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Biomedical subjects

K Kaidbey

Publications and source records attributed to K Kaidbey.

6 recordsLinked to original sources

Effects of topical ammonium lactate on cutaneous atrophy from a potent topical corticosteroid.

BACKGROUND: Topical corticosteroids produce atrophic changes in skin, including thinning of the epidermis and decrease in dermal ground substance. We observed that 12% ammonium lactate produced an increase in the thickness of epidermis and increased amounts of dermal glycosaminoglycans. OBJECTIVE: Our purpose was to determine whether 12% ammonium lactate could minimize cutaneous atrophy produced by a potent topical corticosteroid. METHODS: Clobetasol propionate, 12% ammonium lactate, and both agents were repetitively applied under occlusive patches as well as in open patches on the forearms of human volunteers for 3 to 4 weeks. Biopsy specimens were analyzed for thickness of the epidermis and dermal glycosaminoglycans by image analysis. RESULTS: Twelve percent ammonium lactate produced a significant sparing of atrophy in both the epidermis and dermis without any influence on the bioavailability or antiinflammatory properties of the corticosteroid. CONCLUSION: Twelve percent ammonium lactate may be useful in mitigating the adverse effects of corticosteroid on skin.

Administration, Topical

Persistent light reactivity from systemic quinine.

A 41-year-old black female with psoriasis developed photosensitivity and a Koebner reaction while receiving phototherapy. She had been receiving oral quinine intermittently for muscle cramps. Photobiological evaluation revealed a strongly positive photopatch test to quinine sulfate and a marked persistent reduction in the minimal erythema dose to solar-simulated radiation in the uninvolved skin. There were no abnormal reactions to UVA. The photosensitivity is still present 3 years after the withdrawal of quinine. These features are similar to those observed previously in persistent light reactors to topical photosensitizers.

Adult

Wavelength dependence for DNA synthesis inhibition in hairless mouse epidermis.

Exposure of mammalian skin to ultraviolet radiation (UVR) results in a transient inhibition of scheduled DNA synthesis. The wavelength dependence for this response was investigated in the epidermis of albino hairless mice. Groups of animals were exposed to narrow wavebands of UVR (HPBW 6.6 nm) from a monochromator in the 260-335 nm range. A dose-dependent inhibition of DNA synthesis was observed following exposure to all test wavebands except that centered at 335 nm. An action spectrum constructed from dose-response regression lines showed peak effectiveness at 290 nm. This spectrum bears a close resemblance to published action spectra for the induction of pyrimidine dimers in vivo, suggesting that DNA is the primary chromophore for both events. The DNA synthesis inhibition spectrum bears little resemblance to a published therapeutic action spectrum for the clearing of psoriasis.

Animals

Comparison of methods for assessing photoprotection against ultraviolet A in vivo.

Photoprotection against ultraviolet A (UVA) by three sunscreens was evaluated in humans, with erythema and pigmentation used as end points in normal skin and in skin sensitized with 8-methoxypsoralen and anthracene. The test sunscreens were Parsol 1789 (2%), Eusolex 8020 (2%), and oxybenzone (3%). UVA was obtained from two filtered xenon-arc sources. UVA protection factors were found to be significantly higher in sensitized skin compared with normal skin. Both Parsol and Eusolex provided better and comparable photoprotection (approximately 3.0) than oxybenzone (approximately 2.0) in sensitized skin, regardless of whether 8-methoxypsoralen or anthracene was used. In normal unsensitized skin, Parsol 1789 and Eusolex 8020 were also comparable and provided slightly better photoprotection (approximately 1.8) than oxybenzone (approximately 1.4) when pigmentation was used as an end point. The three sunscreens, however, were similar in providing photoprotection against UVA-induced erythema. Protection factors obtained in artificially sensitized skin are probably not relevant to normal skin. It is concluded that pigmentation, either immediate or delayed, is a reproducible and useful end point for the routine assessment of photoprotection of normal skin against UVA.

Adolescent

UV suppression of mast cell-mediated wealing in human skin.

Prior exposure of normal skin to subthreshold doses of UVR from a "UVA" phototherapy cabinet resulted in a small but significant reduction of the wealing response to intradermally injected codeine phosphate, a mast cell degranulating agent. The flare component of the reaction was not affected, nor were the responses to intradermally injected histamine. Both UVA and UVB from banks of filtered fluorescent tubes appeared to produce a similar but less pronounced effect. Dose-response studies revealed that the inhibition of mast cell-mediated wealing required a certain cumulative threshold dose of UVR (about 35 J/cm2 UVA + 20 mJ/cm2 UVB). The observed reduction in wealing could not be entirely explained by differences in the content of tissue histamine. It is concluded that repeated exposure to a broad range of UV wavelengths can depress the response of mast cells in vivo to degranulating agents by an unknown mechanism. This finding may have relevance to some of the observed therapeutic effects of phototherapy in certain inflammatory dermatoses and especially cutaneous mast cell disorders.

Adult

Persistent photosensitivity following occupational exposure to epoxy resin.

Persistent photosensitivity developed in eight men following occupational exposure to hot epoxy resin fumes. The condition was limited to sites the resin contacted. Small doses of ultraviolet-A light (2 to 5 joules/sq cm) evoked abnormal reactions consisting of erythema, edema, and papules in the clinically involved skin. Positive photopatch tests to epoxy resin were observed in four subjects, and to 4, 4'-isopropylidenediphenol (Bisphenol A) in all. The photosensitivity is most probably due to photocontact allergy to 4,4'-isopropylidenediphenol or to a closely related chemical.

Adult