Pigmentary Disorders of the Skin

| Manon Paradis

C H A P T E R 92

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II. Dermatohistopathologic examination reveals an increased number of melanocytes in the epidermis and the presence of melanin pigment in most keratinocytes.

Differential Diagnosis

I. Pigmented neoplasms of the skin, especially melanocytomas and melanomas

II. Papillomavirus-induced lesions: characterized by slightly rough black-pigmented macules to plaques that may trans-form into squamous cell carcinoma

III. Pigmented epidermal nevi IV. Lentigo profusa

A. Hereditary form of lentigo previously reported in pugsB. May be papillomavirus-induced lesions or pigmented

epidermal nevi V. Aforementioned conditions: hyperkeratotic surface or

thickening

Treatment and Monitoring

I. None indicated: cosmetic condition only II. Benign skin change

Lentigo Simplex in Orange Cats

Defi nition and Causes

I. Multiple lentigines affecting mucocutaneous junctions, especially in orange cats

II. Cause unknown III. Most likely genetically determined

Pathophysiology

I. Hyperpigmented macules or patches result from an in-creased number of skin melanocytes and a hypermelanosis of the keratinocytes of the basal cell layer of the epidermis.

II. Focal proliferation of epidermis is not evident.

Clinical Signs

I. Lesions start as tiny black spots on the lips and often spread to the nose, gingiva, and eyelids (Figure 92-1).

II. Lentigines progressively increase in size (range from 1 to 9 mm in diameter) and number with age and may eventually coalesce.

III. Lesions may start in orange cats <1 year of age. IV. Lentigines are not symptomatic.

DISORDERS OF HYPERPIGMENTATION

Lentigo

Defi nition and Cause

I. In Latin, lentigo (plural, lentigines) is the word meaning lentil-shaped spot.

II. Lentigo describes the well-circumscribed black macules observed in mature dogs.

III. The cause of these lesions is usually unknown. IV. Hyperpigmented (Box 92-1) macules or patches result

from increased numbers of melanocytes in the epidermis, without evidence of focal proliferation.

Clinical Signs

I. Several well-circumscribed black macules develop over several months.

II. Subsequently they become static and remain unchanged for the life of the dog.

III. The most common location is on the ventrum. IV. The condition affects mature dogs. V. It is asymptomatic.

Diagnosis

I. Diagnosis is usually based on history and clinical fi ndings.

Box 92-1

Terminology Pertaining to Pigmentary Changes of Hair and Skin

Term Definition

Hyperpigmentation or Increased pigmentation of the hypermelanosis skin or hair coat in areas that

should be less pigmentedMelanoderma Skin hyperpigmentation Melanotrichia Hair hyperpigmentation Hypopigmentation or Lack of (or decrease in) pigmentation hypomelanosis of the skin or hair coat in areas

that should be pigmentedLeukoderma Depigmented skin or mucosa Leukotrichia Depigmented hair shaft

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902 SECTION 12 | Dermatologic System

Diagnosis

I. Diagnosis is usually based on history and clinical fi ndings. II. Dermatohistopathologic examination reveals marked hy-

permelanosis, predominantly of the basal cell layer of the epithelium, and increased numbers of melanocytes.

Differential Diagnosis

I. Melanocytoma (benign melanoma) II. Malignant melanoma

Treatment and Monitoring

I. None indicated II. Cosmetic condition only

Postinflammatory Hyperpigmentation

Defi nition and Causes

I. Skin hyperpigmentation after infl ammation is very com-mon (especially in dogs), regardless of the inciting cause of the infl ammation.

II. Hyperpigmentation is a common sequela to pyoderma, demodicosis, Malassezia spp. dermatitis, and dermato-phytosis in dogs.

III. Dermatophytosis is one of the few skin diseases of cats in which hyperpigmentation may be seen.

Pathophysiology

I. Exact mechanism of hyperpigmentation after infl amma-tion is unknown.

II. Hyperpigmentation associated with many pruritic diseases results from chronic irritation because of cutaneous friction in addition to infl ammatory processes.

Clinical Signs

I. Postinfl ammatory skin hyperpigmentation can be focal and well circumscribed, patchy, or diffuse.

II. Focal postinfl ammatory melanotrichia is seen occasionally in adult dogs with silver or gray hair coats.

III. Cutaneous hyperpigmentation is uncommon in cats.

Diagnosis

I. Diagnosis is usually based on history and clinical fi ndings. II. Identifi cation of an underlying cause is supportive.

Treatment and Monitoring

I. Identify and treat the underlying cause. II. Melanoderma usually resolves slowly (over weeks to months),

after the underlying cause has been corrected. III. In most cases melanotrichia resolves at the next shedding

cycle.

Hormonal-Associated Hyperpigmentation

Defi nition and Causes

I. Diffuse skin hyperpigmentation may result from endocrin-opathies, such as hyperadrenocorticism, hypothyroidism, hyperestrogenism, and alopecia X.

II. The mechanism of hyperpigmentation is unknown. III. Hyperpigmentation may result from direct and/or indirect

effects of hormones on melanocytes. IV. Tanning of alopecic skin exposed to ultraviolet light—the

most potent stimulus for melanogenesis—may also be a contributing factor.

