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Endocrine alopecia
in dogs
Fabia Scarampella,
DVM, MSc, Dipl.ECVD
Studio Dermatologico Veterinario,
Milan, Italy
Dr. Scarampella received her diploma
from the European College of
Veterinary Dermatology in 2000 and
in 2007 achieved a Master’s Diploma in Evidence Based
Medicine and Health Care Research Methodology. Co-
author of the book “Manuale pratico di Dermatologia
Veterinaria” she has authored textbooks and scientific
journals. She is currently President of the Italian Veterinary
Dermatology Society (SIDEV), scientific co-ordinator of the
Dermatology Itinerary at the Scuola di Formazione
Veterinaria Post Universitaria, and works as a self-
employed professional dealing exclusively with veterinary
dermatology. She is also a consultant and co-creator of the
veterinary dermatology website www.teledermvet.com.
Introduction
The hair follicle is influenced by hormonal activity
in a variety of ways and is capable in its own right
of synthesizing and converting a wide range of
hormones. In the rat, it has been demonstrated
that estradiol, testosterone and the steroids
produced by the adrenal glands delay the start of
the anagen (active growth) phase, while thyroid
hormones accelerate follicular activity (1). In the
dog, certain endocrinopathies (hypothyroidism,
hypercortisolism), functional neoplasia of the
gonads (hyperestrogenism) and certain follicle
dysplasias (cyclic alopecia of the groin) are
associated with alterations of the follicular cycle
and present as symmetrical alopecia.
The aim of this article is to provide an up-to-date
summary on the pathogenesis and the dermato-
logical signs of hormonal diseases that cause
alterations in the follicular cycle, and offer a
diagnostic approach for dogs with non-pruritic
symmetrical alopecia.
KEY POINTS
Non-pruritic symmetrical alopecia in dogs is a
clinical condition commonly associated with
endocrinopathies, functional neoplasia of the
gonads, follicular dysplasia and idiopathic alopecia.
Although unlikely, infectious conditions that can
affect the hair follicle, in particular demodicosis,
should be excluded.
Ultrasonography is advisable for female dogs
presenting with enlarged vulva and teats and for
male dogs that are either cryptorchid or have
alterations in the size/consistency of the testicles.
The initial laboratory examinations should include
hematology, CBC and urine examination.
Dynamic assessment of thyroid function must be
carried out after any adrenal function test.
Cutaneous biopsy may help identify follicular
dysplasia or an idiopathic alopecia (Alopecia X).
Hypothyroidism
Thyroid hormone receptors are present in all
tissues. In the skin, receptors are especially abund-
ant in the sebocytes, the cells of the external follicle
sheath, and the dermal papilla. Because of this, the
thyroid exercises significant influence on the hair
follicle cycle and production of sebum. Thyroid
hormones also control lipogenesis and serum and
cutaneous levels of fatty acids; additionally they
stimulate the proliferation of fibroblasts and the
synthesis of collagen, and (via the regulation of the
synthesis and catabolism of the glycosamino-
glycans) influence the thickness of the dermis.
The thyroid produces thyroxin (T4) and tri-
iodothyronine (T3) in a ratio of 4:1 and in the
circulation these hormones are mainly bound to
plasma proteins. This assists with storing and
regulating the serum concentration of the hormones.
Less than 0.05% of T4 and less than 0.5% of T3 are
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ENDOCRINE ALOPECIA IN DOGS
present in the blood in free form (2). The free
form of T4 (fT4) penetrates the target cell where
80% converts to the free form of T3 (fT3), a
biologically active form.
increases if combined with data obtained from the
clinical examination. Cutaneous alterations are
reported in 60-80% of dogs with hypothyroidism
(3-4) and include bilaterally symmetric alopecia;
hair that is dull and easily epilated, and which
regrows more slowly after clipping (5); skin
that is hyperpigmented and cold to the touch;
desquamative dermatitis variably associated with
signs of follicular keratosis (follicular casts); and
ceruminous otitis externa. Hypotrichosis and
alopecia are particularly evident in the areas
subject to major trauma such as pressure points,
the perineum, the tail, the bridge of the nose and
the neck (Figure 1) . Note that Irish setters may
show hypertrichosis due to retention of hairs in the
telogen (resting) phase and in these subjects the coat
can turn lighter. The loss of color is probably due to
the effect of environmental factors on hair that is
retained longer than normal within the hair follicles.
