Ординатура / Офтальмология / Английские материалы / Dry Eye and Ocular Surface Disorders_Pflugfelder, Beuerman, Elliot Stern_2004

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A

B

Figure 1 Ocular surface conditions associated with ocular cicatricial pemphigoid.

(A) Inflammation. (B) Conjunctival fibrosis. (C) Conjunctival fibrosis.

C

neovascularization (Fig. 1). Because intraocular pressure measurement and fundus examination can be hindered by keratopathy, glaucoma is often underdiagnosed in these patients [4]. The end stage of the disease involves ankyloblepharon, corneal xerosis, and blindness.

II.DIAGNOSIS OF OCP

According to recent consensus nomenclature, OCP belongs to the newly defined heterogeneous group named mucous membrane pemphigoid, which includes presumed autoimmune, chronic inflammatory, subepithelial blistering diseases that predominantly affect mucous membranes and are characterized immunopathologically by linear deposition of immunoglobulins and complement fragments in the epithelial basement membrane zone [5]. Mucous membrane pemphigoid can be associated with skin involvement, although the latter should not predominate. Unlike mucous membrane pemphigoid, which involves extraocular mucosae, vesicles are very rare in OCP, whereas scarring is a consistent feature.

Diagnosis is fairly easy when OCP is associated with lesions of other sites (mouth, nasopharynx, anogenital region, skin, larynx, and esophagus, in decreasing order of frequency). Often, immunopathological proof of mucous membrane pemphigoid has already been obtained by biopsy of these sites, and conjunctival biopsy is therefore unnecessary. However, some forms of mucous membrane

Table 1 Differential Diagnoses of OCP

Nonautoimmune fibrosing conjunctivitis

Bacterial conjunctivitis: Chlamydia trachomatis, Corynebacterium diphtheriae, Streptococcus

Viral conjunctivitis: adenoviral keratoconjunctivitis

Systemic diseases: sarcoidosis, progressive systemic sclerosis, Sjögren’s syndrome Bullous mucocutaneous diseases: Stevens-Johnson syndrome, toxic epidermal

necrolysis

Miscellaneous: ocular rosacea, atopic keratoconjunctivitis, iatrogenic conjunctivitis, conjunctival trauma, chemical burns, irradiation, porphyria cutanea tarda, erythroderma ichthyosiform congenita, self-induced cicatricial conjunctivitis

Autoimmune mucocutaneous diseases Paraneoplastic pemphigus Epidermolysis bullosa acquisita Bullous pemphigoid

Linear IgA disease Dermatitis herpetiformis Lichen planus pemphigoides (Paraneoplastic) lichen planus

pemphigoid can share not only clinical but also immunopathological features of OCP. Fortunately, most of them require the same therapy as OCP [6]. When the disease is restricted to the conjunctiva, the most clinically challenging non-autoimmune differential diagnoses are ocular rosacea, atopic keratoconjunctivitis, and iatrogenic conjunctivitis (drug-induced pseudopemphigoid) [7]. Table 1 lists the main differential diagnoses of OCP. Treatment failure of suspected OCP should challenge the diagnosis.

Definite diagnosis of OCP relies on the demonstration of linear immune deposition along the basement membrane zone of the conjunctiva, other mucosae, or skin. A direct causal relationship between these deposits and progressive subepithelial scarring is possible but not proven. Many basement membrane zone components have been recognized as mucous membrane pemphigoid candidate epitopes [5]. In OCP, the β4 component of integrin α6β4 was identified as a conjunctival target autoantigen [8–10]. The diagnosis of OCP can still be difficult, however, especially when the eye is the only site of involvement. Indeed, autoantibodies directed against the basement membrane zone are very rarely detected [3], conjunctival biopsy specimens are more difficult to obtain and process than those harvested from the oral mucosa or skin, and immunopathological techniques used to detect basement membrane zone deposits are not perfectly sensitive, even in typical cases. When biopsy is noncontributory, the decision to treat the disease as OCP is thus based on the clinical impression alone.

The polymorphism of the disease, and poor access to reference immunopathology laboratories for some ophthalmologists, may explain why OCP is often diagnosed late, when conjunctival fibrosis is already at an advanced stage (stage III) [11].

III.OCP: A THERAPEUTIC CHALLENGE

Treatment challenges in OCP include not only the choice of drug(s), but also the timing of treatment initiation, its duration, and the route of administration. Well-designed randomized controlled studies are scarce, because OCP is a rare, chronic, and sometimes asymmetric disease with numerous clinical variants. Published trials have involved a variety of drugs, used as monotherapy, in combination, or sequentially [5].

The choice and monitoring of potentially toxic systemic drugs to control inflammation is also a challenge, especially in elderly patients. Moreover, followup must be long enough to draw definite conclusions, because OCP is a chronic disease and prolonged spontaneous remissions have been reported [3,12]. In the case of presumed (non-biopsy-proven) OCP inexorably progressing to blindness, the practitioner is faced with the decision to use potentially life-threatening immunosuppressive drugs; this underlines the need for exhaustive clinical and laboratory investigations in order to rule out all differential diagnoses.

As in other ocular inflammatory diseases, the activity and progressive nature of OCP must first be established, in order to select the most effective and least toxic drugs. Disease progression should be assessed using one of the three recommended grading systems (Table 2; Figs. 2A–2C). In our opinion, Foster’s modified grading system [13] is the most precise tool to assess progression of fibrosis (Fig. 3). However, the other two grading systems are simpler and therefore more appropriate for multicenter trials involving several observers [2,3].

IV. SYSTEMIC CORTICOSTEROIDS AND LOCAL THERAPIES: LESSONS FROM EARLIER STUDIES

It has been unanimously accepted since the publication of Franke [14] in the early 1900s that untreated OCP almost inexorably leads to severe corneal morbidity and often to bilateral blindness. In the mid 1970s [15–20], the demonstration of circulating antibodies and immune deposits in the epithelial basement membrane zone proved that OCP was a systemic autoimmune disease. It is then not surprising that the efficacy of topically or subconjunctivally administered drugs such as steroids, cyclosporin, and retinoids has not been proven in well-designed studies [3,11]. One trial supported the use of subconjunctival mitomycin [21], but the results were not confirmed in other studies [22]. Dermatologists were the first to treat mucous