[66] Most patients diagnosed as having psoriasis need referral to a dermatologist for further management.[4] Treatment consists of topical (eg, tacrolimus cream) and systemic (eg, methotrexate) immunomodulators, as well as UV light and laser application.[4] Topical treatments are effective in most cases; however, they carry a 40% adherence rate because of the time-consuming application and cosmetic inappropriateness.[65] Phototherapy with PUVA and UVB has been used for several decades with good treatment response in mild cases.[4,67] Moderate to severe cases of psoriasis respond well to combination treatment with phototherapy and biologics.[68]

Granuloma Annulare

Granuloma annulare (GA) is a noninfectious granulomatous skin condition characterized by collagen degeneration, mucin deposition, and palisaded or interstitial histiocytes.[69] Although the exact cause of GA is unknown, a cell-mediated hypersensitivity reaction to an unknown antigen is favored as the mechanism.[70–73] GA presents typically as erythematous to flesh-colored papules coalescing to form an oval or a ring lesion (Fig. 5).[4] GA lesions may resemble tinea corporis infection; however, lack of symptoms, scale, and associated vesicles can be used to help differentiate GA from tinea corporis.[74]

Figure 5.

(A) Localized granuloma annulare: well-circumscribed, erythematous annular plaque on dorsal hand. (B) Generalized granuloma annulare: coalescing erythematous round to oval plaques.

The relation between GA and DM has been controversial.[4,69] Early studies suggested a link between the two conditions,[75,76] but more recent studies have questioned the strength of this association.[77,78] A retrospective study by Studer et al failed to find a statistically significant association between GA and DM;[78] however, patients with both conditions tended to have more chronic and relapsing disease than did nondiabetic patients.[79]

GA often presents asymptomatically but can cause pruritus and/or a burning sensation.[80] Patients with classic features of GA often are diagnosed based on clinical findings alone.[70] In patients with clinically atypical lesions or cases in which other nongranulomatous conditions remain in the differential diagnosis, biopsy should be performed for confirmation.[70] Treatment can be categorized into local, skin-directed therapy and systemic immunomodulatory or immunosuppressive therapy.[70] Treatment selection is based on the severity of the disease and patient preference.[70] Treatment options include topical or intralesional steroids, isotretinoin, dapsone, antimalarials, and phototherapy.[4] For localized disease, topical steroids are the first-line treatment.[80] Intralesional steroids can be used for localized disease that does not respond to topical steroids.[80] Antimalarials, isotretinoin, and systemic biologic therapy (in particular, adalimumab and infliximab) have demonstrated efficacy in the treatment of generalized GA.[70]

Acquired Perforating Dermatosis

Acquired perforating dermatosis (APD) is a chronic skin disorder characterized histologically by transepidermal perforation and elimination of a connective tissue portion of the dermis.[26,81] APD presents as highly pruritic, dome-shaped papules and nodules with an umbilicated central keratin plug.[4,26] Lesions are seen typically on the extensor surfaces of the extremities and trunk, and less often, the head.[25] This condition has been associated with DM, chronic kidney disease, and hemodialysis (often related to diabetic nephropathy).[4,26] APD has been linked specifically to both T1DM and T2DM.[24,25,82] The pathogenesis is poorly understood. Hypotheses include metabolic derangements causing an epidermal or dermal alteration; a deposition of some substance not removed by dialysis, which the immune system then perceives as foreign; and/or microtrauma secondary to scratching/excoriation or a manifestation of microangiopathy.[26,80,82–85]

Diagnosis is clinical and based on characteristic appearance and the patient's history (eg, the diagnosis of associated conditions such as DM and chronic kidney disease). APD in the setting of DM is relatively unresponsive to treatment.[26] Treatment options include avoidance of scratching/excoriation, topical or systemic steroids, phototherapy, retinoids, and antihistamines.[4] Lesions may resolve slowly by avoiding trauma to the area; therefore, symptomatic relief of pruritus is an important treatment strategy.[26] Hemodialysis has not shown therapeutic value, but renal transplant has shown efficacy in clearing lesions.[84]

