OBJECTIVE: To report the serial development of oral mucositis following infusion of bevacizumab in a young woman with a malignant brain tumor and history of cutaneous psoriasis. CASE SUMMARY: A 29-year-old woman with a history of active cutaneous psoriasis and a malignant glioneuronal tumor was treated with bevacizumab for 2.5 years. With each infusion of bevacizumab, she developed oral mucositis within 36 hours. She received temozolomide as part of concurrent therapy with radiation and as maintenance therapy; it was discontinued after continuous therapy for 1.5 years. Bevacizumab 10 mg/kg was added after 7 cycles of maintenance temozolomide, as the tumor had minimal response and evidence of increased perfusion with angiogenesis on imaging studies. All medication, including temozolomide, was evaluated and eventually discontinued, with the exception of bevacizumab, which remained the drug suspected of causing the mucositis. DISCUSSION: Oral mucositis is a frequent adverse effect of cytotoxic chemotherapy, but has not been reported with bevacizumab. The Naranjo probability scale indicated a probable adverse drug reaction. This likely indicates that bevacizumab is one of many drugs known to induce exacerbation of psoriatic disease. We speculate that oral mucositis developed as bevacizumab-induced generation of proinflammatory cytokines within the vascular endothelium, leading to mucosal damage and ulceration. In addition, interruption of reparative angiogenic pathways with bevacizumab likely contributed to the severity of mucositis. CONCLUSIONS: Clinicians should be aware that bevacizumab can potentially exacerbate psoriatic disease.
OBJECTIVE: To report the serial development of oral mucositis following infusion of bevacizumab in a young woman with a malignant brain tumor and history of cutaneous psoriasis. CASE SUMMARY: A 29-year-old woman with a history of active cutaneous psoriasis and a malignant glioneuronal tumor was treated with bevacizumab for 2.5 years. With each infusion of bevacizumab, she developed oral mucositis within 36 hours. She received temozolomide as part of concurrent therapy with radiation and as maintenance therapy; it was discontinued after continuous therapy for 1.5 years. Bevacizumab 10 mg/kg was added after 7 cycles of maintenance temozolomide, as the tumor had minimal response and evidence of increased perfusion with angiogenesis on imaging studies. All medication, including temozolomide, was evaluated and eventually discontinued, with the exception of bevacizumab, which remained the drug suspected of causing the mucositis. DISCUSSION: Oral mucositis is a frequent adverse effect of cytotoxic chemotherapy, but has not been reported with bevacizumab. The Naranjo probability scale indicated a probable adverse drug reaction. This likely indicates that bevacizumab is one of many drugs known to induce exacerbation of psoriatic disease. We speculate that oral mucositis developed as bevacizumab-induced generation of proinflammatory cytokines within the vascular endothelium, leading to mucosal damage and ulceration. In addition, interruption of reparative angiogenic pathways with bevacizumab likely contributed to the severity of mucositis. CONCLUSIONS: Clinicians should be aware that bevacizumab can potentially exacerbate psoriatic disease.