Alopecia in the Dog
World Small Animal Veterinary Association World Congress Proceedings, 2013
Mike Shipstone, BVSc, FANZCVS, DACVD
Dermatology for Animals, Stafford Heights, QLD; School of Veterinary Science, University of Queensland, QLD, Australia

When an animal first presents, the causes of alopecia can be differentiated into 2 broad categories: either there is excessive loss (mostly inflammatory causes) or there is inadequate production (noninflammatory causes). The first step is to decide which path of investigation to follow - remembering that the pet may not be reading the text and have secondary complications, which means it can fit into both categories!

1. Excessive Loss (Inflammatory)

The cause of the alopecia in these cases is loss faster than the follicle is able to replace it. There is nothing fundamentally wrong with the follicular unit either in the signaling for the production of a new shaft or in the production of the shaft.


The hair is lost due to traumatic removal via any of the manifestations of itch, i.e., biting, rubbing, rolling, licking, gnawing. In many cases, the clients are unaware or unwilling to believe that the animal is traumatizing itself. The easiest method of identifying self-trauma is via a trichogram. A normal hair should be finely tapering to the end. Traumatised hair may be broken, split or cracked, and it is this that gives the coat its harsh feel.

The types of allergies that may lead to generalised alopecia are:

 Insect bite hypersensitivity


 Food adverse reactions

The investigation of these was covered in the examination of the pruritic pet and will not be detailed again here.


Whilst most cases of pyoderma present with the classic clinical signs, i.e., papules, pustules, epidermal collarettes and target lesions, some cases will show as a 'moth-eaten,' patchy alopecia. This is particularly so in the short-coated breeds, many of which will not be particularly itchy. The folliculitis leads to interference with the anchoring of the telogen hairs in the follicle, so the hairs are shed.

Malassezia Dermatitis

Overgrowth with excessive number of Malassezia can lead to an increase in pruritus, which leads to traumatic loss of the hair as the animal attempts to relieve the irritation. In addition, some may develop a hypersensitivity to the Malassezia so that even relatively low organism counts may lead to severe pruritus.


Whilst dermatophytes may cause inflammation, they should be considered in any cases of annular alopecia. In most instances, the hair loss is localised rather than generalised, but more widespread loss may occasionally occur. Investigation may be done via Woods lamp examination (positive only for Microsporum canis and then only up to 50% of cases), trichogram and examination for arthrospores (examination is helped by chlorphenolac or potassium hydroxide clearance first), fungal culture or biopsy.


Skin scrapes should be performed in any area of alopecia. It is a simple technique that will quickly rule the presence of the mites in or out. With a few exceptions, demodicosis is readily identified with a deep skin scrape, performed in areas once the skin has been firmly squeezed and scraped until there is capillary oozing present. There are 3 species identified on the dog: Demodex canis, D. cornei (short bodied) and D. injai (long bodied). Whilst D. canis infection is traditionally not pruritic, it may become so with secondary bacterial infection. I have found infection with the short-bodied mites to be reasonably commonly pruritic, and these seem to be controlled quicker and easier than the D. canis.


Also known as 'walking dandruff' because the large mites look like scurf. Infestation is quite pruritic, and hair loss is due to traumatic removal.

2. Inadequate Production (Noninflammatory)

The cause of the alopecia in these cases is inadequate production of new hair because of either abnormalities in morphogenesis (production of a new follicular shaft) or in follicular cycling (signaling for the production of a new shaft).

Hair growth is divided into 4 phases:

 Anagen: Active growth where there is an intact inner root sheath (IRS).

 Catagen: Still actively growing, but the IRS is being actively replaced by trichilemmal cornification.

 Telogen: Inner root shaft (IRS) is completely replaced by trichilemmal cornification. Resting phase of the hair cycle.

 Exogen: The old telogen shaft is shed, and a new anagen hair replaces it. Originally thought to be due to the new shaft applying pressure, now some believe it may be due to enzymatic release in the old telogen follicle (Dunstan 2009).

In most animals, telogen is the longest phase of the hair cycle. The exceptions would be those breeds that require clipping, e.g., Poodle where the telogen predominant cycles have > 50% of the follicles in telogen; but even in the breeds with a telogen predominant cycle, there is variability in the % of follicles in each stage of the cycle (anagen, catagen, telogen [haired and hairless]). It is important to understand that telogenisation does not necessarily mean that there is alopecia present. The only way this can be determined is if horizontal sections are made and the number of hair shafts per follicular unit is determined.