Hypothyroidism is the most common endocrinopathy
in dogs. This disease can have a congenital or
acquired origin. Acquired hypothyroidism can be
primary or secondary. Primary hypothyroidism is
due to insufficient production of hormones by the
thyroid glands, while in the secondary form
glandular dysfunction is the result of insufficient
production of pituitary TSH.
An auto-immune thyroiditis is by far the most
common cause of acquired primary hypothyroidism
and is often associated with the presence of
circulating thyroglobulin antibodies (AbTG).
However, the presence of AbTG alone does not
confirm thyroid dysfunction. The second cause of
acquired primary hypothyroidism is idiopathic
thyroid degeneration in which a gradual replace-
ment of the glandular parenchyma with adipose/
fibrous tissue is observed in the absence of an
inflammatory infiltrate. Secondary hypothyroidism
is very rare and has been observed in combination
with pituitary neoplasia. In these cases, hypo-
thyroidism is accompanied by signs related to
concurrent illnesses such as such as Addison’s
disease, diabetes insipidus and reproductive
dysfunction.
The lack of thyroid hormone also leads to reduced
fibroblast activity and alteration of collagen
metabolism. Cutaneous wounds heal more slowly
and in areas subject to trauma an excessive
deposition of fibrous tissue (corns) may be
observed. In hypothyroid dogs, due to the slowed
glycosaminoglycan catabolism, excess hyaluronic
acid accumulates in the dermis, retaining water.
The myxedema that results gives the skin a greater
thickness and a lower temperature.
Among the systematic clinical signs of hypo-
thyroidism the most common are sleepiness, low
resistance to physical exercise and a tendency of
subjects to suffer more from the cold. Bradycardia
The clinical signs observed in hypothyroid
subjects are fundamental for the diagnosis, and
the predictive value of hormone functionality tests
Figure 1.
Hypothyroidism in a female golden retriever (left). Note the perineal alopecia (right).
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Figure 2.
Figure 3.
Symmetrical bilateral alopecia in a 7-year-old Shih Tzu with
hypercortisolism.
Alopecia, comedones and thinning of the ventral skin in the
same dog.
is a frequent clinical sign. Ocular alterations such
as corneal lipidosis, keratoconjunctivitis sicca and
corneal ulceration may also be observed. Hypo-
thyroid bitches often have persistent anestrus and
infertility, while males can have spermatogenic
defects. Gynecomastia and galactorrhea are
observed in 25% of non-sterilized bitches and
occasionally in neutered bitches and males. This
phenomenon is probably due to an increase in the
serum levels of prolactin induced by TRH over-
production. Hypothyroid subjects often have
mild, non-regenerative anemia and defects in
platelet function. Recurrent pyoderma is also a
common complication.
hyperplasia of both adrenal glands, in particular
in the fasciculata and reticularis zone; the adrenal
glands then produce excessive quantities of
cortisol.
Functional adrenal neoplasias represent 15-20%
of spontaneous hypercortisolism cases in dogs.
These neoplasms (adenomas or adenocarci-
nomas) are usually unilateral; unresponsive to the
hypothalamic-pituitary axis control mechanism,
they autonomously produce large quantities of
cortisol whilst the contralateral adrenal gland
usually atrophies.
Iatrogenic hypercortisolism due to prolonged oral,
parenteral or topical administration of cortisone
will show the majority of clinical signs that are
observed with the spontaneous form of the
disease, as well as suppression of the adrenal
functions and elevation of hepatic enzymes.
