Acanthosis nigricans describes a clinical reaction in dogs characterized by axillary and inguinal hyperpigmentation, lichenification, and alopecia.
Etiology and Clinical Findings
Acanthosis nigricans is a disorder of hyperpigmentation that has no sex predilection. Primary acanthosis nigricans is a genodermatosis that can occur in many breeds but particularly Dachshunds. Clinical signs are usually present by 1 yr of age in this breed. Secondary acanthosis nigricans can occur in any breed of dog and at any age; it is most common in breeds predisposed to diseases that result in inflammation of the axillary or inguinal region due to conformational abnormalities, obesity, endocrinopathies (eg, hypothyroidism, hyperadrenocorticism, sex hormone abnormalities), axillary and inguinal pruritus associated with atopic dermatitis, food allergy, contact dermatitis, primary disorders of keratinization, and skin infections (eg, staphylococcal pyoderma, Malassezia dermatitis).
Clinical signs start with increased pigmentation in the axillary and/or inguinal region. In primary acanthosis nigricans, the hyperpigmentation is initially diffuse and noninflammatory. It tends to develop uniformly in the affected areas. In secondary acanthosis nigricans, the distribution is patchy and often starts with a lacey appearance. It may not occur in all areas at the same time. Inflammation is mild but becomes more severe with time. Lesions in secondary acanthosis nigricans are not necessarily present in both the axillary and inguinal region, nor are they necessarily symmetric. In primary acanthosis nigricans, the development of secondary inflammatory lesions (ie, lichenification) most commonly occurs as a result of conformational friction. Secondary acanthosis nigricans is triggered by inflammation and/or friction. Lesions can develop into severe areas of hyperpigmentation, with marked lichenification, hair loss, and seborrhea. Often, these areas are odiferous and may be painful. The edges of these lesions are often erythematous; this is a sign of secondary bacterial and/or yeast pyoderma. With time, lesions may spread to the ventral neck, groin, abdomen, perineum, hocks, periocular area, and pinnae. Pruritus is variable and is usually the result of secondary microbial overgrowth (staphylococcal or Malassezia dermatitis) or pruritus from the underlying disease.
The physical findings compatible with a clinical diagnosis of acanthosis nigricans are not difficult to recognize. Primary acanthosis nigricans is a diagnosis of exclusion; acanthosis nigricans in a juvenile Dachshund is not always caused by a genodermatosis. A careful history and physical examination should be performed to identify an underlying cause. Skin scrapings should be performed to rule out demodicosis, especially in young dogs. Impression smears should be performed to confirm suspected bacterial and Malassezia infections. Depending on the nondermatologic signs, endocrine function tests for thyroid and adrenal disease may be useful; endocrine skin diseases are not pruritic unless accompanied by secondary skin infections. Intradermal skin testing, a food trial, or both may be necessary. Skin biopsies are usually not necessary to confirm primary disease and are usually not helpful in identification of the underlying disease associated with secondary disease, with the possible exception of primary seborrhea. In some cases, skin biopsy can identify secondary bacterial infections not previously recognized. The presence of such infections is common; secondary infections are underdiagnosed in this condition. In most cases, it is useful to treat the secondary bacterial and/or Malassezia infections before proceeding with other diagnostic tests.
Primary acanthosis nigricans in Dachshunds is not curable. In some dogs, lesions do not progress beyond a cosmetic problem. If inflammation is present, early cases may respond to antimicrobial shampoo therapy and local topical glucocorticoids, eg, triamcinolone acetate spray or betamethasone valerate ointment. As lesions progress, more aggressive systemic therapy may be useful. The following systemic therapies have been used, alone or in combination, with varying degrees of success: vitamin E, 200 IU, PO, bid, for 2–3 mo; systemic glucocorticoids, 1 mg/kg, PO, sid for 7–10 days, then on alternate days; melatonin, 2 mg/dog, SC, sid for 3–5 days, then weekly or monthly as needed. The concurrent treatment of secondary bacterial or Malassezia infections is helpful and is required before systemic glucocorticoids are administered; antimicrobial therapy is compatible with the other therapies. Antiseborrheic shampoos are often beneficial for removing excess oil and odor but must be used frequently (ie, 2–3 times/wk).
In secondary acanthosis nigricans, most of the lesions will resolve after identification and correction of the underlying cause. Some residual lacey hyperpigmentation may remain. Treatment of secondary bacterial and yeast overgrowth is critical. If the dog has not been previously treated for a staphylococcal bacterial infection of the skin, empiric therapy with narrow-spectrum drugs such as oral trimethoprim-sulfonamide (15–30 mg/kg, bid), erythromycin (10–20 mg/kg, tid), or lincomycin (15–30 mg/kg, bid) are indicated. Cephalexin (30 mg/kg, bid) may be the most cost-effective drug in large dogs. Dogs receiving longterm therapy or multiple drug courses should be treated based on bacterial culture and sensitivity; methicillin-resistant staphylococci are becoming more common. Yeast infections may be successfully treated with concurrent oral itraconazole, ketoconazole, or fluconazole (5–10 mg/kg). Affected dogs benefit greatly from appropriate antimicrobial therapy and antiseborrheic shampoos (2–3 times/wk). If the lesions are caused by friction, emollients may be beneficial.
Clinical signs resolve slowly, possibly over months.
Last full review/revision July 2011 by Karen A. Moriello, DVM, DACVD