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Canine recurrent flank alopecia: A synthesis of theory and practice

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Canine recurrent flank alopecia is a non-inflammatory, non-scarring alopecia of unknown etiology and has a visually striking clinical presentation. Although this disease entity is relatively common in the northern hemisphere, there is only scant information in the literature regarding case descriptions. The aim of this article was to review the literature and to describe clinical presentations recognized in practice, which are not always extensively documented in the literature.
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Vlaams Diergeneeskundig Tijdschrift, 2014, 83 275
Vlaams Diergeneeskundig Tijdschrift, 2014, 83 Review 275
BSTRACT
Canine recurrent ank alopecia is a non-inammatory, non-scarring alopecia of unknown
etiology and has a visually striking clinical presentation. Although this disease entity is relatively
common in the northern hemisphere, there is only scant information in the literature regarding
case descriptions. The aim of this article was to review the literature and to describe clinical
presentations recognized in practice, which are not always extensively documented in the
literature.
SAMENVATTING
Caniene recurrente ankalopecia wordt klassiek gekenmerkt door een niet-inammatoire alopecia
met onbekende etiologie. Deze dermatose wordt getypeerd door unieke huidsymptomen. Alhoewel de
aandoening relatief frequent voorkomt in het noordelijk halfrond en dus ook in België, is er slechts
beperkte informatie over te vinden in de literatuur. Het doel van dit overzichtsartikel is om enerzijds
een samenvatting te geven van de literatuur en anderzijds de verschillende klinische presentaties
die herkend worden in de dagelijkse praktijk maar niet vaak beschreven worden in de literatuur, te
documenteren.
A
INTRODUCTION
Canine recurrent ank alopecia (CRFA) is a visu-
ally striking disease characterized by cyclic episodes
of non-inammatory hair loss (or coat changes) that
can recur annually (Miller et al., 2013a). Several
names have been proposed for this unique canine alo-
pecic disease (canine ank alopecia, seasonal ank
alopecia, idiopathic cyclic ank alopecia, cyclic folli-
cular dysplasia) but none of the names t perfectly:
visually complete hair loss is not always seen, alo-
pecia is not always conned to the ank area, and
some dogs only experience one episode throughout
their entire lives (Paradis, 2009). This intriguing dis-
ease was rst reported in 1990 by Danny Scott (Scott,
1990). He described a clinically distinct form of wax-
ing and waning non-scarring alopecia in ve ovario-
hysterectomized dogs. Later, it became evident that
dogs of either sex and reproductive status could be
affected. Although the disease is well-recognized in
practice, it remains poorly documented in the veter-
inary literature. The aim of this article is to make a
synthesis of the current knowledge from the literature
Canine recurrent ank alopecia: a synthesis of theory and practice
Caniene recurrente ankalopecia: synthese van theorie en praktijk
1S. Vandenabeele, 1J. Declercq, 2H. De Cock, 1S. Daminet
1Department of Medicine and Clinical Biology of Small Animals, Ghent University, Belgium
2Veterinary Pathology Services/Medvet, Antwerpen, Belgium
s.vandenabeele@ugent.be
and the different clinical presentations that are recog-
nized in practice, but which are not extensively men-
tioned in the literature.
ETIOLOGY AND PATHOGENESIS
The exact etiology of CRFA remains unknown.
Studies evaluating thyroid function, reproductive
hormones and growth hormones in affected dogs
have not revealed abnormalities (Curtis et al., 1996;
Daminet and Paradis, 2000). However, a localized
change in the amount or sensitivity of the hair follicle
receptors cannot be excluded (Miller et al., 2013a).
