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1/15. Photoinduced dermal pigmentation in patients taking tricyclic antidepressants: histology, electron microscopy, and energy dispersive spectroscopy.

    Two patients had been taking long-term tricyclic antidepressant therapy. Each developed a blue to slate-gray hyperpigmentation in sun-exposed areas. On histologic examination there were refractile golden brown granules free in the dermis along collagen bundles. Similar pigment was present in macrophages and along the basement membrane zone. The granules stained for melanin, but not for iron, and were bleached by the permanganate method. Electron microscopy showed varying size and shaped electron-dense granules within lysosomes and free in the dermis, which, in unstained sections, showed a less dense peripheral halo. This peripheral halo was also evident on light microscopy. Energy dispersive spectroscopy showed these granules to be rich in copper and sulfur (elements present in tyrosinase and pheomelanin, respectively). We believe that this represents a drug-melanosome complex, which is most likely caused by chronic photoactivation.
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2/15. 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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3/15. Photodistributed blue-gray pigmentation of the skin associated with long-term imipramine use.

    A 72-year-old white woman presented with progressively increasing slate-gray pigmentation of the face and extensor aspect of the forearms, which she had been suffering from for 8 years. She had been taking imipramine for approximately 30 years. Her other medications included ranitidine and anacin. physical examination revealed slate-gray hyperpigmentation of the skin photodistributed on the face (Figs 1, 2) and extensor aspects of the forearms. Relative sparing of the skin folds, mucous membranes, sclerae, teeth, and nails was noted. The remainder of the physical examination revealed no abnormalities. skin biopsy specimens from the right cheek and right forearm were obtained. Histologic examination revealed collections of variably sized, round to ovoid, yellow-brown globular deposits in the upper and mid dermis (Fig. 2). The deposits were identified within macrophages and free within the dermis. The epidermis was unremarkable and free of deposits. The deposits stained for melanin with a Fontana-Masson stain, but did not stain for iron.
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4/15. Pigmented squamous cell carcinoma of the cheek skin probably arising from solar keratosis.

    We report a rare case of pigmented squamous cell carcinoma (SCC) of the cheek skin probably arising from solar keratosis. An 80-year-old man was referred to our clinic because of a black skin nodule in the right cheek. The nodular lesion was 1 cm in diameter, dome-shaped, hard, sharply demarcated, partially erosive and telangiectatic at the border. The lesion was completely excised under the clinical diagnosis of probable seborrheic keratosis. Microscopically, cutaneous horn and mildly atypical squamous epithelia suggestive of previous solar keratosis were present in the surface of the lesion. The lesion consisted of atypical squamous cells with keratinization and intercellular bridges, and it was regarded as SCC. The SCC cells were seen to invade lightly into the upper dermis, where lymphocytic infiltrations and melanophages were noted. Characteristically, heavy deposition of melanin pigment was recognized in the SCC cells as well as in proliferated dendritic and pigment blockade melanocytes that were scattered or colonized within the SCC cell nests. Masson-Fontana stain revealed numerous melanin granules in the SCC cells, as well as in dendritic and pigment blockade melanocytes. Immunohistochemically, the SCC cells were positive for cytokeratins and epithelial membrane antigen, and negative for S-100 protein and HMB45 antigen. Dendritic and pigment blockade melanocytes were negative for cytokeratins, epithelial membrane antigen, and HMB45 antigen, but positive for S-100 protein. The present case suggests that SCC cells of the skin may induce proliferation of melanocytes. The differential diagnosis and the histogenesis of pigmented SCC of the skin are discussed.
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5/15. Chronic actinic dermatitis with vitiligo-like depigmentation.

    This report describes two patients suffering from severe chronic actinic dermatitis. Unusual widespread vitiligo-like depigmentation occurred during the course of the disease. The progression of these lesions was triggered by the chronic actinic dermatitis. Loss of pigment and complete absence of tyrosinase positive melanocytes were found in depigmented skin of both cases. Immunohistological investigation of the inflammatory infiltrate in case 2 revealed a predominance of CD-8 positive cytotoxic/-suppressor lymphocytes. Analysing the adjacent pigmented epidermis of progressive depigmenting lesions a dense exocytosis of CD-8 T-cells was notable. This distribution suggests cytotoxic destruction of melanocytes as the cause for the vitiligo-like depigmentation.
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6/15. amyloidosis cutis dyschromica. dna repair reduction in the cellular response to UV light.

