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Myalgias and Arthralgias Associated With Paclitaxel

Paclitaxel-induced myalgias and arthralgias occur in a significantfraction of patients receiving therapy with this taxane, potentiallyimpairing physical function and quality of life. Paclitaxel-inducedmyalgias and arthralgias are related to individual doses; associationswith the cumulative dose and infusion duration are less clear. Identificationof risk factors for myalgias and arthralgias could distinguisha group of patients at greater risk, leading to minimization of myalgiasand arthralgias through the use of preventive therapies. Optimalpharmacologic treatment and possibilities for the prevention of myalgiasand arthralgias associated with paclitaxel are unclear, partially dueto the small number of patients treated with any one medication. Theeffectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) is themost frequently documented pharmacologic intervention, although noclear choice exists for patients who fail to respond to NSAIDs. However,the increasing use of weekly paclitaxel could necessitate daily administrationof NSAIDs for myalgias and arthralgias and leave patients at riskfor adverse effects. This concern may also limit the use of corticosteroidsfor the prevention and treatment of paclitaxel-induced myalgias andarthralgias. Data from case reports suggest that gabapentin (Neurontin),glutamine, and, potentially, antihistamines (eg, fexofenadine [Allegra])could be used to treat and/or prevent myalgias and arthralgias. Giventhe safety profile of these medications, considerable enthusiasm existsfor evaluating their effectiveness in the prevention and treatment ofpaclitaxel myalgias and arthralgias, particularly in the setting ofweekly paclitaxel administration.

Latest Article

Association Between the Rates of Synchronous and Metachronous Metastases: Analysis of SEER Data

Patients with cancer are usually staged based on the presence of detectable regional and/or distant disease. However, staging is inexact and cM0 patients may have microscopic metastases (cM0pM1) that later cause relapse and death. Since the clinical tools used to stage patients are fairly similar for different tumors, the ratio of the rates of metachronous to synchronous metastases should be similar for different tumors (hypothesis #1). Improvements in diagnostic tools should have caused the ratio of metachronous-to-synchronous metastases to have decreased over time (hypothesis #2). Finally, the fraction of patients with either metachronous or synchronous metastases should have declined over time due to increased screening and earlier diagnoses (hypothesis #3). To test these hypotheses, Surveillance, Epidemiology, and End Results (SEER) data from 1973-1998 were analyzed for 19 solid tumors. A linear relationship was seen between the rates of metachronous and synchronous metastases, with modestly strong correlation coefficients, consistent with hypothesis #1. Over time, changes in staging methods have not significantly altered the ratio of metachronous/synchronous metastases, contrary to hypothesis #2. Also over time, a decrease in the number of patients with metastases was found, consistent with hypothesis #3. Therefore, the rate of anticipated metachronous metastases can be estimated from the rate of clinically evident metastases at presentation. Changes in screening/staging of disease over time may have reduced the overall fraction of patients with metastases.