2 Apr 2024
Davide Immediato and Filippo De Bellis outline causes, diagnosis and treatment of pruritus in canines.
Image © Mila / Adobe Stock
Pruritus is defined as an “unpleasant sensation that triggers a desire to scratch”1-4, and it is divided into acute and chronic pruritus.
Pruritus can be an alarm system to remove damaging or harmful substances from the skin1,3, but it could also be an important feature of many dermatological conditions affecting both humans and animals3,5. It is the most common complaint in canine dermatology, and can affect the quality of life of dogs and their owners4,6.
In 2007, in humans, members of the International Forum for the Study of Itch proposed an aetiological classification of pruritus4,7. An adaptation of this classification was recently proposed in dogs, with six distinct origins: dermatological, systemic, neurological, psychogenic, mixed, and other (Table 1)4,7.
| Table 1. Classification of pruritus in dogs, adapted from Olivry and Baeumer (2017)7 | |
|---|---|
| Type of pruritus | Causes |
| 1. Dermatological | Secondary to skin diseases such as ectoparasites, allergies, infections or neoplasia |
| 2. Systemic | Secondary to organ diseases, none recognised in dogs |
| 3. Neurological | Secondary to disease/disorders of the central or peripheral nervous system (for example, syringomyelia or acral mutilation syndrome) |
| 4. Psychogenic-psychosomatic | Secondary to behavioural conditions such as acral lick dermatitis or tail chasing |
| 5. Mixed | Association of co-existing diseases such as atopic dermatitis with secondary superficial pyoderma |
| 6. Other | Undetermined origin |
Whereas most other forms of itch are shared between species, an important difference between dogs and humans is the lack of recognised systemic pruritus associated with chronic liver or kidney disease in animals7. In this article, the authors will focus mostly on pruritic dermatological conditions.
The sensation of pruritus can be linked to either activation of epidermal nerve fibres that can belong to pruriceptors (a specialised class of itch-provoking neurones), or a highly specific activation pattern5,8. The chemical mediators that control the neuronal activity originate from complex interactions between keratinocytes, inflammatory cells and nerve endings, along with immune cascades and epidermal barrier function9. Several factors such as skin pH, skin barrier integrity, irritant exposure and the microbiome can modulate the impact of these interactions on neurons5,10-12. Studies have shown that alkaline skin pH enhances serine protease activity and may increase the perception of pruritus3; moreover, central factors such as anxiety, boredom or competing cutaneous sensations (such as pain, touch, heat and cold) can increase or reduce the sensation of pruritus3.
The most common causes of pruritus in dogs include allergies (food and/or environmental), parasites, and infections (bacterial and/or fungal)4,13. Frequently, one or more causes of pruritus can be present simultaneously (for example, a patient with atopic dermatitis may also have fleas and a secondary yeast infection).
Furthermore, itching may increase in intensity when more than one cause overlaps with another (for example, an atopic dog with secondary parasitic infestation)13.
Diagnosis of pruritus requires a methodical work-up and successful treatment depends on the identification of the underlying causes.
Antipruritic management requires a multimodal approach that includes aetiological, topical and systemic symptomatic treatment4.
The evaluation of a pruritic dog requires a step-by-step approach that should lead to a definitive diagnosis14. The differential diagnoses and possible complicating factors need to be narrowed down using information obtained from a detailed clinical history, physical and dermatological examination, diagnostic procedures, and response to treatment (Panel 1)14.
Basic sampling methods and diagnostic tests, which may be required to rule out most of the common differentials, are flea combing, skin scraping, hair plucking and cytological examination14.
The most common infectious conditions that can be associated with pruritus in dogs are staphylococcal pyoderma and yeast dermatitis (typically Malassezia species, although Candida species may also be rarely seen)13-15.
The typical lesions of superficial pyoderma are papulo-pustular eruption and epidermal collarettes, which are often distinctive, making a possible diagnosis; however, confirmation via cytology is always required14. In the case of Malassezia species infection, the most common clinical signs include erythema and kerato-sebaceous scale, with or without hyperpigmentation, lichenification and malodour16.
