CHAPTER | 9 Hereditary, Congenital, and Acquired Alopecias

Excessive Shedding

Alopecic Breeds

Canine Hypothyroidism

Canine Hyperadrenocorticism (Cushing’s disease)

Postclipping Alopecia

Alopecia X (adrenal sex hormone imbalance, congenital adrenal hyperplasia, castration-responsive dermatosis, adult-onset hyposomatotropism, growth hormone–responsive dermatosis, pseudo-Cushing’s disease, follicular arrest of plush-coated breeds, hair cycle arrest)

Feline Paraneoplastic Alopecia/Dermatitis

Feline Hyperadrenocorticism

Sex Hormone Dermatosis—Intact Male Dogs

Sex Hormone Dermatosis—Intact Female Dogs

Congenital Hypotrichosis

Color Dilution Alopecia (color mutant alopecia)

Black Hair Follicular Dysplasia

Canine Pattern Baldness

Idiopathic Bald Thigh Syndrome of Greyhounds

Canine Recurrent Flank Alopecia (seasonal flank alopecia, cyclic flank alopecia, cyclic follicular dysplasia)

Miscellaneous Canine Follicular Dysplasias

Feline Preauricular and Pinnal Alopecias

Anagen and Telogen Defluxion

Traction Alopecia

Alopecia Areata

Feline Psychogenic Alopecia (neurodermatitis)

Excessive Shedding

Features

Shedding is a normal phenomenon in dogs and cats, but some animals shed more than others—a common owner complaint. Some animals shed more in spring and fall, and others shed excessively year round. In spite of continual hair loss, no alopecia or skin abnormalities are associated. Although hairs may epilate easily, focal areas of alopecia cannot be created.

Top Differentials

Differentials include superficial pyoderma, dermatophytosis, demodicosis, anagen or telogen defluxion, and causes of endocrine alopecia.

Diagnosis

1 Based on history, clinical findings, and rule out other differentials.

Alopecic Breeds

Features

These dogs and cats are bred deliberately to produce hairless offspring. Alopecic breeds include the Mexican Hairless dog, Chinese Crested dog, Inca Hairless dog, American Hairless terrier, and Sphinx cat.

Generalized truncal alopecia at birth is typical. Mild secondary pyodermas or seborrhea may develop in dogs. Sphinx cats, because of reluctance to groom, often become greasy, seborrheic, and malodorous. Comedones and milia are common.

Diagnosis

1 Based on signalment, history, and clinical findings.

2 Dermatohistopathology: atrophic, decreased numbers or complete absence of hair follicles. Adnexa are often similarly affected. Follicular dilatation and hyperkeratosis are common.

Treatment and Prognosis

1 Antiseborrheic follicular flushing (comedolytic) antibacterial shampoo baths and conditioners should be used as needed for secondary seborrhea and pyoderma.

2 The prognosis is good. These animals are meant to be hairless.

FIGURE 9-3 Alopecic Breeds.

This Chinese Crested demonstrates the characteristic pattern of alopecia typical of this breed.

FIGURE 9-4 Alopecic Breeds.

A Mexican Hairless dog with generalized alopecia.

FIGURE 9-5 Alopecic Breeds.

A Sphinx cat, demonstrating the almost total alopecia typical of this breed.

FIGURE 9-6 Alopecic Breeds.

Numerous comedones caused by occlusion of dystrophic hair follicles. As these breeds age, comedones and milia are common.

FIGURE 9-7 Alopecic Breeds.

Numerous comedones on the trunk of an adult Chinese Crested.

FIGURE 9-8 Alopecic Breeds.

The Chinese Crested with facial alopecia typical of the breed.

FIGURE 9-9 Alopecic Breeds.

Numerous comedones on the inner thigh of a Chinese Crested.

FIGURE 9-10 Alopecic Breeds.

Numerous comedones on the abdomen.

FIGURE 9-11 Alopecic Breeds.

Over time, the occluded follicles form milia, which appear as white, papular lesions.

FIGURE 9-12 Alopecic Breeds.

Numerous comedones and milia on the neck of an older Chinese Crested.

