Hormonal Dermatoses in Dogs

Clinically, there is always alopecia, symmetrical, on the flanks and the trunk, initially sparing the extremities and the head. Alopecia is an absence of hair or very low density in a given area. This symptom, also called depilation, is present in any hormonal disturbance, with varying intensity, and is associated with poor quality coat (woolly, dull), especially on friction areas.

Endocrine alopecia is linked to a disruption of the hair cycle or the function of the hair follicle. The mechanisms involve either an excess or a deficit in hormone secretion. Inadequate hormone production results in non-specific signs (weight gain or loss, polyuria-polydipsia, fatigue, cardiac, renal, hepatic, neurological disorders).

Pruritus (itching) is very rarely present at the start of development but may appear during secondary microbial infections or complications, which sometimes poses a diagnostic trap. Similarly, other skin conditions are possible, such as seborrheic oleosa, ceruminous otitis, alopecia of the nose bridge or tail end.

The diagnosis of hormonal dermatoses is delicate and requires meticulous work both clinically and in the interpretation of hormonal blood levels. Endocrine diseases can have a severe prognosis, and some are fatal when linked to cancerous tumor growth, or if not properly treated.

This thematic sheet will hence detail:

• Cushing’s syndrome
• hypothyroidism
• hormonal dermatoses of sexual origin

Cushing’s syndrome

This involves chronic saturation of the body with an excess of glucocorticoid production by the adrenal glands (endogenous hypercorticism) or by excessive intake (exogenous or iatrogenic hypercorticism). The secretory abnormality is due either to an adrenal tumor or a pituitary tumor causing overstimulation of the adrenals by the production of a specific molecule, ACTH.

The adrenal glands are two glands located above the kidneys (hence their name) which secrete various hormones (adrenaline, androgens, aldosterone, glucocorticoids).
In adrenal hypercorticism, one can distinguish between non-aggressive tumors (adenomas) and malignant tumors (adenocarcinomas), with obviously differing prognoses. In pituitary origin, these are adenomas thus resulting in generally slower developing hypercorticism.

Clinical and epidemiological presentations

The breeds primarily affected are Poodles, Dachshunds, and Terriers. It is a senior dog disease (average age 11 years).

Excessive glucocorticoid saturation leads to a systemic disease, not just dermatological. General symptoms include increased drinking, as well as appetite, a pendulous abdomen (increased liver size), fatigue, muscle wasting, and reproductive problems.

The skin signs manifest as alopecia distributed on the flanks, bilateral, symmetrical, without itching, with thinning of the skin, more visible cutaneous blood vessels, comedones, and subsequently bacterial, fungal or parasitic infections (demodicosis) and thus scratching.

Complications are frequent, especially if the disease is not detected early: urinary infections (renal, bladder), heart failure linked to high blood pressure, and clot formation (embolisms).

In cats, Cushing’s syndrome is frequently associated with diabetes mellitus, which should therefore be looked for simultaneously.

Diagnosis

It relies on classic blood analyses (haematology, biochemistry) and hormonal tests (ACTH test, dexamethasone suppression tests). These tests highlight an excessive internal corticoid production. Sometimes, they allow distinguishing between pituitary involvement (adenoma) and one of the 2 adrenal glands (adenoma or carcinoma). Imaging is also very important to specify the origin of hypercorticism: ultrasound, CT or MRI provide fundamental details to guide treatment.

Treatment

The current medical treatment is based on the use of a molecule that blocks glucocorticoid synthesis by the adrenals, trilostane. Trilostane is very effective both in pituitary and adrenal-based hypercorticisms, with few side effects. Your vet will adjust the dosage over the first few weeks depending on clinical response and blood checks. Other medications were used prior to trilostane, such as o,p’-DDD, isotretinoin, ketoconazole, various neurotransmitters, with inconsistent results and high costs.

Surgical treatment is interesting for operable adrenal tumors, i.e., without metastasis (especially pulmonary), nor involvement of the vena cava. It requires an experienced surgeon, and subsequently needs rigorous medical follow-up.
The survival rate varies from a few weeks to several years, averaging 2 years in pituitary origin, and 4 years after surgery for a non-metastasized adrenal tumor. Note that medical complications are the cause of more than half of deaths.

Hypothyroidism

It is a rare hormonal disease due to decreased production, action, or lack of activity of thyroid hormones (T3, T4) in the body. They are produced by the thyroid gland located in the neck, consisting of two lobes. Hypothyroidism is probably overdiagnosed, based on insufficiently rigorous clinical or blood criteria. The evolution of this dysendocrinism is often slow, over several years, and symptoms are sometimes mild and non-specific given the varied effects of thyroid hormones.

