Cutis laxa (CL) is a rare disease of the connective tissue that affects the elastic fibers (EFs) throughout the dermis, creating a characteristic clinical appearance of premature aging with sagging and inelastic skin that generates furrows and wrinkles. It can be subdivided into inherited and acquired, the latter rarer than the former.1,2 Inherited CL results from monogenic defects that impair EFs assembly, whereas ACL results from EFs degradation.3

There are two forms of acquired cutis laxa (ACL), type I and type II. Type I ACL can either be localized or generalized and involve visceral organs, such as respiratory, cardiovascular, gastrointestinal, and urogenital systems.1,4 Type II ACL is localized post-inflammatory elastolysis, where skin elasticity occurs over the inflammatory area without involving visceral organs.1,2,4

We present the case of a 30-year-old man with type I ACL with renal, pulmonary, and digestive involvement and its response to intensive immunosuppressive treatment. A search of PubMed using the keywords cutis laxa, acquired cutis laxa, acquired elastic fiber disease, acquired disorders of elastic tissue, skin laxity, disorder of elastolysis, primary elastolysis, generalized elastolysis, Marshall syndrome, was performed to identify other cases reported in the literature.