Canine Hypothyroidism

Features

This endocrinopathy is most often associated with primary thyroid dysfunction caused by lymphocytic thyroiditis or idiopathic thyroid atrophy. It is common in dogs, with highest incidence in middle-aged to older dogs. Young adult large and giant-breed dogs also are occasionally affected. Congenital hypothyroidism is extremely rare.

A variety of cutaneous symptoms can be seen. Alopecia on the bridge of the nose occurs in some dogs as an early symptom. The hair coat may be dull, dry, and brittle. Bilaterally symmetrical alopecia that spares the extremities may occur, with easily epilated hairs. Alopecic skin may be hyperpigmented, thickened, or cool to the touch. Thickened and droopy facial skin from dermal mucinosis, chronic seborrhea sicca or oleosa, or ceruminous otitis externa may be present. Seborrheic skin and ears may be secondarily infected with yeast or bacteria. In some dogs, the only symptom is recurrent pyoderma or adult-onset generalized demodicosis. Pruritus is not a primary feature of hypothyroidism and, if present, reflects secondary pyoderma, Malassezia infection, or demodicosis. Noncutaneous symptoms of hypothyroidism are variable and may include aggression, lethargy or mental dullness, exercise intolerance, weight gain or obesity, thermophilia (cold intolerance), bradycardia, vague neuromyopathic or gastrointestinal signs, central nervous system involvement (e.g., head tilt, nystagmus, hemiparesis, cranial nerve dysfunction, hypermetria), and reproductive problems (e.g., decreased libido, prolonged anestrus, infertility). Puppies with congenital hypothyroidism are disproportionate dwarfs with short limbs and neck relative to their body length.

Top Differentials

Differentials include other causes of endocrine alopecia, superficial pyoderma, Malassezia dermatitis, and demodicosis.

Diagnosis

1 Rule out other differentials.

2 Hemogram and serum biochemistry panel: nonspecific findings may include a mild, nonregenerative anemia, hypercholesterolemia, or elevated creatine kinase.

3 Dermatohistopathology: usually, nonspecific endocrine changes or findings consistent with pyoderma, Malassezia dermatitis, or seborrhea are seen. If present, dermal mucinosis is highly suggestive of hypothyroidism, but this can be a normal finding in some breeds (e.g., Shar pei).

4 Serum total thyroxine (TT₄), free thyroxine (FT₄) by equilibrium dialysis, and endogenous thyroid-stimulating hormone (TSH) assays: low TT₄, low FT₄, and high TSH are highly suggestive of hypothyroidism, but false-positive and false-negative results can occur, especially with TT₄ and TSH. For example, although TT₄ is a good screening test, it should not be used alone to make a diagnosis because its serum level can be artificially increased or decreased by several factors, such as nonthyroidal illness, autoantibodies, and drug therapy (Box 9-1).

Treatment and Prognosis

1 Any secondary seborrhea, pyoderma, Malassezia dermatitis, or demodicosis should be treated with appropriate topical and systemic therapies.

2 Levothyroxine 0.02 mg/kg PO should be administered every 12 hours until symptoms resolve (approximately 8–16 weeks). Some dogs then can be maintained with 0.02 mg/kg PO every 24 hours; others require lifelong twice-daily dosing to maintain remission.

3 Dogs with concurrent heart disease should be started on levothyroxine more gradually. Treatment should begin with 0.005 mg/kg PO every 12 hours; dosage should be increased by 0.005 mg/kg every 2 weeks until 0.02 mg/kg every 12 hours is being administered.

4 After 2 to 4 months of therapy, serum TT₄ level should be measured 4 to 6 hours after medication administration and should be in the high normal to supranormal range. If the level is low or within the normal range, and if minimal clinical improvement has been seen, the dosage of levothyroxine should be increased and the serum TT₄ level checked 2 to 4 weeks later.

5 If signs of thyrotoxicosis from oversupplementation (e.g., anxiety, panting, polydipsia, polyuria) occur, the serum TT₄ level should be evaluated. If the level is markedly elevated, medication should be temporarily stopped until adverse effects abate; it then should be reinstituted at a lower dose or a less frequent dosage schedule.