Noninflammatory alopecia develops because of either an abnormality in the formation of the hair shaft (dysplasia) or a failure of the follicle to continuously cycle.

Dysplasia is a proliferative process that results in a defect in the quantity or quality of the structural proteins (and/or lipids) that form a hair shaft. The resultant shaft is abnormal and fragile so that growth is impossible. It is associated with the following features:

 It is a proliferative process, so it becomes apparent during anagen not telogen.

 Dysplasias are associated with abnormalities of the shaft (so any alopecic disease lacking this is not a dysplasia).

 Although dysplasias may become atrophic, atrophic diseases do not become dysplastic (Dunstan 2009).

Alopecia due to hair cycle abnormalities may be caused by anagen inhibition, catagen induction and/or prolongation of telogen.

The alopecia is characterized by three basic morphological features that may be present singly or in combination:

 Miniaturisation of the hair shafts

 Increase/persistence in haired telogen follicles

 Increase in hairless telogen follicles (Dunstan 2009)

As no new hair growth is occurring, the hair is gradually lost as a result of frictional forces, leading to the characteristic but often nonspecific clinical appearance which characterizes these forms of alopecia.

There has been a range of different diseases that have been associated with hair cycling abnormalities, and some include the following.

Hair Cycling Abnormalities


Clinical Signs

No sex predilection, but neutered are at greater risk, and 6–10 years > risk. Onset of disease begins earlier (2–3 years old) in large/giant breeds. It is known as the 'great imitator' due to the wide variety of clinical signs that may be manifested.

Classic cutaneous clinical signs are:

1.  Bilaterally symmetric truncal alopecia (spares extremities) - hypotrichosis in frictional areas first. Large/giant breeds lose hair on lateral surface of extremities. Advanced cases loss of all but head and distal extremities.

2.  Dull, dry, brittle, easily removed hair coat - fails to regrow post clipping.

3.  Mucin accumulation. This can lead to myxedema (thick, puffy skin that's cool to touch) - most prominent on the face "tragic" expression.

4.  Hyperpigmentation

5.  Seborrhoea - Commonly seen due to the effects of thyroid hormone on serum and cutaneous fatty acid concentrations. Clinically it may present as dryness, greasiness, or seborrhoeic dermatitis.

6.  Susceptibility to skin infections.

7.  Lack of pruritus. Generally hypothyroidism is not a pruritic disease, unless complicated by secondary infections (bacteria/Malassezia).

Unusually, hypertrichosis (due to retarded turnover of hairs) may be seen, particularly in Boxers and Irish setters. The coat may become lighter in colour because the retained hairs are bleached.

Other changes that may be seen include:

1.  Ceruminous otitis or the medial pinnae and canals become dry and scaly. The changes may predispose the ears to Malassezia and/or bacterial infections.

2.  Bacterial infections

3.  Poor wound healing and easy bruising

4.  Comedone formation - usually over the ventral abdomen

Noncutaneous Cx

There is a wide range of clinical signs affecting the CNS; neuromuscular, gastrointestinal and cardiovascular systems; ocular changes; changes to CBC and reproduction (along with heat-seeking behavior); and weight gain despite unchanged dietary input.

NB hypothyroidism can occur concurrently with other endocrinopathies, be secondary to others (e.g., Cushing's), or be part of a polyglandular problem (e.g., diabetes mellitus, hypoadrenocorticism and thyroiditis occur due to autoimmune disease).


Hypothyroid dogs normally present with a gamut of clinical signs. There are some important clues in identifying a suspected hypothyroid dog: middle aged, recurrent pyoderma in older animals that responds completely to antibiotics (NB some atopics will also present in a similar manner; however, it is generally in a younger dog), a history of heat seeking, lethargy, weight gain whilst on a constant level of feeding, poor libido or abnormal cycling - these all raise the index of suspicion.

Because of the variety of clinical signs and the fact no one test is definitive, a range of tests may be necessary:


 Normocytic normochromic, nonregenerative anaemia is seen in 30% of cases due to folic acid, B12 metabolism deficiency.

 Microcytic hypochromic anaemia may occasionally be seen due to iron metabolism deficiency.

 Microbiological assays

 Hyper-cholesterol (50–75% of cases), CPK elevation (< 50% of cases), urine analysis - normal.