Infection is generally a secondary cause of pruritus13,14; any microbial overgrowth can trigger the production of an inflammatory skin response by activating and recruiting inflammatory cells, which subsequently release inflammatory and pruritogenic substances17.
In a recent publication, it has been stated that pruritus is increased by the presence of pathogens. Human strains of Staphylococcus aureus may directly trigger pruritus to enhance infectious spread via bacterial serine protease V8, encoded by sspA.
In experimental studies, mice infected with V8-deficient multi-resistant Staphylococcus aureus (MRSA) exhibited both reduced itch and dermatitis, whereas injection of purified bacterial V8 protease intradermally was sufficient to induce itch and skin damage18.
The notion that pathogens directly activate sensory neurons to promote sensory responses like itch and pain suggests the importance of infection control in patients already affected by pruritogenic diseases such as atopic dermatitis.
Parasites typically associated with pruritus in dogs include those infesting the skin surface, such as fleas, lice, Otodectes species, Cheyletiella species and chiggers (Eutrombicula species, Walchia species); the superficial aspect of the skin (for example, the stratum corneum and epidermis) such as Sarcoptes canis; or the deep portions of the skin (especially the follicles), such as Demodex canis and Demodex injai13.
The three most common types of allergies associated with pruritus in dogs include flea allergy, food allergy and atopic dermatitis. Dogs may be affected by one or more of these conditions, or even all three concurrently.
Apart from a flea allergy, the work-up of the other hypersensitivity disorders is more complex and considered when all the other non-allergy causes of pruritus are investigated and resolved13.
Obtaining an accurate and complete medical history is extremely important in pruritic patients3,13. The most important information to obtain includes the date/age of the lesions’ onset, original locations, initial appearance, progression and/or regression of lesions, and any previous treatments3.
The presence, location and degree of pruritus are important criteria, and it is helpful to grade the pruritus on a scale of 0 (no itching at all) to 10 (as bad as the pet has ever appeared to itch)19. It is also helpful to determine whether the pruritus initially involves normal skin or whether skin lesions precede or appear at the same time as the pruritus3. It is also important to ask about previous skin problems (for example, a dog presented for paw licking and groin pruritus that has had multiple ear infections).
It is necessary to enquire about the animal’s environment and the skin health of other in-contact animals and humans. Additionally, it is also important to have accurate information on the pet’s diet3,13. At this point, the clinician usually has a general idea of the problem and is ready to proceed with a careful physical examination.
The examination starts by observing the dog from a distance to have a general impression of the animal’s overall health, its attitude and the distribution of any lesions. This is followed by a complete physical examination3,13. Lesion distribution (for example, localised, multifocal, generalised, symmetrical or non-symmetrical) is important to create a list of differential diagnoses. Symmetric lesions usually reflect an internal cause (endocrine, metabolic, or immune-mediated disease); non-symmetric lesions are usually a result of infections, certain ectoparasites, or neoplasia3.
As previously mentioned, it is always important to firstly evaluate the presence of infectious or parasitic skin conditions as a cause of pruritus13. If parasitic infestation or bacteria/yeast infection are found, their elimination may provide a better baseline assessment of the patient’s true pruritic status13.
Furthermore, in light of the recent observation that pruritus can be further augmented by the presence of microorganisms18, it becomes of paramount importance to rule out superficial pyoderma as a possible primary pruritus cause or complicating factor.
Failure to eliminate non-allergic causes may interfere with an accurate assessment of the patient’s condition, potentially skewing the results of an allergy work-up13,14. Should the pruritus persist after the elimination of infections or parasites, an allergic work-up would then be warranted.
Cutaneous cytology is a valuable tool in the evaluation of pruritic dogs, and the initial work-up should always include skin and/or ear cytology3,13. The equipment required includes a clean microscope slide, a coverslip, a stain and a microscope3. Bacteria can be seen as basophilic-staining organisms. Although identification of the exact species is not possible, it is possible to distinguish cocci from rods3.
