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Overview of Acanthosis Nigricans

By Karen A. Moriello, DVM, DACVD, Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison

Acanthosis nigricans is 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. There is 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 or postinflammatory hyperpigmentation can occur in any breed of dog and at any age; it is most common in breeds predisposed to conditions 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 develop in all areas at the same time. Inflammation is mild but becomes more severe with time. Lesions of postsecondary inflammation are not necessarily present in both the axillary and inguinal region, nor are they necessarily symmetric. In primary acanthosis nigricans, secondary inflammatory lesions (ie, lichenification) most commonly develop as a result of conformational friction. Postinflammatory hyperpigmentation 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 primary acanthosis nigricans are not difficult to recognize. Postinflammatory hyperpigmentation is a clinical sign of an underlying disease and should be aggressively evaluated through a careful history and physical examination to identify the underlying trigger. Skin scrapings should be performed to exclude demodicosis, and impression smears should be performed to confirm suspected bacterial and Malassezia infections. Postinflammatory inflammation associated with endocrinopathies is not pruritic, and testing for thyroid and adrenal disease may be useful in older dogs; endocrine skin diseases are not pruritic unless accompanied by secondary skin infections. Intradermal skin testing and/or a food trial may be necessary. Skin biopsies are usually not necessary to confirm primary disease and are usually not helpful in identification of 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/day, PO, for 7–10 days, then on alternate days; melatonin, 2 mg/day/dog, SC, 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 postinflammatory hyperpigmentation, 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, therapy with narrow-spectrum drugs based on culture and susceptibility and/or use of topical chlorhexidine spray or baths is recommended. Culture is recommended to minimize development of methicillin-resistant staphylococci. Yeast infections may be successfully treated with concurrent oral itraconazole or ketoconazole (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.