The main cause of hypothyroidism is immune-mediated inflammation, called lymphocytic-plasmacytic thyroiditis. There are also congenital, medical, or treatment-related causes (surgery or radiotherapy).

Symptoms first appear when ¾ of the thyroid is non-functional, explaining its insidious and chronic nature. The actual frequency of the disease is very low, and many diagnoses are likely made in excess.

Clinical and epidemiological presentation

There are no clear racial predispositions, though Labrador Retrievers, Golden Retrievers, Bernese Mountain Dogs, Leonbergers, and Setters are at risk. A familial genetic transmission has been suggested in some breeds (Setter, Boxer, Old English Sheepdog, Beagle, Dalmatian, German Mastiff).

Hypothyroidism predominantly affects adult dogs, aged between 6 and 10 years, though large and at-risk breeds seem to be affected younger.

Symptoms can be general and/or dermatological, but there is a wide range of clinical signs due to the multiple actions of thyroid hormones, particularly on growth, the nervous system, and the use of oxygen and nutrients. Hypothyroidism is thus a multi-systemic disease: dogs may present with general and/or skin involvement simultaneously.

Classically, fatigue, lethargy, and weight gain are described but are not systematic. Also reported are neuromuscular issues (polyneuropathies, muscle weakness, vestibular syndrome), cardiovascular (bradycardia), haematological (non-regenerative anemia, coagulation disorders), immune (reduced defences), ocular (lipid corneal deposits), reproductive disorders, obesity, and growth delays in congenital forms.

From a dermatological perspective, clinical signs are again varied as thyroid hormones affect hair growth (anagen phase), sebum production, and synthesis of the epidermis’ stratum corneum.

Even if the symmetrical non-pruritic alopecia of the flanks, neck, and tail (“rat tail”), due to lack of regrowth is common, it is not characteristic. The muzzle and friction zones may be involved, with hypermelanosis (blackish coloration) and skin thickening. The coat is dull, thin, dry, and easily pluckable with slow regrowth after clipping. Dandruff and a kerato-seborrheic state are sometimes observed. Bacterial or fungal (yeast) infectious complications are also possible, as well as ceruminous otitis externa.

Diagnosis

It must be rigorous and correlate clinical signs, biological tests, and hormone dosage to avoid unnecessary treatment of ‘false’ hypothyroids.

The clinical suspicion is based on chronic fatigue and slowly progressive fatigue not to be confused with physiological aging, and/or general symmetrical non-pruritic hair loss or a lack of regrowth. Obviously, other chronic pathologies are likely to manifest as a fatigue syndrome and should be considered. Alopecic dermatoses such as congenital coat anomalies (dilute coat alopecia, recurrent flank alopecia, follicular dysplasia) or certain other hormonal diseases such as hypercorticism will be part of the differential diagnosis.

The biological confirmation of the decrease in thyroid hormone secretion must therefore be correlated with strong clinical suspicion. A blood test may show moderate anemia (decrease in red blood cells and hematocrit level) and an increase in cholesterol and triglyceride levels. Skin biopsies are not specific and indicate an endocrine origin.

The measurement of total T4 (thyroxine) along with TSH (thyroid-stimulating hormone) is the reference test. In practice, the T4 value must be very low or even collapsed (less than 12 nmol/l) and the TSH value increased (more than 0.55 ng/ml) except at the very end of progression. Free T4 measurement is also possible.

Other tests are possible, such as antibody search, thyroid imaging (ultrasound, scintigraphy) but with limited interest in dogs. Finally, a therapeutic trial is possible, with thyroid supplementation over a few weeks and observation of effects, even if the effect on hair regrowth is systematic.

Treatment consists of oral administration of levothyroxine at a dose of 10μg/kg, twice a day: two veterinary presentations exist. This dose may be doubled in cases of insufficient response in certain (rare) cases. The dosage used is higher than that used in humans in whom the absorption and activity of the thyroid extract is different. Side effects are rare and reversible: behavioural disorders, diarrhoea, increased water intake. The ease of therapeutic management should not justify unwarranted treatments, based on a too rapid diagnosis or not supported by a solid clinical base.

The positive response is first observed on the general signs within 1 to 4 weeks, then on hair regrowth and skin improvement in about 2 months.
Biological follow-up is carried out after one to two months with a blood test to check the T4 level, which should be above 20 nmol/l (ideally between 25 and 45). Subsequently, regular checks throughout the year, coupled with clinical monitoring, are sufficient.

Cases of ‘false’ hypothyroidism due to reactive drop exist, particularly during other hormonal diseases, chronic infections, renal or hepatic insufficiency, or during prolonged therapies (corticosteroids, phenobarbital in epilepsy). It is important to know how to identify them to avoid unnecessary supplementation of the animals.