Hypercortisolism
Glucocorticoids influence hair growth and follicle
pigmentation by means of specific intracellular
receptors present within the cells of the inter-
follicle epidermis and the basal cells of hair
follicles. Although it has been demonstrated in
mice that suppression of these hormones has a
marked effect on follicle growth (6) the exact
molecular mechanism by which this effect is
produced in dogs is not yet known. Hypercortisolism
may be due to excessive production of cortisol by
the adrenal glands (spontaneous hypercortisolism);
or follow administration of excessive quantities
of cortisol (iatrogenic form). In spontaneous
hypercortisolism, the disease is caused by a
neoplasm of the frontal lobe or, more rarely, the
intermediate lobe, of the pituitary or by the
presence of adrenal tumors. The pituitary form
accounts for 80-85% of all cases of spontaneous
hypercortisolism. Here the pituitary produces an
excessive quantity of ACTH and causes bilateral
Spontaneous hypercortisolism is seen in adult
dogs but especially older animals. Clinical signs
are largely the result of excessive quantities
of cortisol. These signs are numerous and their
appearance is conditioned by many factors, in
particular by the location of the neoplasia
(pituitary or adrenal), the age of the subject and
the breed affected. In dogs affected by a pituitary
adenoma the clinical signs tend to manifest
themselves gradually, while in dogs affected by a
pituitary carcinoma or adrenal neoplasm the
appearance of clinical signs are much faster.
Subjects of advanced age are more sensitive to
the catabolic effects of the glucocorticoids and
manifest symptoms more quickly than young
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ENDOCRINE ALOPECIA IN DOGS
Figure 5.
Alopecia and gynecomastia in a bulldog with ovarian cysts.
Figure 4.
Ulcerated firm plaques on the neck of a dog with cutaneous
calcinosis (iatrogenic hypercortisolism).
subjects. Small-sized breeds tend to manifest the
disease in the classic manner and with a greater
number of clinical signs than large-sized breeds.
of the anagen phase and tend to keep the follicle in
the telogen phase (7-8).
Hyperestrogenism as a cause of alopecia is only
reported in the dog and results most commonly
from ovarian cysts; less often the cause is an
estrogen-secreting ovarian or testicular neoplasia.
Hyperestrogenism secondary to ovarian cysts is
most common in the British bulldog and manifests
itself in adults (2-7 years). On the other hand
hyperestrogenism secondary to ovarian neoplasia
has no breed predisposition and manifests itself in
subjects of advanced age.
The presence of PU/PD is the most common initial
symptom and can precede the typical cutaneous
manifestations of the disease by 6-12 months.
Cutaneous signs such as loss of hair sheen,
presence of dry scale, and a slight hypotricosis may
be noted initially but in time alterations in coat
pigmentation and bilaterally symmetric alopecia
can be observed (Figure 2) . The skin of dogs
affected by hypercortisolism is thin, hypotonic and
non-elastic (Figure 3) . Phlebectasia, the presence
of ecchymosis and petechiae after slight trauma,
scaling, comedones and (especially in the iatrogenic
form) cutaneous calcinosis may all be observed.
Cutaneous calcinosis is commonly observed on the
back of the neck, the axillae and the inguinal
regions and manifests itself as hard, whitish
papules and plaques. In time the plaques become
ulcerated and very pruritic (Figure 4) . Pyoderma
and demodicosis are complications commonly
associated with this hormonal disease. Pyoderma
in dogs affected by hypercortisolism typically
manifests itself with the presence of elongated,
non-follicular pustules and mild inflammation.
Infections respond poorly to antibiotic treatment.
