In 1891, Schweninger and Buzzi1 originally described macular atrophy under the title, Multiple Benign Tumor-like New Growths of the Skin. Since then, the few and isolated case reports of the condition have failed to bring forth any substantial evidence of etiologic relationship. The clinical features of the various reported cases of macular atrophy are strikingly similar to the classic description of Schweninger and Buzzi.1 Combes2 and later Chargin and Silver3 showed that both primary and secondary macular atrophy have a similar histologic picture and suggested that toxic substances, whatever their nature, may be assumed to play a role in the production of the degenerative process. Scull and Nomland4 believed that secondary macular atrophy, irrespective of the causative disease, occurs subsequent to a subclinical destruction of the elastic tissue in the upper dermis by an inflammatory infiltrate. Butterworth5 reported a case of