6 The prognosis is good with lifelong replacement thyroxine therapy, although hypothyroidism-induced neuromuscular abnormalities may not completely resolve.

FIGURE 9-13 Canine Hypothyroidism.

An obese Rottweiler with hypothyroidism. Note that the hair coat lacks the bilaterally symmetrical alopecia that is considered characteristic of this disease.

FIGURE 9-14 Canine Hypothyroidism.

Generalized truncal alopecia in an adult collie.

FIGURE 9-15 Canine Hypothyroidism.

Mild alopecia on the bridge of the nose may be an early lesion of hypothyroidism.

FIGURE 9-16 Canine Hypothyroidism.

Alopecia and hyperpigmentation with no evidence of secondary superficial pyoderma on the trunk.

FIGURE 9-17 Canine Hypothyroidism.

Generalized seborrhea sicca can be caused by numerous underlying conditions, including hypothyroidism.

FIGURE 9-18 Canine Hypothyroidism.

General alopecia of the tail caused by hypothyroidism.

FIGURE 9-19 Canine Hypothyroidism.

Alopecia on the lumbar area and tail head. Note the similarity to flea allergy dermatitis and postclipping alopecia.

FIGURE 9-20 Canine Hypothyroidism.

Alopecia of the tail tip.

FIGURE 9-21 Canine Hypothyroidism.

The hair of this affected Irish Setter became faded over time as a result of the follicular arrest that occurs with hypothyroidism.

FIGURE 9-22 Canine Hypothyroidism.

Severe fading of the hair coat with partial alopecia in a hypothyroid Irish Setter.

FIGURE 9-23 Canine Hypothyroidism.

Same dog as in Figure 9-22. The extremely faded hair coat also demonstrates partial alopecia (the matting is not typical of this disease).

FIGURE 9-24 Canine Hypothyroidism.

Same dog as in Figure 9-22. Faded hair is apparent on the dorsal surface of the foot. Note the abnormal nails, which developed as a result of the metabolic effects of hypothyroidism.

FIGURE 9-25 Canine Hypothyroidism.

Same dog as in Figure 9-22. Abnormal nails developed as a result of the abnormal metabolism caused by the disease.

FIGURE 9-26 Canine Hypothyroidism.

Generalized fading caused by the lack of normal follicular cycling and hair renewal.

FIGURE 9-27 Canine Hypothyroidism.

A tragic facial expression is characteristic of this disease.

Canine Hyperadrenocorticism (Cushing’s disease)

Features

Spontaneously occurring hyperadrenocorticism is associated with excessive production of endogenous steroid hormones (principally glucocorticoids, but sometimes mineralocorticoids or sex hormones) by the adrenal cortex. The disease is caused by a hyperfunctioning adrenal tumor (15%–20% of cases) or pituitary tumor (80%–85% of cases). Pituitary-dependent hyperadrenocorticism (PDH) is caused by excessive production of adrenocorticotropic hormone (ACTH), usually from a pituitary microadenoma or macroadenoma. Iatrogenically induced disease occurs secondary to excessive administration of exogenous glucocorticoids. Iatrogenic hyperadrenocorticism can occur at any age and is common, especially in chronically pruritic dogs and dogs with immune-mediated disorders that are controlled with long-term glucocorticoids. Spontaneously occurring hyperadrenocorticism is also common and tends to occur in middle-aged to older dogs, with an increased incidence noted in Boxers, Boston terriers, Dachshunds, Poodles, and Scottish terriers.

The hair coat often becomes dry and lusterless, and slowly progressing, bilaterally symmetrical alopecia is common. Alopecia may become generalized, but it usually spares the head and limbs. Remaining hairs are easily epilated, and alopecic skin is often thin, hypotonic, and hyperpigmented. Cutaneous striae and comedones may be seen on the ventral abdomen. The skin may be mildly seborrheic (fine, dry scales), bruise easily, and exhibit poor wound healing. Chronic secondary superficial or deep pyoderma, dermatophytosis, or demodicosis is common and may be the client’s primary complaint. Calcinosis cutis (whitish, gritty, firm, bonelike papules and plaques) may develop, especially at the dorsal midline of the neck or ventral abdomen, or in the inguinal area.