Because the disease is more prevalent in certain
breeds, such as Boxers, Airedales, Schnauzers, Eng-
lish bulldogs, Affenpinschers, Griffon Korthals and
Bearded collies, a genetic predisposition is suspec-
ted (Paradis, 2009; Waldman, 1995; Fontaine et al.,
1998). Duration of daylight exposure or changes in
light exposure appear to play a role in the develop-
ment of the lesions. Several observations support the
role of light in the pathogenesis of this disease. Firstly,
276 Vlaams Diergeneeskundig Tijdschrift, 2014, 83
there is the seasonal nature and often annual recur-
rence of the disease. Interestingly, the onset of CRFA
in the northern hemisphere is the reverse of what is
seen in Australia and New Zealand, which means that
in both hemispheres, the onset of alopecia coincides
with the months with a shorter duration of daylight
(Miller et al., 2013a; Paradis, 2012, Basset et al.,
2005). Secondly, some cases that have been reported
in the literature describe the development of lesions
in dogs that were kept in abnormal light conditions;
one dog in the northern hemisphere developed lesions
in the summer when kept in a dark room (Waldman,
1995; Ando and Nagata, 2000). Light therapy has
anecdotally been tried with success as a preventive
therapy. In another study, dogs exposed to 100-200
Watt during 15 to 16 hours from September till April
did not develop alopecia (Paradis, 1998).
There are two important photo-dependent hor-
mones in the body: melatonin and prolactin. Melatonin
is primarily synthesized in the pineal gland and acts
at the level of the pars tuberalis of the pituitary. Its
production is proportional to the length of the dark
period. Decreased retinal daylight exposure results
in increased melatonin production. Melatonin is im-
portant for reproduction, thermoregulation, coat color
and hair cycling (Paradis, 2000; Stankov et al., 1994).
It is known to be involved in the moulting of several
mammalian species. Melatonin implants have been
used in foxes and minks to manipulate seasonal coat
changes (Valtonen et al., 1995; Rose et al., 1984).
Because of the familial incidence, the associa-
tion with light exposure and the positive effects of
melatonin supplementation, a decreased endogen-
ous melatonin production in genetically predisposed
animals is suggested to play a role in the pathogen-
esis of this disease (Paradis, 1995). Melatonin may
act directly on the hair follicle or indirectly through
modulation of melatonin stimulating hormone (MSH)
and/or prolactin (Paradis, 1995; Fischer et al., 2008).
Prolactin levels are known to inversely correlate with
melatonin levels (Messenger, 1993). The increase of
melatonin levels and subsequent decrease in prolactin
levels induce the formation of a winter coat in sheep
(Paradis, 2000; Nixon et al., 2002). Hair follicle cyc-
ling is governed by seasonal changes to produce a
summer and winter moult, and the other photo-de-
pendent hormone, prolactin, has been implicated
as a principal regulator of this process (Messenger,
1993). Prolactin is synthesized in the pineal gland. It
has been shown to inhibit growth of anagen follicles
in mice and sheep (Nixon et al., 2002; Craven et
al., 2006). It is believed to have inhibitory effects
at different stages of the hair follicle cycle with the
ability to reduce hair length, shorten anagen, induce
shedding or lengthen the telogen phase (Nixon et al.,
2006; Craven et al., 2006; Thompson et al., 1997).
Prolactin may thus very well be an important player
in CRFA but no studies have been done to assess its
potential role.
CLINICAL PRESENTATION
The age of onset has a wide range: from one year
of age to eleven years, with most cases developing
clinical signs for the rst time between three and six
years of age (Miller et al., 2013a; Paradis, 2009; Para-
dis, 2012). Numerous breeds can be affected, but there
seems to be a breed predilection in the Boxer, English
bulldog, Airedale, Griffon Korthals, Affenpinscher,
Labrador retriever, Golden retriever, Bouvier des
Flandres, Dobermann and Schnauzer (Miller et al.,
2013a; Paradis, 2009; Waldman, 1995; Fontaine et
al., 1998; Cerundolo; 1999). Dogs of either sex and
reproductive status can be affected. In practice, the
typical clinical presentation of CRFA is a bilateral
symmetrical, geographic-shaped, non-scarring and
non-inammatory alopecia in the thoracolumbar
area. It is further characterized by a rapid onset of
Figure 1. Classical presentation of canine recurrent
ank alopecia. A four-year-old Rhodesian ridgeback
with bilateral symmetrical, geographic shaped alopecia
on the thoracolumbar area and marked lesional hyper-
pigmentation.
Figure 2. Facial presentation with complete alopecia of
the dorsal muzzle in a Golden retriever.