 Thyroid Testing

 Total T4 (TT4), Total T3 (TT3)
The evaluation of baseline total T3 and total T4 has been subject to controversy, as the levels of each will fluctuate during the day and are affected by numerous factors other than thyroid function alone. Added to this is the fact that the tests themselves are imprecise with varying rates of specificity and sensitivity.
A positive test in the absence of supportive clinical signs does NOT equal a diagnosis of hypothyroidism.

 Free T4 (fT4)
More consistent measure - because fT4 determines availability to the cells and TT4 may change (in response to illness, drugs, etc.) without changing fT4.

 Serum TSH Measurement
This is the most reliable method in humans. The combination of low fT4 together with elevated endogenous thyroid-stimulating hormone (TSH) seems to be the most reliable method currently available.

 Function Studies

 TSH Stimulation
Vastly superior to basal hormone determination. Bovine TSH is no longer commercially available; however, recent pilot studies have suggested that human TSH may be a viable alternative. This still requires further validation before it can be recommended.

 TRH Stimulation
This test is unreliable (Frank 1996).

Generally, the changes are nonspecific, but suggestive changes include vacuolated hypertrophied arrector pili muscle, increased dermal mucin, thick dermis. The other use of the biopsy is to rule out other differentials, e.g., Demodex, infections, follicular dysplasia.


Cause and Pathogenesis

1.  Iatrogenic
Due to an excessive administration of some form of glucocorticoid. Even topicals can produce clinical signs typical of hyperadrenocorticism.

2.  Pituitary-dependent hyperadrenocorticism (PDH)
80–85% of spontaneous cases of hyperadrenocorticism are due to PDH. It is due to either micro or macro pituitary neoplasia. These are functional tumours, producing excessive adrenocorticotropic hormone (ACTH), which leads to bilateral adrenal hyperplasia.

3.  Adrenal tumour

a.  15–20% of cases

b.  Usually affects only one adrenal, although rare reports of bilateral tumour occur (which are difficult to differentiate from PDH-induced hyperplasia on ultrasound)

c.  The tumour functions autonomously excessive cortisol negative feedback on corticotropin-releasing factor (CRF) and ACTH atrophy of other adrenal and all cells in affected adrenal

Clinical Signs

Tends to be in middle-aged animals with no definitive sex predilection. Occasionally seen in young animals (6–9 months), but they usually show retarded growth with the classic clinical signs.

Breeds: Boxer, Boston terrier, poodle, dachshund - but all breeds can be affected.

Iatrogenic - can affect any animal.

 PU/PD > 100 mL/kg/day (32–85%)

 Polyphagia ~ 80–90%

 Cutaneous changes


 Early - becomes dull, more difficult to groom

 Later - hairs lost hypotrichosis/alopecia; symmetrical of trunk with sparing of the head and extremities

 Short-coated breeds may appear 'moth eaten'

 Failure to regrow shaved area

 Colour change

 Tips - due to sun bleaching because hairs are not shed

 Entire shaft - appears to be mediated by sex hormones

 Thin hypotonic skin

 Easy bruising (petechiae, ecchymoses)




 Calcinosis cutis

 Poor wound healing (may see stria - because of limited fibrous tissue)

 Secondary infections - pyoderma, seborrhoea, demodicosis (5+%)

 Musculoskeletal changes

 Skeletal muscle weakness and atrophy (75–80%)

 Abdominal enlargement (90–95%)

 Myotonia or pseudomyotonia


 Other changes


 Persistent anoestrus

 Clitoral enlargement (not seen in iatrogenic hyperadrenocorticism), excess ACTH stimulation of sex hormone production

 Testicles - small, soft, flaccid

 Respiratory complications

 Behavioral changes

 Neurologic changes

 Hepatic enlargement

 Dystrophic calcification


 Sudden acquired retinal degeneration syndrome (SARDS)

Sex Hormone Dermatoses

The direct relationship between excessive sex hormones and skin and coat changes, are well understood and documented in the overproduction syndromes. In males these include Sertoli cell tumour, Leydig (interstitial cell tumour) and in females, granulosa cell tumour and ovarian cysts. These conditions generally respond to de-sexing. However, in castration-responsive dermatosis, oestrogen- and testosterone-responsive dermatoses, and congenital adrenal hyperplasia, the cause and effect relationship is much less clear and remains controversial. It may be that the problem lies not with the serum level of hormone but rather the sensitivity of follicle receptors, or it may be due to some inherent follicular abnormality.


