Cases reported "Blepharitis"

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1/5. Discoid lupus erythematosus masquerading as chronic blepharoconjunctivitis.

    PURPOSE: To recognize discoid lupus erythematosus (DLE) as a treatable cause of chronic blepharoconjunctivitis. DESIGN: Retrospective observational case series. PARTICIPANTS: Records of 5 patients with biopsy-proven DLE were reviewed. methods: Clinical and pathology records were examined. MAIN OUTCOME MEASURES: patients' clinical and histopathological characteristics and response to treatment were assessed. RESULTS: Clinical features included meibomian gland dysfunction, blepharitis, chalazia, trichiasis, madarosis, conjunctivitis, chronic eyelid edema, and eyelid plaques. Histopathology showed hyperkeratotic epithelium, degeneration of the basal cell layer, and a perivascular lymphocytic infiltrate. There was delayed diagnosis in all cases, ranging from 4 months to 25 years. All of the patients responded to systemic hydroxychloroquine therapy. CONCLUSIONS: Heightened awareness of eyelid DLE may lead to earlier detection and specific therapy for this chronic disorder.
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ranking = 1
keywords = gland
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2/5. Discoid lupus erythematosus of the eyelids associated with staphylococcal blepharitis and Meibomian gland dysfunction.

    Lower eyelid involvement occurs in 6% of patients with discoid lupus erythematosus (DLE). Eyelid lesions are rarely the initial manifestation of DLE. We describe a 25-year-old woman presenting with discoid lesions of the lower eyelids, staphylococcal blepharitis and Meibomian gland dysfunction, who later developed a discoid lesion on the chin. Histopathological and immunofluorescence studies of a biopsy specimen from this lesion established the diagnosis of DLE. We are unaware of any previously reported cases of DLE presenting with discoid eyelid lesions associated with staphylococcal blepharitis and Meibomian gland dysfunction. DLE should be considered as a differential diagnosis in chronic blepharitis that persists despite usual medical management and eyelid hygiene. Misdiagnosis may lead to eyelid margin deformities, necessitate a complicated full-thickness biopsy, and delay diagnosis of systemic lupus.
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ranking = 6
keywords = gland
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3/5. The masquerade syndrome.

    Malignant lesions of the lid and ocular adnexae may present with striking inflammatory signs and this has most often been described with meibomian gland carcinoma and given the name of the masquerade syndrome. This paper presents examples of lid malignancies which have not only masqueraded as predominantly inflammatory lesions but whose origin was further obscured by the nature of the spread of the tumour in lid and conjunctiva. Recognition of the true nature of the malignancy only follows biopsy of the centre of the lesion which is fully justified in an older patient presenting with unilateral chronic, unresponsive inflammation especially involving the canthus and bulbar conjunctiva as well as the lid. Histological confirmation of the nature of the peripheral spread of the tumour is also of importance since pagetoid spread has been shown to be associated with more aggressive neoplasia and increased mortality.
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ranking = 1
keywords = gland
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4/5. Conjunctivalization of meibomian glands following cryosurgery for basal cell carcinoma of the eyelid.

    cryosurgery on the eyelids destroys the cellular elements in the frozen region, but preserves the collagenous supporting structures. cells from the neighborhood colonize this framework during wound healing. The Authors describe a peculiar change in the meibomian glands, which obviously developed by this mechanism in a lid treated by cryotherapy for a basal cell carcinoma. The collagenous lodges of the meibomian glands, denuded of their sebaceous cells by the therapy, were epithelialized by ingrown conjunctival epithelium. This situation seems to promote the spread of and maintain acute and chronic exogenous inflammation in the tarsal plate.
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ranking = 6
keywords = gland
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5/5. lichen planus and Sjogren-type sicca syndrome in a patient with chronic hepatitis c.

    We report a 54-year-old Japanese male with lichen planus and Sjogren-type sicca syndrome, accompanied by the latent complication of chronic hepatitis c. The patient first showed erythematous and erosive lesions with white irregular striae in the buccal mucous membrane, and blepharitis and hyperemia of conjunctiva in his eyes. He later had two small erosions on the glans penis, and flat-topped violaceous papules on the dorsa manus and nape. A biopsy specimen of the lower lip lesion demonstrated a lichenoid tissue reaction at the basement membrane zone, and lymphocytic focal accumulations in the salivary glands. Immunohistochemical study of this specimen revealed CD45RO- (T) cells associated with the expression of hla-dr antigens predominantly in both the lichenoid tissue reaction and the lymphocytic sialadenitis. Objective keratoconjunctivitis sicca was confirmed by the Schirmer and Rose-Bengal tests. Anti-dna antibody was positive; however anti-SS-A, and anti-SS-B antibodies were negative. Increased levels of transaminase enzymes, TTT, ZTT, and IgG were observed in first laboratory examinations; thereafter, antihepatitis C virus (HCV) antibodies and HCV-rna were detected. The high serum amylase level, in which salivary amylase predominated, was normalized by etretinate therapy in parallel with the clinical improvement of the oral LP lesions. Our case is considered to support the hypothesis that an etiologic association may be present among lichen planus, sjogren's syndrome, and chronic hepatitis c.
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ranking = 1
keywords = gland
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