Vlaams Diergeneeskundig Tijdschrift, 2014, 83 277
alopecia between the months of November and April
in the northern hemisphere. The actual month of on-
set does not appear to be related to breed, age, sex
or reproductive status (Miller et al., 2013a; Paradis,
2012). Hair regrowth can rarely take up to 18 months
and permanent alopecia can be seen in chronic re-
current patients. Often, the area of alopecia remains
visually recognizable, because regrown hair has a
slightly different texture and/or color (Miller et al.,
2013a; Paradis, 2012). Hyperpigmentation in the alo-
pecic area may be striking but is not always present.
The presence or absence of hyperpigmentation in re-
sponse to light exposure depends on the breed and
within certain breeds depends on the individual pig-
mentation prole of the dog. In some breeds and some
individuals, hypermelanization of the skin resulting
from endogenous production of factors that stimulate
the melanocytes has never been noticed. Breed re-
lated lack of hyperpigmentation is usually seen in the
Wirehaired pointer, Dalmatian, Dobermann, Vizsla
and Weimaraner (Paradis, 2009; Declercq, 2008).
The classical distribution of the lesions is the lat-
eral to dorsolateral thorax and lumbar region. Lesions
consist of well-circumscribed patches of alopecia ex-
hibiting a geographic and irregular pattern (Figure 1).
The alopecic area ranges in size from 2 cm to almost
the entire thoracolumbar area. Lesions most com-
monly are bilateral symmetrical, but one side is com-
monly more affected then the other. Unilateral lesions
have been recognized. At the time of onset, there is
lesional increased epilation (Miller et al., 2013a).
Several atypical presentations (facial presentation,
generalized presentation, ank alopecia without an
episode of visual ank alopecia and ank alopecia with
interface dermatitis) have been recognized in practice
(Declercq, 2008; Vandenabeele, 2007; Vandenabeele,
2014). They are called atypical because the distribu-
tion of the alopecia is not conned to or absent in the
thoracolumbar area, or because instead of alopecia,
there is only a discoloration and texture change of the
coat. The factors that unify all of these cases are the
often recurrent nature of the rapid onset of the non-
pruritic lesions between November and April (except
for the dogs with discoloration of the coat, where coat
color changes and texture changes are seen later in the
year and have an onset between April and September)
and the spontaneous hair regrowth (Declercq, 2008;
Cerundolo and Rest, 2013).
Facial presentation
In these patients, alopecia of the dorsal muzzle
and sometimes associated mild alopecia in the peri-
ocular region are seen (Figure 2). This is most com-
monly noticed in the Golden retriever and Labrador
retriever (Declercq, 2008; Cerundolo and Rest, 2013;
Vandenabeele, 2007).
A visually more striking variation of this presenta-
tion is seen in the Bordeaux dog. These dogs present
with alopecia and hyperpigmentation of the dorsal
muzzle and facial folds. The affected dogs have no
alopecia in the thoracolumbar area. The authors of
the present study have also seen a Cane corso with
this presentation, where the dog had three episodes of
alopecia on the facial folds in three consecutive years
(Figure 3). The alopecia started in April and hair re-
growth was seen in July (Vandenabeele, 2014).
Generalized form
In these dogs, alopecia is present in the thora-
columbar area and other regions, such as the dorsal
muzzle, periocular regions, base of the ears, peri-
neum and base of the tail (Miller et al., 2013a; De-
clercq, 2008; Cerundolo and Rest, 2013) (Figure 4).
This multifocal non-scarring alopecic form has been
described in some Airedales, Golden retrievers, Grif-
fon Korthals, Dobermanns, Wirehaired pointers and
Giant Schnauzers (Paradis, 2009). Spontaneous re-
growth is seen simultaneously in all of the affected
areas.
Flank alopecia without an episode of visual alo-
pecia
Coat color changes and/or changes in texture of
the coat are seen in the ank and thoracolumbar area,
without a visual episode of alopecia. These coat color
changes are irregular in distribution and may have a
geographic pattern. In the literature, aurotrichia has
been described in Schnauzers without preceding alo-
pecia (White et al., 1992). Interestingly, in the study
Figure 3. Facial presentation with alopecia and hyper-
pigmentation of the dorsal muzzle and facial folds in a
Cane Corso (Picture courtesy of Ilona Schwarzkopf).
