CONSIDERABLE interest has recently been aroused by Kveim's report1of the production of an unusual cutaneous reaction in patients with sarcoidosis by the intracutaneous injection of heated saline suspensions of tissue obtained from persons with active disease. Kveim found that after the transient inflammatory response caused by the trauma of such an injection had subsided, a small, indurated papule developed at the test site within a variable period of time. This delayed papular reaction was distinctive in that it often required weeks to attain its maximum size and usually remained visible for many months thereafter. Microscopic examination of tissue from sites of such reactions showed a histologic structure essentially the same as that of the lesions of the natural disease. Since control injections of Frei antigen and old tuberculin injected simultaneously with the suspensions of tissue into the same patients produced no comparable response, and, since the sarcoid material
AN INCREASED interest in incontinentia pigmenti is indicated by the recent articles of Carney, 1 Epstein and others, 2 Haber, 3 and Findlay, 4 who regard this disease not merely as a skin disease but preferably as a widespread syndrome comprising various congenital disorders. In Japan, Kitamura and Chan 6 described, in 1938, a baby girl showing the characteristic pigmented patterns of incontinentia pigmenti as the first Japanese case of this disease. Since then, 21 cases of incontinentia pigmenti have been observed in this country. However, as most of them * were reported in Japanese medical journals during the recent war, they are unknown to world dermatologists, with the exception of the first case of Kitamura and Chan, which at that time was abstracted in Dermatologische Wochenschrift . 7 So the relative frequency of this disease among the Japanese people, which is now presumed from the above-mentioned number of the observed
ANIMAL experiments suggest1and clinical observations confirm2that the topical application of pantothenic acid, a nutritional factor of the vitamin B group, favors regeneration and functional recovery of damaged epithelium in dermatoses of various causes.3 Response obtained by one of us with derivatives of pantothenic acid when administered in massive doses orally, in combination with vitamin E, in the treatment of certain phases of lupus erythematosus and in granuloma annulare,4stimulated interest in a study of the therapeutic value of Panthoderm*(a water-miscible cream containing 2% pantothenyl alcohol), topically, for lesions of lupus erythematosus. Study was accordingly undertaken of this material as a topical therapeutic adjuvant to the internal regimen mentioned above. Panthoderm was used, topically, by 26 private-practice patients with lupus erythematosus. Patients are classified according to the disease phase presented: The longest period of therapy was 13 months; the average, 8 months. Of
For the past year and a half, the department has been interested in the use of some of the new chelating compounds in the field of clinical dermatology. The most extensive experience with these has been with the local use on the scalp. Another phase of the study, under the direction of Dr. Cleveland Denton, has been with the use of these compounds in nickel and chromium hypersensitivity, and the third phase of the study is the use of disodium calcium ethylenediaminetetraacetic acid (EDTA) complex in routine wet-dressing techniques. Ethylenediaminetetraacetic acid is one of the chelating compiunds whose function is to grab or grip various ions, especially the metallic ions. In regard to the use of soaps, these chelating agents briefly funtion as water softeners by combining not only with iron or other heavy metals, but aso with the calcium and magnesium ions of hard water. These chelates also maintain
A variety of adverse reactions to quinidine have been reported since Frey1in 1918 found the drug to be more effective in cardiac arrythmias than its levorotary isomer quinine. These reactions are of two types, acquired sensitivity and drug toxicity.2 Manifestations of acquired sensitivity are thrombocytopenic purpura,*fever,† and skin eruptions. The toxic reactions are characterized by cinchonism, the commonest adverse reaction; cardiac standstill or ventricular tachycardia; syncope; convulsions, and respiratory difficulties.‡ Most patients with acquired sensitivity also experienced manifestations of cinchonism. Goldschlag15in 1942 reported the occurrence of a symmetrical eczematoid dermatitis from quinidine. After his patient had taken the drug for a period of two months, a scaling, pruritic, edematous eruption appeared on the exposed areas of the skin. On two occasions the eruption disappeared promptly after quinidine was discontinued. However, when quinidine was given again, the eruption recurred as a severe pruritic, violaceous-colored,
