Metabolic Syndrome, Central Obesity and Insulin Resistance are Associated with Adverse Pathological Features in Postmenopausal Breast Cancer

Aims: Obesity is associated with both an increased risk of postmenopausal breast cancer and increased mortality rates. The mechanism is unclear, and central (visceral) obesity, insulin resistance, altered sex steroids and altered adipokines are mooted as possible factors. These features may cluster in the so-called metabolic syndrome. The relevance of metabolic syndrome to the biology of breast cancer is unknown, and this was the focus of the present study. Materials and methods: All postmenopausal women with newly diagnosed breast cancer (n = 105) were recruited. A detailed clinical history was carried out, as well as a body composition analysis, metabolic screen and measurement of adipokines and inflammatory markers. Results: The median age was 68 years (40-94 years) and the mean body mass index was 28.3 +/- 5.2 kg/m(2), with 87% of patients centrally obese. Metabolic syndrome was diagnosed in 39% of patients, and was significantly associated with central obesity (P < 0.005) and increased inflammation, with C-reactive protein levels doubling in metabolic syndrome patients compared with non-metabolic syndrome patients (10.3 vs 5.8 mg/l; P = 0.084). Patients with a later pathological stage (II-IV) were significantly more likely to be obese (P = 0.007), centrally obese (P = 0.009), hyperglycaemic (P = 0.047) and hyperinsulinaemic (P = 0.026); 51% had metabolic syndrome compared with 12% for early stage disease. Patients with node-positive disease were significantly more likely to be hyperinsulaemic (P = 0.030) and have metabolic syndrome (P = 0.028) than patients with node-negative disease. Discussion: The data suggest that metabolic syndrome and central obesity are common in postmenopausal breast cancer patients, and that metabolic syndrome may be associated with a more aggressive tumour biology. (C) 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.