278 Vlaams Diergeneeskundig Tijdschrift, 2014, 83
by White et al. (1992), the onset of the discoloration
of the coat from silver or black hairs turning into a
gold colored coat occurred during the months of April
till September. This is later than what has been ob-
served in the other forms of ank alopecia. One of the
Schnauzers had two consecutive episodes of aurotri-
chia (White et al., 1992). Idiopathic aurotrichia has
also been described in a Bichon frisé (month of onset
not reported) (Miller et al., 2013b). The authors of
the present study have seen recurrent aurotrichia in
a Poodle, Lhasa apso, Cocker and Yorkshire terrier
during the months of April till September (Figure 5).
It is currently unknown why the coat color change of
these dogs occurs at that time of the year. Possibly,
the changes in the hair coat represent the recovery
phase of the disease and are actually new grown hairs.
Flank alopecia in non-related dogs in the same
household has been anecdotally noted. The case de-
scription of the ank alopecia in the Affenpinschers
of Waldman (1995) mentions that multiple Affen-
pinschers developed ank alopecia in the winter,
when kept in the conservatory, where there was no ar-
ticial heating or lighting. The authors of the present
study have seen “an outbreak” of ank alopecia in
a breeding facility where multiple Bichon frisé dogs
developed alopecia at the same time. No more recur-
rences were seen when the day-night cycle was adjus-
ted in the breeding facility. Another example which
was observed by the authors of the present study is
a household with three non-related English Stafford-
shire terriers where the three dogs develop ank alo-
pecia simultaneously every year between December
and February.
Flank alopecia with interface dermatitis
This entity was rst described in 2003 by Rachid
in Boxers and is characterized by a combination of
ank alopecia and interface dermatitis/folliculitis
(Rachid et al., 2003; Mauldin, 2005). In Europe,
this presentation of ank alopecia has been repor-
ted by Van der Luer in an English bulldog (Van der
Luer and Bonestroo, 2010). Also, the authors of the
present study have seen this presentation in an Eng-
lish bulldog. The distribution of the lesions is very
similar to the classical presentation of ank alopecia,
with lesions conned to the thoracolumbar area. The
difference is the concurrent presence of non-painful
and non-pruritic multifocal circular scaly and crusted
depigmented plaques within the alopecic area (Figure
6). The alopecia and the interface dermatitis demon-
strate concurrent courses of remission and recurrence
in these patients. The relationship between the two
types of lesions is not known (Rachid et al., 2003;
Mauldin, 2005). The possibility of a superimposed
erythema ab igne (chronic radiant heat dermatitis) on
CRFA lesions in some of those cases has been sug-
Figure 4. Generalized presentation of canine recurrent ank alopecia in a Wirehaired pointer. Note alopecia of the
pinnae, anks and distal extremities.
Vlaams Diergeneeskundig Tijdschrift, 2014, 83 279
gested (Paradis, 2009). However, the hypopigment-
ation bordered by the hyperpigmentation is unique
to erythema ab igne (Declercq and Vanstapel, 1998).
Moreover, histopathological changes typical of ery-
thema ab igne, such as keratinocyte atypia and karyo-
megaly and a variable number of wavy eosinophilic
elastic bres (“red spaghetti”), are not seen in CRFA
with interface dermatitis (Declercq and Vanstapel,
1998; Walder and Hargis, 2002; Rachid et al., 2003;
Mauldin, 2005).
DIAGNOSIS
If a dog is presented with a history of annual re-
curring alopecia presenting with the typical lesions
from November to April and spontaneous regrowth is
evident, the diagnosis of CRFA can be made based on
the history and striking clinical ndings (Miller et al.,
2013a; Paradis, 2012).
If a dog is presented for a rst episode of CRFA
with the typical clinical presentation endocrinopath-
ies, such as hypothyroidism, breed specic hair cycle
abnormalities, color dilution alopecia, post-shaving
arrest, erythema ab igne (chronic radiant heat
dermatitis), glucocorticoid injection reaction and
post-rabies vaccination panniculitis need to be ruled
out (Declercq, 2008).
