A New Perspective on Canine Keratoconjunctivitis Sicca

Kaswan, Renee L.; Salisbury, M. A.

doi:10.1016/s0195-5616(90)50052-2

Cited by 116 publications

(126 citation statements)

References 36 publications

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“…The condition is common in humans (Caffery et al, 1996) and in dogs (Kaswan, Pappas and Wall, 1996) : certain breeds of dog being particularly prone to a condition similar to Sjogren's syndrome in man (Grauwels, 1979 ;Sansom and Barnett, 1985a ;Barnett and Sansom, 1985 ;1987 ;Carrington et al, 1987b). In such cases, there is commonly an immune-mediated destruction of lacrimal tissue (Kaswan and Salisbury, 1990), a decrease in conjunctival goblet cell density (Grauwels, 1979) and accumulation of copious quantities of abnormal viscous mucus (Sansom and Barnett, 1985a). Thus, the dog presents a model of spontaneous KCS which is particularly useful for the examination of fundamental disease mechanisms, and the development of new therapies (Kaswan and Salisbury, 1990 ;Kaswan, 1994 ;Kaswan, Bounous and Hirsh, 1995).…”

Section: -4835\98\120709j10 $3000\0mentioning

confidence: 99%

Biochemical Analysis of Ocular Surface Mucin Abnormalities in Dry Eye: The Canine Model

Hicks

Corfield

Kaswan

et al. 1998

Experimental Eye Research

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confidence: 99%

Biochemical Analysis of Ocular Surface Mucin Abnormalities in Dry Eye: The Canine Model

Hicks

Corfield

Kaswan

et al. 1998

Experimental Eye Research

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“…The finding that topical cyclosporine ameliorates the condition strengthens this hypothesis but yet to date no studies have reported the detailed phenotype of the mononuclear inflammatory cell infiltrate in the lacrimal tissue from affected eyes. While Izci and colleagues (2002) have reported changes in the inflammatory cell populations in KCSaffected animals treated with topical cyclosporine they did not document the initial quantitative findings in the lacrimal tissue of these animals and compare this with cell numbers in normal lacrimal tissue (Kaswan and Salisbury, 1990). Here we sought to do exactly that.…”

Section: Discussionmentioning

confidence: 96%

“…No other immunomodulatory agents such as tacrolimus had been used in these animals. The reduction in inflammatory cell numbers caused by use of cyclosporine (Kaswan and Salisbury, 1990;Williams, 1997bWilliams, , 2008 would have negated the results were dogs on treatment to have been used. While we have no direct evidence on the time-course of recovery in inflammatory lesions in iKCS, it is reported that cessation of topical cyclosporine treatment leads to recurrence of inflammatory disease in under one month (Williams et al, 1995), hence the choice of three months to ensure that lacrimal pathology would have reverted to pre-treatment levels.…”

Section: Methodsmentioning

confidence: 99%

“…While work over twenty years ago showed that the infiltrating cell population in lacrimal and nictitans glands of such dogs was lymphocytic in nature (Kaswan et al, 1984), further work characterizing these populations is lacking. The ameliorative lacrimostimulatory action of the immunomodulatory drugs cyclosporine (Kaswan and Salisbury, 1990;Olivero, 1991), tacrolimus (Berdoulay et al, 2005) and pimecrolimus (Nell et al, 2005) further suggests an immune-mediated disease process in this condition although these calcineurin inhibitors may exert their lacrimogenic influence through mechanisms other than, or in addition to their immuno-modulatory action (Williams, 1997a;Gao et al, 1998;Yoshida et al, 1999). One paper has evaluated the changes in lacrimal gland lymphocyte populations after the use of cyclosporine but without first characterising the cells infiltrating the gland (Izci et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Immunohistochemical evaluation of lymphocyte populations in the nictitans glands of normal dogs and dogs with keratoconjunctivitis sicca

Williams¹,

Tighe²

2018

Open Vet J.