An oestrogen receptor pathway has been shown to regulate the anagen-telogen transition in mice. Oestradiol inhibits anagen initiation, shortens the anagen period, promotes catagen, and lengthens the duration of the resting phase. This is thought to be due to stimulation of bone morphogenic protein 4 (BMP4) expression in the follicular papilla. BMP4's interaction with its receptor results in down-regulation of a range of signaling molecules and hair growth inhibition (Frank 2009).


Hyperandrogenism is not generally associated with alopecia in dogs, as intact males do not develop hair growth in the presence of testosterone nor do they lose it in response to testosterone secretion. It has been shown that the hair follicles of dogs lack the ability to convert testosterone to dihydrotesterone (DHT), which is the mechanism by which hair loss occurs in sensitive human males (Frank 2009).


1.  Sertoli cell tumour

a.  Cause and pathogenesis
Blood oestrogen is not always elevated. Also hyperoestrogenism could be local, with peripheral aromatisation of androgens to oestrogen.

b.  Clinical signs

i.  Feminisation syndrome:

a)  Incidence depends on location of testes (15% in scrotum, 50% inguinal, 70% abdominal)

b)  More likely with larger tumours and increasingly severe as tumour size increases

ii.  Bilaterally symmetrical alopecia, gynecomastia, pendulous prepuce, attraction of other male dogs

iii.  Depressed libido, aspermatogenesis, galactorrhoea

iv.  Other testicle often atrophied

v.  Prostate - enlarged (oestrogen induced squamous metaplasia)

vi.  Bone marrow depression - rare (non-regenerative anaemia, thrombocytopaenia, leukopenia)

2.  Interstitial cell tumour

a.  Boxers predisposed

b.  No tendency for cryptorchid testes to develop the tumour

c.  Most cause no skin changes

d.  If present, see: tail gland hyperplasia, macular melanosis, prostate hyperplasia

e.  Changes due to increase in testosterone secretion

3.  Hypogonadism (castration-responsive dermatosis)
This is a decrease or abnormality in functional activity.

a.  Cause and pathogenesis
Most dogs have palpably normal testes and no pathology on histology once castrated. Hair loss may be due to some unmeasured sex hormone, failure of peripheral conversion of sex steroids, a follicular receptor defect in which follicles change sensitivity to sex hormones.

b.  Clinical signs

i.  Truncal alopecia that mimics testosterone-responsive hypothyroidism, Cushing's

ii.  Plush-coated breeds seem predisposed

iii.  Most 1–4 years

iv.  Initial clinical signs: coat becomes dry and brittle with loss of primary hairs leaving a "puppy-like" coat; dark hairs lighten; alopecia develops around the collar, flanks, perineum and caudomedial thighs. Rarely hair loss may progress to include the entire trunk, sparing only the head and legs. Hyperpigmentation of the skin is common.

c.  Treatment
Castration may be curative with regrowth in 2–4 months. Most maintain this coat permanently, but some will lose it 2–4 years after castration. Some of these may then be successfully treated with testosterone!

4.  Hyperandrogenism
Hypertestosteronaemia (usually associated with testicular interstitial cell tumour)

a.  Clinical signs

i.  Idiopathic

a)  Severe seborrhoea - most severe on face, ears, feet, axillae and groin

b)  Secondary infections common

ii.  Testicular neoplasia

a)  Hyperplasia of circumanal and tail glands (both composed of hepatoid cells)

b)  Doughnut-like appearance around anus. May become severe enough that multiple nodules/cysts develop

c)  Some develop macular hyperpigmentation of the tail gland, perianal area, scrotum, ventral tail and ventral abdomen

b.  Treatment

i.  Castration

ii.  In idiopathic, skin returns to normal in 2–4 months; behavioral changes may last longer

iii.  Glandular hyperplasia - castration stops progression, but some of the hyperplasia is irreversible

iv.  Macular hyperpigmentation fades in 6 months

5.  Congenital adrenal hyperplasia (adrenal sex hormone imbalance)
Mimics that seen in growth hormone-responsive or gonadal sex hormone dermatoses but fails to respond to growth hormone or neutering. The cause has not been fully determined, but a partial deficiency in one or more of the adrenal enzymes is thought to be responsible. The defect results in a partial deficiency of aldosterone or cortisol, which leads to an increase in ACTH adrenal hyperplasia and increased adrenal sex hormone production (progesterone or androgens). An alternative hypothesis is an inherent increased production of the adrenocortical sex hormones. It should be noted that whilst increased hormone (especially progesterone) has been recorded, a deficiency of the enzymes has not been documented. To further confuse matters, Schmeitzel (1995) found a decrease in growth hormone and an increase in the adrenal androgens in both normal and bald Pomeranians.