Polyuria and polydipsia (water intake >100 mL/kg/day) and polyphagia are common. Muscle wasting or weakness, a pot-bellied appearance (from hepatomegaly, fat redistribution, and weakened abdominal muscles), increased susceptibility to infection (conjunctival, skin, urinary tract, lung), excessive panting, and variable behavioral or neurologic signs (expanding pituitary tumor) are often present.

Top Differentials

Differentials include other causes of endocrine alopecia, follicular dysplasia, alopecia X, superficial pyoderma, demodicosis, and dermatophytosis.

Diagnosis

1 Hemogram: neutrophilia, lymphopenia, and eosinopenia are often seen.

2 Serum biochemistry panel: an elevated alkaline phosphatase enzyme level is typical (90% of cases). Mildly to markedly elevated alanine transaminase activity, as well as elevated cholesterol, triglyceride, or glucose levels, may occur.

3 Urinalysis: the specific gravity is usually low, and bacteriuria, proteinuria, or glucosuria may be present. Subclinical urinary tract infections are common.

4 Urine cortisol/creatinine ratio: usually elevated. A nonspecific screening test that is not diagnostic by itself because false-positive results are common (stress-induced, seen with many other illnesses). To minimize the effects of stress, a home-collected urine sample should be used, instead of one obtained at the veterinary hospital.

5 Dermatohistopathology: often shows nondiagnostic changes consistent with any endocrinopathy. Dystrophic mineralization (calcinosis cutis), thin dermis, and absent erector pili muscles are highly suggestive of hyperadrenocorticism, but these changes are not always present.

6 Abdominal ultrasonography: may demonstrate adrenal hyperplasia or tumor.

7 Computed tomography (CT) or magnetic resonance imaging (MRI): may detect a pituitary mass.

8 Adrenal function tests:

ACTH stimulation test (cortisol): an exaggerated poststimulation cortisol level is highly suggestive of endogenous hyperadrenocorticism, but false-negative and false-positive results can occur. In iatrogenic cases, an inadequate response to ACTH stimulation is typical. Note: Reconstituted cosyntropin (ACTH solution) can be stored frozen at −20°C in plastic syringes for up to 6 months with no adverse effects on its bioactivity.

ACTH stimulation test (17-hydroxyprogesterone): exaggerated basal and poststimulation 17-hydroxyprogesterone levels may be seen in endogenous hyperadrenocorticism, but false-negative and false-positive results can occur. 17-Hydroxyprogesterone, a progestin, is an adrenal gland–produced precursor of cortisol.

Low-dose (0.01 mg/kg) dexamethasone suppression test: inadequate cortisol suppression is highly suggestive of endogenous hyperadrenocorticism, but false-negative and false-positive results can occur. Suppression at 4 hours followed by escape from suppression at 8-hour sampling is characteristic of PDH.

High-dose (0.1 mg/kg) dexamethasone suppression test: used to help differentiate between adrenal neoplasia and pituitary-dependent hyperadrenocorticism. Lack of cortisol suppression is suggestive of adrenal neoplasia, whereas cortisol suppression suggests pituitary disease.

Endogenous ACTH assay: used to help differentiate between adrenal neoplasia and pituitary-dependent hyperadrenocorticism. An elevated ACTH level is suggestive of pituitary disease, whereas a depressed ACTH level is suggestive of adrenal neoplasia.

Treatment and Prognosis

1 Any concurrent infection (e.g., pyoderma, demodicosis, urinary tract infection) should be treated with appropriate therapy. Any secondary pyoderma, otitis externa, or Malassezia dermatitis should be treated with appropriate therapy. Controlling and preventing secondary infection is an essential component of managing atopic dogs. Bathing every 3 to 7 days and treating the ears after every bath helps disinfect the skin and ear canals, preventing the recurrence of secondary infection.

2 The treatment of choice for iatrogenic Cushing’s cases is to progressively taper, then discontinue glucocorticoid therapy.

3 Treatment of choice for adrenal neoplasia is adrenalectomy.

Dogs with inoperable adrenal tumors or metastases may benefit from mitotane or trilostane therapy.

