Basal cell carcinoma in chronic arsenicism occurring in Queensland, Australia, after ingestion of an asthma medication

Citation
W. Boonchai et al., Basal cell carcinoma in chronic arsenicism occurring in Queensland, Australia, after ingestion of an asthma medication, J AM ACAD D, 43(4), 2000, pp. 664-669
Citations number
36
Categorie Soggetti
Dermatology,"da verificare
Journal title
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
ISSN journal
01909622 → ACNP
Volume
43
Issue
4
Year of publication
2000
Pages
664 - 669
Database
ISI
SICI code
0190-9622(200010)43:4<664:BCCICA>2.0.ZU;2-T
Abstract
Background: Ingestion of trivalent inorganic arsenic has long been recogniz ed as a cause of basal cell carcinomas (BCCs) anti has been reported most o ften in Taiwan and Singapore. Objective: Our purpose was to study the clinical and histologic characteris tics of BCCs occurring in Australian Caucasians as a consequence of chronic arsenicism due to ingestion of an arsenic-containing medication. Methods: Self-referred persons with a history of ingestion of Bell's Asthma Medication were interviewed, and skin examinations were performed. Local a ge- and sex-matched patients with BCCs were used to compare the distributio n and histologic subtypes of BCCs in arsenic-exposed and sporadic cases. Results: Thirty-six persons (21 male, 15 female; mean age, 57 years) partic ipated, all of whom had been exposed to the asthma medication early in life (mean age, 13 years) for a mean duration of 5 years. Each person had at le ast one cutaneous sign of chronic arsenicism, either self-reported or on ex amination, and all except one had a history of either BCC or squamous cell carcinoma of the skin, with self-reports of 20 to 2000 skin lesions removed per person. The mean age at first presentation with a BCC Nas 33 years, bu t neither latency nor number of skin lesions appeared to be related to dura tion of exposure to arsenic. BCCs in persons exposed to arsenic occurred mo re often on sun-protected sites compared with BCCs in age- and sex-matched sporadic cases (P < .001), but the distribution and histologic subtypes bet ween these two groups were similar. Conclusion: We have described BCCs in arsenic-exposed Australians and shown that they occur predominantly in sun-protected locations. Although the rep orted number of skin lesions is very high, the latency and number do not ap pear to be related to the duration of arsenic exposure. The histologic type s of the BCCs occurring in arsenic-exposed persons are not different from s poradic BCCs.