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1/105. Photoallergy induced by quinidine.

    An 82-year-old woman presented with a lichenified dermatitis over light-exposed areas. The eruption cleared upon withdrawal of quinidine and recurred on re-administration of the drug. Though quinidine has not been recognized as a photo-sensitizing agent, upon review of the literature we have uncovered other cases which meet the criteria and justify including this drug among those capable of causing such reactions.
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2/105. Photolocalized tinea facialis.

    The case of a 34-year-old white woman with tinea facialis that persisted for nine months prior to diagnosis is presented. The confluent plaquelike erythematous eruption of the face with eyelid lichenification that flared outdoors was thought to represent polymorphic light eruption and was refractory to antibiotics, corticosteroids (topical and systemic), and antimalarials. A KOH preparation was positive when the dermatosis spilled onto the mandibular region, and restaining of the initial skin biopsy revealed fungal hyphae. Complete resolution was accomplished with griseofulvin and MicTin. tinea cab be added to the list of infectious agents that have a photosensitivity component. The fungus possibly "photolocalizes" to sun-damaged areas, ie, areas of increased capillary permeability. This case illustrates the importance of including tinea in considering diagnoses of sun-exposed lesions of the face.
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3/105. Jessner's lymphocytic infiltrate and probable discoid lupus erythematosus occurring separately in two sisters.

    We describe two sisters with clinical and histological features suggestive of Jessner's lymphocytic infiltrate in one and discoid lupus erythematosus in the other. The occurrence of these two entities in one family now gives credence to the theory that Jessner's lymphocytic infiltrate is in the same disease spectrum as lupus and probably also polymorphic light eruption.
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4/105. Polymorphic light eruption occurring solely on an area of naevoid telangiectasia.

    We report the case of a 60-year-old woman presenting with polymorphic light eruption occurring solely on an area of acquired naevoid telangiectasia. We have hypothesized that increased blood flow in the telangiectatic skin may reduce the threshold for expression of photosensitivity by permitting enhanced inflammatory cell trafficking to the overlying tissue.
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5/105. Polymorphic light eruption occurring in common variable hypogammaglobulinaemia, and resolving with intravenous immunoglobulin therapy.

    A 55-year-old woman with a past history of lower respiratory tract infections presented with a photosensitive eruption. Polymorphic light eruption (PLE) was diagnosed on the basis of the temporal relationship to sun exposure and the diagnosis was supported by positive monochromator irradiation tests in the ultraviolet A wavelength spectrum. Investigation of the patient's immune status identified low levels of all immunoglobulin (Ig) subtypes consistent with common variable hypogammaglobulinaemia. Intravenous Ig replacement therapy, instituted to minimize risks from bacterial infections, was commenced and over the ensuing months resulted in a complete resolution of the PLE. PLE is considered to represent a type IV hypersensitivity reaction directed against a cutaneous autoantigen induced by exposure to ultraviolet light. In PLE, nonspecific immunomodulatory mechanisms of intravenous Ig may be active, such as a reduction in the synthesis of cytokines and a blockage of the IgG Fc receptors on macrophages.
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6/105. Polymorphous light eruption. A case report and consideration of the hardening mechanism.

    BACKGROUND: Polymorphous light eruption (PLE) is a common form of photodermatosis. The pathogenesis of the disease and the mechanism of the hardening phenomenon, however, have not been clarified. observation: We report a 62-year-old Japanese woman with PLE. Provocation and hardening induction testing revealed that hardening was induced at the sites irradiated by a sufficient dose of UV for reproduction of the lesion. Topical steroid could prevent a positive reaction but not the hardening induction. The expression of adhesion molecules and CD1a was decreased at the hardening site. CONCLUSION: From these results, the hardening phenomenon in our case might be due to immunosuppression by UV exposure supported by the down-regulation of cell adhesion molecule expression and partially due to the depletion of endogenous antigens which cause a delayed-type hypersensitivity reaction.
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7/105. A case of actinic prurigo in thailand.

