Immune thrombocytopenia (ITP) - could it be part of autoimmune/inflammatory syndrome induced by adjuvants (ASIA)?

Immune thrombocytopenia (ITP) is a complex autoimmune disorder characterized by thrombocytopenia and an increased bleeding risk, arising from autoantibody-mediated platelet destruction and impaired megakaryocyte function. The pathogenesis of ITP involves a multifaceted interplay of genetic predispositions, immune dysregulation, and environmental triggers, though the precise mechanisms remain uncertain. Several infectious agents, mostly viruses, have been implicated in both acute and chronic ITP through mechanisms such as molecular mimicry, direct bone marrow suppression, and immune dysregulation. Vaccinations, particularly those containing adjuvants like aluminum and those capable of inducing molecular mimicry, have also been associated with ITP, either as a new onset or as a relapse in preexisting cases. The role of drugs, particularly quinine, quinidine and certain antibiotics, in inducing ITP through various immunological pathways further illustrates the diverse etiologies of this condition. The multiple triggers of the disease raise the question of whether ITP may be classified as an autoimmune/inflammatory syndrome induced by adjuvants (ASIA). This condition encompasses a range of autoimmune and inflammatory symptoms triggered by adjuvants, such as silicones, polypropylene meshes, metal implants, and mineral oils present in various medical materials and medications. Similar to that observed in some cases of ITP, adjuvants can trigger autoimmune or autoinflammatory responses via molecular mimicry, epitope spreading, and polyclonal activation. This narrative review explores the underlying environmental factors related to ITP and examines ITP triggers that could potentially support an association between ITP and ASIA syndrome.

Should we be targeting type 1 interferons in antiphospholipid syndrome?

Systemic autoimmune diseases are characterized by increased production of type I interferon (IFN-1) and upregulation of IFN-1-inducible genes, suggesting an important role of the IFN-1 pathway in their pathogenesis. Recent studies have demonstrated increased IFN-1 expression in both primary and secondary antiphospholipid syndrome (APS), along with increased toll-like receptor type 9 activity and plasmacytoid dendritic cell function. The increasing knowledge of the association between IFN-1 and APS pathology may provide a rationale for conducting clinical trials to assess the efficacy of IFN-1-targeting drugs in reducing APS-related complications. In this narrative review, we summarize the current knowledge on the role of IFN-1 in APS pathogenesis, explore its clinical implications, and examine the existing evidence regarding therapeutic options that have been investigated to date.