Increased Incidence of Metabolic Syndrome after Hematopoietic Stem Cell Transplantation.

Metabolic syndrome (MS), formerly known as X-syndrome, is a clinical and laboratory entity involving obesity, hypertension, and borderline fasting glucose, high triglyceride and low HDL cholesterol levels, that is considered to be a counterpart of insulin resistance with overweight playing a key role; increased insulin, leptin, adiponectin and resistin levels link its various features and some common flanking findings such as hypercholesterolemia, hyperuricemia and hyperferritinemia. Clinical and laboratory data reminiscent of metabolic syndrome are commonly observed after hematopoietic stem cell transplantation (HSCT). We evaluated the body mass index (BMI), routine lipid and glucidic markers, and common endocrinologic parameters in 37 HSCT recipients (19 males; median age 45 years, range 26–60; 22 autologous, 15 allogeneic) whose continuous CR lasted at least five years; insulin (baseline and after an oral glucose test), leptin, resistin, TNF-alpha and adiponectin levels were also detemined. Diabetic HSCT recipients were excluded. The control group consisted of 23 healthy volunteers of comparable age and sex without a family history of diabetes. In comparison with the controls, the HSCT recipients had significantly increased levels of TNF (median 10.05 vs 9.3 pg/mL, p=0.034), insulin (13.6 vs 10.1 mIU/mL, p=0.029) and leptin (13.71 vs 3.69 ng/mL, p= 0.02); there were no significant differences in adiponectin and resistin levels, BMI or the other considered parameters. In comparison with the other HSCT recipients, the 16 patients with higher baseline insulin levels (>15 mIU/mL) had significantly higher leptin levels (median 23.665 vs 8.3, p<0.001), and also different total cholesterol (231 vs 202 mg/dL, p<0.01), HDL-cholesterol (58 vs 68 mg/dL, p<0.01), triglyceride (150 vs 92 mg/dL, p<0.01) and ferritin levels (635 vs 491 ng/mL, p<0.01). This preliminary investigation show an increased prevalence of MS findings in HSCT recipients, and a relationship between baseline insulin levels and some common laboratory features of MS. Unlike in spontaneously occurring cases, obesity does not seem to play a primary role; furthermore, BMI and adiponectin were not significantly increased. However, the significant increase in TNF (another inducer of insulin resistance) suggests a possible pathogenetic sequence of post-HSCT MS linking TNF, insulin and leptin. The association between MS and the development of cardiovascular diseases is well known, but HSCT may, in alternative ways, induce a long-term metabolic derangement that affects the life expectancy of patients already cured of their baseline neoplastic disease.