In healthy dogs, the average number of cocci and rods per oil immersion field is less than two3,20. When large numbers of bacteria are found, a condition of bacterial overgrowth is present and may contribute to pruritus and disease3.
Direct tape impression smears are one of the most effective methods for detecting Malassezia species3. Malassezia pachydermatis is an inhabitant of the skin in healthy dogs. The presence of more than one or two yeast organisms per high-power field is not diagnostic of Malassezia dermatitis, but this may indicate that yeasts are present in abnormally high numbers and may be contributing to the pathologic changes seen3,21.
Additionally, animals may develop a hypersensitivity reaction to Malassezia species and exhibit clinical signs when only a few organisms are present3.
The initial work-up of the pruritic dog should also include skin scrapings13. The equipment required includes mineral oil, a scalpel blade (with or without a handle), microscope slides, coverslips and a microscope3.
Not all skin scrapings are performed in the same way. Success in finding parasites is enhanced if the technique of scraping is adapted to the specific parasite that the clinician expects to find3.
Superficial skin scrapings are indicated to diagnose surface and superficial mites (such as sarcoptic mites and Cheyletiella species); deep skin scrapings for the diagnosis of Demodex mites3,13,14.
Examination of debris obtained by flea combing or with surface tape impressions may help demonstrate superficial ectoparasites such as Cheyletiella species, fleas, “flea dirt” and lice3,13.
Surface tape impression is obtained by pressing a clear acetate tape to the hair surface. The tape is then stuck with pressure on a microscope slide and examined3. In the flea-combing technique, large areas of the body are combed and the material and scale that fall on the table, or a sheet of paper placed under the patient, are collected and placed on a slide with mineral oil. A coverslip is then put on top of the material and the slide is examined under the microscope3.
For patients with a history of repeated antibiotic administration, deep pyoderma, or failure to respond to empirical antibiotic therapy, bacterial culture and sensitivity testing need to be considered13.
A skin biopsy should not be used as an alternative diagnostic tool to evaluate patients for infection, parasitic infestation and/or skin allergies, but should be considered to provide further information and to help rule out other causes of pruritus, such as cutaneous lymphoma, patient with atypical presentation (for example, persistent diffuse erythema or scale, ulceration or involvement of mucocutaneous junctions), or in cases where, despite appropriate antibiotic and antiparasitic treatment, no evidence of improvement has been observed13.
While the clinical signs in a dog with flea infestation are variable, the location of skin lesions and pruritus are commonly found at the level of the lumbosacral area, tail base and caudomedial thighs14,22.
Good flea control is an important step in the work-up of any pruritic dog, even in areas where fleas are considered uncommon14, and even if flea allergy is not considered to be a likely differential13. Drugs in the isoxazoline class are widely used to control ectoparasitic infestation in dogs23; however, in certain circumstances (for example, patients with pre-existing neurologic disease or seizure history), these drugs should be used with caution, if at all13,23,24.
For these patients, other drugs (such as monthly indoxacarb, dinotefuran or weekly imidacloprid) may be sufficient13. Regardless of the agent(s) chosen, treatment of the patient and all in-contact animals must be maintained for a minimum of 12 weeks to be certain that the local flea population has been eliminated13,14.
Food-related pruritus can be caused by two different mechanisms: one is a non-immune mediated reaction (food intolerance), and the other is immune-mediated, which includes immunoglobulin E (IgE) mediated hypersensitivity (food allergy)14,25.
Because reactions to food components can present clinically as canine atopic dermatitis, it is impossible to clinically distinguish between atopic dermatitis and canine adverse food reactions14,26. In any patient presented with non-seasonal clinical signs, adverse food reactions can only be ruled out by strict elimination diet trials, since accurate diagnostic commercial tests are not available13,14,27.