It is of interest that certain breeds that are predis-
posed for CRFA, such as the Boxer, Airedale and Ger-
man pointers, are also predisposed for hypothyroid-
ism (Dixon et al., 1999; Paradis, 2009). Hypothyroid-
ism usually presents as a slowly progressive alopecia,
as opposed to the rapid onset of alopecia in CRFA.
Usually, other coat changes are present in hypo-
thyroid dogs such as a scaly or dull and brittle hair
coat. Concurrent pyoderma and otitis are an occa-
sional complaint in hypothyroid dogs (Paradis, 2009).
Slow hair regrowth in clipped areas and a rat tail are
other clinical ndings suggestive of hypothyroidism.
In CRFA, the quality and quantity of the coat in the
non-lesional skin are normal. Another difference is
that metabolic signs (weight gain, lethargy) are gen-
erally seen with hypothyroidism, but not in dogs with
CRFA (Paradis, 2009).
Color dilution alopecia causes an initially dorsally
oriented, slowly progressive diffuse, partial alopecia.
A variable degree of alopecia can also be noted on
the head and rarely, the extremities. Various breeds
such as Dobermann, Chihuahua, Italian Greyhound,
Yorkshire terrier, Whippet are predisposed for color
dilution alopecia. It is associated with diluted colors
of brown and black. These coat colors are referred to
as blue, gray, fawn and red (Laukner, 1998). Affected
dogs present with clinical signs before the age of 1
year and rarely later in life (Laukner, 1998).
There is a variety of breed-specic alopecic dis-
eases in dogs that have erroneously been classied as
follicular dysplasia. Because these forms of alopecia
are not developmental abnormalities and do not rep-
resent one specic disease, it has been decided that
hair cycle abnormalities would be a better denomina-
tion for this form of alopecia (Cerundolo et al., 2009).
These hair cycle abnormalities have a true breed pre-
disposition and have been reported in the Portuguese
water dogs, Chesapeake Bay retriever, Curly Coated
retriever and Irish water spaniels (Cerundolo et al.,
2009; Laffort-Dassot et al., 2002; Cerundolo et al.,
2005). The alopecia in these breeds can wax and
wane, but there is no seasonal inuence and the hair
regrowth is never complete in these breeds. The caudal
thighs and ventral neck are often involved and these
are areas that are not affected in dogs with CRFA.
Moreover, these dogs do not respond to melatonin
treatment (Cerundolo et al., 2009; Cerundolo
et al., 2005).
In post-clipping alopecia, there is a lack of regrowth
at the site of previous clipping (Miller et al., 2013c).
Figure 5. Presentation of canine recurrent ank alope-
cia without noticeable alopecia. Note the difference in
coat color in an irregular pattern in the thoracolumbar
area in this Poodle.
Figure 6. Flank alopecia with interface dermatitis in
a 3-year-old English bulldog. Note the thoracolumbar
distribution of the lesions with the presence of crusted
depigmented plaques within the alopecic area (Picture
courtesy of Anja Bonte).
280 Vlaams Diergeneeskundig Tijdschrift, 2014, 83
Especially, if the dog was clipped in the thoracolumbar
or dorsal area (as might be seen with epidural anes-
thesia), clinical resemblance with CRFA is possible.
This disease usually effects Nordic breeds such as the
Siberian husky, Alaskan malamute, Samoyed, Pom-
eranians and Chow Chows without age or sex pre-
dilection (Miller et al., 2013c; Gross et al., 2005a). It
has been proposed that in those breeds, hair regrowth
might take a lot longer because of a prolonged telo-
gen phase that possibly developed to save energy in
those cold climates. In this case, the prolonged telo-
gen phase is responsible for the post-clipping alope-
cia (Credille, 2000). These breeds are not predisposed
for CRFA, but post-clipping alopecia can be seen in
other breeds too. Post-clipping alopecia is diagnosed
by the signalment, the history of previous clipping
and clinical presentation (Miller et al., 2013c; Gross
et al., 2005a). Endocrinopathies, such as hypothyroid-
ism, hyperadrenocorticism and alopecia X should be
ruled out.
If a dog presents with unilateral alopecia in the
thoracolumbar or dorsolumbar area, erythema ab igne
and injection reactions need to be ruled out.
