Iododerma

IODODERMA (jododerma tubero-bullosum, jododerma tuberosum fungoides, s. anthracoides, jododerma ecthymatosum vegetans), diverse toxic exanthems, most often in the form of banal acne (see Acne), arising from the intake of iodine preparations. Less frequently encountered are dermatoses morphologically similar to urticaria, erythema, erythema multiforme exudativum, purpura, erysipelas, pemphigoid rash, pemphigus vegetans, varioliform rash, erythema nodosum, and eczema. Nodular iododerma is a rare dermatosis, first described by Besnier in 1882 under the name acne anthracoide jodo-potassique. It is observed in individuals with an idiosyncrasy to iodine. Its preferred localization is the region of the head and nose. With symptoms of itching and burning, acneiform pustules, infiltrated at the base, arise initially; these, by merging, turn into tumors, often of a fungoid character, blue-purple in color, ranging in size from a pea to a pigeon's egg, in the center of which blisters often form [see separate table (col. 303-304), fig. 1]. These nodules are painful and soft to the touch, of a spongy consistency, and bordered by a wide inflammatory rim. Increasing in size, they undergo softening and disintegration in the center, yielding an ulcerated, vegetating surface, partly covered with black-brown crusts. At the periphery of the lesion, new acneiform eruptions are noticeable. After healing, pigmentation usually remains, less often smooth scars. The mucous membranes of the oral cavity (Jesionek, Rille, et al.) and the stomach (Neumann, Polland) are affected extremely rarely. Sometimes the tumors are accompanied by general symptoms, diarrhea, and albuminuria. In severe cases, a fatal outcome is possible. In pemphigoid toxidermia, characterized by intense inflammatory exudation, with which tuberous iododerma is sometimes combined, it can lead to localized gangrene. A strict distinction between both of these forms is impossible. Histologically: sharp infiltration of the papillary layer and the dermis proper, consisting mainly of polymorphonuclear leukocytes, lymphocytes, eosinophils, and isolated plasma cells. Giant cells are observed rarely. Elastic and collagenous tissues disappear. Skin appendages are gradually destroyed. Edema and proliferation of the epithelium with the formation of microabscesses are noted. Vessels are sharply dilated; there is swelling and proliferation of the endothelium, thickening of the intima, and sometimes endo- and perivasculitis of large vessels. Sometimes atypical proliferation of the epithelium creates a false impression of a malignant neoplasm (Montgomery et al.). According to Pellizzari et al., the basis of iododerma is inflammation of the vessels, arising as a result of irritation of the vasomotor apparatus. The hypothesis of Adamkiewicz and Heitzmann regarding skin irritation due to the deposition of free iodine in the excretory ducts of the sebaceous glands is not very plausible. The microbial theory has many adherents. Diseases of the kidneys, liver, and heart, malnutrition, severe infections (e.g., syphilis), and constitutional features play the role of a predisposing factor. In diagnosis, a number of dermatoses showing similarity to iododerma are taken into account, such as: vegetating syphilids, mycosis fungoides, pemphigus vegetans, fungous tuberculosis, rhinoscleroma, condyloma, and bromoderma. Treatment. Usually, iododerma disappears spontaneously with the cessation of iodine intake. The application of anti-inflammatory lotions or ointments promotes healing. Rarely, it is necessary to scrape out the growths with a sharp curette. Sodium chloride is useful orally (Ullmann; 10-12 g per day) or intravenously; alkaline-carbonate waters promote the elimination of iodine.