The most common food allergens in dogs are beef, dairy, chicken products, wheat, soy, lamb, pork, fish and corn14,28. A diet trial is performed by instituting a strict trial with a diet containing commercial or home-cooked novel (such as rabbit, kangaroo, venison, horse, and so forth) or hydrolysed protein13,14. Both approaches are valid, but neither is guaranteed to succeed13.
No consensus exists on the length of a diet trial, even if one recent publication has recommended a minimum of eight weeks13,29. Furthermore, providing anti-inflammatory/antipruritic support for the first few weeks of the trial may shorten the diet trial duration13,30. Ideally, all elimination diets should be followed by rechallenge with the dog’s previous diet13.
Atopic dermatitis is considered to be a clinical diagnosis by exclusions13. The allergens involved may be seasonal (such as pollen) or non-seasonal (such as dust mites)14.
In the initial phase, pruritus can be associated with primary skin lesions (such as erythema and occasionally papules)31,32, and face, concave aspect of the ear pinnae, ventrum, axillae, inguinal area, perineal area and distal extremities are the most commonly affected areas31. However, variations of the affected body sites have been reported in different breeds33.
In chronic stages, secondary skin lesions will occur due to self-trauma, chronic inflammation and secondary infections (such as excoriations, alopecia, lichenification, hyperpigmentation, crusting and seborrhoea)14. It is paramount that all reasonable differential diagnoses are ruled out or under control before the diagnosis of atopic dermatitis is made13.
A tool known as “Favrot’s criteria” has been developed to help diagnose atopic dermatitis (Panel 2)3,13,14.
These criteria do not prove that a patient has or does not have atopic dermatitis, and do not replace an allergy work-up13,14, but can provide useful information about which clinical signs (and combination of signs) may best support a diagnosis of atopic dermatitis13.
Once a clinical diagnosis has been made, several factors may play a role in the decision making of whether an allergy test (intradermal allergy testing and/or allergen IgE serology) is necessary14.
Although allergy testing (serology or intradermal) is often used to “diagnose” atopic dermatitis, these cannot reliably discriminate between healthy and atopic dogs, and can only support a clinical diagnosis of atopy13,14,34. The results of these tests are used to identify the offending allergen(s) and to formulate an allergen-specific immunotherapy13,14.
Glucocorticoids exhibit a strong antipruritic effect due to the reduction of cutaneous inflammation and, because of their antipruritic mode of action, are likely to be of high value in dogs with inflammatory skin diseases7,35.
Glucocorticoids express their antipruritic effect four hours after oral administration4. The initial dose is 0.5mg/kg to 1mg/kg, once daily or twice daily, for three to seven days for prednisolone, and 0.4mg/kg to 0.8mg/kg once daily for five to seven days for methylprednisolone. After an induction dose, the frequency of administration can be gradually reduced to an every other day regimen4.
Adverse reactions are reported in between 10% and 100% of treated dogs, with polyphagia, polyuria and polydipsia being the most common4,36,37. Other reported adverse events were digestive disorders (vomiting, diarrhoea or loose stools), and superficial pyoderma4,36,37. The use of systemic glucocorticoids for long-term management is not recommended, or only with great care if a low dose is administered at 48 or 72-hour intervals. Adrenal insufficiency can be minimised with an every other day regimen, but adrenal insufficiency may occur at any pharmacologically active dose. Dose reduction and discontinuation should be gradual to avoid adrenal insufficiency4.
Hydrocortisone aceponate 0.0584% solution, applied daily at an average dose of two applications per 100cm2, significantly reduces pruritus38, and the frequency of administration could be progressively decreased without loss of efficacy39.
Hydrocortisone aceponate is also a good treatment option for rapidly relieving pruritus in dogs with flea bite hypersensitivity40. It seems to be a safe molecule due to its metabolic pathway (that is, in the skin with no systemic absorption)4. Because of its potential local thinning effect, its use is not recommended in dogs suffering from other systemic diseases that have an impact on skin integrity (such as Cushing’s disease)4.
