Ocular Allergy as a Risk Factor for Dry Eye in Adults and Children

Edoardo Villani; Giovanni Rabbiolo; Paolo Nucci

Disclosures

Curr Opin Allergy Clin Immunol. 2018;18(5):398-403. 

In This Article

Ocular Allergy and Tear Film Instability

A growing number of articles report the association between ocular allergy and decreased tear film break-up time (BUT). This phenomenon is more evident in allergic kerato-conjunctivitis, and it seems to be correlated with the severity of the ocular surface disease, as suggested by a comprehensive study published by Hu et al.[15] who reported a BUT of 3.1 ± 1.6 s vs. 4.5 ± 1.0 s vs. 11.4 ± 1.0 s (P < 0.01), respectively, in AKC, VKC, and healthy controls.

More recent studies, comparing children affected by SAC, PAC, and even allergic rhinitis to age-matched healthy individuals, demonstrated that also these conditions affect the tear film stability.[12–14,16] These articles provided essential information on this issue but, reporting very heterogeneous BUT values and adopting a threshold value of 10 s (validated only in adults), they also indirectly highlighted our current poor knowledge of pediatric dry eye.

Significantly, a few studies on tear film stability in intermittent forms of ocular allergy reported that VKC patients seem to show a shortened BUT even in the quiet phases of the disease,[11] whereas SAC patients don't have decreased tear film stability outside the pollen season.[17]

In the vicious cycle of DED, tear film instability may be due to different mechanisms, including meibomian glands and lipid layer changes on the one hand and mucins alterations on the other.[18,19]

A few imaging studies assessed meibomian glands in different forms of ocular allergy,[20] including AKC, VKC, and PAC. They showed morphological changes, probably related partly to ocular surface inflammation and partly to continuous mechanical stress to the tarsal tissue by eye rubbing. Functional implications of these morphological changes have been suggested, but they need to be further investigated. Only one study, published more than 10 years ago by Suzuki et al.,[21] assessed the alterations of the tear film lipid layer in ocular allergy. This research showed increased lipid layer thickness in patients with SAC and reported a surprising negative correlation between lipid layer thickness and BUT.

The impact of ocular allergy on secreted and membrane-associated mucins has been studied a bit more in depth, at least in severe forms.

Preclinical studies on mouse models suggested that histamine, leukotrienes, and prostaglandins directly stimulate goblet cell secretion, whereas inflammatory cytokines as IL-13, TNFα, and IFNγ have opposing effects on the regulation of secretion, proliferation, and apoptosis of these cells.[22]

Several in-vivo studies from the Keio University reported a depletion of MUC5AC in patients with AKC and VKC,[15,23] particularly in eyes with corneal shield ulcers.[24] The decreased tear concentration of this gel-forming mucin is widely accepted as a feature of all forms of DED.[18]

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