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July 1992

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

Author Affiliations

From the Departments of Dermatology (Drs Moriwaki, Nishigori, Horiguchi, and Imamura) and Experimental Radiology (Dr Takebe), Faculty of Medicine, Kyoto (Japan) University; and the Department of Dermatology, Kitano Hospital, Osaka, Japan (Dr Toda).

Arch Dermatol. 1992;128(7):966-970. doi:10.1001/archderm.1992.01680170098015

• 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)