Abstract 5018

Background:

Obesity was associated with a more than 2-fold greater risk of myelodysplastic syndrome (MDS) in a recent epidemiological study (Ma et al, Am J Epidemiol. 2009 June 15; 169(12): 1492–1499). The impact of obesity on outcome of disease in patients with an established diagnosis of MDS has not been studied. We examined the prognostic value of obesity in a large cohort of lower risk MDS patients treated at the Moffitt Cancer Center (MCC).

Methods:

Data were collected retrospectively from the Moffitt Cancer Center (MCC) MDS database and individual charts reviewed. The primary objective was to evaluate the impact of obesity on overall survival (OS) in lower risk patients with MDS. Patients with low or intermediate-1 (int-1) risk disease by International Prognostic Scoring System (IPSS) were included. Obesity was defined as a body mass index (BMI) ≥ 30 (Standard definition) measured at time of referral to MDS program at MCC. Patients were divided into two groups according to BMI ≥ 30 or BMI < 30. All analyses were conducted using SPSS version 19.0. Chi square and independent t-test were used to compare baseline characteristics between the 2 groups for categorical and continuous variables, respectively. The Kaplan–Meier method was used to estimate median overall survival. Log rank test was used to compare Kaplan–Meier survival estimates between two groups. Cox regression was used for multivariable analysis.

Results:

Between January 2001 and December 2009, 479 low/int-1 IPSS risk MDS patients were included. Among those, 132 (27.6%) had BMI ≥ 30 and 325 (67.8%) had BMI <30; BMI was missing in 22 patients (4.6%). The baseline characteristics between the two groups were comparable. No difference was noted in mean age, WHO subtype, karyotype, MD Anderson risk model group, red blood cell transfusion dependency (RBC-TD), or serum ferritin (Table-1).

Table-1

Baseline Characteristics

BMI < 30 n= 325BMI ≥ 30 n=132p-value
Age ≥ 60  232 (71%) 91 (69%) 0.65 
Karyotype Good 253 (77.8%) 106 (80.3%) 0.15 
Intermediate 46 (14.2%) 21 (15.9%) 
Poor 24 (7.4%) 3 (2.3%) 
Unknown 2 (0.6%) 2 (1.5%) 
MDAS Low 144 (44.3%) 48 (36.4%) 0.6 
Int-1 63 (19.4%) 55 (41.7%) 
Int-2 15 (4.6%) 24 (18.2%) 
High risk 4 (1.2%) 5 (3.8%) 
WHO type RA 73 (22.5%) 33 (25%) 0.7 
RARS 51 (15.7%) 20 (15.2%) 
RCMD 71 (21.8%) 34 (25.8%) 
Del 5q 16 (4.9%) 3 (2.3%) 
RAEB 101 (31.1%) 37 (28%) 
MDS-U 13 (4%) 5 (3.8%) 
RBC-TD  143 (44.4%) 48 (36.6%) 0.3 
Ferritin>1000 (ng/ml)  76 (32.5%) 29 (30.5%) 0.4 
HMA (yes)  145 (44.6%) 67 (50.8%) 0.13 
BMI < 30 n= 325BMI ≥ 30 n=132p-value
Age ≥ 60  232 (71%) 91 (69%) 0.65 
Karyotype Good 253 (77.8%) 106 (80.3%) 0.15 
Intermediate 46 (14.2%) 21 (15.9%) 
Poor 24 (7.4%) 3 (2.3%) 
Unknown 2 (0.6%) 2 (1.5%) 
MDAS Low 144 (44.3%) 48 (36.4%) 0.6 
Int-1 63 (19.4%) 55 (41.7%) 
Int-2 15 (4.6%) 24 (18.2%) 
High risk 4 (1.2%) 5 (3.8%) 
WHO type RA 73 (22.5%) 33 (25%) 0.7 
RARS 51 (15.7%) 20 (15.2%) 
RCMD 71 (21.8%) 34 (25.8%) 
Del 5q 16 (4.9%) 3 (2.3%) 
RAEB 101 (31.1%) 37 (28%) 
MDS-U 13 (4%) 5 (3.8%) 
RBC-TD  143 (44.4%) 48 (36.6%) 0.3 
Ferritin>1000 (ng/ml)  76 (32.5%) 29 (30.5%) 0.4 
HMA (yes)  145 (44.6%) 67 (50.8%) 0.13 

MDAS MD Anderson Score risk group, int-1 intermediate-1, int-2:intermediate-2, RA: refractory anemia, RARS refractory anemia with ring sideroblasts, RCMD refractory cytopenia with multilineage dysplasia, RAEB refractory anemia with excess blasts, MDS-U MDS unclassified, RBC-TD red blood cell transfusion dependency, HMA hypomethylating agent

The median OS was 59 mo (95%CI 48–70) in patients with BMI <30 compared to 44 (95%CI 38–50) in patients with BMI ≥ 30. (p=0.03). There was no difference in rate of AML transformation according to BMI, 12.9% and 15.7% respectively for BMI ≥ 30 and BMI <30. (P=0.3). In Cox regression analysis obesity predicted inferior OS (Hazard ratio (HR) 1.7 (95%CI 1.15–2.4) (P=0.007) after adjustment for age, MD Anderson risk group, serum ferritin, RBC-TD, use of hypomethylating agents and tobacco use.

Conclusion:

Our data suggest that obesity is an independent adverse prognostic factor for OS in patients with lower risk MDS. Obesity may be associated with other comorbidities and metabolic dearrangements that contribute to the pathogenesis of the underlying disease.

Disclosures:

No relevant conflicts of interest to declare.

Author notes

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Asterisk with author names denotes non-ASH members.

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