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Amyloidosis Cutis Dyschromica:  DNA Repair Reduction in the Cellular Response to UV Light

Shin-ichi Moriwaki, MD; Chikako Nishigori, MD, PhD; Yuji Horiguchi, MD; Sadao Imamura, MD, PhD; Ken-ichi Toda, MD; Hiraku Takebe, PhD
Arch Dermatol. 1992;128(7):966-970. doi:10.1001/archderm.1992.01680170098015.
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• 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.(Arch Dermatol. 1992;128:966-970)


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