Publication Only: Lymphoma biology & translational research
NHLs are an etiologically, clinically &histologically heterogeneous group oflymphoproliferative disorders. Obesity has beenfound to be a risk factor through dysregulation of alarge spectrum of inflammatory & adipositycytokines in many types of cancer.
We aimed to Study the association between obesityas measured by body mass index (BMI), and risk of NHL development by evaluating the role ofinflammatory cytokines, (IL-6, IL-10, IFN-gamma& CRP) & adipokines (leptin & adiponectin).
All patients (n;45) as well as Healthy controls (n;43) subjected to Complete history and Physicalexamination assessment of the body mass index (BMI), Ann Arbor Clinical staging, laboratoryworkup in form of:Routine laboratory investigations, Pan CT, bonemarrow and excisional biopsy of the involvedlymph node for cytochemical studies. Specificmarker assessment; IL-6, IL-10, IFN-Y, CRP,Leptin & Adiponectin by ELISA kits.
We had investigated 45 NHL patients. Female were (n;16),while male were (n; 29). The Median age at the time of diagnosis was 55years. Also, 43 age and sex matched healthy controls (HC) were enrolled. They were 30 patients having diffuse large B-celllymphoma (DLBCL) (66.67%), 8 patients havingmucosa-associated lymphoid tissue-B variant (MALT) (17.78%), and 7 patients having follicularlymphoma (FL) (15.56%). All the inflammatory markers (IL-6, IL-10, IFN-γ& CRP) together with adiponectin werestatistically higher in NHL cases than control. (Pvalue0.001). We studied different variables affecting cytokinesin our NHL patients & we found that genderaffected leptin level only, which was higher infemales than males. (P-value 0.001). Among other studied variables we found no othersignificant correlations affecting inflammatorycytokines and adipokines in our NHL patients. Important scale in our work was subgrouping ourpatients into two groups regarding their BMI, firstgroup (Group A) (n. 16 patients) with BMI < 25 kg/m2 and second group (Group B) (n. 29patients) with BMI ≥ 25 kg/m2 and studying levelsof inflammatory & adiposity markers in bothgroups. The inverse association between leptin and NHLrisk was slightly strengthened (p-value was 0.61and became 0.001) with higher levels in the secondgroup with BMI ≥ 25 kg/m2. Other inflammatory markers weren't significantcorrelated with BMI except the unexpected higherlevels of IL 6 & CRP in non obese patients. We noted in our study that stage of the disease didnot affect levels of inflammatory or adipositymarkers, except in late stage of disease (stage VI)which was associated with higher level ofadiponectin only (p-value 0.014). Also, we didn't find any significant differencebetween de-novo and relapse diseases regardinginflammatory markers as well as adipositymarkers.
Our findings support the hypothesis that obesityhas a major role in the development of NHL. Weobserved positive significant correlation betweenIL-6, IFN-γ, CRP and adiponectin with increasedrisk of NHL development. These findings supporta role for subclinical inflammation and chronic Bcellstimulation in lymphomagenesis.