    BACKGROUND--amyloidosis cutis dyschromica, a special type of primary cutaneous amyloidosis, is assumed to be a congenital disorder and sun exposure is thought to be the major causal factor. Herein we report a case of this rare disease and dna repair characteristics of UV damages in the fibroblasts derived from the patient. OBSERVATIONS--A 24-year-old Japanese woman showed hyperpigmented and hypopigmented xerotic lesions in sun-exposed skin since she was 10 years old; deposits of amyloid material were detected in the papillary dermis. The fibroblasts were hypersensitive to UV-B, but not so sensitive to UV-C. Unscheduled DNA synthesis of the patient's cells after UV-C exposure was lower than that of normal cells at 3 hours and both reached the same level at 6 hours. After UV-B exposure, unscheduled DNA synthesis of the patient's cells was lower than that of normal cells at least until 6 hours after UV exposure. CONCLUSION--Although the origin of amyloidosis cutis dyschromica is unknown, hypersensitivity to UV-B with possible dna repair defects is suggested to be the cause of this disease.
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7/15. Experimental production of DLE lesion with a single exposure to UVB (2.7 MEDs) radiation.

    Keratotic erythematous lesions developed on the face, ears, neck, and upper back of a 38-year-old man. The patient had a history of photosensitivity to sunlight manifested by the development of new lesions. One week after an MED (2.7 mJ/cm2) was determined using UV-B light, persistent erythema with fine scales were observed at test sites irradiated over 72 mJ/cm2. These lasted for at least 2 months. A biopsy specimen obtained from the test site irradiated at 72 mJ/cm2 showed liquefaction degeneration of the basal cell layer. Within the upper part of the dermis, perivascular and disseminated lymphocytic infiltrates were seen. However, when irradiated again under the same conditions 7 and 12 months after the initial phototest, no persistent erythema was observed.
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8/15. quinidine photosensitivity.

    A 55-year-old woman developed a dermatitis confined to light-exposed areas while taking quinidine gluconate, warfarin sodium, furosemide, spironolactone, and digoxin after cardiac surgery. Phototesting indicated a normal erythematous response to 290- to 320-nm ultraviolet radiation, but she developed erythema from 6 joules/sq cm of 320- to 400-nm radiation (ultraviolet A [UV-A]), a much lower dose than needed to produce a reaction in normal individuals. Two days after she discontinued quinidine and warfarin, phototesting showed no reaction to as much as 20 joules/sq cm of UV-A. One week after resuming quinidine (but not warfarin), she again reacted to 8 joules/sq cm of UV-A. No reactivity was elicited when the preparation was applied to the skin or injected into the dermis either with or without subsequent UV-A irradiation.
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9/15. Musk ambrette and chronic actinic dermatitis.

    A patient with persistent photosensitivity and positive photopatch tests to musk ambrette and an after-shave lotion is reported. Phototests showed extreme sensitivity to UV radiation, especially UVB. patch tests with the European Standard Series and some plant allergens were negative. histology showed a granulomatous reaction with epithelioid and giant cells in the dermis.
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10/15. Actinic reticuloid. A clinical, pathologic, and action spectrum study.

    A 54-year-old man suffered from a chronic dermatitis that was more severe on light-exposed areas. skin biopsy specimens revealed histopathologic findings consistent with those seen in mycosis fungoides. Ultrastructural studies demonstrated the existence of lymphoid cells with hyperconvoluted nuclei, typical of the mycosis fungoides cell or Sezary cell, within the epidermis, dermis, and peripheral blood. Light testing with a monochromator showed abnormal photosensitivity to both short- and long-wave ultraviolet light as well as to the violet, blue, and green wavelengths of visible light. The features of this patient's disease indicate actinic reticuloid.
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