In our study, TVAT was confirmed to be a prognostic risk factor that reached statistical significance. Although the median OS not reached in non-sarcopenic and sarcopenic patients, the non-sarcopenic patients had a trend to better OS. BMI status of the patients was not different in terms of OS, although a non-significant trend was favoring normal weighed patients. In patients younger than 40 years, TVAT may be a better prognostic factor than TSI due to healthy muscle structure.
In chronic conditions, decreased muscle volume was shown to be related to poor prognosis rather than obesity and fat, especially in metabolic diseases. The role of the potential role of the muscle catabolism in disease physiopathology is still under investigation.[26, 27] Sarcopenia is a frequent phenomenon in cancer patients which is also related to poor survival.[28–31]
The frequently studied parameter in breast cancer patients is body mass index (BMI), which is calculated as weight in kilograms divided by height in squared meters. for. In patients with class 2 or 3 obesity (BMI > 35) survival found to be worse control groups in a pooled analysis. The lower levels of obesity had conflicting results in several studies.[32–34]
The literature was evaluating sarcopenia and TVAT in breast cancer mainly composed of metastatic and adjuvant studies. Although multiple studies designed to evaluate the prognostic value of body composition in breast cancer, to our knowledge, our study is the first for young breast cancer patients.
Bette et al. reported sarcopenia was a better prognostic indicator than visceral adiposity. Low muscle volume related to decreased survival and considered to be a better marker than BMI. Although this trial had the largest patient number, the age factor cut-off was determined as 55 years, which was inaccurate for young breast cancer. Also, the proportion of the young breast cancers was not specified.
Five studies only reported the prognostic effect of sarcopenia in breast cancer. Three studies were designed in a metastatic patient group while two studies composed by non-metastatic patients.[18, 20–23] Only one of these studies demonstrated an increased risk of death in sarcopenic patients. In another study, which reported sarcopenia to have a relation with over-all mortality in non-metastatic breast cancer patients, had a small number of events and evaluated TSI after chemotherapy. Also, the composition of the muscle reported being an important factor in over-all mortality. Rier et al. found low muscle radiodensity was associated with increased overall mortality in the metastatic state. This finding was speculated to be related to inflammatory conditions, and immune system were supported by more trials.[36–38]
One previous study reported a relationship between mortality and muscle density in metastatic patients in terms of very low mean cut-off value when compared with non-metastatic patients.[21, 35] The difference was hypothesized for the accumulation of fat tissue among muscles with the increased stage and disease burden, which also explained the difference in the cut-off value of muscle density in these populations.
Our study had compatible results with earlier studies in terms of visceral adiposity. Three previous studies reported decreased distant disease-free and overall survival in locally advanced breast cancer in patients with high visceral adiposity.[18, 19, 35] Even TVAT was found to be an independent risk factor in our study for young breast cancer patients, it may be more important in the de-novo metastatic population.
Although other studies had young patient populations, our study specifically designed to investigate the body composition of young breast cancer to avoid the change in time via life-style changes and co-morbidities. The effect of muscle tissue on prognosis may be lesser important than adipose tissue in young breast cancers.
The cross-sectional design of the study had limitations to evaluate patient characteristics. All CT or PET-CT images gathered at the time of diagnosis, which may have a difference between de-novo metastatic and recurrent patients. Also, the small patient population does not allow subgroup analysis for recurrent or de-novo metastatic patients. Small numbers of recurrences do not allow disease-free survival analysis. The effect of lifestyle interventions, tolerance of adjuvant treatment, and toxicity profiles cannot be evaluated due to the retrospective design of the study.