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Journal of Clinical Oncology, Vol 23, No 10 (April 1), 2005: pp. 2434-2435
© 2005 American Society of Clinical Oncology.
DOI: 10.1200/JCO.2005.05.890

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CORRESPONDENCE

Elevated Body Mass Index Predicts for Longer Overall Survival Duration in Men With Metastatic Hormone-Refractory Prostate Cancer

Susan Halabi

Department of Biostatistics and Bioinformatics and CALGB Statistical Center, Durham, NC

Eric J. Small

Urologic Oncology Program, University of California at San Francisco, San Francisco, CA

Nicholas J. Vogelzang

Nevada Cancer Institute, Las Vegas, NV

To the Editor:

In recent articles, Amling et al1 and Freedland et al2 reported that an elevated body mass index (BMI) is associated with an elevated risk of biochemical failure in hormone-sensitive patients. Further, in an analysis of 1,681 deaths from prostate cancer, Calle et al3 found a statistically significant linear trend in mortality with elevated BMI. We asked the question as to whether an elevated BMI also predicts for shorter overall survival among 1,216 men with hormone-refractory prostate cancer enrolled on eight clinical trials conducted by the Cancer and Leukemia Group B (CALGB).

Data on eight multicenter clinical trials conducted by CALGB between 1992 to 2002 were pooled.4 The patient population consisted of men with prostate cancer who had progressive disease who had failed at a minimum both androgen deprivation therapy and antiandrogen withdrawal. Eligible patients had progressive prostate cancer during androgen deprivation therapy (with documented castrate levels of testosterone), an Eastern Cooperative Oncology Group (ECOG) performance status of 0 to 2, and adequate hematologic, renal, and hepatic functions.

We have used the definition of the National Institutes of Health for classifying patients as: normal (< 25 kg/m2), overweight (25 to 29 kg/m2), mildly obese (30 to 34 kg/m2), and moderately to severely obese (≥ 35 kg/m2). The proportional hazards model was used to explore the prognostic significance of BMI as both a categorical and a continuous factor.

Among the 1,216 patients, 45% had a Gleason sum of 8 or higher, and the median age was 71 years. Thirty-five percent of patients had measurable disease, and 89% had an ECOG performance status of 0 to 1. The median BMI was 27.7 kg/m2 (interquartile range, 25.2 to 31.0 kg/m2). Twenty three percent (281 of 1,216) of the patients had normal BMI, 46% (563 of 1,216) had overweight BMI, 22.9% (278 of 1,216) had mild obesity, and 7.7% (94 of 1,216) were moderately and severely obese (≥ 35 kg/m2).

In univariate analysis, BMI was a statistically significant predictor of overall survival. The median survival times were: 10.6 months for normal patients (95% CI, 8.32 to 12.16), 14.3 for overweight men (95% CI, 13.4 to 16.1), 15.4 for mildly obese men (95% CI, 13.5 to 18.0), and 17.0 months (95% CI, 14.0 to 21.49; log-rank P < .001) for moderately to severely obese men. The hazard ratio (HR) was 0.97 (95% CI, 0.96 to 0.98; P < .001). When BMI was considered as a categorical variable, compared with men with normal BMI, the HRs of overweight men were 0.72 (95% CI, 0.62 to 0.84; P < .0001); for mildly obese patients, 0.69 (95% CI, 0.58 to 0.83; P < .0001); and for moderately and severely obese men, 0.58 (95% CI, 0.45 to 0.76; P < .0001). In multivariate analysis adjusting for race, performance status, hemoglobin, prostate-specific antigen, lactate dehydrogenase, alkaline phosphatase, and Gleason scores, BMI remains a statistically significant predictor of overall survival. Compared with men with normal BMI, the adjusted HRs of overweight patients were 0.78 (95% CI, 0.66 to 0.91; P < .001); for mildly obese patients, 0.85 (95% CI, 0.71 to 1.02; P < .082); and for moderately to severely obese men, 0.58 (95% CI, 0.45 to 0.76; P < .0001). Thus, contrary to our initial hypothesis, an elevated BMI predicts for longer overall survival. One obvious hypothesis for this observation is that men with the most advanced cancer have cachexia, resulting in weight loss and possibly height loss, and a "normal BMI." Patients with less advanced cancer continue to have a normal appetite and maintain their basal (and often elevated) BMI. Regardless of the explanation, our findings confirm an impact of obesity on the behavior of human prostate cancer. Investigating the mechanism(s) by which obesity affects the growth of human cancer seems to be a fruitful area of research.

Authors' Disclosures of Potential Conflicts of Interest

The authors indicated no potential conflicts of interest.

REFERENCES

1. Amling CL, Riffenburgh RH, Sun L, et al: Pathological variables and recurrence rates as related to obesity and race in men with prostate cancer undergoing radical prostatectomy. J Clin Oncol 22:439-445, 2004[Abstract/Free Full Text]

2. Freedland SJ, Aronson WJ, Kane CJ, et al: Impact of obesity on biochemical control after radical prostatectomy for clinically localized prostate cancer: A report by the Shared Equal Access Regional Cancer Hospital Database Study Group. J Clin Oncol 22:446-453, 2004[Abstract/Free Full Text]

3. Calle EE, Rodriguez C, Walker-Thurmond K, et al: Overweight, obesity, and mortality from cancer in s prospectively studies cohort of U.S. adults. N Engl J Med 348:1625-1638, 2003[Abstract/Free Full Text]

4. Halabi S, Small EJ, Kantoff PW, et al: A prognostic model for predicting overall survival in men with advanced prostate cancer. J Clin Oncol 21:1232, 2003[Abstract/Free Full Text]


Related Reply

  • In Reply:
    Stephen Freedland
    JCO 2005 23: 2435 [Full Text]



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