a.  Clinical signs

i.  Pomeranians, Chow Chow, Keeshond, Samoyed

ii.  Starts 1–2 years; M > F; response to neutering often poor

iii.  First changes: loss of primary hair in friction areas (collar, tail base, posteromedial thighs); then loss of all primary hairs puppy-like coat

iv.  Secondary hairs then lost and underlying skin hyperpigments

v.  Complete truncal hair loss is rare

b.  Treatment

i.  Neutering; many regrow (often to lose it 2–3 years later)

ii.  op DDD 15–25 mg/kg/day or trilostane (5 mg/kg/day). Aim is to reduce baseline cortisol concentration to low normal with some response to ACTH stimulation.

iii.  NB must be used with caution as there is the possibility of creating an Addisonian animal without altering the hair coat.

6.  Testosterone-responsive dermatosis
Pathogenesis unknown - hypoandrogenism has been suggested but never documented

a.  Clinical signs

i.  Seen in old neutered males

ii.  First changes: dull dry coat ± seborrhoeic changes

iii.  Dark colours may fade before hair loss noted

iv.  Hair loss truncal, slowly progressive

b.  Treatment

i.  Methyltestosterone 1 mg/kg (max 30 mg)

ii.  Should see response in 3 months change to maintenance (1–2 x weekly)

c.  Adverse effects: Seborrhoea oleosa, cholestatic liver disease, aggression


1.  Hyperoestrogenism

a.  Cause and pathogenesis
Cystic ovaries, ovarian tumours (most granulosa-theca cell origin)

b.  Clinical signs

i.  Bilaterally symmetrical alopecia - beginning in perineal, inguinal and flank regions; may spread to entire trunk

ii.  Nipples and vulva enlarged

iii.  Comedones (ventrum, vulva)

iv.  Secondary seborrhoeic changes

v.  Abnormal cycle, pyometra, endometritis

c.  Diagnosis
History; physical exam; rule out hypothyroidism, Cushing's, follicular dysplasia; elevated blood oestrogen; ultrasound; laparoscopy; response to ovariohysterectomy

d.  Treatment: Spay

2.  Congenital adrenal hyperplasia (adrenal sex hormone imbalance)

Non-Hormonal Alopecia

Pattern Baldness

Three syndromes recognised:

1.  Pinnal alopecia dachshunds

a.  Male and rarely female dachshunds

b.  Slowly lose hair from pinnae 6–9 months, progresses to complete loss by 8–9 years

c.  Other parts of the coat are normal; exposed skin hyperpigments

2.  American Water Spaniel and Portuguese Water Dog

a.  Hair loss noted at ~ 6 months - restricted to ventral neck, caudomedial thighs and tail

3.  Primarily dachshunds, also recognised in Boston terriers, Chihuahuas, Whippets, Manchester terriers and Greyhounds

a.  Almost exclusively in females

b.  6 months; hair loss from postauricular area, along ventral neck and entire ventrum, caudomedial thighs

c.  Close inspection - multiple fine hairs are still present

d.  (DDx: oestrogen responsive - this develops later 2–4 years and leaves no residual hairs)

e.  Biopsy: miniaturization of follicles with normal adnexa

Follicular Dysplasia

Colour Dilution (Mutant) Alopecia

Cause and Pathogenesis

 Cause unknown; coat colour genes play significant role

 Dilute hairs have larger pigment granules (macromelanosomes) and although lighter in colour, contain more melanin than non-dilute hairs

Clinical Signs

 Recognised in blue/fawn Dobermans, dachshunds, blue Chow Chows, blue Standard Poodles, blue Great Danes, blue Italian Greyhounds, and blue Whippets and others, including mongrels with blue coats

 Age depends on coat colour: gray - 6 months, less dilution steel blue 2 years

 Two forms


 Initial clinical signs may be dorsal, recurrent bacterial folliculitis or hypotrichosis - only hairs in dilute areas involved

 Antibiotics lead to resolution but the follicles remain hairless or regrow slowly. Repeated infection progressive hypotrichosis/alopecia

 Hair loss

 Secondary pyodermas may occur but clearly come after the hair loss; typically lose from dorsum first and then spread

 Initial hair loss due to shaft fracture (large clumped melanin causes structural weakness)

 With time, less tendency to regrow


Early - alopecia is due to shaft fracture, so minimise trauma from shampooing and excess grooming. The disease is incurable, although shampoos like benzoyl peroxide remove scales, and hydrating sprays or rinses improve the skin appearance as well as oral eicosapentaenoic acid.

