Cutaneous leukocytoclastic vasculitis in a patient treated with carboplatin for uterine carcinoma

Abstract

Cutaneous leukocytoclastic vasculitis (LCV) is a histopathological term used to refer to in lammation of the small vessels, including arterioles, capillaries and postcapillary venules, in the skin. The main morphological features of LCV are fibrinoid necrosis of the vessel wall with mainly neutrophilic infiltration and leukocytoclasis. LCV can be idiopathic or triggered by several causes, such as medications, underlying infection and malignancies. IgA vasculitis is a type of LCV with IgA-dominant immune deposits in the vascular wall. We report a rare case of skin-limited IgA vasculitis a ter treatment with carboplatin in a patient with uterine cancer. To our knowledge, this is the first reported case of LCV (in our case, skin-limited IgA vasculitis) connected to carboplatin treatment. A 57-year-old patient with uterine carcinoma was treated with surgery. A terwards, she received postoperative chemotherapy with pegylated liposomal doxorubicin (PLD) in combination with carboplatin. When the disease progressed, the patient received carboplatin monotherapy; a ter the third round of carboplatin therapy, she developed IgA vasculitis of the skin without systemic involvement. Chemotherapy with carboplatin was discontinued. She was treated symptomatically, and a ter six months, the skin lesions resolved and had not reappeared as of her last visit. Carboplatin can induce LCV, and clinicians should be aware of this potential e fect for the proper management of a fected patients.

DKC1 aggravates gastric cancer cell migration and invasion through up-regulating the expression of TNFAIP6

“…TNFα-stimulated gene-6 (TNFAIP6), also known as TSG6, is a member of the hyaluronic acid–binding protein family and exhibits a pivotal role in the protease network associated with inflammation (Evrard et al 2021 ; Yu et al 2016 ; Rajer et al 2021 ). TNFAIP6 has been also joined in extracellular matrix (ECM) remodeling, cell adhesion, and migration to regulate cancer progression.…”