Skin Disease in the Cuna Indians

McFADDEN, Archibald W.

doi:10.1001/archderm.1961.01580180129020

Cited by 19 publications

(4 citation statements)

References 2 publications

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“…The role of tanning is clearly seen in patients with vitiligo where the depigmented skin is much more sensitive to UV irradiation (13). Individuals with constitutively pigmented skin are less susceptible to sunburn and skin cancer than fair-skinned individuals (12,14). Tanning caused by UVA, but not UVB, has been shown to be less protective against UVB-induced erythema but equally protective against UVB-induced DNA damage (10).…”

Section: Discussionmentioning

confidence: 99%

Long‐wave UVA offers partial protection against UVB‐induced immune suppression in human skin

Skov

Villadsen

Ersbøll

et al. 2000

APMIS

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Ultraviolet-B (UVB, 280-320 nm) interferes with the generation of cell-mediated immunity to contact allergens applied epicutaneously on the irradiated site. To investigate whether pretreatment with UVA-1 (340-400 nm) protects against the UVB-induced immune suppression we sensitized human volunteers with diphenylcyclopropenone (DPCP) on normal buttock skin (n= 12), on UVB-irradiated buttock skin (n=21), on buttock skin pretreated with UVA-1 (n= 12), and on buttock skin pretreated with UVA-1 and thereafter irradiated with UVB (n=22). Sensitization on UVB-irradiated skin reduced the immunization rate to DPCP compared with sensitization on non-irradiated skin (p<0.01) and skin pretreated with UVA-1 (p<0.01). In contrast, the immunization rate in the group of volunteers sensitized on skin pretreated with UVA-1 before UVB irradiation was significantly higher than the immunization rate in the group of volunteers sensitized on UVB-irradiated skin alone (p<0.05). These results indicate that pretreatment with UVA-1 under certain conditions offers partial protection against the UVB-induced reduction in the immunization rates to epicutaneous allergens.

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Section: Discussionmentioning

confidence: 99%

Long‐wave UVA offers partial protection against UVB‐induced immune suppression in human skin

Skov

Villadsen

Ersbøll

et al. 2000

APMIS

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“…Tanning is widely believed to be a photoprotective response of UVR-exposed skin, which decreases damage from subsequent UVR exposure (Kollias et al, 1991;Mawn and Fleischer, 1993;McGinley et al, 1998). Much of the work to date on natural photoprotection, however, is based on constitutive pigmentation (McFadden et al, 1961;Young et al, 1985;Lookingbill et al, 1995;Lock-Andersen et al, 1997). It has further been suggested that the signi®cance of stratum corneum in photoprotection may be greater in fair skinned individuals than in pigmented individuals (de Fine et al, 1997), especially in albino or vitiliginous skin where the stratum corneum may represent the only source of protection.…”

mentioning

confidence: 99%

Repeated Ultraviolet Exposure Affords the Same Protection Against DNA Photodamage and Erythema in Human Skin Types II and IV but is Associated with Faster DNA Repair in Skin Type IV

Sheehan

Cragg

Chadwick

et al. 2002

Journal of Investigative Dermatology

118

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We have investigated the photoprotective properties of induced pigmentation using erythema and epidermal DNA photodamage as endpoints. Previously unexposed buttock skin of 12 young, healthy adults (six skin type II and six skin type IV) was exposed daily (Monday to Friday) for 2 wk (days 1-12) with 0.65 minimal erythema dose of solar simulated radiation. Mean skin type IV minimal erythema dose was 1.8-fold greater than for skin type II. Compared to skin type II, solar simulated radiation treatments produced less erythema and more tanning in skin type IV. To assess DNA photodamage, biopsies were taken and prepared for paraffin sections that were stained with a monoclonal antibody for thymine dimers. Thymine dimers were quantified by image analysis. The single exposure data (0.65 and 2 minimal erythema dose) showed that DNA damage was related to physical dose (J per cm2) independent of skin type. Our data also showed that DNA photodamage accumulates in both skin types with repeated, suberythemal doses of solar simulated radiation. On day 12, there were more thymine dimers in skin type IV than skin type II, again indicating that physical rather than biologic dose determines the level of DNA damage. Comparisons on days 12 and 19, however, showed a much greater loss of thymine dimers in skin type IV, suggesting better thymine dimer repair. Protection factors for erythema and thymine dimers were calculated and shown to be about 2 in both skin types. This provides further indirect evidence that DNA is a chromophore for erythema, but also suggests that a tan may not be the major factor in natural photoprotection.

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“…The deaths of five of these albinos were attributed to skin cancer eroding through the eyes, skull or large blood vessels. A study of the Cuña Indian albinos of Panama found that the incidence of actinic keratosis in albinos was nearly l00% after the age of 7 years 52 . In South Africa, Kromberg et al .…”

Section: Complicationsmentioning

confidence: 99%

Oculocutaneous albinism

Okulicz

Shah

Schwartz

et al. 2003

Acad Dermatol Venereol

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Oculocutaneous albinism represents a group of inherited skin disorders characterized by a generalized reduction of cutaneous, ocular and pilar pigmentation from the time of birth. Oculocutaneous albinism types 1 and 2 are the most common, but several other types have been described. A defect in the melanin synthesis pathway, resulting in reduced formation of melanin, is responsible for oculocutaneous albinism. Aetiology, clinical manifestations, diagnosis and management are discussed.

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Skin Disease in the Cuna Indians

Cited by 19 publications

References 2 publications

Long‐wave UVA offers partial protection against UVB‐induced immune suppression in human skin

Long‐wave UVA offers partial protection against UVB‐induced immune suppression in human skin

Repeated Ultraviolet Exposure Affords the Same Protection Against DNA Photodamage and Erythema in Human Skin Types II and IV but is Associated with Faster DNA Repair in Skin Type IV

Oculocutaneous albinism

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