J Neurol Surg B Skull Base 2017; 78(S 01): S1-S156
DOI: 10.1055/s-0037-1600540
Oral Presentations
Georg Thieme Verlag KG Stuttgart · New York

Aspirin, Nonsteroidal Anti-inflammatory Drugs and Vestibular Schwannoma Growth

Jacob B. Hunter
1   Vanderbilt University Medical Center, Nashville, Tennessee, United States
,
Brendan P. O'Connell
1   Vanderbilt University Medical Center, Nashville, Tennessee, United States
,
Marc L. Bennett
1   Vanderbilt University Medical Center, Nashville, Tennessee, United States
,
Alejandro Rivas
1   Vanderbilt University Medical Center, Nashville, Tennessee, United States
,
George B. Wanna
1   Vanderbilt University Medical Center, Nashville, Tennessee, United States
,
Reid C. Thompson
1   Vanderbilt University Medical Center, Nashville, Tennessee, United States
,
David S. Haynes
1   Vanderbilt University Medical Center, Nashville, Tennessee, United States
› Author Affiliations
Further Information

Publication History

Publication Date:
02 March 2017 (online)

 

Objective: To investigate whether the use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) impact growth of vestibular schwannoma (VS).

Study Design: Retrospective case series.

Setting: Single academic, tertiary care center.

Patients: Patients with VS who underwent at least two MRI studies prior to intervention.

Intervention(s): Serial MRI studies

Main outcome measure(s): Tumor growth, defined as a ≥2 mm increase in the maximum tumor diameter between consecutive MRI studies, or between the first and last available study.

Results: 548 VS patients met inclusion criteria, with 164 (29.9%) taking some form of aspirin. Both age (p = 0.001) and the presence of diabetes (p = 0.023) were significantly associated with aspirin use. Controlling for patient age and presence of diabetes, aspirin use was not significantly associated with VS tumor growth (p = 0.828). Subset analysis was performed based on aspirin dosage; no significant association between dosage and growth was observed (p = 0.168). In addition, ninety-two patients (17.0%) were taking at least one NSAID, not including aspirin, at the time of clinical presentation. There was no significant difference in the percentage of VS that grew between NSAID users and non-users (p = 0.502). Recognizing that different NSAIDs have different affinities for inhibiting cyclooxygenase-2 (COX-2), we separated NSAIDs into four categories based on COX-2 selectivity, including those patients who took aspirin: high, moderate, poor, and weak. COX-2 selectivity was not significantly associated with VS tumor growth (p = 0.159).

Conclusions: While previous studies have suggested a relationship between aspirin use and VS growth, no significant association was present in our series of 548 observed VS. Furthermore, there was no apparent relationship between VS growth, aspirin dosage, NSAID use and COX-2 selectivity.