Rubeosis Faciei

Rubeosis faciei (RF), also termed rubeosis faciei diabeticorum, is a relatively common microangiopathic complication associated with DM.[4,86] RF presents as flushing of the face, leading to a generalized reddish complexion.[4,17] One study identified RF in 3.2% of patients with DM,[3] whereas an older study performed in Jerusalem found that RF occurred in up to 59% of hospitalized patients with DM.[87] The appearance of RF often is a sign of poor glycemic control.[4,17] Hyperglycemia in patients with DM is believed to result in sluggish microcirculation, which can lead to facial venous dilatation.[86] If recognized, RF should alert clinicians to look for other microangiopathic complications such as retinopathy.[4,86]

Diagnosis is clinical and based on characteristic appearance. The mainstay of treatment is strict glycemic control, which can improve the appearance of RF and prevent complications of microangiopathy in other organ systems.[4,17,50]

Periungual Telangectasias

Periungual telangectasias (PT) represents another reddish color change seen in diabetic skin, specifically of the proximal nailfold.[26] PT presents as nailfold erythema, dilated capillaries around the nail bed visible to the naked eye, fingertip tenderness, and thick cuticles.[4] PT arises in the nail beds of patients with DM after the loss of capillary loops and dilatation of the superficial vascular plexus.[4,26] One study identified PT in 49% of patients with DM.[88] PT is believed to represent underlying diabetic microangiopathy.[89]

The diagnosis of PT can be made clinically. Other than occasional fingertip tenderness, patients often are asymptomatic[26] and no treatment is necessary.[4]


Onychodystrophy presents as excessive nail thickening and deformity, which may cause the accumulation of debris and subsequent infection of the toe that should be treated as a diabetic ulcer.[4] The condition itself may cause diabetic foot ulcers.[90,91] In patients with DM, onychodystrophy often is the result of poor peripheral circulation and diabetic nephropathy.[4]

Diagnosis can be made by clinical appearance. Poorly fitting shoes may cause repeated trauma and worsening of the injured site.[4,21] Proper nail care, well-fitting shoes, and immediate attention to nail infections are the mainstays of treatment.[4]

Lichen Planus

Lichen planus (LP) is a chronic inflammatory disease affecting the skin, mucous membranes, scalp, and nails.[92] It occurs in 0.4% to 1.9% of the population[92] and commonly affects individuals older than 45 years.[93] LP has a higher prevalence in patients with DM, with various studies demonstrating it in 2% to 4% of patients with either T1DM or T2DM.[94,95] It is classically described by the "four P's": pruritic, purple (violaceous), polygonal, and papules or plaques.[4] Cutaneous LP presents as grouped, symmetric, erythematous to violaceous, flat-topped, and polygonal papules distributed mainly in the flexural aspects of arms and legs (Fig. 6);[96] variants may include ulcerative and perforating types.[4] Oral lesions also may occur; these can burn, be asymptomatic, or be painful.[97] LP in the mucous membranes usually presents as white lace-like lesions that are found in the lateral buccal mucosa, sometimes involving the lips, gingivae, and tongue.[98] The exact pathogenesis of LP remains unclear, but it has been postulated to be a T-cell–mediated autoimmune process, resulting in damage of keratinocytes.[99–101]

Figure 6.

Cutaneous lichen planus: violaceous, flat topped papules (A) Leg, (B) forearm, and (C) oral lichen planus: reticulated white lines of the buccal mucosa.

The diagnosis of LP often can be made based on clinical findings.[4] If clinical diagnosis is uncertain, then biopsy is indicated.[4] Multiple treatment options exist, but few higher-order treatment studies have been conducted because of the typical spontaneous remission of LP.[95,102] Cutaneous LP often resolves spontaneously within 1 to 2 years, whereas LP affecting mucosal membranes may be more persistent and resistant to treatment.[101] Even with treatment, recurrences are common.[101] High-potency topical corticosteroids are the first-line therapy for cutaneous LP.[103] It should be noted that medium- to low-potency topical corticosteroids are recommended for the face and intertriginous areas because high-potency steroids in these areas cause steroid-induced atrophy.[4] Intralesional corticosteroids should be used for thicker lesions.[4,104] Another important component of cutaneous LP treatment focuses on pruritus control[102] and often can be achieved with oral antihistamines (eg, hydroxyzine).[102] With generalized involvement, phototherapy can be added to the treatment regimen.[4] Systemic glucocorticoids, phototherapy with PUVA and UVB, and oral acitretin can be beneficial for patients who are not candidates for topical corticosteroid therapy.[4]