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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Antiphospholipid syndrome (APS) is an autoimmune thrombotic disorder characterized by arterial and venous thrombosis in the presence of antiphospholipid antibodies. Bullous pemphigoid (BP) is an autoimmune blistering skin disease that is rarely associated with APS. Catastrophic antiphospholipid syndrome (CAPS) is a life-threatening form of APS marked by rapidly developing multiorgan thromboses. We report a case of CAPS triggered by BP in a patient with long-standing primary APS.
A 64-year-old man with a history of chronic disseminated intravascular coagulation due to aortic dissection, deep vein thrombosis, and cerebral infarction had developed nephrotic syndrome 11 years earlier. Renal biopsy and positive antiphospholipid antibodies confirmed primary APS, and plasma exchange, corticosteroids, warfarin, and antiplatelet therapy improved renal function from a serum creatinine level of 4.0 mg/dL to 2.0 mg/dL with long-term stability.
Five months before admission, he developed generalized bullae and was diagnosed with BP based on an elevated BP180 antibody titer (5760 U/mL). The lesions improved with minocycline, nicotinamide, and prednisolone, and the antibody titer decreased to 1200 U/mL. One week before admission, bullous lesions and inflammation recurred (CRP 10.84 mg/dL). He was hospitalized and treated with vancomycin, meropenem, intravenous immunoglobulin, and methylprednisolone (40 mg/day), which led to temporary improvement.
On hospital day 14, inflammation worsened again, accompanied by melena and coagulopathy with a prolonged PT-INR. Endoscopy revealed bleeding gastric and duodenal ulcers with fragile esophageal mucosa. Warfarin was discontinued, and endoscopic clipping was performed, but melena persisted. Despite transfusions, hemorrhagic shock developed, and he died on hospital day 21. Autopsy revealed widespread thrombi not only in the gastrointestinal tract but also in multiple systemic organs, leading to the diagnosis of catastrophic antiphospholipid syndrome (CAPS) complicated by gastrointestinal bleeding.
In patients with APS who present with complex conditions such as severe bleeding or concomitant autoimmune diseases like bullous pemphigoid, CAPS should be considered in the differential diagnosis. Even when the clinical presentation is dominated by bleeding or inflammation, early initiation of plasma exchange therapy may be essential to prevent fatal thrombotic complications.
