Practice Dilemma: The Itchy Dog

While it doesn’t always feel it, as we come into March spring is finally on its way, after what has really felt like a long, hard winter. However, along with (hopefully) warmer weather and longer days, in practice that means one thing – we’re coming back into allergies season again!

“Lucy” Hamish is a case in point. An elegant, snow-white and fastidious Westie six months of the year… and an itchy, pink-stained and frequently hairless misery the other six months. As you look at her (extensive) clinical records, it’s clear that Lucy is a walking pharmacy – she’s being treated with two separate atopy medications, and has regular antibiotic prescriptions as well as a complex immunotherapy regime.

While there are of course pharmaceutical options to be explored – rescue corticosteroids also feature extensively on Lucy’s history – perhaps it’s time to consider the pathology from a different angle. In particular – how effective is her skin’s barrier function?

The outer layer of skin, the stratum corneum, comprises squames (flattened “dead” corneocytes packed with keratin), cemented together by a lipid-rich matrix. Together, these comprise the “barrier” – protecting the deeper sensitive tissues from water loss dehydration, bacterial invasion, and penetration of immunoreactive substances. We can envisage this as squame “bricks” held in place and “waterproofed” by lipid “mortar” (Nishifuji and Yoon, 2013).

Only when foreign immunoreactive material – such as pollens, arthropod secretions or bacterial products – reach the dendritic cells and the IgE-primed mast cells in the deeper layers of the skin can allergic reactions occur. Failure of the skin barrier to prevent entry of allergens, and thus triggering a hypersensitivity response, is now widely considered to be a key factor in the pathogenesis of atopic dermatitis (Santoro et al, 2015).

The lipid component of this barrier is rich in long-chain free fatty acids, ceramides, and cholesterol. The manufacture of these products may be a rate limiting step, and therefore oral supplementation is believed to act as to “reinforce” this barrier, reducing allergen penetration in the long term (see Raballi, 2016, for a review of the theory).

Of particular importance are Linoleic Acid (LA) and Alpha Linoleic Acid (ALA, believed to have a “sparing” effect on sparse dermal LA reserves). Other fatty acids are of course important, especially for their anti-inflammatory properties. However, disruption of the healthy lipid balance in the stratum corneum is a key factor in atopic dogs, and so restoration of this balance should in theory help to slow or even reverse the failure of the barrier function (Chermprapai et al 2018).

So is there any clinical evidence that this will work?

Yes, actually, there is. A number of studies have demonstrated the effects of oral essential fatty acid supplementation. These include a randomised controlled trial by Saevik and others (2004), which showed that a 2 month course of essential fatty acid supplementation reduced both pruritis score and the requirement for anti-inflammatory medication. The study has been repeated fairly recently, demonstrating a ciclosporin-sparing effect (Müller et al, 2016). Another study by Bond and Lloyd (1992) demonstrated a deterioration of atopic patients when transferred from an EFA-rich supplement onto a high lipid, low EFA equivalent.

So in Lucy’s case, will EFA supplements, such as YuDERM, help you manage an acute flare up? No, probably not. However, the available evidence suggests that it will help to prevent Lucy from getting to that point in the first place. So, we should really be thinking of YuDERM and similar products as being adjunctive treatments – not replacing pharmaceuticals, but supplementing their effects and reducing the requirement. After all, many of the pharmaceuticals we use (most anti-inflammatories, monoclonal anti-IL-31 antibodies, and JAK inhibitors such as oclacitinib) are treating the clinical signs (the itch), not the underlying pathology. By protecting the barrier at the same time as reducing the itch-scratch cycle, we are addressing multiple parts of the jigsaw simultaneously.

Now, while you wait for your Dermatology colleague to get back… how about brushing up on your dermatology knowledge? We have a series of webinars by Sarah Warren, BVetMed MSc (Clin. Onc.) CertVD MRCVS, Veterinary Dermatologist coming up – so watch out for our “Spring into Skin” course!

References:

Bond R, Lloyd DH. A double-blind comparison of olive oil and a combination of evening primrose oil and fish oil in the management of canine atopy. Vet Rec. 1992 Dec 12;131(24):558-60. PMID: 1481346.

Chermprapai S, Broere F, Gooris G, Schlotter YM, Rutten VPMG, Bouwstra JA, (2018) Altered lipid properties of the stratum corneum in Canine Atopic Dermatitis, Biochimica et Biophysica Acta (BBA) – Biomembranes 1860(2): 526-533

Müller MR, Linek M, Löwenstein C, Röthig A, Doucette K, Thorstensen K, Mueller RS. (2016) Evaluation of cyclosporine-sparing effects of polyunsaturated fatty acids in the treatment of canine atopic dermatitis. Vet J.;210:77-81.

Nishifuji K and Yoon JS (2013). The stratum corneum: the rampart of the mammalian body, Veterinary Dermatology 24(1): 60-72

Reballi E (2016) Using essential fatty acids in canine atopic dermatitis, Veterinary Times, July 18, 2016

Saevik BK, Bergvall K, Holm BR, Saijonmaa-Koulumies LE, Hedhammar Å, Larsen S and Kristensen F (2004), A randomized, controlled study to evaluate the steroid sparing effect of essential fatty acid supplementation in the treatment of canine atopic dermatitis. Veterinary Dermatology, 15: 137-145.

Santoro D, Marsella R, Pucheu‐Haston CM et al. (2015) Review: pathogenesis of canine atopic dermatitis: skin barrier and host–micro‐organism interaction. Vet Dermatol 2015; 26: 84–e25

Remove unfortunately and reword slightly – too suggestive that derm needs to be avoided!

Was trying to avoid the dreaded “Specialist” term, but I see what you mean…