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Oxaliplatin, a third generation novel platinum compound is the most effective first line chemotherapeutic agent for colorectal cancer (CRC) in combination with 5FU and leucovorin. It is indicated for pancreatic, gastric and testicular cancers combined with bevacuzimab, capecitabine, irinotecan and other cytotoxic agents. However, moderate to severe hypersensitivity reactions (HSR) during or after oxaliplatin infusion usually require cessation of chemotherapy or substitution of the key therapeutic drug which largely interferes with improved patient prognosis. This mini-review showcases recent and accepted opinions/approaches in oxaliplatin induced HSR management. Physicians and oncologists have varying attitudes regarding the decision to rechallenge the patient after an HSR experience, efficacy of desensitization protocols, effectiveness and selection of drugs for premedication and possibilities of cross sensitivity to other platinum agents (e.g. carboplatin). A brief insight into underlying molecular mechanisms and clinical manifestations of oxaliplatin induced HSR is offered. We have also discussed the management of oxaliplatin induced HSR and risk stratification for a successful and complete chemotherapeutic plan.

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Background: To assess the frequency and severity of gastrointestinal adverse effects in advanced colorectal carcinoma patients treated with four different schedules of FOLFOX. Materials and Methods: Patients (median age 61 years) who underwent surgery were included in the study. All had measureable disease at CT scan, ultrasonography or clinical examination. Toxicity was graded on a scale of 1-5 according to the general grade definition of CTC v2.0. The severity of adverse effects (Grade 3 and 4) assessed in each treatment arm was compared. Results: Differences between the incidence rates of 3 and 4 toxicity and all grades of toxicity for all parameters in GI toxicity were very highly significant (p<0.001). Severe gastrointestinal symptoms of toxicity were noted with FOLFOX7 (oxaliplatin 130 mg/m 2 ). Grade 3 diarrhea was reported in 25% patients and grade 4 diarrhea in 4% in the FOLFOX7 treatment arm. Grade 2 vomiting was very frequently reported in the FOLFOX4 treatment arm (oxaliplatin 85mg/m 2 ). Grade 2 stomatitis was reported in 42% patients treated with mFOLFOX6 (oxaliplatin 100mg/m 2 ). Differences in the incidence rate of nausea, diarrhea and stomatitis among all treatment arms of FOLFOX were significant (p<0.05) . Conclusions: Severe diarrhea is associated with FOLFOX7 treatment. No grade 3 or 4 GI toxicity was reported in patients of the mFOLFOX6 arm.

Introduction: Chemotherapy-induced hepatotoxicity in cancer patients often results in cessation of therapy and prevents completion of the treatment plan. The entire pathological description and comparison of hepatic damage induced by oxaliplatin or cisplatin in combination with 5-fluorouracil (5-FU) is not adequately reported. This study reports histopathological assessment of hepatotoxicity of a non-tumor bearing organ in rats treated with 5-FU, oxaliplatin and cisplatin (CDDP). Material and methods: Changes in hepatic biochemical profile of 36 albino Wistar rats equally divided into different treatment groups with cisplatin, oxaliplatin, 5-FU, cisplatin plus 5-FU and oxaliplatin plus 5-FU were compared with a group of rats treated with normal saline (control group). At the end of treatments, hepatic tissues were taken for blinded histopathological assessment by light microscopy. Results: Serum glutamate pyruvate transaminase and serum glutamic-oxaloacetic transaminase levels were disrupted in rats treated with 5-FU alone and in combination with cisplatin or oxaliplatin. Hepatocellular injuries, e.g. sinusoidal dilatation, venular fibrosis and centrilobular vein injury induced by oxaliplatin were intensified in treatment groups also receiving 5-FU, manifested as massive architectural distortion, periportal fibrosis, hepatic cord degeneration and cystic lesions with demarcated margins. Hepatocellular degenerative sequence and abnormally dilated central hepatic vein was shown in the cisplatin plus 5-FU treatment group with hemorrhage and blood filled sinusoids. Conclusions: Oxaliplatin-associated cystic lesions were intensified in rats treated with a combination of 5-FU and oxaliplatin.