Veterinary Dermatology 2002, 13, 131139

Blackwell Science, Ltd

The effects of capsaicin topical therapy in dogs with atopic

dermatitis: a randomized, double-blinded, placebo-controlled,
cross-over clinical trial
ROSANNA MARSELLA, CONSTANCE F. NICKLIN and CAROLINE MELLOY
Blanche Saunders Dermatology Laboratory, University of Florida, Gainesville, FL 32610-0126, USA
(Received 6 September 2001; accepted 15 January 2002)

Abstract The efficacy of twice daily topical application of capsaicin (0.025%) for the management of pruritus
in dogs with atopic dermatitis (AD) was evaluated in double-blinded, placebo-controlled study. Twelve dogs with
AD were randomly assigned to either 0.025% capsaicin or vehicle lotion applied twice daily for 6 weeks. After a
4-week wash-out period, treatments were switched. Significant improvement was reported by owners
(P = 0.0006), but not by investigators. Owners noted temporary worsening of pruritus after the first week of capsaicin therapy. Overall capsaicin was well tolerated. Substance P (SP) concentrations in the skin did not correlate
with the severity of the pruritus and did not change significantly over time and between treatments. Lesional skin
had less SP than nonlesional skin (P = 0.03). These observations suggest that topical capsaicin should be further
evaluated as an adjunctive antipruritic agent in dogs with AD.
Keywords: atopic dermatitis, capsaicin, dogs, Substance P

I N T RO D U C T I O N
Atopic dermatitis (AD) is one of the most common
allergies in dogs. Estimated prevalence ranges from 15
to 30% of the canine population.1 Despite the fact that
AD is extremely common, the pathogenesis of this disease is not completely established and the therapeutic
options currently available are limited. Thus, evaluation of the role of mediators involved in canine AD
and their pharmacological manipulation would be of
great benefit.
In humans there is increasing evidence that neuropeptides, such as Substance P (SP), are involved in
the pathogenesis of AD.24 In humans, SP release is
triggered by various stimuli, including histamine.5
Intradermal injection of SP causes wheal and flare
reactions.6,7 Receptors for SP have been identified on
human mast cells8 and their stimulation triggers
degranulation and histamine release9,10 and further
release of SP.11 Substance P is released after allergen
challenge in humans with atopic disease12,13 and contributes significantly to the recruitment of eosinophils
in allergic rhinitis.14
Distribution and density of several neuropeptides
were examined in lesional and nonlesional skin of
atopic patients and in normal controls using immunohistochemistry.15,16 Substance P immunoreactivity was
Correspondence: Rosanna Marsella, Department of Small Animal
Clinical Sciences, College of Veterinary Medicine, PO Box 100126,
University of Florida, Gainesville, FL 32610-0126, USA. Tel.: +1352-392-4700 (ext. 5756); Fax: +1-352-392-6125; E-mail:
MarsellaR@mail.vertmed.ufl.edu
2002 Blackwell Science Ltd

present in all atopic patients but not in controls.15 The

distribution density of the cutaneous nerve fibres was
higher in patients with AD than in normal controls,
and the diameter of these fibres was larger, because of
the large number of axons in each nerve fibre.17 These
studies support a role for neuropeptides in the pathogenesis of human AD, and an imbalance between various neuropeptides (vasoactive intestinal polypeptide
vs. SP) might reflect diverse roles in the modulation of
AD lesion.16
A neurogenic component for AD is also supported
by the fact that keratinocytes are a source for neurotrophins such as nerve growth factor, that are required
not only for survival and regeneration of sensory neurons, but also to control the responsiveness of these
neurons to external stimuli.18 In addition, in individuals
with AD, itching seems to be elicited by a different
physiological pathway to that in nonatopic individuals
supporting the need of antipruritic agents influencing
the centrally altered nociception of atopic patients.19
The effect of SP on proliferation and cytokine
expression of peripheral blood mononuclear cells in
response to allergens (Dermatophagoides farinae) was
also studied in patients with AD.20 Upon stimulation
with relevant allergens, peripheral blood mononuclear
cells from patients with AD proliferated, whereas those
from healthy controls did not and it was noted that SP
promoted the allergen-induced proliferation. It was
concluded that SP modifies immune responses of
atopic T cells by promoting proliferation and altering
cytokine profiles, and therefore modulates the clinical
manifestations of AD. Therefore, neuropeptides, neuropeptide receptors, neuropeptide-degrading enzymes
131