Clinical Signs

I. Diffuse melanoderma is seen, particularly of hypotrichotic or alopecic skin.

II. Melanotrichia is observed occasionally after treatment of canine hyperadrenocorticism.

Diagnosis

I. Diagnosis is usually based on history and clinical fi ndings. II. Identifi cation of the underlying endocrinopathy is suppor-

tive.

Treatment and Monitoring

I. Identify and treat the underlying endocrinopathy. II. Hyperpigmentation usually resolves slowly (over weeks

to months), after the underlying endocrinopathy has resolved.

DISORDERS OF HYPOPIGMENTATION

Nasal Depigmentation

Defi nition and Causes

I. Acquired hypopigmentation of the nasal planum II. Also known as Dudley nose or snow nose

FIGURE 92-1 Lentigo simplex represented by multiple pigmented macules on the lips and nasal planum of an adult orange cat.

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CHAPTER 92 | Pigmentary Disorders of the Skin 903

III. Idiopathic disorder with genetic predisposition in golden retrievers, yellow Labrador retrievers, Siberian huskies and Alaskan malamutes

IV. Loss of pigment production by melanocytes of the nasal planum

Clinical Signs

I. Affected dogs are born with pigmented noses, but the black color of the nasal planum gradually lightens to a light brown (hypopigmentation) or pinkish color (depigmenta-tion) (Figures 92-2 and 92-3).

II. Changes may be permanent or may wax and wane in some dogs.

III. Typically worse during the winter months (hence the collo-quial name snow nose), with some increase in pigmentation in spring and summer.

IV. Other dermatologic lesions such as ulceration and crusts or pruritus are absent.

V. Normal cobble texture of the nasal planum is preserved, as opposed to autoimmune diseases in which the normal surface architecture is destroyed.

Diagnosis

I. Diagnosis is based on history and clinical fi ndings. II. Dermatohistopathologic examination reveals a marked re-

duction of epidermal melanin granules.

Differential Diagnosis

I. Vitiligo (see following section) II. Cutaneous (discoid) lupus erythematosus III. Pemphigus erythematosus IV. Epitheliotropic lymphoma (mycosis fungoides)

V. Uveodermatologic syndrome (Vogt-Koyanagi-Harada–like syndrome; Table 92-1)

Treatment and Monitoring

I. No known treatment is available. II. It is a cosmetic problem only. III. The condition is considered a defect in show dogs.

Vitiligo

Defi nition and Causes

I. Vitiligo is an acquired disorder characterized by selective destruction of melanocytes in skin and hair matrix cells, which results in leukoderma and leukotrichia (see Box 92-1).

II. Vitiligo is presumed to be hereditary in some breeds, such as the Belgian shepherd, rottweiler, Doberman pinscher, and Siamese cat.

Pathophysiology

I. Various theories have been proposed to explain vitiligo, including the production of antimelanocyte antibodies.

II. In general, vitiligo is a spontaneous disorder and is not accompanied by infl ammation.

Clinical Signs

I. One or several asymptomatic, possibly symmetrical, macular areas of leukoderma and/or leukotrichia develop, especially of the lips, buccal mucosa, muzzle, nasal planum, and footpads.

II. Depigmentation is usually permanent, but spontaneous repigmentation may occur.

III. It is usually fi rst noted in young adulthood. IV. The disorder is uncommon in dogs and rare in cats.

FIGURE 92-2 Depigmentation of the nasal planum in an adult Alaskan malamute (also called Dudley nose or snow nose).

FIGURE 92-3 Depigmentation of the nasal planum in an adult yellow Labrador retriever.

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TABLE 92-1

Miscellaneous Acquired Pigmentary Disorders

DISORDER DEFINITION AND CAUSE DIAGNOSIS CLINICAL SIGNS TREATMENT AND MONITORING

Melanotrichia Cats demonstrating Diagnosis is based on Melanotrichia develops No treatment is required of feline acromelanism (dark compatible history at the site of skin Melanotrichia usually acromelanism extremities or points), and clinical fi ndings infl ammation or after resolves at the next such as the Siamese and Changes are confi ned clipping of the truncal shedding cycle Himalayan breeds, develop to cats with area temporary coat color acromelanism changes consisting of melanotrichia after infl ammation or hair clipping Acquired Acquired pigment changes Diagnosis is based on Miniature schnauzers No known treatment aurotrichia are seen in the hair coat compatible history develop patches of exists (“gilding of miniature schnauzers, and physical golden hair in a Spontaneous resolution syndrome”) presumably caused by a examination previously normal, occurs in 6-24 months shift in eumelanins and fi ndings gray or black coat pheomelaninsMalnutrition Malnutrition is the cause— Diagnosis is based on Black hair changes to Feed a balanced diet specifi cally trace element suggestive history reddish or brown hair Condition normally defi ciencies such as and physical resolves when the copper and zinc, examination underlying cause is as well as low dietary fi ndings removed tyrosine or phenylalanineEndocrinopathies Lightening of the hair coat Diagnosis is based on Old retained hair shafts Treat the underlying occurs in dogs with suggestive history, become dry, frizzy, and cause Sertoli cell tumors, physical examination lighter in color Condition normally alopecia X, fi ndings, and resolves when the hypothyroidism, or appropriate diagnostic underlying cause is hyperadrenocorticism tests removedEnvironmental Color changes occur after Diagnosis is based on Old retained hair shafts Avoid excessive exposure factors exposure to chronic suggestive history become dry, frizzy, and to causative ultraviolet light or other and physical lighter in color environmental factors environmental elements examination Condition resolves (e.g., chlorine, detergents) fi ndings when the underlying

