Dithiocarbamate therapy for nickel dermatitis.

Increased internal exposure to nickel can cause an exacerbation of nickel contact dermatitis. Nickel ions are chelated by diethyldithiocarbamate (DDC) and thereby inactivated. An oral dose of about 1 g DDC/day was given to a patient. The nickel excretion in the urine increased about tenfold; the nickel elimination in scalp hair did not increase. The slightly negative nickel balance did not exhaust the nickel content of the organs appreciably with a dose of 1.2 g DDC/day for 2 months. At the end of this experiment patch tests with nickel sulphate were still positive though less local therapy was needed, and the cross correlation between the activity of the eczema and the nickel concentration in the urine had lost its former periodicity. It is therefore not yet possible to conclude whether or not DDC may be really of help in the very nickel hypersensitive patient by reducing the exposure to nickel originating in food and other environmental sources.

Factors influencing nickel dermatitis. I.

The nickel concentrations in urine and blood plasma of a very hypersensitive female patient have been followed during two periods of 34 and 42 days each. A limited degree of correlation was found between the course of the nickel concentration in plasma, the nickel concentration in urine and the clinical activity of the dermatitis. Evidently other factors also influence the activity of the dermatitis; among these menstruation and stress might be expected to play a role.

Factors influencing nickel dermatitis. II.

The nickel concentrations in urine and other data of a very hypersensitive female patient have been followed during two periods exceeding 30 days each. Only a limited degree of correlation was found between the course of the nickel concentration in urine and the clinical activity of the dermatitis. In order to better evaluate the measure of the correlation and the influence of some other factors upon the activity of the dermatitis, a pathway analysis scheme has been constructed. Consideration of this scheme reveals the need for more extensive data regarding the nickel ion climate in the body.

Nickel content of plasma, urine and hair in contact dermatitis.

The nickle (Ni) concentrations of blood plasma, urine and scalp hair do not differ between hypersensitive and non-hypersensitive subjects. Those who are occupationally exposed have about ten times the control content of nickel in the plasma, urine and hair, whether hypersensitive or not. During vacations the Ni contents of their plasmas and urines decrease sharply. Oral administration of only 5 mg Ni (as the sulphate) increases the Ni concentration of plasma and urine to ten times the normal for more than the subsequent 24 h.

Magnesium content of the hair in alopecia areata atopica.

The magnesium content of hair from alopecia areata atopica patients, from nonatopic dermatological patients and from normal controls has been studied using atomic absorption spectroscopy. The two groups of patients had lower means and ranges than did the normal subjects, but the overlap was considerable. It is suggested that the lower levels found in the patients may be due to the nonspecific 'metabolic cost' of the skin diseases.

Occupational cobalt and chromium dermatitis in an offset printing factory.

A case history of three offset printers and the atomic absorption analysis of their contact materials is described. Though the factory direction and personnel felt strongly about cooperating in order to combat the disease, it became apparent that the prescribed measures had not been effectively carried out. The chemical analysis of the materials proved to be a necessary supplement to the patch testing procedure.