Amyloidosis cutis dyschromica. DNA repair reduction in the cellular response to UV light

Arch Dermatol. 1992 Jul;128(7):966-70. doi: 10.1001/archderm.128.7.966.

Abstract

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.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Amyloidosis / etiology*
  • Amyloidosis / pathology
  • Colony-Forming Units Assay
  • DNA / biosynthesis
  • DNA Repair / radiation effects
  • Female
  • Fibroblasts / radiation effects
  • Fibroblasts / ultrastructure
  • Humans
  • Photosensitivity Disorders / complications*
  • Photosensitivity Disorders / pathology
  • Skin / cytology
  • Skin / pathology*
  • Ultraviolet Rays

Substances

  • DNA