Cyclic Flank Alopecia

 Localised cyclic follicular dysplasia - tends to occur in autumn or spring (regrow in other seasons)

 The aetiology is unclear, with deficiency or partial deficiency of melatonin secretion proposed. It may be that the condition is not due to melatonin deficiency, but is melatonin responsive.

 Airedale, British Bull, Boxer, Schnauzer - higher risk

 Clinically it presents as non-scarring alopecia in the thoracolumbar region. Usually bilaterally symmetric, well demarcated, with marked hyperpigmentation

 Spontaneous regrowth may occur and may be completely normal hair or different colour, texture, or both

 Prognosis is variable - from one episode to repeated episodes (± getting worse) to permanent loss

Follicular Dysplasia of Siberian Husky and Other Breeds

 Siberian husky, Malamute

 First seen at 3–4 months, guard hairs lost from trunk, slowly progressive. Coat turns reddish colour. Distal limbs spared. Clipped areas don't regrow.


 1–4 years, begins in flank, progresses slowly to dorsum and entire flank. Complete truncal hair loss not recognised.

 Airedale, English Bulldog, Staffordshire

 2–4 years. Flank and saddle most commonly affected.

 Irish Water Spaniel, Portuguese Water Dog, Curly Coat Retriever

 2–4 years. Periocular, flank, saddle

 Early spontaneous hair growth can occur but not of normal quality

 Biopsy (Portuguese Water Dog)

 Prominent apoptosis of keratinocytes in inner and outer root sheath, vacuolar alteration of IRS, pigmentary clumping intraluminally in follicular epithelium, dissolution of anagen bulb

 The dysplasia is due to abnormal melaninisation of the pilosebaceous unit.

Black Hair Follicular Dysplasia

Rare - dogs with bi or tri colour lose the black hairs only at early age.

Cause and Pathogenesis


 Due to abnormalities of pigment transfer and cuticle abnormalities

 Affected animals have disorderly proliferation of matrix hairs, abnormalities of pigment transfer, which leads to further weakening

Clinical Signs

 Recognised in cross breeds and pure (including Bearded Collie, Basset, Papillion, American Cocker)

 Born normal, coat changes by 4 weeks - black hairs become dull progressive hair loss until all black are gone

 Hair loss is due to shaft fracture; stubble may remain


1.  Dunstan RW. A common sense approach to the morphology of the hair follicles - readdressing points of follicular confusion. 24th Proceedings of the North American Veterinary Dermatology Forum. Savannah; 2009.

2.  Feldman EC, Nelson RW. Canine and Feline Endocrinology and Reproduction. 2nd ed. Philadelphia: WB Saunders; 1996.

3.  Frank L. Comparison of thyrotropin releasing hormone (TRH) to thyrotropin (TSH) stimulation for evaluating thyroid function in dogs. J Am Anim Hosp Assoc. 1996;32:481.

4.  Frank L. Of hormones and hair - hormonal mechanisms of canine alopecia. 24th Proceedings of the North American Veterinary Dermatology Forum. Savannah; 2009.

5.  Scott D, Miller W, Griffin C, eds. Muller and Kirk's Small Animal Dermatology. 5th ed. Philadelphia: WB Saunders.

6.  Schmitzel LP, Lothrop CD, Rosenkrantz WS. Congenital adrenal hyperplasia like syndrome. In: Kirk's Current Veterinary Therapy XIII. Philadelphia: WB Saunders; 1995:600–604.

7.  Spales AH, Gruffyd-Jones TJ, Watson PR, et al. Assessment of dose and time responses to TRH and thyrotropin in dogs. J Small Anim Pract. 1995;36:245.

8.  Williams DA, Scott-Montcrief C, Bruner J, et al. Validation of immunoassay for canine TSH and changes in serum concentration following induction of hypothyroidism in dogs. J Am Vet Med Assoc. 1996;209:1703.


Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Mike Shipstone, BVSc, FANZCVS, DACVD
Dermatology For Animals and
School of Veterinary Science, University of Queensland,
QLD, Australia

MAIN : Dermatology : Canine Alopecia
Powered By VIN