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R. Marsella et al.

and neurotrophins participate in a complex, interdependent network of mediators that modulate skin
inflammation, wound healing and the skin immune
system.
Capsaicin is an alkaloid derived from the seed and
membranes of plants of the nightshade family (active
principle of chilli pepper). The exact mechanism of
action is unknown. The effects of capsaicin on SP
appear to be principally on type C sensory neurons.21
These unmyelinated slow-conducting fibres of the
type C group have been implicated in mediating cutaneous pain and the itch sensation.22 Repeated application of topical capsaicin abolishes pain and itch.
Capsaicin has been successfully used in people with contact allergy,23,24 chronic prurigo,25 pruritic psoriasis,26
hydroxyethyl starch-induced pruritus,27 haemodialysisrelated pruritus,28 uraemic pruritus,29 cold and heat
urticaria30 and aquagenic pruritus.31 Relief is usually
noted within 14 days and persists for a few weeks. It
is hypothesized that capsaicin works by depleting the
sensory nerve endings of SP.3234 In addition, inhibition of nuclear factor B activation and thus, modulation of the production of inflammatory mediators may
be important.35
Little information is available on the role of SP in
canine pruritus. However, SP acts as a primer of canine
neutrophils and may act as a mediator of neurogenic
inflammation.36 The objectives of this study were to
investigate the efficacy of capsaicin topical therapy on
pruritus in dogs with AD and the effects of this therapy
on cutaneous SP concentrations to evaluate a possible
correlation between pruritus and the presence of SP in
the skin.

MATERIALS AND METHODS

Animals
This project was reviewed and approved by the Institutional Animal Care and Use Committee and Clinical
Research Review Committee. Twelve privately owned
dogs with AD were selected. A signed consent form
was obtained in all cases. The following criteria were
used to select the dogs that participated in this study.
Inclusion criteria were a diagnosis of AD, which was
based on suggestive history, compatible clinical signs,
and at least three positive reactions on intradermal
skin testing using a panel of 57 allergens. A positive
reaction was considered a reaction that scored 2 or
higher on a scale of 04, in which 0 was the score given
to the negative control (saline) and 4+ was the score of
the positive control (histamine) 15 min after the injections.

Exclusion criteria were the presence of other pruritic

skin diseases (e.g. food allergy and scabies) and the
presence of secondary ear and skin infections (e.g. staphylococcal pyoderma and Malassezia dermatitis).
Other exclusion criteria were the use of topical, oral
steroids and antihistamines in the 2 weeks prior to the
study and injectable steroids in the 2 months prior to
the study. During the study only heartworm prevention
and flea control (monthly application of Frontline,
Merial Limited, Iselin, NJ, USA) were allowed.
Once selected, dogs were randomly divided into two
groups (A and B). Assignment to treatment was randomized by coin toss, in that a coin toss prior to enrolling
the first dog determined the treatment of that first
dog. The remaining dogs were enrolled in alternating
treatments until all of the dogs were enrolled. This
allowed for equal distribution of dogs assigned to each
treatment and minimized order of treatment effects.
Division was blinded to investigators and owners.
Group A received application of capsaicin lotion
(0.025%),37 whereas group B received a placebo lotion
(vehicle) to affected areas twice daily for 6 weeks. At
the end of the first treatment period, there was a 4-week
wash-out period before the treatments were crossed
over. The capsaicin lotion was compounded from oleoresin capsicum liquid USP, which contained 17.7%
capsaicin. This was reduced to 0.025% in a lotion base
containing 2/3 emollient cream and 1/3 preserved
water. Concentration, frequency of application, duration of treatment and wash-out periods were decided
based on studies in people.2331,37 Systemic absorption
and maximum dose of capsaicin allowed are not a concern in people. However, in this study a maximum daily
amount of 2.5 mg (10 mL) of capsaicin for a 30 kg dog
(0.08 mg kg1) was used. This choice was based on clinical experience. Dogs were distracted after lotion application or an Elizabethan collar was used to prevent
licking until the lotion was absorbed. Owners were
requested to return the bottle of lotion at the completion of each treatment period, which helped to verify
owner compliance.
Evaluation of clinical signs
Owner scored pruritus on a weekly basis using the criteria outlined in Table 1. Owners were asked to record
on a data sheet their weekly score of pruritus, and they
returned the data sheet at the end of each treatment
period. Using the criteria indicated in Table 2, the
investigator (RM) evaluated and scored pruritus
before and after each treatment period. Scores ranged
from 0 to 5, with higher numbers indicating more
severe clinical signs.

