Cutis laxa (CL) is a rare connective-tissue disorder characterized by loose, inelastic skin due to defects in elastic fiber production or structure. Acquired cutis laxa (ACL) typically develops in adulthood and may follow inflammatory or immune-mediated events, though idiopathic cases remain uncommon. We report a 29-year-old male with a 10-year history of progressive skin laxity affecting the face, neck, and upper back. There were no preceding infections, drug exposures, or inflammatory skin conditions. Medical, surgical, and family histories were unremarkable. Examination revealed redundant, wrinkled skin with markedly reduced recoil in the involved areas, without joint hypermobility or systemic features suggestive of connective-tissue disease. Laboratory tests and imaging were normal. Histopathology demonstrated diminished and fragmented elastic fibers throughout the dermis, confirmed by Verhoeff-Van Gieson staining, consistent with ACL. This case represents an idiopathic, localized adult-onset form of ACL. The characteristic histological findings, along with the absence of systemic involvement, support the diagnosis. It is important to distinguish this condition from others, such as Ehlers-Danlos syndrome, anetoderma, and pseudoxanthoma elasticum, since overlapping clinical features can lead to misdiagnosis. Idiopathic ACL is rare and often under-recognized, and this case represents the first reported regional idiopathic instance, to the best of our knowledge, from Saudi Arabia. Overall, this case highlights the value of careful clinical assessment and histological evaluation in patients with slowly progressive, non-inflammatory skin laxity.

Light and heavy chain deposition disease (LHCDD) is a clonal plasma cell or monoclonal B-cell dyscrasia characterized by deposition of monoclonal immunoglobulin light and heavy chains. LHCDD mainly belongs to monoclonal gammopathy of renal significance (MGRS), including a spectrum of kidney disorders caused by a monoclonal protein (M-protein) secreted by a small plasma cell clone or other B-cell clones in patients who do not meet the diagnostic criteria for multiple myeloma or other B-cell malignancies. It may also occur as a renal complication of overt multiple myeloma. We report a 27-year-old man who presented clinically with chronic nephritic syndrome and was diagnosed with LHCDD confirmed by renal biopsy, accompanied by hypocomplementemia and bronchiolitis obliterans (BO). Notably, he initially developed acquired cutis laxa (CL) four years before renal dysfunction. Progressive dermatologic manifestations prompted repeat skin biopsies, revealing deposition of γ1 heavy chains, restrictive lambda light chains and complement components (C3, C4 and C1q) along dermal elastic fibers, establishing monoclonal gammopathy of dermatologic significance (MGODS) before systemic involvement. This case illustrates a rare constellation of MGRS, MGODS, and BO in a young adult and provides unique histologic and serologic evidence of classical complement pathway activation. Our findings support a potential immune-mediated mechanism underlying tissue injury in both renal and extrarenal manifestations of monoclonal gammopathy, highlighting the diagnostic value of early tissue biopsy and the importance of complement assessment in such cases.

We report a rare case of coexisting elastosis perforans serpiginosa and acquired cutis laxa in a patient with Wilson's disease following prolonged penicillamine therapy. This represents two rare but important dermatologic complications of long-term chelation therapy that clinicians should be aware of, given the potential for underlying elastin disruption to also affect systemic tissues.

Cutis laxa is a rare connective tissue disorder, characterized by a reduced number and abnormal properties of elastic fibers throughout the dermis, creating a clinical appearance of premature aging. It can be subdivided into inherited and acquired, the latter rarer than the former, and skin involvement may be localized or generalized. The etiology of acquired cutis laxa (ACL) remains unknown and there is no definitive treatment. We present the case of a 30-year-old man diagnosed with type I ACL with progressive systemic involvement at the renal, pulmonary, and digestive levels. Histological analysis of the skin revealed reduction and fragmentation of elastic fibers. Immunosuppressive treatment was started with prednisone, cyclophosphamide, and rituximab, with which a complete response to proteinuria was achieved and the progression of lung damage was limited. Autoimmune, infectious, and neoplastic diseases were ruled out.