Erythema ab igne is a typically unilateral derma-
tosis that occurs at the site of repeated exposure to
moderate heat. Lesions are commonly seen at the
dorsolateral thoracic region and consist of irregular
branching areas of alopecia with erythema and hypo-
pigmentation bordered by hyperpigmentation (Miller
et al., 2013d; Gross et al., 2005b; Walder and Hargis,
2002; Declercq and Vanstapel, 1998) (Figure 7). The
distribution of the lesions and the irregular alopecia
are similar to CRFA, especially ank alopecia with
interface dermatitis. The hypopigmentation bordered
by the hyperpigmentation is unique to erythema ab
igne (Declercq and Vanstapel, 1998). Histopatholo-
gical changes consist of keratinocyte atypia and karyo-
megaly, scattered apoptotic or vacuolated basal cells
with an interface dermatitis, adnexal atrophy and a
variable number of waxy eosinophilic elastic bres
(“red spaghetti”) (Gross et al., 2005b). Erythema ab
igne is diagnosed by a history of chronic access to
heat sources, such as a heating pad, electric blanket,
burning stove or heat lamp, with typical clinical signs
and typical dermatopathological changes (Miller et
al., 2013d; Gross et al., 2005b; Walder and Hargis,
2002; Declercq and Vanstapel, 1998). It is of interest
to note that glucocorticosteroid injections also can
cause either alopecia or changes in coat color and
coat texture (Declercq, 2008; Miller et al., 2013e)
(Figure 8). The alopecia is focal and often there is
a concurrent atrophy of the skin with slight scaling.
Mineralized injected material in the deep dermis can
be seen or palpated; moreover, the underlying mus-
culature can be atrophic in severe cases (Miller et al.,
2013e). Another type of injection reaction, post-ra-
bies vaccination panniculitis can be seen at the site
of rabies vaccine deposition and is considered to be
one of the vasculopathic syndromes under the group
of ischemic dermatopathy (Gross et al., 2005c). Typi-
cally, the lesion is noted two to three months post
vaccination. The lesion consists of a focal alopecia
with minimal inammation. The alopecic area may
vary in size, and erythema is minimal or absent. Le-
sional hyperpigmentation can be seen (Miller et al.,
2013e). Injection reactions can be diagnosed by his-
tory, clinical presentation and histopathology (Miller
et al., 2013e; Gross et al., 2005b).
If a client does not want to wait for spontaneous
regrowth, a biopsy and histopathological examina-
tion are warranted. In active lesions, the fairly typical
histopathological changes consist of infundibu-
lar hyperkeratosis extending to secondary follicles
and sometimes even into the sebaceous gland ducts
(Figure 9). The hair follicles demonstrate an atrophic
base and may be malformed. These fore-mentioned
changes create a specic dysplastic appearance of
the hair follicles resembling a malformed foot, hence
called “witch’s feet” or “octopus-like hair follicles”
(Gross et al., 2005d). The size of the adnexae is nor-
mal, but sebaceous glands may be melanized. Melanin
aggregates may also be present in the follicular lumen
(Bagladi et al., 1996; Miller and Dunstan, 1993). The
timing of the biopsies greatly inuences the histo-
pathological changes (Gross et al., 2005d; Paradis,
2009). When patients are biopsied early in the disease
Figure 7. Clinical presentation of erythema ab igne.
Note the alopecia with erythema and hypopigmenta-
tion bordered by hyperpigmentation (arrow) on the
ank of this mixed breed dog subjected to a heat lamp
post whelping.
Figure 8. Focal discoloration of the coat with concur-
rent atrophy of the skin in a Weimaraner caused by a
glucocorticosteroid injection.
Vlaams Diergeneeskundig Tijdschrift, 2014, 83 281
process, most follicles are in the telogen or catagen
phase. However, more often, patients are biopsied
when the alopecia has been present for several months
and is in the regression phase. If biopsied then, the
follicles will often already be in anagen phase, and
the infundibular orthokeratotic hyperkeratosis might
not be prominently present (Fontaine et al., 1998).
This is similar to what can be seen when the disease
presents with just coat discoloration. In those cases,
follicular hyperkeratosis and anagen follicles can be
seen. The described follicular changes are suggest-
ive but not pathognomonic for CRFA (Gross et al.,
2005d; Paradis, 2009). Dysplastic hair follicles and
abnormal melanin aggregation occur in both follicu-
lar dysplastic diseases and endocrine skin diseases
(Rothstein et al., 1998).