    Actinic prurigo is a separate entity from the polymorphous light eruption that affects American Indians. It has been reported mainly from North and south america, with only few reported cases from Britain or asia. We report a case of actinic prurigo in a Thai girl who showed cheilitis and pruritic papules on exposed areas for three years. We were able to induce populovesicular lesions by three consecutive irradiations with 100 J/cm2 UVA and 2 minimal erythematous dose of UVB. However, three weeks after irradiation, a prurigo papule developed at the UVB irradiated site.
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8/105. A case of actinic prurigo showing hypersensitivity of skin fibroblasts to ultraviolet A (UVA).

    We here report a patient with actinic prurigo. He had had erythematous papulovesicular eruptions on the sun-exposed sites from fall to early summer for 4 years. The lesions healed leaving atrophic scars. The histology showed epidermal necrosis and dermal dense perivascular lymphohistiocytic infiltration and edema. His minimal erythema doses to ultraviolet B (UVB) and UVA were normal and lowered, respectively. skin lesions were produced by repeated irradiation with UVA plus UVB, but not with UVA alone. Then he was diagnosed as having actinic prurigo. skin fibroblasts from the patient were hypersensitive to UVA. We believe that the hypersensitivity relates to the pathomechanisms of the photosensitivity in the case. UVA sensitivity of fibroblasts may be useful for differentiating actinic prurigo, hydroa vacciniforme, and other similar photosensitive disorders.
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9/105. Photo-accentuated eruption and vascular deposits of immunoglobulin a associated with hepatitis a virus infection.

    skin rash associated with hepatitis a virus infection has rarely been reported. We describe a patient with hepatitis a virus infection who presented a rubelliform rash markedly accentuated in sun-exposed areas; direct immunofluorescence studies of the lesion revealed immunoglobulin (Ig) A deposition on the endothelial cells in the upper dermis. Oral rechallenge tests of the previously administered drugs failed to reproduce the eruption. The preferential setting of immune complexes containing IgA at sites of sun exposure and sunlight as a triggering factor might have been responsible for the development of the eruption in this patient. Eruptions associated with hepatitis A virus infections may be more frequent than commonly thought. Because of difficulty to exclude the possibility of drug eruptions, these cases might have been overlooked. In patients with such a disorder, a careful clinical workup such as IgM antibodies for hepatitis a virus at diagnosis and during follow-up is especially recommended.
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ranking = 7
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10/105. Cutaneous porphyria in a neonate with tyrosinaemia type 1.

    A term infant born to consanguineous parents presented at birth with hypoglycaemia, thrombocytopenia, coagulopathy and hyperbilirubinaemia associated with polycythaemia due to delayed cord clamping. Despite phototherapy and correction of polycythaemia by partial exchange transfusion, coagulopathy, hypoglycaemia and conjugated hyperbilirubinaemia persisted, suggesting hepatic failure. Metabolic work-up led to the diagnosis of tyrosinaemia type 1 on day 4. Two--(2-nitro-4-trifluoromethylbenzoyl)--1,3 cyclohexanedione (NTBC) treatment, started on day 5, resulted in progressive clinical improvement and unambiguous biochemical response. Severe skin purpuric lesions occurred in areas exposed to phototherapy. These resolved slowly after its discontinuation. urine analysis sampled just before and 6 days after starting NTBC treatment showed high levels of type 1 coproporphyrin isomers. Such findings do not seem directly related to tyrosinaemia type 1 where succinylacetone inhibits delta-aminolevulinic acid (delta-ALA) dehydratase and where the accumulation of delta-ALA results in neurotoxicity without photosensitivity. CONCLUSION: We describe a cutaneous form of porphyria in a neonate presenting with severe liver failure due to tyrosinaemia type 1. This porphyria is tentatively attributed to a secondary accumulation of coproporphyrins due to cholestasis, as reported in the bronze baby syndrome and recently described in neonates with purpuric phototherapy-induced eruption, rather than to a primary defect of porphyrin metabolism. The hypothesis of a direct effect of tyrosinaemia type 1 on porphyrin excretion is also discussed.
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