Topical treatment with a 0.015% triamcinolone acetonide solution applied on lesional skin twice daily for seven days, followed by dose reduction to once daily for seven days and then every other day for two weeks, was reported to be effective4.
Antihistamines are competitive inhibitors at the H1 receptor, one of the four known receptors for histamine7. The activation of the H1 receptor plays a central role in the pathophysiology of immediate-type hypersensitivity reactions7.
Antihistamines that cross the blood-brain barrier (“first-generation” antihistamines like diphenhydramine) are believed to be more antipruritic than the “second-generation” antihistamines such as cetirizine or loratadine7.
Antihistamines targeting H1 receptors have been used for decades for the treatment of atopic dermatitis in humans. Despite their common usage, two recent guidelines highlighted that a lack of evidence exists suggesting their efficacy as antipruritic drugs in humans7. The efficacy of antihistamines, both first-generation and second-generation, have been tested in different studies; most of them did not report a strong antipruritic effect7,41,42.
Despite scientific results, anecdotally, evidence exists of a low to medium efficacy of antihistamines as antipruritic medications4,7 and, more recently, the consensus practice guidelines for the treatment of canine atopic dermatitis, included the antihistamines as drugs with modest and variable antipruritic effects43.
With the use of antihistamines, sedation is the main but infrequently reported side effect, mainly observed with the first-generation molecule. The side effects can be minimised by dose reduction4,42.
Oral ciclosporin is a calcineurin inhibitor that acts mainly (but not exclusively) as a T-cell inhibitor, along with the ability to target other cells, such as dendritic cells, eosinophils, mast cells and keratinocytes5,7.
Furthermore, the antipruritic effect of ciclosporin is also secondary to a direct effect on several pruritogenic nerve receptors7.
The recommended dose in dogs is 5mg/kg once daily, and takes four to six weeks to have its clinical effect. Studies have shown that by the second month of administration, dogs were controlled with an every other day dose regimen39,40,44.
The most common side effects include vomiting and diarrhoea, followed by anorexia/dysorexia, polyphagia, flatulence, hypersalivation, abdominal pain and weight loss4. Additional side effects may include infectious skin complications (bacterial, fungal), gingival hyperplasia or papillomatous lesions4.
Medium-term to long-term hypertrichosis was rarely reported and other very rare side effects included lethargy, weakness, skin lesions, pruritus and neurological problems4.
Repeat urinalyses have been recommended to screen for occult urinary tract dysbiosis or infection45.
Janus kinase (JAK) inhibitors include a group of molecules that inhibit the enzymes involved in cellular signal transduction after binding cytokines to their receptor; for this reason, the effect of the JAK inhibitors varies depending on which of the four JAKs (JAK1-3, TYK2) is interested5,7.
Oclacitinib is a JAK1-predominant inhibitor that principally blocks the signalling of cytokines involved in allergy, inflammation and pruritus (such as IL-2, IL-4, IL-6, IL-13, IL-31, and so forth)46. The recommended dose of oclacitinib is 0.4mg/kg to 0.6mg/kg twice daily for 14 days, then 0.4mg/kg to 0.6mg/kg once daily47.
The pruritus reduction is observed four hours post-administration46, and further to its antipruritic effects, oclacitinib is associated with an improvement in clinical lesions and delays in the development of clinical lesions37. Reported adverse effects include dermatological signs (such as otitis, pyoderma or pododermatitis), gastrointestinal signs (such as, anorexia, vomiting and diarrhoea), and urinary tract infection/cystitis7,47.
No association between daily administration of oclacitinib and malignancies/benign skin masses developing has been reported48. Blood analysis (complete blood count and biochemistry) of dogs treated with oclacitinib showed values in the reference ranges47.
Lokivetmab is a caninised monoclonal antibody that binds and neutralises canine IL-317,49. Lokivetmab is administered subcutaneously at a dose of 1mg/kg or 2mg/kg depending on the country (in the UK and the rest of Europe, it is licensed at a dosage of 1mg/kg), and the level and duration of the response are dose dependent4.