CLINICAL MANAGEMENT
Dogs with this disease are otherwise healthy, and
the disease should be considered as a cosmetic dis-
ease. As spontaneous hair regrowth does occur (al-
beit potentially incomplete with recurrent episodes),
benign neglect can be a valid treatment option (Miller
et al., 2013a; Paradis, 2009).
Because of a variable timing of the spontaneous
regrowth and the unpredictable course of the alope-
cic periods, evaluation of treatment, either curative
or as a preventive measure is very difcult to assess
objectively.
Melatonin is considered the initial treatment of
choice, if treatment is requested (Miller et al., 2013a).
The optimal dose, best route of administration and
the duration of treatment and best time of initiation
of treatment are currently unknown, as placebo-con-
trolled studies have not yet been published. A success
rate of 50-75% has been reported based on anecdotal
information (Paradis, 2009). Melatonin implants
at 12mg/dog have been successfully used as a pre-
ventative treatment in dogs with recurrent episodes
of CRFA (Paradis, 2000). Oral melatonin can be ad-
ministered at a dose of 3 to 6 mg per dog twice to
three times daily during 4 to 6 weeks (Paradis, 2000).
This duration of treatment is based on a study in mink
showing that melatonin induces the anagen hair cycle
within a 4- to 6-week period (Paradis, 2000). How-
ever, once the hair cycle is restarted, melatonin is no
longer necessary for continuous growth and matura-
tion of the pelage (Valtonen et al., 1995). Treatment
should be initiated shortly after the onset of the alo-
pecia or 1 to 2 months before the anticipated onset of
the alopecia. Melatonin is a safe drug, without side
effects, but due to its interaction with reproductive
hormones, it should not be used in breeding animals
(Paradis, 2000).
In summary, canine recurrent ank alopecia is a
fascinating disease unique to dogs with an unknown
pathomechanism and with several clinical presenta-
tions. The proposed name does not t perfectly for
this disease entity. The course of the disease and its
response to melatonin therapy are unpredictable.
ACKNOWLEDGEMENT
The authors wish to thank dr Anja Bonte and dr
Ilona Schwarzkopf for providing the clinical picture
of CRFA with interface dermatitis (Figure 6).
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0033-12_AML_advertentie_100916.indd 1 16/09/10 14:59
... In other forms, a hereditary background is suspected because of a clear breed predisposition, and these cases typically exhibit later onset of the clinical phenotype. Examples of such disorders are alopecia X [22][23][24][25][26] and recurrent flank alopecia (RFA) [27,28]. The cause of these disorders remains unknown. ...
... Typical RFA is characterized by recurrent episodes of well demarcated, hyperpigmented areas of alopecia that affect several canine breeds, including Boxers, Rhodesian Ridgebacks, and Airedale Terriers [27][28][29][30][31]. The hair on the affected parts will usually regrow within a few weeks with recurrent loss the following year [31][32][33]. ...
... The hair on the affected parts will usually regrow within a few weeks with recurrent loss the following year [31][32][33]. RFA is not correlated with the sex of the individual [34] and always affects adults [27]. Previous studies have shown that the onset of RFA is influenced by the photoperiod [31,34]. ...
Article
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Non-inflammatory alopecia is a frequent skin problem in dogs, causing damaged coat integrity and compromised appearance of affected individuals. In this study, we examined the Cesky Fousek breed, which displays atypical recurrent flank alopecia (aRFA) at a high frequency. This type of alopecia can be quite severe and is characterized by seasonal episodes of well demarcated alopecic areas without hyperpigmentation. The genetic component responsible for aRFA remains unknown. Thus, here we aimed to identify variants involved in aRFA using a combination of histological, genomic, and transcriptomic data. We showed that aRFA is histologically similar to recurrent flank alopecia, characterized by a lack of anagen hair follicles and the presence of severely shortened telogen or kenogen hair follicles. We performed a genome-wide association study (GWAS) using 216 dogs phenotyped for aRFA and identified associations on chromosomes 19, 8, 30, 36, and 21, highlighting 144 candidate genes, which suggests a polygenic basis for aRFA. By comparing the skin cell transcription pattern of six aRFA and five control dogs, we identified 236 strongly differentially expressed genes (DEGs). We showed that the GWAS genes associated with aRFA are often predicted to interact with DEGs, suggesting their joint contribution to the development of the disease. Together, these genes affect four major metabolic pathways connected to aRFA: collagen formation, muscle structure/contraction, lipid metabolism, and the immune system.
