Differential diagnosis of non-inflammatory alopecia in dogs

Clinically, non-inflammatory alopecia is the absence of hair without other skin lesions.

There are various mechanisms of non-inflammatory alopecia:

1. Follicular cycle arrest in endocrine diseases, telogen effluvium, anagen defluxion, post clipping alopecia. It usually produces partial or complete alopecia with symmetrical, generalised or regional distribution.
2. Congenital or acquired genetic defects: congenital alopecia (fig.1), follicular dysplasias and dystrophies, alopecia X, pattern baldness (fig. 2). It appears with partial or complete alopecia of regional or generalised distribution.
3. Inflammatory origin but clinically noninflammatory: alopecia areata, post-injection vasculitis, cicatricial alopecia, traction alopecia. Usually produces focal or multifocal complete alopecia.

Alopecia due to follicular cycle arrest

Hair is produced in the anagen phase. The telogen phase is a resting phase, in which the hair remains in the hair follicle until the follicle enters the anagen phase and synthesises a new hair that pushes out the “old” hair, producing the shedding of hair (old hair is replaced by new hair). If there is no activation of the hair follicle cycle, the old hair falls over time, producing alopecia.

Post-clipping alopecia: This occurs in plush coat breeds (e.g. Nordic) whose hair cycle has a very long catagen and telogen phase, and the anagen phase can take up to a year to activate. If shaving is carried out during the follicular inactivity phase, the hair can delay its emergence for months. Biopsy confirms the diagnosis by ruling out other processes.

Endocrine diseases

A defect or excess of certain hormones inhibits or prevents the activation of the anagen phase. The first dermatological signs are the presence of dry, dull, discoloured hair, which falls out easily, leading to progressive alopecia (fig.3). Alopecia begins in areas with increased friction, such as the neck, pressure areas, flanks or thighs, and progresses to other trunk areas. It does not usually affect the head or limbs. The skin is generally hyperpigmented, and comedones, seborrhoea and secondary infections are common.

The biopsy suggests endocrinopathy but cannot differentiate between the different endocrine diseases.

Dermatological lesions may be the first clinical signs of the disease, but other systems and organs are affected, and if the condition is not diagnosed can produce serious health issues.

Hypothyroidism is the most common endocrine disease in dogs. Thyroid hormones are necessary for the activation of the follicular cycle. In addition to the characteristic progressive alopecia of endocrine disorders, hair loss on the tail (rat tail) and alopecia of the nasal bridge have been described.
Accumulation of glycosaminoglycans in the dermisleads to myxedema as a cause of the tragic face expression. Frequent secondary nfections are associated with impaired skin barrier and immune system function.

In addition to dermatological signs, general clinical signs, cardiovascular, ocular, reproductive, gastrointestinal, muscular and peripheral neuropathy may occur. Common clinicopathological changes are normocytic and normochromic anaemia, neutropenia, thrombocytopenia, hypercholesterolaemia, and hypertriglyceridaemia.

The presence of low thyroid hormone levels (TT4) is very common in sick animals and  can lead to diagnostic errors. Diagnosis should be based at least on the measurement of  TT4 and TSH together. Complex cases may require complete panels such as the Thyroid profile Dog, including T4, fT4, T3, fT3, TSH, thyroglobulin Ab, T4 Ab*, T3 Ab* and/or the  TRH stimulation test.

Hyperadrenocorticism (HAC)

Hyperadrenocorticism can be spontaneous (associated with pituitary micro, macroadenomas or adrenal gland neoplasia) or iatrogenic.

High levels of glucocorticoids inactivate the follicular cycle, cause atrophy of the adnexal,  inhibit fibroblast proliferation and produce alterations in cornification. In 90% of cases,  here are cutaneous manifestations: alopecia, skin atrophy (fig.4), comedones, poor healing, distension of scars, desquamation, xerosis and predisposition to secondary  infections. Calcinosis cutis is not very common but is a very characteristic lesion of hyperadrenocorticism.

Other clinical signs include polydipsia/polyuria, abdominal dilatation, hepatomegaly,  muscle atrophy, exercise intolerance, anestrus and metabolic complications: diabetes  mellitus, systemic hypertension, urinary tract disorders, acute pancreatitis, CNS and  neuromuscular disorders, and pulmonary thromboembolism.

The diagnosis of HAC usually requires the combination of several tests.

• Skin biopsy – is orientative
• Urinary cortisol/creatinine index is a screening test. It is not diagnostic, but average  values in the absence of renal disease rule out HAC with high confidence
• ACTH stimulation test
• Suppression test with Dexamethasone at low doses (0.01mg/kg IV). Evaluate cortisol at  T0 and four h and eight h after administration
• Suppression test with high dose Dexamethasone (0.1 -0.5 -1mg/kg IV).
• Ultrasonography of the adrenal glands.
• Computed tomography – in case of pituitary tumour

Sex hormone imbalance. The skin clinical picture is caused by oestrogen excess in males due to testicular tumours (fig.6), usually Sertoli cell tumours, but also seminomas and interstitial cell tumours. In females cystic ovaries can be a cause and less frequently ovarian neoplasia. It can be caused by exogenous oestrogen, including percutaneous penetration of oestrogen used by owners. The progressive bilateral alopecia usually starts in the perigenital area, extending to the abdomen, thighs, breasts, flanks and neck. Hyperpigmentation, lichenification, secondary infections and oily skin with a foul odour are common.
Other clinical signs include gynecomastia and enlarged nipples; enlargement of the vulva in females and in males: pendulous prepuce, linear preputial erythema (fig. 5) and attraction of the animal to other males.
Excess oestrogen can lead to irreversible bone marrow aplasia.
Diagnosis usually requires ultrasonography and biopsy. In addition, sex hormone (Adrenal Profile: 17 OH-progesterone, androstenedione, estradiol) can be determined.

Congenital  or acquired genetic defects

Alopecia X– It is prevalent in Pomeranians and other breeds such as Chow-chow, Samoyeds, Siberian Huskies and miniature Poodles. There is a progressive loss of primary and later secondary hair until complete alopecia, starting on the neck, perineum or caudal thighs and progressing to complete alopecia of the trunk, excluding the head and limbs.

Diagnosis is based on a compatible biopsy together with tests that rule out endocrine disease. Alopecia X is an aesthetic process in an otherwise healthy animal, whereas an endocrinopathy is a disease that can have severe consequences for the animal‘s health.

Congenital alopecia or hypotrichosis produces an absence of hair at birth or in the first months of life. There are selected breeds with congenital alopecia – e.g. Chinese Crested dog (fig.1).