Hypothyroidism is therefore a dysendocrinia with multiple, general, and dermatological repercussions, characterized mainly by fatigue and symmetrical alopecia with lack of regrowth. Oral supplementation with thyroid extracts is relatively simple to implement but must be justified by a well-established diagnosis and not based on clinical suspicion or dubious analyses. Be particularly mindful of dermatoses resulting in non-inflammatory alopecia that may suggest hypothyroidism. Your vet can perform the necessary diagnostic tests, if required.

Hormonal dermatoses of sexual origin

These are rare dermatoses secondary to endocrine imbalances caused by gonadal, ovarian, and testicular tumors, and are mainly accompanied by general signs. We distinguish hyperestrogenism in the female and three types of testicular tumors in the male.

Hyperestrogenism or ovarian imbalance in the female

This dysendocrinia is the result of excessive oestrogen exposure due to a secreting ovarian tumour or ovarian cysts, and manifests as ovarian cycle abnormalities, genital, skin and haematological signs. Oestrogens slow down hair growth, particularly in the peri-genital, peri-anal regions, flanks, posterior thighs, and abdomen.

These are diseases of the older bitches (average 10 years), characterised by bilateral symmetrical hair loss, beginning in the peri-genital, perineal region, with progressive extension forward. Alopecia is sometimes accompanied by hyperpigmentation and/or skin thickening, seborrheic dermatitis, comedones, and infectious complications.

Haematological and gynaecological signs are also present. Uterine infections (pyometra), vulvar hypertrophy, mammary swelling or phantom pregnancies (pseudogestational lactation), as well as severe anaemia due to the action of oestrogens, may be observed.

Distinction must classically be made with other hormonal dermatoses, congenital alopecia and certain dermatoses such as demodicosis or extensive ringworms. Additional imaging tests (X-ray, ultrasound), along with a haemogram showing anaemia and suggestive symptoms, will help confirm the suspicion. Repeated hormonal assays of estradiol and progesterone may be useful.
Surgical removal by ovariohysterectomy is curative but should be accompanied by chemotherapy in the presence of metastases. In this latter case or if associated haematological signs are present (anaemia), the prognosis will be much more reserved.

Hyperandrogenism or dermatoses due to testicular tumours in males

Three types of testicular tumours are distinguished in males: benign behaviour leydigomas, seminomas, and sertolinos which rarely metastasize (about 10% of cases).

Clinically, bilateral symmetrical alopecia is classically observed, beginning in the peri-genital, perineal region with progressive extension towards the front (abdomen, flanks, thorax, neck). It is accompanied by hyperpigmentation, erythema along the sheath, comedones, and a thin, dull coat. Seborrheic conditions and infectious complications are frequent, with subsequent appearance of itching.

Leydigomas produce testosterone and result in peri-anal tumours (circumanalomas), while sertolinos and seminomas secrete oestrogens. In the latter case, a feminization syndrome is observed: characterized by penile atrophy, mammary swelling, behavioural changes (attracting other males) or haematological alterations (anaemia and decrease in blood cell line cells) or biological changes (increase in calcium level). A prostatic syndrome (hypertrophy) characterized by urethral blood loss, urinary disorders (infections, abnormal urinations) or defecation issues (difficulty expelling stools) is possible.

Here again, the diagnosis is based on imaging (testicular ultrasound), blood tests (hematology), and hormonal assays (testosterone and oestrogen dosage). If the extension assessment shows no metastases, the curative treatment is castration of both testicles, including the one that does not appear clinically affected. Otherwise, chemotherapy or even radiotherapy are possible.

Alopecia X

This is a dermatosis of the young adult, primarily affecting Nordic dog breeds, with a suspected genetic origin associated with a deficiency in the synthesis of sexual hormones or a defect in their action on the hair.

The coat becomes sparse and appears woolly (‘puppy coat’) due to a loss primarily of primary hairs and a persistence of secondary hairs. Over time, hair loss spreads to friction areas (neck, back of the thighs) while preserving the extremities and face. Dry skin and hyperpigmentation accompany the alopecia.

The diagnosis is based on a body of presumption combining clinical appearance, exclusion of other non-inflammatory and non-itchy alopecic dermatoses, and histopathological examination. Sex hormone assays are difficult to interpret.

Various treatments have been proposed with varying success rates: sterilisation, insertion of a deslorelin implant blocking the synthesis of fertility hormones, trilostane, melatonin. Local care with hydrating and emollient topicals and the supply of essential fatty acids ω3-ω6 are important to combat skin dryness.

Conclusion

Hormonal dermatoses in dogs initially present with an identical clinical appearance characterised by symmetrical trunk hair loss, no itching, and hyperpigmentation of the skin. General signs are systematically present, explaining that these are serious diseases, with a delicate diagnosis, requiring careful and regular follow-up.