cause is removedUveodermatologic It is considered an immune- Diagnosis is based on Often acute onset of anterior Prednisone is syndrome mediated disease, with compatible history or panuveitis occurs administered 2 mg/kg melanocytes as the target and physical Possible retinal detachment, PO SID or divided Hair, skin, and the uveal tract examination fi ndings secondary glaucoma, and BID initially, then of the eyes are affected Histopathology of blindness may occur tapered once signs are Alaskan sled dogs and skin biopsies is Depigmentation of eyelids, controlled oriental breeds are diagnostic: lichenoid nose, lips, footpads, Azathioprine (1-2 mg/kg predisposed; also dermatitis with scrotum, and (sometimes) PO SID) may be documented in the many macrophages, haired areas of the body needed in addition to Australian shepherd, Irish uncommon apoptotic is seen prednisone for setter, golden retriever, cells in the basal cell Oral and cutaneous diffi cult to control St. Bernard, and other layer, pigmentary ulcerations are possible cases breeds incontinence in in severe forms See also Chapter 102 It may affect dogs of all ages depigmented areas Mild cutaneous signs include depigmentation of skin and hair, as well as mild scaling and erythema of affected areas Generalized or focal vitiligo is a classic fi nding

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CHAPTER 92 | Pigmentary Disorders of the Skin 905

Diagnosis

I. History of acquired depigmentation of one or several macular areas of skin, mucosa, or hair, with no history of previous trauma is highly suggestive.

II. Dermatohistopathologic examination reveals normal skin except for the absence of melanocytes and melanin.

Differential Diagnosis

I. Nasal depigmentation (Dudley nose, snow nose) II. Uveodermatologic syndrome (Vogt-Koyanagi-Harada–like

syndrome) III. Certain autoimmune diseases: cutaneous lupus erythema-

tosus, pemphigus erythematosus, pemphigus foliaceus IV. Alopecia areata: leukotrichia possibly seen in resolving

lesions V. Epitheliotropic lymphoma (mycosis fungoides) VI. Postinfl ammatory or posttraumatic hypopigmentation

Treatment and Monitoring

I. No known treatment is available. II. Vitiligo is a cosmetic disorder that does not affect the

animal’s quality of life.

Postinflammatory Hypopigmentation

Defi nition and Causes

I. It is an acquired hypopigmentation of previously normal skin and hair after destruction of melanocytes.

II. Potential causes include trauma, burns, and infection. III. A number of infl ammatory diseases may begin with hypo-

pigmentation of the nose and occasionally the lips, such as cutaneous lupus erythematosus, pemphigus erythematosus, pemphigus foliaceus, and uveodermatologic syndrome.

Pathophysiology

I. Selective destruction of melanocytes occurs in skin and hair matrix cells.

II. Secondary leukoderma and leukotrichia develop.

Clinical Signs

I. Leukoderma and/or leukotrichia develop at a site of pre-vious skin trauma.

II. Depigmentation is usually permanent.

Diagnosis

I. Acquired depigmentation occurs at the site of previous trauma, infection, or infl ammation.

II. It can occur in any breed of dog or cat.

Differential Diagnosis

I. Vitiligo and other hypopigmenting disorders II. Epitheliotropic lymphoma (see Chapter 91)

Treatment and Monitoring

I. Repigmentation may occur after treatment of the under-lying cause.

II. Sunscreen applied before sun exposure may prevent sunburn in the hypopigmented skin.

III. Depigmented skin may be prone to sunburn and subsequent actinic dermatitis.

MISCELLANEOUS ACQUIRED PIGMENTARY DISORDERS

See Table 92-1.

BibliographyAlhaidari Z: An approach to disorders of pigmentation. p. 66. In Foster

A, Foil C (eds): British Small Animal Veterinary Association Manual of Small Animal Dermatology. 2nd Ed. British Small Animal Veterinary Association, Quedeley, United Kingdom, 2003

Alhairdari Z, Olivry T, Ortonne JP: Melanocytogenesis and melano-genesis: genetic regulation and comparative clinical diseases. Vet Dermatol 10:3, 1996

Medleau L, Hnilica KA: Small Animal Dermatology. A Color Atlas and Therapeutic Guide. 2nd Ed. WB Saunders, Philadelphia, 2006

Scott DW, Miller WH, Griffi n CE: Mueller and Kirk’s Small Animal Dermatology. 6th Ed. WB Saunders, Philadelphia, 2001

Yu S, Rogers QR, Morris JG: Effect of low levels of dietary tyrosine on the hair color of cats. J Small Anim Pratct 42:176, 2001

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