Cases reported "Lichen Planus"

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1/44. Unilateral linear lichen planus with mucous membrane involvement.

    Linear lichen planus is a rare distinctive variant of lichen planus (LP) characterized by a pruritic eruption of lichenoid, violaceous papules in a linear distribution that sometimes assume a Blaschko line pattern. We describe a 33-year-old woman who presented with a 4-month history of a slightly pruritic unilateral linear array of papular lesions on the left side of her neck that were clinically and histologically consistent with linear LP. Two months after the onset of her skin disease she developed typical lesions with a lacy white pattern on the left lateral aspect of her tongue and the left buccal mucosa with a striking predominance for the left side. Clinically the lesions on the patient's neck were similar to lichen striatus or lichenoid epidermal naevus, a variant of linear verrucous epidermal naevus. However, the histological features and the fact that later in the course of her disease the patient developed typical LP of the oral mucosa suggest that this patient has the rare condition of linear LP with unilateral restriction.
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2/44. Demonstration of antibody to 230 kDa bullous pemphigoid antigen in lichen planus-like keratosis.

    We describe a 67-year-old man with lichen planus-like keratosis associated with anti-230 kDa bullous pemphigoid antigen (BPAG1) autoantibody. The patient had noticed solitary dark brown macule more than 6 years previously on his left chest. Histological findings showed hypergranulosis, irregular acanthosis, liquefaction degeneration of basal cells, band-like infiltration of lymphocytes at the subepidermal portion, and a cleft at the basement membrane zone (BMZ), resulting in the formation of subepidermal blisters. Direct immunofluorescence findings of perilesional skin showed a linear deposition of IgG at BMZ. On indirect immunofluorescent study using normal human skin, circulating IgG autoantibody to BMZ was present in the patient's serum at a titer of 1:80. The antigen located on the epidermal site of normal skin split by 1M NaCl was reacted with the patient's serum. Immunoblot analysis using epidermal extracts demonstrated the presence of IgG antibody directed to BPAG1 in the patient's serum. These observations suggest that the presence of an antibody to BPAG1 could be caused by the damage of basal cells following lichen planus-like keratosis.
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3/44. IgG autoantibodies from a lichen planus pemphigoides patient recognize the NC16A domain of the bullous pemphigoid antigen 180.

    lichen planus pemphigoides (LPP) most likely encompasses a heterogeneous group of subepidermal autoimmune blistering disorders occurring in association with lichen planus. We describe the case of a 49-year-old patient with features characteristic of LPP. Direct immunofluorescence microscopy studies demonstrated linear deposits of C3 along the cutaneous basement membrane, while circulating IgG autoantibodies directed against the epidermal side of skin separated by 1 M NaCl were detected. The patient's serum contained IgG autoantibodies immunoblotting a recombinant form of bullous pemphigoid antigen 180 (BP180), but not the COOH-terminus of BP230. By using deletion mutants, it was found that IgG reactivity was restricted to the NC16A domain of BP180, the region harboring the major antigenic sites targeted by IgG autoantibodies from patients with the bullous pemphigoid group of disorders. Our findings provide support to the idea that a subset of patients with LPP have a distinct form of bullous pemphigoid associated with lichen planus.
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4/44. Cicatrizing conjunctivitis associated with paraneoplastic lichen planus.

    PURPOSE: To report two cases of cicatrizing conjunctivitis associated with paraneoplastic lichen planus. methods: case reports. RESULTS: Two patients were examined because of redness and discomfort in both eyes. A 63-year-old woman with follicular, small-cleaved cell lymphoma had cicatrizing conjunctivitis, stomatitis, vulvitis, and skin lesions. A 25-year-old man with malignant thymoma had cicatrizing conjunctivitis, erosive stomatitis, and penile papules. Histopathologic studies of conjunctiva and skin biopsy specimens in the first patient and labial biopsy specimens in the second revealed lichen planus. CONCLUSION: Paraneoplastic lichen planus is a possible cause of cicatrizing conjunctivitis associated with inflammatory skin and mucous membrane disease.
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5/44. Oesophageal lichen planus.

    We present a case of lichen planus affecting the oesophagus of an 80-year-old woman. Symptomatically, the lesions manifested themselves as dysphagia requiring repeated oesophageal dilatations. The patient was unable to tolerate several conventional treatments and so pulsed methylprednisolone was given with some beneficial short-term effects. Due to potential for malignant change in lichen planus of the mucous membranes it is important to remember this complication and investigate patients with oesophageal symptoms.
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6/44. lichen planus with involvement of all twenty nails and the oral mucous membrane.