Score

Definition

1
2
3
4
5

Mild pruritus (scratching, rubbing, chewing or licking for < 10% of day)
Mild-moderate pruritus (scratching, rubbing, chewing or licking for 10 30% of day)
Moderate pruritus (scratching, rubbing, chewing or licking for 30 50% of day)
Moderate-severe pruritus (scratching, rubbing, chewing or licking for 50 75% of day)
Severe pruritus (scratching, rubbing, chewing or licking all the time, even at night)

2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 131139

Table 1. Criteria for the evaluation and

scoring of pruritus by the owner

Capsaicin for canine atopic dermatitis

Table 2. Criteria for the evaluation and
scoring of pruritus by the investigator

133

Score

Definition

1
2
3
4

No pruritus (no evidence of self-trauma)

Mild-moderate pruritus (15 mild excoriations, involving only one part of the body)
Moderate pruritus (evident excoriations in more than one part of the body)
Moderate-severe pruritus (evidence of pyotraumatic dermatitis, or deep ulcerations
that are self inflicted, or scratching, licking or chewing 15 times during the visit)
Severe pruritus (scratching, chewing or licking constantly, self mutilation if left
unattended)

Skin biopsies
To measure SP, full-thickness to 6 mm skin biopsy
specimens were taken from all dogs (one biopsy from
normal skin and one from lesional skin) at the beginning and end of each treatment group. Skin specimens
were obtained under local anaesthetic (0.5 mL per site
of lidocaine hydrochloride 2%; Phoenix Pharmaceutical Inc., St. Joseph, MI, USA) using a disposable skin
biopsy punch (Miltex Instrument Company, Lake Success, NY, USA). Sites were sutured routinely.
Each sample was cut in half and both halves were
snap frozen in liquid nitrogen. Skin samples were transferred to a 70 C freezer (Harris UltraLow, Harris
Manufacturing, Inc., Asheville, NC, USA) until processed for extraction of SP and ELISA analysis.
Substance P concentrations were expressed per g
weight of the tissue, as described previously.38 40
Extraction of Substance P
All samples were weighed (Model A250, Denver
Instrument Company, Arvada, CO, USA) and minced.
The minced sample was placed in 1.25 mL of 1 glacial acetic acid in ethanol and vortexed. The sample
was then homogenized for 30 s using a tissue homogenizer (Omni International TH, Omni International,
Inc., Warrenton, PA, USA). Pieces left on the homogenizer were collected with forceps, placed in an additional 1.25 mL 1 glacial acetic acid in ethanol and
homogenized for an additional 30 s. This was combined with the original homogenized sample and any
remaining pieces were also added. The homogenized
sample was then boiled for 10 min and centrifuged
(Harrier 18/80, SANYO Gallenkamp PLC, Leicester,
UK) at 3000 g, 20 C for 15 min. The supernatant was
saved, and the pellet was homogenized again by adding
1.25 mL 1 glacial acetic acid in ethanol and repeating
the above process. Within 5 min of the extraction process, 500 KIU of aprotonin/mL was added to the supernatant. The supernatants from both extractions were
mixed and stored at 70 C until purified.
Purification
The samples were purified as directed in the protocol
provided with the Substance P Immunoassay kit (R &
D Systems, Minneapolis, MN, USA). Briefly, an equal
volume of 1% trifluoroacetic acid (TFA) was added to
the sample. The sample was then centrifuged at 6514 g,
5 C for 15 min. The supernatant was collected and
added to a 200 mg C18 column (Accubond, J & W
Scientific, Folsom, CA, USA) that had been activated
with 1 mL acetonitrile and 15 mL 1% TFA, respectively.

