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The axillary microflora of 229 subjects was characterized quantitatively and the results correlated with whether the odor was pungent body odor or instead a faint "acid odor". The axillary flora was found to be a stable mixture of Micrococcaceae, aerobic diphtheroids and Propionibacteria. Significantly higher numbers of bacteria were recovered from the axilla of those with pungent axillary odor than in those with acid odor. Aerobic diphtheroids in high numbers were recovered in all subjects having typical body odor. These included lipophilic as well as large-colony diphtheroids. When droplets of apocrine sweat placed on the forearm were inoculated with various bacteria which reside in the axilla, only diphtheroids generated typical body odor. Cocci produced a sweaty odor attributable to isovaleric acid.

In five patients developing axillary contact dermatitis subsequent to the use of an antiperspirant containing propantheline bromide patch testing was performed. Three patients reacted to propantheline bromide. The other two patients exhibited positive patch test reactions to the proprietary product; in these cases, the active ingredient was not tested individually. In all five patients, in addition to the antiperspirant, at least one other contact allergen was identified. In case of localized adverse reactions due to topical treatment of hyperhidrosis axillaris patch testing is recommended. If contact allergy to propantheline bromide is revealed, one should be aware of cross sensitization to methantheline bromide.

Seven patients with hyperhidrosis of the palms or soles resistant to topical application of aluminum chloride solution were treated successfully with tap water iontophoresis. After an average of 10 or 11 treatments 80% sweating suppression was found on palms and 74% suppression on soles. As side effects of treatment discomfort and transient skin irritation were observed depending on the amperage used. The effect lasts up to several weeks; however, maintenance treatment on an individual schedule is required.

Suntan is known to be protective against sunburn resulting from medium-wavelength ultraviolet radiation. Protection against UV-B by UV-A-induced pigmentation was studied by the evaluation of the erythema produced and by histologic alterations in the epidermis, including sunburn cell counts. Six subjects were deeply tanned with UV-A (mean cumulative dose, 700 joules/sq cm). The minimal erythemal dose to UV-B (300 +/- 5 nm) was established for each subject in normal skin and in UV-A-tanned areas. The UV-A tan provided measurable protection against UV-B-induced erythema. Following UV-B irradiation, 36 to 93 sunburn cells were counted per 10 mm of epidermal surface length in histologic sections of untanned skin as compared with four to seven sunburn cells in UV-A-tanned skin.

The diagnostic procedure in two patients suffering from persistent light reaction is described. In addition a modification of standard 8-methoxypsoralen-UVA (PUVA) schedule is presented which is necessary because of the extreme sensitivity to UV electromagnetic wave lengths in this photodermatosis. Both patients were able, for the first time in 8 years, to resume normal outdoor activities.