Lokivetmab administration in dogs with non-seasonal moderate to severe atopic dermatitis showed a strong antipruritic effect and moderate efficacy in reducing skin lesions7,50. Reported mild to moderate adverse reactions include otitis externa, dermatitis, pyoderma, erythema, vomiting, anorexia, lethargy, pruritus and diarrhoea, which, in most cases, resolved spontaneously4,50.
Topical tacrolimus is a calcineurin inhibitor with similar mechanisms of action and pharmacokinetic profiles as the one reported for ciclosporin5,7,51. It has several uses in veterinary dermatology, and it is mainly used for immune-mediated disease.
Despite its anti-inflammatory action, the effect of 0.1% tacrolimus ointment to control pruritus in dogs has only been assessed in one study, in which only partial improvement in pruritus scores was reported7.
Cytotoxic drugs, such as azathioprine, mycophenolate mofetil or methotrexate, act to inhibit the cells (such as T-cells) that cause inflammation and the associated pruritus7. In recent years, their usage to control pruritus in human has increased; however, information on their action in pruritus control in dogs is limited7.
Phosphodiesterase-4 (PDE4) inhibitors show an anti-inflammatory effect by increasing the cyclic adenosine monophosphate (cAMP) in immune cells and keratinocytes7. The anti-inflammatory action of topical and oral PDE4 inhibitors has been recently confirmed in human clinical trials7. In dogs, the usage of arofylline in atopic patients showed a good reduction of pruritus after four weeks of treatment52. Unfortunately, the occurrence of vomiting is a common side effect that may limit its usage7,52.
ALIAmides are a family of fatty acid amides sharing a common mechanism of action: the autacoid local injury antagonism (ALIA)53.
The cannabinoid receptors CB1 and CB2 are expressed on sensory nerve fibres, keratinocytes and mast cells7. Treatment with topical cannabinoid receptor agonists has been observed reducing histamine-induced pruritus and vasodilation in humans5,7. Palmitoylethanolamide (PEA) is an endogenous arachidonic acid-derived fatty acid amide that targets the peroxisome proliferator-activated receptor (PPAR)-alpha7,53. PEA has a cannabinoid-like effect, binding directly to CB1 or CB27. PEA was also shown to activate and then desensitise one of the principal neuronal receptors involved in itch transmission, the transient receptor potential vanilloid 1 (TRPV1)7. In a recent study, PEA was used in dogs with non-seasonal mild to moderate atopic dermatitis and mild to severe pruritus levels, and was found to significantly reduce pruritus in dogs7,53.
Interferon-gamma has been proven effective as an antipruritic treatment in dogs with atopic dermatitis7,43. Its mode of action is not yet proven, but might be due to the inhibition of type two pro-allergic cytokines such as IL-4 and IL-137.
Capsaicin is a vanillylamide, and its main action results from the binding to TRPV1. The binding of capsaicin to TRPV1 results in calcium and sodium influx, nerve depolarisation and substance P release, which causes an initial intense burning sensed as pain or pruritus7,55.
Repeated applications of capsaicin lead to the exhaustion of substance P nerve reserves, which result in long-lasting nerve desensitisation, and consequent reduction of pain and pruritus7,54,55. The topical application of capsaicin has been proven effective in controlling localised pruritus in humans7,54,55.
Only one study reports the effect of a six-week treatment of topical 0.025% capsaicin applied twice daily to control pruritus in animals, which showed a reduction of the pruritus score7,54.
Topical anaesthetics block the voltage-gated sodium channels in the cell membrane of postsynaptic neurons, with consequent inhibition of the generation of electric potentials.
The use of 1% pramoxine (pramocaine) lotion is effective in controlling uraemic pruritus in humans5,7,56. In veterinary medicine, only one trial exists where the antipruritic effect of pramoxine-containing cream rinses has been tested in dogs with atopic dermatitis, showing a satisfactory reduction in pruritus that lasted for 48 hours after its application7,56.
