An Eicosapentaenoic Acid Supplement Versus Megestrol Acetate Versus Both for Patients With Cancer-Associated Wasting: A North Central Cancer Treatment Group and National Cancer Institute of Canada Collaborative Effort

2004 ◽  
Vol 22 (12) ◽  
pp. 2469-2476 ◽  
Author(s):  
Aminah Jatoi ◽  
Kendrith Rowland ◽  
Charles L. Loprinzi ◽  
Jeff A. Sloan ◽  
Shaker R. Dakhil ◽  
...  

Purpose Studies suggest eicosapentaenoic acid (EPA), an omega-3 fatty acid, augments weight, appetite, and survival in cancer-associated wasting. This study determined whether an EPA supplement—administered alone or with megestrol acetate (MA)—was more effective than MA. Patients and Methods Four hundred twenty-one assessable patients with cancer-associated wasting were randomly assigned to an EPA supplement 1.09 g administered bid plus placebo; MA liquid suspension 600 mg/d plus an isocaloric, isonitrogenous supplement administered twice a day; or both. Eligible patients reported a 5-lb, 2-month weight loss and/or intake of less than 20 calories/kg/d. Results A smaller percentage taking the EPA supplement gained ≥ 10% of baseline weight compared with those taking MA: 6% v 18%, respectively (P = .004). Combination therapy resulted in weight gain of ≥ 10% in 11% of patients (P = .17 across all arms). The percentage of patients with appetite improvement (North Central Cancer Treatment Group Questionnaire) was not statistically different: 63%, 69%, and 66%, in EPA-, MA-, and combination-treated arms, respectively (P = .69). In contrast, 4-week Functional Assessment of Anorexia/Cachexia Therapy scores suggested MA-containing arms experienced superior appetite stimulation compared with the EPA arm, with scores of 40, 55, and 55 in EPA-, MA-, and combination-treated arms, respectively (P = .004). Survival was not significantly different among arms. Global quality of life was not significantly different among groups. With the exception of increased impotence in MA-treated patients, toxicity was comparable. Conclusion This EPA supplement, either alone or in combination with MA, does not improve weight or appetite better than MA alone.

2002 ◽  
Vol 10 (1) ◽  
pp. 71-75 ◽  
Author(s):  
Aminah Jatoi ◽  
Jun-ichi Yamashita ◽  
Jeff A. Sloan ◽  
Paul J. Novotny ◽  
Harold E. Windschitl ◽  
...  

2005 ◽  
Vol 23 (5) ◽  
pp. 495-503 ◽  
Author(s):  
Evanthia Galanis ◽  
Jan C. Buckner ◽  
Matthew J. Maurer ◽  
Joel M. Reid ◽  
Mary J. Kuffel ◽  
...  

2007 ◽  
Vol 38 (2-4) ◽  
pp. 87-94 ◽  
Author(s):  
Steven R. Alberts ◽  
Jonathan R. Sande ◽  
Nathan R. Foster ◽  
Fernando J. Quevedo ◽  
Robert R. McWilliams ◽  
...  

2010 ◽  
Vol 28 (18) ◽  
pp. 3002-3007 ◽  
Author(s):  
Shauna L. Hillman ◽  
Sumithra J. Mandrekar ◽  
Brian Bot ◽  
Ronald P. DeMatteo ◽  
Edith A. Perez ◽  
...  

Purpose In March 1998, Common Toxicity Criteria (CTC) version 2.0 introduced the collection of attribution of adverse events (AEs) to study drug. We investigate whether attribution adds value to the interpretation of AE data. Patients and Methods Patients in the placebo arm of two phase III trials—North Central Cancer Treatment Group Trial 97-24-51 (carboxyamino-triazole v placebo in advanced non–small-cell lung cancer) and American College of Surgeons Oncology Group Trial Z9001 (imatinib mesylate v placebo after resection of primary gastrointestinal stromal tumors)—were studied. Attribution was categorized as unrelated (not related or unlikely) and related (possible, probable, or definite). Results In total, 398 patients (84 from Trial 97-24-51 and 314 from Trial Z9001) and 7,736 AEs were included; 47% and 50% of the placebo-arm AEs, respectively, were reported as related. When the same AE was reported in the same patient on multiple visits, the attribution category changed at least once 36% and 31% of the time. AE type and sex (Trial Z9001) and AE type and performance status (Trial 97-24-51) were associated with a higher likelihood of AEs being deemed related. Conclusion Nearly 50% of AEs were reported as attributed to study drug on the placebo arm of two randomized clinical trials. These data provide strong evidence that AE attribution is difficult to determine, unreliable, and of questionable value in interpreting AE data in randomized clinical trials.


Cancer ◽  
2018 ◽  
Vol 124 (7) ◽  
pp. 1455-1463 ◽  
Author(s):  
David Schiff ◽  
Kurt A. Jaeckle ◽  
S. Keith Anderson ◽  
Evanthia Galanis ◽  
Caterina Giannini ◽  
...  

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