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Asia induced by hyaluronic acid, tattoos, hyaluronidase and polypropylene mesh
Olga Vera-Lastra1, Javier Juárez Medrano2, Brayan Assael Carrasco Pérez3
1Departamento de Medicina Interna, Unidad Médica de Alta Especialidad, Hospital de Especialidades Dr. Antonio Fraga Mouret, Centro Médico Nacional, "La Raza", Instituto Mexicano del Seguro Social, Mexico; División de Estudios de Posgrado, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico.
Abstract:
The growing use of cosmetic fillers, tattoos, and surgical meshes has brought increasing attention to their potential inflammatory and immunologic complications. Autoimmune/inflammatory syndrome induced by adjuvants (ASIA) proposes a framework for systemic manifestations reported after exposure to these materials in susceptible individuals. Although hyaluronic acid is a natural component of the extracellular matrix with low immunogenicity and high biocompatibility, Hyaluronic acid fillers (HAF) have been associated with delayed inflammatory and granulomatous foreign-body reactions, and ASIA. Treatment includes corticosteroids and immunosuppressive (IS) agents and hyaluronidase which dissolves injected HAF, but it can cause allergic reactions. Tattoo pigments may provide a persistent immunological stimulus. Proposed mechanisms include cytokine-mediated immune activation, oxidative stress, and the release of nuclear antigens that may promote autoantibody production. Reported manifestations range from local inflammatory reactions to uveitis, sarcoidosis, and systemic autoimmune conditions. Treatment includes corticoids, IS, pigment removal and Lasser may be considered in selected cases. Similarly, Polypropylene Mesh (PPM) used in hernia and pelvic organ prolapse repair induces a persistent foreign-body response. Selected clinical reports describe ASIA-like manifestations after implantation, but population-based studies have not demonstrated an increased risk of defined systemic autoimmune disease. Across these exposures, delayed symptom onset, nonspecific manifestations, and the absence of a specific biomarker complicate diagnosis and causal attribution. Early recognition requires careful assessment of exposure history, local and systemic findings, and alternative diagnoses. Distinguishing established local complications from suspected systemic ASIA is essential to guide individualized treatment, while further controlled studies are needed to clarify causality and therapeutic outcomes.