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Idiopathic canine keratoconjunctivitis sicca (iKCS) is a common condition of the canine eye involving a deficiency in aqueous tear production which is commonly held to have an immune-mediated, as most probably an autoimmune aetiopathogenesis. Yet to date no direct evaluation has been made of the inflammatory cell populations in the lacrimal tissue of dogs with iKCS. Here we sought to quantify T and B lymphocyte populations in the lacrimal tissue of the nictitans glands of dogs with iKCS those with neurological KCS (nKCS)and also in dogs with tear production within the recognized normal levels and no ocular surface signs of KCS. Nictitans glands were obtained from 10 healthy dogs with no signs or history consistent with KCS at post-mortem or after enucleation. Nictitans glands were also obtained at parotid duct transposition surgery from ten dogs with idiopathic KCS and three with neurogenic KCS. Histological sections form the lacrimal tissue were processed immunohistochemically with primary monoclonal antibodies recognizing the T lymphocyte CD3 antigen and the B lymphocyte CD79a antigen. Cell numbers were counted in 10 randomly sampled representative high-power fields in five sections. Statistical significance of differences in cell numbers was determined using analysis of variance with significance achieved at p=0.05.Nictitans glands from dogs with iKCS showed elevated numbers of T and B lymphocytes compared with those from dogs with normal tear production. The increase in the T cell population was highly statistically significant (p=0.0025) while the increase in B cells, while statistically significant was less pronouncedly so (p=0.049). T and B lymphocyte numbers were not significantly elevated in nictitans glands from dogs with neurogenic KCS compared with those in dogs with normal tear production. The elevation in the T cell population seen in dogs with idiopathic KCS strongly supports the widely held assumption that this disease is an immune-mediated and probably autoimmune. The lack of increase in T cell populations in dogs with nKCS strongly suggests that the changes in iKCS are causing the tear deficiency and not resulting from it.

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“…22,23 Previous studies have shown that topical CsA 1-2% can be used safely and effectively in human eyes status post penetrating keratoplasty for allograft rejection, vernal keratoconjunctivitis, keratoconjunctivitis sicca, immune-mediated keratitis, necrotizing scleritis and stromal herpetic keratitis. [24][25][26][27][28][29] Considerable evidence exists that topical cyclosporin A reduces the lacrimal gland infiltrate and improves tear production in keratoconjunctivitis sicca dogs, [30][31][32][33] and a few clinical studies indicate that systemic or topical cyclosporine improves some objective or subjective signs of keratoconjunctivitis sicca in patients with or without Sjogren's syndrome. [34][35][36] Therefore, it appears that cyclosporin A may target the tear deficient aspect of dry eye by modulating the immune reactivity and inflammatory processes of both senescence-related dry eye as well as the dry eye condition associated with Sjogren's syndrome.…”

Section: Discussionmentioning

confidence: 99%

The use of topical cyclosporin A in ocular graft-versus-host-disease

Kiang

Tesavibul

Yee

et al. 1998

Bone Marrow Transplant

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Summary:Ocular manifestations of GVHD include keratoconjunctivitis sicca, cicatricial lagophthalmos, sterile conjunctivitis, persistent corneal epithelial defects, corneal ulcers and corneal melting. Conventional initial therapy such as lubrication and topical steroids is directed to treat decreased tear production and ocular surface abnormalities. The purpose of this study was to illustrate the possible benefit of topical cyclosporin A 1% (CsA) as an adjunct in managing ocular surface abnormalities in five cases of GVHD refractory to conventional therapy. Five clinical case reports of chronic GVHD patients in whom conventional therapy was inadequate to stop the progression from its initial presentation are described. Patient presentation varied in severity on a spectrum of mild to moderate diffuse punctate epithelial erosions to sterile necrotizing corneal melts. Although systemic therapy for GVHD consisting of systemic immunosuppressants (ie cyclosporin A and corticosteroids) was given to these patients, this therapy was insufficient in managing the ocular manifestations of the disease. Topical CsA was added to the treatment regimen and the progression of the ocular disease was recorded. The addition of topical CsA 1% probably helped in controlling the epithelial keratitis and melting process in our reported cases and we conclude that topical CsA may be an appropriate modality in managing ocular surface abnormalities in patients with ocular GVHD after conventional treatments have been tried. However, a further randomized clinical prospective study is needed to evaluate the efficacy of topical CsA in managing these problems in GVHD patients.

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A New Perspective on Canine Keratoconjunctivitis Sicca

Cited by 116 publications

References 36 publications

Biochemical Analysis of Ocular Surface Mucin Abnormalities in Dry Eye: The Canine Model

Biochemical Analysis of Ocular Surface Mucin Abnormalities in Dry Eye: The Canine Model

Immunohistochemical evaluation of lymphocyte populations in the nictitans glands of normal dogs and dogs with keratoconjunctivitis sicca

The use of topical cyclosporin A in ocular graft-versus-host-disease

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