Mitotane for adrenal tumors: one should give 50 mg/kg PO every 24 hours with food for 7 to 14 days. An ACTH stimulation test is performed every 7 days. If inadequate cortisol suppression persists, increase the mitotane dosage to 75–100 mg/kg/day for an additional 7 to 14 days, while monitoring with ACTH stimulation tests weekly. When adequate adrenal suppression is demonstrated, maintenance mitotane therapy is initiated as described below.

4 The traditional (historical) medical treatment of choice for PDH is mitotane 50 mg/kg PO administered every 24 hours with food. The daily dosage is continued until the basal serum or plasma cortisol level normalizes and does not increase after ACTH stimulation. Control is usually achieved within 5 to 10 days of initiation of therapy, so the patient should be closely monitored with ACTH stimulation tests performed every 7 days. Monitoring water and food intake before and during induction may be useful. Water and food intake often markedly decreases when adequate adrenal suppression has been achieved. If signs of adrenal insufficiency (e.g., anorexia, depression, vomiting, diarrhea, ataxia, disorientation) develop, mitotane therapy should be stopped and hydrocortisone 0.5 to 1.0 mg/kg PO every 12 hours administered, until symptoms resolve.

To maintain remission after mitotane induction, mitotane PO with food 50 mg/kg administered once weekly, or 25 mg/kg twice weekly. Dogs that relapse during maintenance therapy should be reinduced with daily mitotane for 5 to 14 days or until recontrolled, then maintained with 62 to 75 mg/kg once weekly, or 31 to 37.5 mg/kg twice weekly. A great deal of patient variability occurs, requiring close monitoring.

5 A more recent treatment option and the current recommendation for the medical treatment of PDH is trilostane. At this writing, its optimal dosing regimen has not yet been determined, but many investigators are using the following protocol:

Dogs <5 kg: give 30 mg PO with food q 24 hours

Dogs between 5 and 20 kg: give 60 mg PO with food q 24 hours

Dogs between 20 and 40 kg: give 120 mg PO with food q 24 hours

Dogs >40 kg: give 240 mg PO with food q 24 hours

Assess efficacy by monitoring clinical signs and evaluating results of ACTH stimulation tests 10 days, 4 weeks, and 12 weeks after the start of therapy, then every 3 months thereafter. ACTH stimulation tests should be performed 4 to 6 hours after trilostane dosing. A post-ACTH cortisol level <150 nmol/L (but >20 nmol/L) is usually consistent with good control. However, optimal clinical control has also been reported with post-ACTH cortisol concentrations between 150 and 250 nmol/L, so blood work results should always be interpreted alongside clinical signs. If the dog is not clinically well controlled and post-ACTH cortisol concentrations are >150 nmol/L, the dose of trilostane should be increased. Dose adjustments should be made in increments of 20 to 30 mg/dog. A wide range of trilostane doses to induce and maintain remission have been reported in dogs, with the therapeutic dose for most dogs between 4 and 20 mg/kg/day. Some dogs may require twice-daily dosing if duration of effect is inadequate. Clinical signs such as polydipsia/polyuria/polyphagia often start to improve within the first 10 days of treatment, but alopecia and other skin changes may take 3 or more months to improve. If signs of adrenal insufficiency (depression, inappetence, vomiting, diarrhea) develop at any time during therapy, or if post-ACTH cortisol concentrations (measured 4–6 hours after trilostane dosing) are <20 nmol/L, trilostane should be stopped for 5 to 7 days, then reinstituted at a lower dose. Note: Although trilostane appears to be well tolerated by most dogs, sudden death has been reported in dogs with concurrent heart problems. Trilostane is also contraindicated in pregnant and lactating dogs, dogs with primary hepatic disease, and dogs with renal insufficiency.

6 Other alternative, but less consistently successful, medical treatments for PDH include the following:

Ketoconazole 15 mg/kg PO with food q 12 hours

Selegiline (l-deprenyl) 1–2 mg/kg PO q 24 hours

7 An effective treatment (where available) for PDH is microsurgical transsphenoidal hypophysectomy. This procedure requires a highly skilled neurosurgeon and specialized veterinary facilities that have access to advanced pituitary imaging techniques. Postoperative complications may include hypernatremia, keratoconjunctivitis sicca, diabetes insipidus, and secondary hypothyroidism.

