DOI: 10.1093/bjd/ljag086.054 ISSN: 0007-0963

P027 An unusual cause of forearm discoloration and swelling in a patient with chronic lymphocytic leukaemia

Supriya Sharma, Clemency Britton, Nikita Cliff-Patel

Abstract

An 89-year-old man with chronic lymphocytic leukaemia diagnosed in 2017, stable on the Bruton tyrosine kinase inhibitor acalabrutinib since 2021, was referred with progressive purple–brown discoloration of both forearms and marked swelling of the right arm. The discoloration began on the right forearm 2 years earlier and gradually spread circumferentially. In February 2025 he developed sudden-onset, pitting swelling of the right forearm and hand, which improved with elevation. Over subsequent months, similar discoloration appeared on the left forearm without swelling. There was no history of trauma or infection. Examination showed striking violaceous–brown discoloration of both forearms with a sharp proximal cutoff; the right forearm and hand were markedly swollen and indurated. There was associated lower-limb oedema but no palpable lymphadenopathy. Duplex ultrasonography excluded upper-limb deep-vein thrombosis. Computed tomography of the neck, chest, abdomen and pelvis demonstrated extensive subcutaneous oedema of the distal right forearm and hand without venous or lymphatic obstruction or disease progression. Given the clinical appearance in the context of malignancy and suspected lymphoedema, lymphangiosarcoma was a major concern. A deep incisional biopsy of the right forearm and a punch biopsy of the left forearm were performed. Both showed florid dermal oedema, extensive red blood cell extravasation with conspicuous haemosiderin deposition and a mild perivascular inflammatory infiltrate, without vascular proliferation or malignancy. Bruton tyrosine kinase inhibitors are known to cause bleeding and bruising through effects on platelet signalling and vascular integrity. The case was discussed in a clinicopathological meeting, where the findings were felt to represent a drug-related vasculopathic process with secondary lymphatic dysfunction rather than malignancy. Management was conservative with limb elevation and lymphoedema support, and acalabrutinib was subsequently discontinued and switched to zanubrutinib. This case highlights a striking clinicopathological mimic of angiosarcoma and underscores the importance of clinicopathological correlation in patients receiving targeted therapies.

More from our Archive