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Available studies on metabolic syndrome (MS) after hematopoietic stem cell transplantation (HSCT) are retrospective with heterogeneous inclusion criteria, and little is known about the early post-transplant phase. In our prospective study, clinical and laboratory data were collected in 100 HSCT recipients, 48 allogeneic and 52 autologous, at baseline, at + 30, + 100 and + 360 days. At baseline, MS was observed in 24 patients, significantly associated with insulin resistance and leptin on multivariate analysis. At + 30, the diagnosis of MS was confirmed in 43 patients, significantly related to insulin resistance and allogeneic transplants. If the whole series was considered, patients with MS had significantly higher mortality from any cause. The baseline presence of any MS feature was a predictor of + 30 MS. Isolated occurrences of MS features were related to hyperleptinemia and hyperinsulinemia, except in the case of low HDL cholesterol, linked to adiponectin and resistin. Our data confirm that patients undergoing HSCT have a high prevalence of MS, with hyperleptinemia playing a major role. The early peak of new MS cases is primarily attributable to insulin resistance, notably but not exclusively immunosuppression-induced; the subsequent long-term increase in MS cases may be an effect of persistent adipokine imbalance.

Background: Hematopoietic stem cell transplantation (HSCT) is used in the treatment of several hematological and non-hematological disorders. An increasing number of long-term survivors recover from their primary disease, but they are at risk of adverse late effects, including metabolic syndrome (MS), which seems to be common in long-term survivors of HSCT., Aim: To compare common metabolic parameters and adipohormone profiles in post-transplant and spontaneously occurring or "classic" MS patients., Subjects and Methods: Post-transplant MS patients (15 women and 14 men; 49.8±9.3 yr) were compared to "classic" MS patients (15 women and 14 men; 52.9±8.0 yr). For each subject a record of conventional clinical parameters was made; moreover, serum leptin, insulin, quantitative C-reactive protein (CRP), tumor necrosis factor-α [TNF-α], and adiponectin concentrations were measured., Results: The patients with post-HSCT MS had significantly higher levels of leptin, CRP, and TNF-α than the patients with "classic" MS. A generalized linear model comprising serum insulin (p=0.022), body mass index (p<0.001), gender (p<0.001), and group (i.e. healthy, post-HSCT with MS, or suffering from "classic" MS; p<0.001) explained serum leptin variability (adjusted R(2)=0.741). Serum leptin concentrations and BMI were related in the patients with "classic" MS but not in those with post-HSCT MS., Conclusions: A possible pathogenetic mechanism in the development of MS after HSCT could be hyperleptinemia. A potential interaction among circulating leptin, components of MS, and immune function might explain the role of this adipokine in mediating cardiovascular risk after HSCT.

Our purpose was to determine the prevalence and features of metabolic syndrome (MS) in a series of long-term hematopoietic stem cell transplantation (HSCT) survivors. We assessed the clinical, metabolic and endocrinological data, and plasma TNF, leptin, resistin and adiponectin levels relating to 85 HSCT recipients. MS was diagnosed on the basis of the National Cholesterol Education Program-Adult Treatment Panel III criteria. Its prevalence was compared with that observed in an Italian population, and its relationship with the clinical and laboratory parameters was assessed univariately and multivariately. Twenty-nine HSCT recipients had MS instead of the 12.8 expected (P<0.0001), with hypertriglyceridemia being the most common feature. Univariate analysis indicated that high insulin and leptin levels, low-adiponectin levels and hypogonadism were significantly related to a diagnosis of MS; multivariate analysis indicated plasma leptin, insulin resistance, age and hypogonadism. We conclude that HSCT recipients are at increased risk of a form of MS that has particular clinical features. Plasma leptin levels are independently related to MS, thus suggesting that leptin resistance may play a role as a pathogenetic clue, as in other conditions in which MS occurs as a secondary phenomenon. MS deserves consideration as a life-threatening complication in patients who are probably cured of their underlying disease.