The typical clinical signs of both conditions in the
female are bilateral symmetrical alopecia of the
perineum and the inguinal/groin regions. In
chronic cases, alopecia can affect friction points
( e.g. collar) and may eventually affect the whole
trunk. On the skin of the abdomen and the vulva
numerous comedones are often present, and hair
is dry and dull. Bitches often present with estral
cycle abnormalities, gynecomastia and vulva
enlargement (Figure 5) . Endometritis and sub-
sequently pyometritis are common.
Sertolioma, a tumor of the Sertoli cells in the
testes, can induce the appearance of alopecia and
a feminization syndrome in around 1/3 of subjects
affected. These dogs have high levels of circulating
estrogens and the effects of this alteration are
cutaneous, hematological, prostatic and behavioral
abnormalities. There is no breed predisposition
and the neoplastic disease is manifested in adult,
usually older, dogs. The distribution of the
alopecia is similar to that described for females.
Hyperestrogenism
Estrogens are mainly produced by the ovary and,
in both sexes, the adrenal cortex, the liver and the
mammary glands. Hair follicles are themselves
capable of synthesizing estrogens from androgens
by enzymatic action. Estrogens are powerful
modulators of follicle growth and delay the start
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Figure 7.
Figure 6.
Estrogen-secreting testicular neoplasia: alopecia and teat
enlargement in a dog with Sertolioma.
Estrogen-secreting testicular neoplasia. Note the erythematous
linear dermatitis along the prepuce.
The skin in the affected areas is normally hyper-
pigmented and the hair dry, dull and woolly. A
suggestive cutaneous sign is a linear erythema
along the prepuce and the scrotum (Figures 6 and
7) . Other signs are increased teat size, a pendulous
prepuce, little interest in females in heat, prostatic
hypertrophy, thrombocytopenia and anemia.
it is advisable to perform a skin biopsy. Histological
examination will help confirm a suspected follicular
dysplasia associated with pigmentation anomalies
or a recurrent flank alopecia.
However if the problem persists, or is associated
with systemic signs such as polyuria and/or
polyphagia, or if on microscopic examination hair
bulbs are observed to be mostly in the telogen
phase, the presence of hypercortisolism and hypo-
thyroidism must be considered. Initial laboratory
examination should include hematology, CBC and
urinalysis. These tests may demonstrate anomalies
consistent with endocrinopathies and exclude
other diseases such as chronic kidney disease,
diabetes mellitus and certain hepatic diseases.
Note that in subjects where clinicopathological
alterations suggest an endocrinopathy, assessment
of the thyroid function must always be carried
out after adrenal function tests because an
increase in plasma cortisol may reduce serum
T4 levels.
Diagnostic protocol for non-
pruritic symmetrical alopecia
When presented with a case of non-pruritic
symmetrical alopecia, initially all bacterial, fungal
and parasitic diseases that can affect the hair
follicle should be considered. Microscopic exam-
ination of the hair at this stage of the diagnostic
procedure can be useful and is summarized in
Table 1 . If these causes can be excluded, the presence
of metabolic diseases, functional neoplasia of the
gonads (ovarian neoplasia or Sertolioma), ovarian
cysts and follicular dysplasia must be considered.
A general physical examination should be
performed; if alterations are observed in the
dimensions and consistency of the testicles of a
male dog, or if there is a persistent increase in
size of the vulva and teats and alterations in the
estral cycle in a female, it is advisable to request
a testicular or abdominal ultrasound with
possibly biopsy of the gonads.
The main clinico-pathological alterations encountered
in dogs with hypercortisolism and hypothyroidism
are presented in Table 2 . If hypercortisolism is
suspected, endocrine screening tests should be
considered (9-10) (see Cut-out and keep on
pages 47-48 ):
If microscopic examination detects alterations of the
hair shaft, such as deformations of the cortex and
presence of melanin (macro-melanosomes), or if the
alopecia is seasonal and located in the groin region,
Note false positives are possible for each of these
tests and it is extremely important that results are
interpreted in conjunction with the history and
clinical condition of the patient. In cases where a
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