8 For calcinosis cutis, adjunctive topical treatment with dimethyl sulfoxide (DMSO) gel every 24 hours may help resolve the lesions. During DMSO therapy, serum calcium levels should be monitored periodically because hypercalcemia is a potential adverse effect of this treatment.

9 The prognosis ranges from good to poor, depending on the cause and severity of the disease, with the average survival time for dogs with PDH being approximately 2.5 years after diagnosis.

FIGURE 9-28 Canine Hyperadrenocorticism.

An adult Labrador demonstrates the typical potbellied appearance. Generalized muscle wasting, which causes the abnormal posture, is also seen. Note that the hair coat is generally in good condition and does not demonstrate bilaterally symmetrical alopecia.

FIGURE 9-29 Canine Hyperadrenocorticism.

An adult Labrador with an adrenal tumor, demonstrating severe muscle wasting, which causes the abnormal body confirmation.

FIGURE 9-30 Canine Hyperadrenocorticism.

Same dog as in Figure 9-29. The potbellied appearance and alopecia are apparent.

FIGURE 9-31 Canine Hyperadrenocorticism.

Same dog as in Figure 9-29. Generalized seborrhea sicca can be secondary to numerous underlying diseases but was caused by hyperadrenocorticism in this dog.

FIGURE 9-32 Canine Hyperadrenocorticism.

Severe abdominal distention and alopecia with breakdown of the ovariohysterectomy scar caused by muscle and collagen wasting in this dog with iatrogenic hyperadrenocorticism.

FIGURE 9-33 Canine Hyperadrenocorticism.

Close-up of the dog in Figure 9-32. As tissue wasting progressed, the scar became thin and the tissue was pulled apart.

FIGURE 9-34 Canine Hyperadrenocorticism.

The papular rash was caused by secondary superficial pyoderma.

FIGURE 9-35 Canine Hyperadrenocorticism.

Numerous comedones on the abdomen of a dog. Comedones are a common feature of Cushing’s disease and demodicosis.

FIGURE 9-36 Canine Hyperadrenocorticism.

Phlebectasia (an erythematous papular lesion) is an unusual and unique lesion associated with Cushing’s disease.

FIGURE 9-37 Canine Hyperadrenocorticism.

Extensive calcinosis cutis covering the dorsum of a dog with iatrogenic Cushing’s disease.

FIGURE 9-38 Canine Hyperadrenocorticism.

Calcinosis cutis in the axillary region of a Boxer with iatrogenic hyperadrenocorticism. Note that the entire alopecic, hyperpigmented, papular plaque can be lifted like plate.

FIGURE 9-39 Canine Hyperadrenocorticism.

Calcinosis cutis demonstrating the alopecic, hyperpigmented, papular plaque typical of this syndrome. White papular lesions may appear as pustules, but the calcified material is difficult to express.

FIGURE 9-40 Canine Hyperadrenocorticism.

Mild calcinosis cutis lesions appear as erythematous papules or pustules. At this stage, they can be easily confused with lesions typical of superficial pyoderma.

FIGURE 9-41 Canine Hyperadrenocorticism.

Calcinosis cutis on the tongue.

FIGURE 9-42 Canine Hyperadrenocorticism.

Calcinosis cutis with a severe inflammatory dermatitis in the inguinal skin fold.

FIGURE 9-43 Canine Hyperadrenocorticism.

Close-up of the dog in Figure 9-42. The erythematous, papular plaque was caused by a combination of calcinosis cutis and secondary infection.

FIGURE 9-44 Canine Hyperadrenocorticism.

Symmetrical truncal alopecia in a dog with hyperadrenocorticism.

FIGURE 9-45 Canine Hyperadrenocorticism.

Same dog as in Figure 9-44. The sparse hair coat was bilaterally symmetrical. This dog was mildly pruritic because of a secondary superficial pyoderma.