The sample was eluted by applying 3 mL of a 60:40

solution of acetonitrile: 1% TFA. The eluant was collected in a plastic tube and dried using a SpeedVac
concentrator (ASE 1010, Savant Instruments, Holbrook,
NY, USA). This was then stored at 70 C until assayed.
Immunoassay
Samples were reconstituted with assay buffer, and the
concentration of SP in each sample was determined
using the Substance P Immunoassay kit (R & D Systems) following the protocol provided with the kit. The
coefficient of variation of this assay is 4.56.7% intraassay and 4.27.3% interassay. This assay can detect SP
concentrations < 8.0 pg mL1. Each assay included
total activity, nonspecific binding, maximum binding
and substrate blank wells as a means of quality control.
Prior to processing and analysing the study samples,
normal canine skin was spiked with known concentrations of SP to validate the process and assay.
Statistics
Data were analysed using least squares analysis of variance (LS) with all main effects and interactions
included in the model. Differences among treatments
or groups and times were analysed using orthogonal
contrast analysis. A value of P < 0.05 was considered
significant. Clinical scores were rank transformed
prior to analysis. Means and SEM were calculated
using the untransformed data. However, all P-values
were representative of the rank transformed data. Tests
for heterogeneity of regression were conducted to evaluate time trends between treatments. The analysis was
performed at the highest significant order of regression.
Pearson product moment correlation was used to
evaluate correlation between the severity of pruritus
and the concentration of SP in the skin. An r-value
> 0.80 was considered positive. All analyses were performed using the statistical software The SAS System for
Windows version 8.1 (SAS Institute, Cary, NC, USA),
and all results are reported as mean SEM, unless
otherwise indicated.

RE S U L T S
No difference was detected between periods, indicating
that order of treatment did not have an effect, so capsaicin and placebo data were pooled and reanalysed.
Twelve dogs with AD completed this double-blind,
cross-over study. The dogs age ranged from 1.5 to
6.5 years (mean, 3.6 years). Five dogs were Retrievers
2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 131139

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R. Marsella et al.

Table 3a. Actual scores of pruritus by owner

Placebo

Capsaicin

Dog no.

Wk 0

Wk 1

Wk 2

Wk 3

Wk 4

Wk 5

Wk 6

Wk 0

Wk 1

Wk 2

Wk 3

Wk 4

Wk 5

Wk 6

1
2
3
4
5
6
7
8
9
10
11
12

0.75
3
1
3
0.5
4
3
3
3
2
2
1

1
3.5
1
3.5
0.5
4
4
3
3
2
2
1

1
4
2
4
2
4
3.5
2.5
2.5
3
2
1

1.5
4
2
4
2
3
3.5
2
2.5
3
2
1

2
4.5
2
4
3
3
3
3
2.5
3
2
1

2
5
3
3.5
2
3
3
2.5
2.5
3
2
1

2
5
3
4
1
3
3
2
2.5
4
2
1

0.5
4
2
3
3
3
3
4
3
3
1
3

1
3
3
3
3
4
3
3.5
5
4
2
3

1
2.5
3
3
2
3
2.5
3
4
3
2
3

1.5
2.5
3
3
3
3
2.5
2
4
1
2
3

2
2.5
2
2
4
3
2
2

2
2
4

2
2.5
1
2
3
2
2
2.5

1
2
3

2
2.5
1
2
2
2
1.5
2.5

0
2
3

Figure 1. Scatter plot indicating the owner clinical scores of pruritus over time.

(either Labrador or Golden), whereas the other dogs

included a Beagle, Shar-Pei, Boston Terrier and mixed
breeds. Eight dogs were castrated males, whereas four
were spayed females.
Owner scores of pruritus
At week 0, the capsaicin group had significantly higher
pruritus scores than the placebo group (Table 3a;
P = 0.02). Despite this disadvantage, by week 6, the
capsaicin group had significantly lower scores than the
placebo group (P = 0.005). Within the placebo group
there was no significant difference between week 0 and
week 6. Within the capsaicin group, there was a significant decrease from week 0 to week 6 (P = 0.0006).
In the capsaicin group, scores worsened after the
first week of treatment, but this worsening was not
significant (Fig. 1).
Investigator scores of pruritus
According to the investigator, scores of pruritus for 11
of the 12 dogs either improved or remained the same
while on the capsaicin treatment, but this improvement
was not significant (Fig. 2, Table 3b). There were no
2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 131139

Table 3b. Actual scores of pruritus by investigator

Placebo

Capsaicin

Dog no.

Week 0

Week 6

Week 0

Week 6

1
2
3
4
5
6
7
8
9
10
11
12

2
3
2.5
3
2.5
2
3
3
3
2
1
2

1.5
4
3.5
2
1
1
2
2
4
3.5
3
1.5

1
3
2
2.5
2
2.5
3
2.5
2.5
1
2
4.5

2
2
2
2.5
2
1.5
2
2
3
1
2
1

significant changes in pruritus score during the placebo

treatment, and there was no significant difference
between treatment groups at week 0 or week 6.
Substance P concentrations in the skin
Cutaneous concentrations of SP were not significantly
different overtime and in between treatment groups

Capsaicin for canine atopic dermatitis

135

Figure 2. Scatter plot indicating the investigator clinical scores for pruritus over time.