Mu-opioid receptor agonists induce mast cell histamine release7. Recent data suggest that stimulation of Mu-opioid receptors induces pruritus, while Kappa-opioid receptors antagonise it5.
Several trials have reported the antipruritic effect of the Mu-opioid receptor antagonists (such as naloxone, naltrexone and nalmefene) in controlling cholestatic pruritus, chronic urticaria and atopic dermatitis in humans7,57.
In veterinary medicine, the use of Mu-opioid receptor antagonists (naltrexone or nalmefene) has been tested in dogs with acral lick dermatitis with a good antipruritic effect7,57.
Gabapentin and pregabalin are gamma-aminobutyric acid (GABA) structural analogues (GABAergics)5. These drugs work by binding to the alpha-2-delta subunit of voltage-dependent calcium channels, mainly at the spinal cord level, inhibiting the presynaptic calcium influx and decreasing the glutamate release and associated synaptic transmission5.
Furthermore, these molecules also inhibit the inflammation-induced release of substance P and calcitonin-gene-related peptide5,7. Anecdotal evidence exists of the antipruritic efficacy of gabapentin and/or pregabalin in humans with neuropathic pruritus7.
Oral gabapentin and pregabalin were also effective in controlling pruritus in a cavalier King Charles spaniel with Chiari-like malformation and associated syringomyelia7. Evidence for the antipruritic effect of gabapentin and pregabalin in other canine pruritic skin conditions and/or other forms of neuropathic pruritus is lacking7.
The selective serotonin reuptake inhibitors (SSRIs) fluoxetine, fluvoxamine, paroxetine and sertraline are effective in relieving pruritus, albeit partially, in humans5,7,58. Similarly, tricyclic antidepressants (TCAs), such as amitriptyline and doxepin, appear to have some antipruritic efficacy in patients with dermatologic, systemic, neuropathic and psychogenic pruritus5,7.
Only a few reports exist of the use of SSRIs and TCAs in dogs to treat pruritic diseases7. In dogs, as in humans, the dosages should be increased until the desired effect occurs, or side effects develop7. SSRI fluoxetine and TCA clomipramine appeared effective in controlling the obsessive-compulsive licking behaviour of acral lick dermatitis, whereas SSRIs and TCAs (particularly doxepin) were not effective in controlling pruritus in atopic dogs7.
In contrast, the use of oral amitriptyline led to a good to excellent pruritus control in one-third of the treated patients7.
Pentoxifylline is a methylxanthine derivative and a non-selective phosphodiesterase inhibitor3. Inhibition of the phosphodiesterase produced an increased intracellular concentration of cAMP, which has numerous cell-stabilising and anti-inflammatory properties3.
In a study, the use of pentoxifylline at 25mg/kg twice daily was found to be effective in controlling pruritus in dogs with atopic dermatitis. Furthermore, it was effective as a steroid-sparing agent and in combination with allergen-specific immunotherapy. Side effects were mild and rare, including nausea, vomiting and diarrhoea59.
In refractory cases, or in cases when the therapeutic dose needs to be reduced due to side effects, it may be important to consider the association of different molecules to enhance the anti-pruritic effects of certain medications.
Pruritus is a clinical manifestation with a multifactorial aetiology. To work up the pruritus, it is important to have a step-by-step approach, starting with getting an accurate clinical history, followed by a screening for infectious or parasitic causes (for example, skin cytology, skin scrapes, hair plucks and coat brush). Once those causes have been ruled out and/or controlled, an allergy work-up should be started, focusing on a diet trial first, followed by an environmental allergens investigation (intradermal allergy test versus allergy IgE serology).
The treatment of pruritus needs to be tailored to the patient and, in some circumstances, association of different molecules may be required to obtain a better clinical response or reduction of the therapeutic dosage.
In cases of relapses or flares, it is paramount to review the case and rule out secondary infection/parasitic infestation before considering the molecule to be ineffective.
