Search

BACKGROUND: Proteinuria is a common adverse event of vascular endothelial growth factor (VEGF) inhibitors. It is unclear, however, whether proteinuria has an adverse effect on treatment course and increases treatment discontinuation in a real-world setting. OBJECTIVES: To describe our experience with proteinuria in patients receiving VEGF inhibitor therapy in a real-world community setting and provide a review of literature related to VEGF inhibition--induced proteinuria. METHODS: A retrospective analysis was conducted of 139 adults receiving treatment with a VEGF inhibitor (bevacizumab or an oral tyrosine kinase inhibitor). Patients were assessed to describe new or worsening proteinuria and its impact on the course of therapy (rates of withholding therapy, treatment discontinuation) and adverse events. RESULTS: Proteinuria occurred or worsened in 78 (56%) patients, and nonsteroidal anti-inflammatory drug (NSAID) use was more common in this group than in patients without proteinuria (42% vs 23%, respectively; P=.017). The patients with proteinuria had a longer duration of therapy (8.2 months vs 3.9 months for patients without proteinuria; P=.005) and had similar discontinuation rates as a result of documented adverse events (12% vs 23%; P=.072). The effects on serum creatinine and blood pressure were comparable between groups. The patients who had proteinuria ≥2+ were more likely than those with no or less severe proteinuria to have treatment withheld (59% vs 36%, respectively; P=.02), but treatment discontinuation as a result of documented adverse events remained similar between the patients with and without ≥2+ proteinuria (9% vs 19%, respectively; P=.163). CONCLUSION: Proteinuria resulting from VEGF pathway inhibitor therapy does not have an adverse impact on treatment course and does not increase treatment discontinuation as a result of adverse events. The study data support previous evidence that advocates for a possible decrease in the frequency of urine protein monitoring with bevacizumab treatment. Further exploration of the potential impact of NSAIDs on having proteinuria is necessary to help inform therapy. [ABSTRACT FROM AUTHOR]

Purpose: A case of embolia cutis medicamentosa (Nicolau syndrome) in a patient receiving monthly intramuscular fulvestrant injections is presented. Summary: An 85-year-old woman receiving monthly fulvestrant injections in the outpatient setting developed a necrotic lesion at the fulvestrant injection site on her right buttock. Her medical history is notable for metastatic breast cancer with bone metastases. Prior to developing the necrotic lesion, the patient was receiving monthly fulvestrant injections for 6 years. Other potential causes such as infection and pressure necrosis were ruled out clinically. After 185 days of wound care involving multiple surgical debridements, topical therapy, and frequent follow-up appointments, the patient's wound resolved with 100% epithelialization. Nicolau syndrome has been reported with other non-vesicant, injectable medications such as antibiotics and corticosteroids; however, it has not been previously reported with fulvestrant. Conclusion: Nicolau syndrome developed in the right buttock of a patient with metastatic breast cancer following an intramuscular fulvestrant injection. Healthcare practitioners need to be cognizant of this adverse effect with intramuscular injections in order to recognize and refer patients for wound care evaluation early in the evolution of this syndrome. Proper injection technique is recommended to reduce the risk of this idiopathic adverse effect. [ABSTRACT FROM AUTHOR]

Background: Vascular endothelial growth factor (VEGF) inhibitors are known to cause hypertension. The purpose of this study was to assess the impact of blood pressure (BP) elevations on outcomes in patients receiving VEGF inhibitors. Methods: This retrospective chart review analyzed patients receiving treatment with VEGF inhibitors. The primary endpoint was time to progression (TTP) in those with or without significant increase in BP (increase in systolic BP greater than 20 mm Hg or greater than 10 mm Hg increase in diastolic BP). Secondary endpoints included treatment interruption, therapy discontinuation due to documented adverse effect, and time to BP elevation. Subgroup analyses were completed in those receiving bevacizumab and oral tyrosine kinase inhibitors. Results: A total of 155 patients were included and 93 patients (60%) experienced a significant increase in BP. Median time to development of an elevated BP was 47 days. Patients with significant increases in BP had a longer median TTP compared to patients without (8.1 months vs 4.4 months, p = 0.002). No differences were present between groups in treatment interruption or discontinuation due to a documented adverse effect and outcomes were similar in those receiving bevacizumab and oral tyrosine kinase inhibitors. In the analysis of the impact of severity of BP elevations, those with severe BP elevations were more likely to have treatment interrupted but discontinuation rates were similar across groups. Conclusion: Development of significant BP elevations may be a marker of therapeutic response to VEGF inhibitors and does not limit treatment duration, even in those with severe elevations. [ABSTRACT FROM AUTHOR]