Table 4. Substance P concentrations in the

skin before and after treatment. Results are
reported as mean SEM on a per g tissue
weight basis

Table 5. Substance P concentration in lesional

and nonlesional skin expressed as mean (pg/
g). SEM was 117.7 pg g1 at all times

Substance P
(pg g1)
Capsaicin
Placebo
P-values
(capsaicin vs. placebo)

Week 0

Week 6

P-values
(Week 0 vs. Week 6)

1088.24 83.22
987.89 83.22

1021.12 83.22
899.51 83.22

0.5743
0.4607

0.4031

0.3127

Substance P
(pg g1)

Week 0

Week 6

P-value
(Week 0 vs. Week 6)

Capsaicin

Lesional skin
Non-lesional skin

955.58
1220.91

1054.85
987.39

0.5570
0.1746

Placebo

Lesional skin
Non-lesional skin

765.35
1210.43

850.42
948.6

0.6144
0.1300

(Tables 4 and 5). Over all times and treatments, lesional

skin had significantly less SP than nonlesional skin
(906.55 58.85 and 1091.83 pg g1, respectively, P =
0.0366). However in both groups, at week 0, lesional
areas tended to have less SP than nonlesional areas.
This difference was statistically significant only in the
placebo group (P = 0.0139). At week 6, there was no
difference in SP concentrations between lesional and
nonlesional skin in both treatment groups.

DISCUSSION
In this study, owners perceived a significant decrease
in pruritus after using capsaicin for 6 weeks. As the
investigator did not report a significant change,
the investigators evaluation did not agree with the
owners evaluation. This difference in evaluation
between owners and investigator could be due to
several factors.

The investigator (RM) only evaluated the animal

during the time of the recheck visits in an unfamiliar
and stressful environment that may have interfered
with normal behaviour. Also, the investigator evaluated pruritus based on pruritic acts and signs of selftrauma, but it is important to note that some animals
with significant pruritus may not always cause significant trauma to their skin. Thus, the investigators evaluation of pruritus has some innate limitations. For this
reason, owners evaluations were deemed important
and were included in the design of this study. Owners
can be very attentive evaluators, as they are familiar
with their pets behaviour and level of discomfort. They
also see the animal on a regular basis and in its normal
environment.
In humans, capsaicin has been used successfully for
a variety of pruritic skin conditions.2331 Capsaicin may
be less effective at decreasing pruritus caused by AD than
for other pruritic skin diseases.41 In one study, capsaicin
pretreatment significantly reduced itch sensations in
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R. Marsella et al.

control subjects, whereas in AD patients, no differences

were seen.41 In the same study, capsaicin effectively
suppressed histamine-induced itching in healthy skin
but had less effect in AD.41 A similar situation could
exist in dogs with AD.
A variety of concentrations has been used in humans,
ranging from 0.025 to 0.5%.2331,35,37,42 It is possible
that a more frequent application or a higher concentration would have resulted in more pronounced efficacy.
However, in humans it is suspected that higher concentrations could more frequently lead to adverse effects
and sensitization43 and in order to avoid reactions a
low concentration was selected for this study.
In the capsaicin group, pruritus scores worsened
after the first week of treatment even though this worsening was not statistically significant. This worsening
might have been related to a release of SP caused by
repeated application of capsaicin, as this is one of the
reported mechanism of action of capsaicin.44 Alternatively, the worsening may have been caused by a direct
stimulation of nociceptors by capsaicin, as reported
previously in other species.44,45 Unfortunately, no skin
biopsies were taken after the first week to measure
cutaneous SP concentrations, thus, no conclusive
answer can be given for this observation.
In this study, clinical improvement with capsaicin
treatment as noted by owners did not correspond to a
decrease in cutaneous concentrations of SP. One possible explanation for this finding is that capsaicin exerts
its beneficial effects in ways other than depleting SP.
Capsaicin has long been known to act selectively on a
subpopulation of neurons to produce initial excitation,
followed by a prolonged neuroinhibitory action but the
cellular basis for these effects is not well understood.
Capsaicin binds to a specific membrane receptor
(vanilloid receptor or VR-1),46 which is either tightly
coupled to, or indeed is, a relatively nonselective cation
channel. Binding of capsaicin to this receptor allows
both sodium and calcium ions to flow down their
concentration gradients, causing initial depolarization
and neurotransmitter release.47 Prolonged exposure to
capsaicin produces desensitization or neuroinhibition,
which can be both capsaicin-specific and nonspecific.
The latter is characterized by a loss of responsiveness
to all stimuli and is probably associated with the neurotoxic effect of this agent. Whereas in earlier studies,
depletion of SP was considered the main mechanism
of action of capsaicin22,33,42,48 it is now accepted that
several other mechanisms are involved in the desensitization, including receptor inactivation, blockage of
voltage-activated calcium channels, intracellular accumulation of ions leading to osmotic changes, activation
of proteolytic enzyme processes, modulation of the
production of inflammatory mediators by inhibition
of nuclear factor B activation, and degeneration and
reversible loss of nerve fibres.35,47,4952 Thus, it is possible that the improvement noted in this study could
have been caused by a mechanism not related to SP
depletion. It is also currently unknown whether dogs
have the capsaicin receptor.
2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 131139

