242 Background: Cisplatin is a widely used chemotherapeutic in treating malignancies. A common side effects of cisplatin is kidney injury, or nephrotoxicity. This can be a reason for discontinuation of treatment. The majority of the cisplatin is removed from the body by urination. Mannitol is a compound that has been thought to help negate cisplatin-induced nephrotoxicity. Mannitol is a diuretic, causing increased amount of urination, enhancing excretion of cisplatin. Mmultiple studies that indirectly looked into the effect of mannitol in preventing kidney damage in patients receiving cisplatin. However, there are limited prospective data that evaluate the effect of mannitol in preventing cisplatin-induced nephrotoxicity. In this study, we determine the effects of pre-hydration with mannitol on reducing the risk of cisplatin-induced nephrotoxicity, as opposed to normal saline pre-hydration in patients receiving cisplatin. Methods: 50 patients eligible to receive chemotherapy with cisplatin chemotherapy were identified and randomized to receive 1L saline alone (A) or saline plus mannitol (B) before and after chemotherapy. (1) NS 1 Liter pre chemo- > chemo - > NS 1 Liter post chemo; (2) NS + Mannitol pre chemo - > chemo - > NS + Mannitol post chemo. Serum creatinine and BUN were drawn on days 1 (baseline), 5, and 14 Results: Renal function as measured by BUN/Cr ration, GFR, creatinine, and BUN between group (A) and (B) are similar at baseline (BL), day 1, 5, and 14. Cisplatin caused acute decline in renal function as determined by ser Cr, BUN to ser Cr ratio and GFR, however, the addition of mannitol to NS pre-hydration did not change the outcome. The decline in renal function is limited to grade 1 and most patients recover. Conclusions: Mannitol does not prevent acute nephrotoxicity in patients receiving cisplatin. This underscores the importance of adequate hydration in patients treated with cisplatin.[Table: see text]
the study, 14 (61%) were females, 15 (65%) non-smokers, median age of 50 years (23-76). All patients had adenocarcinoma and were tissue positive for ALK by immunohistochemistry 14 (61%) and/or FISH 16 (70%). Nineteen patients (83%) had stage IV disease at diagnosis, with brain involvement in 7 patients (37%), bone in 11 (48%) and liver in 2 (11%). The median number of ALK inhibitors received was 2 (0-4). Twenty-one patients (91%) received ALK inhibitors (5 crizotinib, 3 ceritinib, 13 next-generation inhibitors) and 2 chemotherapy, with an objective response rate of 48%. Five out of 8 patients (63%) that were treatment naïve (baseline) or progressive disease (PD) at the time of collection, were positive for EML4-ALK by liquid biopsy, 1 of 4 samples (25%) at baseline, and 4 of 4 samples (100%) at PD, were positive by liquid biopsy. EML4-ALK variant 1 was detected in two (40%) and variant 3 in three patients (60%). All 26 samples collected during objective response or stable disease (100%) were negative for EML4-ALK by liquid biopsy. The ALK resistance mutation panel was performed on 2 samples from patients with PD, and both were detected positive for ALK resistance mutations, L1196M (variant 1) and G1202R (variant 3), respectively. Conclusion: The monitoring of ALK fusions on exosomal RNA by liquid biopsy is applicable in the clinic and closely correlated to disease control. ALK mutations detection using liquid biopsy can be an accurate tool for assessing the resistance to ALK inhibitors. Updated results from up to 30 patients will be available for the final presentation.
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