No abstract

One of the clinical consequences of aberrant cytokines production in patients with end stage renal disease (ESRD) may be impaired erythropoiesis. To determine the interleukin (IL)-10 levels in ESRD patients on regular hemodialysis (HD) with good and poor response to recombinant human erythropoietin (Epo). Two groups of ESRD-HD patients were evaluated; 48 high epo HD patients and 32 low epo HD patients were evaluated for some laboratory tests and Interleukin-10 by ELISA. The production of IL-10 is decreased in HD with low epo group than high epo group 32.4 +/- 7.9 vs. 45 +/- 6.9 pg/ml (P < 0.001). IL-10 level is well correlated with CRP, ESR, Ferritin, Epo dose, and EPO/Hb ratio in ESRD-HD patients. These findings suggest that IL-10 is playing a part in affecting the response to EPO, even in the absence of any obvious infection or inflammatory condition.

564 Background: Oxaliplatin-based chemotherapy can cause hepatic sinusoidal injury (HSI), portal hypertension, and splenic sequestration of platelets. In the NSABP C-08 study a reduced rate of thrombocytopenia (1.4% vs 3.4%, P <0.01) was seen in the bevacizumab arm. Evidence suggests that bevacizumab may protect against HSI, though the clinical impact of this has not been well examined. Methods: A retrospective review of metastatic colorectal cancer patients treated at MD Anderson Cancer Center from 1/2003 to 1/2010 with ≥3 months of frontline fluoropyrimidine and oxaliplatin (FOLFOX) with or without bevacizumab was conducted. Presence of known liver disease, prior liver surgery, absence of spleen, or adjuvant oxaliplatin were exclusion criteria. Splenic volumes pre, during, and post FOLFOX treatment were determined from CT scans and correlated with platelet counts and treatment. Results: 184 pts (138 FOLFOX/Bev; 46 FOLFOX) were identified. The median number of cycles (9 for each cohort) and the total oxaliplatin dose (P = 0.78) did not differ between the two cohorts. The development of splenomegaly (spleen volume increase of ≥30%) was more common in the non-Bev cohort, 48% vs 32%, P=0.013. The median time to splenomegaly was longer in the Bev cohort, 7.6 vs 5.5 months, P=0.023. When comparing patients with and without splenomegaly, the presence of splenomegaly correlated with thrombocytopenia (<150 platelet count) at 3 months (40% vs. 16%, P=0.0005) and beyond (lower mean platelet counts during 3 to 6 months of treatment, P <0.0001 by Two-way ANOVA). A correlation with thrombocytopenia was also seen in the non-Bev vs. Bev cohort at both 3 months (43% vs 24%, P = 0.006) and beyond (P = 0.003). Conclusions: The addition of bevacizumab to oxaliplatin chemotherapy reduces the frequency of splenic enlargement, which directly correlates with a reduced rate of thrombocytopenia. Further study to understand the hepato-protective mechanism of anti-VEGF therapy is needed.

3544 Background: Oxaliplatin-based chemotherapy can cause hepatic sinusoidal injury (HSI) leading to portal hypertension. This results in splenic sequestration of platelets and thrombocytopenia. Evidence suggests that bevacizumab may protect against HSI, although the clinical impact of this has not been well examined. The purpose of our study was to evaluate rate of thrombocytopenia and splenomegaly as clinical end-points indicative of bevacizumab mediated modulation of oxaliplatin-induced hepatic toxicity. Methods: We performed a retrospective review of metastatic colorectal cancer patients treated at M D Anderson Cancer Center from 1/2003 to 1/2010 with ≥ 3 months of frontline fluoropyrimidine and oxaliplatin (FOLFOX) with or without bevacizumab. Patients with prior liver disease, liver surgery or absence of spleen were excluded. Splenic volumes pre, during and post FOLFOX therapy were determined with CT scans and correlated with platelet counts and treatment. Results: A total of 184 patients [Bev cohort: FOLFOX/Bev (n =138); Non-Bev cohort: FOLFOX alone (n = 46)] were identified. Baseline characteristics (age, gender, spleen size and platelet counts) were similar in both groups. Median number of oxaliplatin cycles for each cohort was 9.00 (p = 0.9). The median total oxaliplatin dose did not differ between the two cohorts (p = 0.9). Development of splenomegaly (volume increase ≥ 30%) was more common in the Non-Bev cohort (48% vs. 32%; p = 0.013). The median time to develop splenomegaly was significantly longer in the Bev cohort (7.6 vs. 5.5 months; p = 0.023). Splenomegaly correlated with a higher rate of thrombocytopenia (defined as platelets < 150K) at 3 months (40% vs. 16%, p = 0.0005) and beyond (during 3 to 6 months of treatment, p < 0.0001). Correspondingly, bevacizumab therapy was associated with lower rates of thrombocytopenia at 3 months (24% in Bev cohort vs. 43% in Non-Bev cohort, p = 0.006) and beyond (p = 0.003). Conclusions: In our cohort, addition of bevacizumab to oxaliplatin chemotherapy reduces the occurrence of splenic enlargement, which correlates with a decreased rate of thrombocytopenia. Further studies to understand the potential hepato-protective mechanism of anti-VEGF therapy are needed.