Over all times and treatments, lesional skin had less

SP than normal skin in this study. This finding contrasts with results reported in human literature,1517
but by itself, does not diminish the importance of SP in
the pathogenesis of pruritus in canine AD. This difference could be due, in part, to the different techniques
used to detect SP in the skin. In our study, SP was
extracted and measured by ELISA for a more objective
measurement, whereas other studies used immunohistochemistry and the criteria selected for evaluation
were more subjective. The other possibility is that SP
may play a role, not by being present in excessive quantities, but by causing an abnormal response. More specifically, an altered (decreased) sensitivity to SP has
already been documented in dogs with AD compared
with healthy controls.53 It is reasonable to hypothesize
that dogs with AD could have an upregulation of the
enzymes (neuropeptide specific peptidases) responsible
for SP degradation5456 leading to an increased metabolism and inactivation. Such enzymes are located
within the target cells or in close proximity to the membranes and to the receptors. Their activity is regulated
by mechanisms of stimulation and inhibition.57 Proinflammatory cytokines, including interleukin (IL)-1
alpha, tumour necrosis factor-alpha (TNF-) and IL6, have been reported to enhance the activity and
expression of neuropeptide-specific peptidases, thus
leading to an increased metabolism of SP.58 If dogs
with AD have an increased concentration of these
cytokines in lesional skin, as it has been described in
humans in AD,59 an increased metabolism of SP could
be a reason for which SP concentrations would appear
decreased despite the significant role for SP in this condition. Another mechanism of abnormal metabolism is
a mutation in these enzymes. Humans with AD have
been reported to have a mutation in the genes responsible for neuropeptide-specific peptidases.60 Whether
this could occur in dogs with AD is unknown, but it is
another possible pathway for abnormal metabolism of
SP in this disease.
In humans, symptoms return 2 4 weeks after discontinuation of capsaicin therapy.37,42 Unfortunately,
the dogs in this study were not followed beyond discontinuation of therapy, so the duration of effect is
unknown. Current research in humans is focusing on
the pharmacological modulation of the vanilloid
receptor and on the identification and modification
of capsaicin analogues (e.g. olvanil).46,47 These compounds have shown improved efficacy and minimal
initial algesic activity and may have a potential
application for canine patients in the future.
In conclusion, it is becoming increasing evident
that the cause of canine AD is a complex interaction
between genetic susceptibility, environmental factors
and abnormal immune responses. It is very likely that
not one single mediator can be proposed to explain
the inflammation and pruritus observed in affected
individuals, and that most likely it is the complex
interactions of these mediators that lead to the clinical
lesions and symptoms of this disease. The knowledge

Capsaicin for canine atopic dermatitis

of the link between the nervous system and the
immune system is still rudimentary, but the importance of this aspect seems to be emphasized by the
effect of stress on manifestations of pruritus, even in
our veterinary medicine patients. Further studies are
necessary to investigate the role of neuropeptides
and the usefulness of compounds that modulate
their release or alter the function of sensory nerves in
the skin.

13.

14.

15.

A C K N OW L E D G E M E N T S
This study was funded by the Morris Animal Foundation.

16.