    A 57-year-old man had had deformities of all ten fingernails for one and a half years before presentation and deformities of all ten toenails for the previous six months. The surfaces of the nails were rough, with excessive longitudinal striations. The bases of the nails were slightly hypertrophic, and the tips were atrophic and itchy. A longitudinal nail biopsy including the nail matrix revealed the typical histology of lichen planus. Reticulated pigmentation, maceration, and erosion on the buccal mucous membrane were also discovered. Histological analysis of the buccal mucous membrane revealed lichen planus intermingled with eosinophils. Immunological blood analysis revealed elevated CD4 T cells and CD4/CD8 ratio. He worked as a tinsmith and had dental metal. The metal series patch test revealed positive reactions to chromate and tin. Treatment with systemic steroids was quite effective in treating the nail lesions.
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7/44. lichen planus pemphigoides with circulating autoantibodies against 200 and 180 kDa epidermal antigens.

    We describe a case of lichen planus pemphigoides with circulating autoantibodies against 200 and 180 kDa epidermal antigens. A 24-year-old man presented pruritic erythematous patches with occasional central blister formation on the face, neck, and trunk and erythematous hyperkeratotic patches on the elbows and feet for 10 months. Histopathological findings of the neck and plantar lesions were consistent with lichen planus. Direct immunofluorescence studies from both lesions showed a linear deposition of IgG and C3 and cytoid bodies along the basement membrane zone. Indirect immunofluorescence studies demonstrated circulating IgG antibodies deposited on the epidermal side of salt-split skin. Immunoblot analysis using epidermal extract showed that the patient's serum reacted with 180 kDa bullous pemphigoid antigen (BPAG2) and a 200 kDa antigen. The cutaneous lesions almost cleared with a low dose of prednisolone and acitretin.
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8/44. PUVA-induced lichen planus pemphigoides.

    A 72-year-old woman had suffered from parapsoriasis en plaque (large plaque type) controlled by topically applied psoralen ultraviolet A (PUVA) therapy. The parapsoriasis lesions gradually disappeared, but numerous tiny red papules with pruritus appeared over the forearms and lower legs 120 days after starting puva therapy. These papules developed to form violaceous plaques. Histological findings demonstrated the characteristics of lichen planus. Two months later, tense bullae developed on the plaques and on uninvolved skin of the limbs. These were subepidermal, with linear deposits of IgG and C3 along the basement membrane zone (BMZ) in immunofluorescence of peribullous skin, and immunodeposits of type IV collagen along the floor of the bullae. We therefore, diagnosed lichen planus pemphigoides (LPP). Using systemic and topical steroid therapy, the lesions rapidly resolved and there has been no recurrence. This case suggests that the combination of basal cell injuries caused by chronic inflammation and puva therapy could expose BMZ components to autoreactive lymphocytes and induce LPP.
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9/44. Previous tuberculosis, hepatitis c virus and lichen planus. A report of 10 cases, a causal or casual link?

    We report 10 cases of lichen planus (LP) and chronic liver disease linked to HCV. The mean age was 63.4 /- 5.1 years (range 51-73), five were female; six patients had an established cirrhosis of the liver, as shown by either a liver biopsy or the ultrasonographic and biohumoral evidence. The remaining four patients had chronic hepatitis. Histological examination confirmed the presence of LP: the localization of the dermatosis was restricted to the skin in four patients, to the mucous membranes in five (4 atrophic erosive and one erosive) while the remaining had mucous-cutaneous localization. A type II cryoglobulinemia was demonstrated in two and a type III in one of the patients, while no one had otherwise circulating autoantibodies (anti-nuclear, anti-smooth muscle, anti-liver kidney microsomal type 1 and anti-mitochondrial antigens) such as other etiological factors of liver disease. In six of the patients the history was positive for previous mycobacterium tuberculosis infection. In clinical practice the patients with chronic liver disease and HCV infection can also suffer from severe extrahepatic manifestations, including lichen planus.
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10/44. Coexistence of lichen planus and bullous pemphigoid. A immunopathological study.

    A 43-year-old white man presented with a generalized eruption of lichen planus and tense blisters within the lichenoid lesions and also on clinically normal skin. Direct immunofluorescence (IF) studies revealed immunological and histopathological characteristics of lichen planus in the lichenoid lesions and of bullous pemphigoid in the bullous lesions, and indirect IF studies showed that the patient had circulating antibasement membrane antibodies. The coexistence of both disorders may indicate a possible link between the pathology in the junctional zone in lichen planus and the appearance of antibasement membrane zone antibodies and bullous lesions, respectively.
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