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Seasonal patterns of hair growth are governed, at least in part, by levels of prolactin in circulation, and although receptors for prolactin (PRLR) have been demonstrated in hair follicles, little is known of their regulation in relation to follicular cycles. In this study, a photoperiod-generated increase in prolactin was used to induce a wool follicle cycle during which changes in PRLR expression in sheep skin were determined by ribonuclease protection assay and in situ hybridisation. mRNA for prolactin and both isoforms of PRLR were also detected in skin by reverse transcription and polymerase chain reaction. As circulating prolactin began to rise from low levels, PRLR mRNA in the skin initially fell. These changes immediately preceded the catagen (regressive) phase of the hair cycle. Further increase in prolactin resulted in up-regulation of PRLR during telogen (dormancy), particularly in the epithelial hair germ, to reach a peak during proanagen (reactivation). In anagen (when follicle growth was fully re-established), PRLR mRNA returned to levels similar to those observed before the induced cycle. Hence, this longer term rise and fall of PRLR expression followed that of plasma prolactin concentration with a lag of 12-14 days. PRLR mRNA was most abundant in the dermal papilla, outer root sheath, hair germ, skin glands and epidermis. Location of PRLR in the dermal papilla and outer root sheath indicates action of prolactin on the growth-controlling centres within wool follicles. These cycle-related patterns of PRLR expression suggest dynamic regulation of PRLR by prolactin, thereby modulating hormonal responsiveness of seasonally growing hair follicles.
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Quantitive collection of night-time urine every 2nd week was used to elucidate the temporal relationship between changes in melatonin production, weight gain, and priming of the winter pelage under natural light conditions and under a long photoperiod (18L: 6D) imposed at different times in four groups of female mink during autumn. In mink maintained outdoors under the natural photoperiod (group 1), melatonin excretion was 1·80 (s.d. 0·80) ng per night (no. = 3) at the beginning of September, thereafter it began to decrease slowly until November when it was only 0·62 (s.d. 0·32) ng per night. These mink had a normal autumn moult during the first half of October and the winter pelage was mature at the end of November. When mink maintained outdoors were transferred to 18L: 6D on 7 September (group 2), excretion of melatonin decreased promptly, autumn moult was disrupted and winter fur priming delayed. Long photoperiod after mid October (group 3), did not interfere with pelage maturation despite the decrease in melatonin production. Mink implanted with melatonin on 14 July (group 4) showed very high melatonin excretion in early September. In these animals the winter pelage growth was unaffected by the long-day conditions; the pelage matured in mid October. Body weight increased in mink of all groups during autumn. This increase levelled off or a weight loss (group 2) was seen along with the final hair maturation. Activation of hair follicles occurred during a 4 to 6 week period. According to these results, melatonin is the photoperiodic signal to autumnal weight increase and autumn moult but seems not to be necessary for later pelage growth and maturation.
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ALOPECIA is characterised by the absence of hair or by its loss from areas where it is normally present. It may be congenital or acquired and may reflect a cutaneous problem or may be the consequence of underlying internal diseases, the recognition of which is fundamental for the health of an animal. A variety of pruritic and non-pruritic diseases, such as those caused by ectoparasites (eg, scabies and demodicosis), dermatophytes, bacterial or yeast infections, and hypersensitivities, may initially show patterns of focal or multifocal alopecia which, if incorrectly managed, can progress to produce a more or less symmetrical generalised alopecia. In this article, however, discussion is restricted to the approach to the diagnosis of diseases causing symmetrical alopecia in dogs, including diseases of the endocrine glands and of the hair follicle unit. These are usually characterised by a non-inflammatory, non-pruritic, progressive alopecia affecting the head, neck, flanks, perineal area and/or thighs.