RE F E RE N C E S
17.
1. Hillier, A., Griffin, C.E. The ACVD task force on canine
atopic dermatitis (I): incidence and prevalence. Veterinary Immunology and Immunopathology 2001; 81: 14751.
2. Tobin, D., Nabarro, G., Baart de la Faille, H. et al.
Increased number of immunoreactive nerve fibers in atopic
dermatitis. Journal of Allergy and Clinical Immunology
1992; 90: 613 22.
3. Pincelli, C., Fantini, F., Massimi, P. et al. Neuropeptides
in skin from patients with atopic dermatitis: an immunohistochemical study. British Journal of Dermatology
1990; 122: 745 50.
4. Heyer, G. Abnormal cutaneous neurosensitivity in
atopic skin. Acta Dermato-Venereologica Supplementum
(Stockholm) 1992; 176: 93 4.
5. Fitzpatrick, T.B., Eisen, A.Z., Wolff, K. In: Dermatology
in General Medicine, Pathophysiology and clinical
aspects, 4th edn, Vol. 1. New York: McGraw-Hill, 1993:
415.
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Rsum Cette tude en double aveugle contre placebo sest intresse valuer lefficacit de lapplication biquotidienne de capsaicine (0.025%) pour le traitement de la dermatite atopique (AD) chez le chien. Douze chiens
prsentant une AD ont t traits au hasard par la solution de capsaicine 0.025% ou par le vhicule, deux fois
par jour pendant 6 semaines. Aprs une priode de wash-out de 4 semaines, les traitements ont t inverss. Une
amlioration significative a t observe par les propritaires (P = 0.0006), mais pas par les investigateurs. Les
propritaires ont dcrit une aggravation temporaire du prurit aprs la premire semaine de traitement par la capsaicine. Globalement la tolrance a t considre comme bonne. Les concentrations de substance P (SP) cutanes
ntaient pas corrles avec la gravit du prurit et nont pas t significativement modifies par le traitement. Les
concentrations taient plus faibles dans la peau lse que dans la peau saine (P = 0.03). Ces observations suggrent que la capsaicine par voie topique mrite des valuations ultrieures comme agent antiprurigineux chez
les chiens AD.
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Resumen Se evalu la eficacia de una aplicacin tpica dos veces al da de capsaicina (0.025%) para el manejo
del prurito en perros con dermatitis atpica (DA), en un estudio doble-ciego, controlado con placebo. A doce
perros con DA les fue aplicado aleatoriamente un tratamiento de 0.025% capsaicina o una locin con excipiente
dos veces al da durante 6 semanas. Despus de 4 semanas de retirada, los tratamientos fueron intercambiados.
Se detect por parte de los dueos una mejora significativa (P = 0.0006), pero no por los investigadores. Los
dueos notaron un empeoramiento temporal del prurito despus de la primera semana del tratamiento con capsaicina. En conjunto la tolerancia a la capsaicina fue buena. La concentracin de sustancia P (SP) en la piel no
se correlacion con la intensidad del prurito y no cambi significativamente a lo largo del tiempo y entre tratamientos. La piel lesionada tena menos SP que la piel no-lesionada (P = 0.03). Estas observaciones sugieren que se
debera valorar con mayor profundidad la capsaicina tpica como agente antiprurtico en perros con DA.
Zusammenfassung Die Wirksamkeit von zweimal tglich lokal angewendetem Capsaicin (0.025%) in der
Behandlung des Juckreizes bei Hunden mit atopischer Dermatitis (AD) wurde in einer Plazebo-kontrollierten
Doppelblindstudie bewertet. Zwlf Hunde mit AD wurden randomisiert einer von zwei Gruppen zugeteilt und
entweder mit 0.025% Capsaicin oder Vehikel behandelt. Nach einer vierwchigen Auswaschperiode wurden die
Behandlungen vertauscht. Signifikante Besserung wurde von Besitzern (P = 0.0006), jedoch nicht von den
Klinikern festgestellt. Nach der ersten Woche Capsaicin Therapie bemerkten Besitzer eine zeitweilige Verschlimmerung des Juckreizes. Capsaicin wurde gut toleriert. Substanz P (SP) Konzentrationen in der Haut korrelierten
nicht mit der Schwere des Juckreizes und nderten sich whrend der Studie und mit den Behandlungen nicht wesentlich. Geschdigte Haut hatte weniger SP als nicht-geschdigte Haut (P = 0.03). Diese Beobachtungen deuten
darauf hin, dass lokales Capsaicin als untersttzendes, antipruritisches Medikament in der Behandlung von Hunden mit AD weiter untersucht werden sollte.

2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 131139