Background: Cytoreductive surgery (CRS) followed by hyper thermic intraperitoneal chemotherapy (HIPEC) is an evolving treatment for peritoneal carcinomatosis (PC). Mitomycin C (MMC), an alkylating agent, is presently the most commonly used chemotherapeutic agent for hyper thermic intraperitoneal treatment. The spleen has a role in the hematologic response after HIPEC and that splenectomy may enhance hematologic toxicity profiles of MMC. We are presenting a case who developed persistent thrombocytosis After Cytoreductive surgery followed by HIPEC.Case presentation: A 48-year-old lady was referred to hematology OPD for first time with findings of persistent thrombocytosis on routine CBC follow-up. She underwent Cytoreductive surgery which include left and right parietal peritonectomy, pelvic peritonectomy, TAH+BSO, small bowel resection, right hemicolectomy, splenectomy plus heated intra operative peritoneal chemotherapy for a low-grade mucinous adenocarcinoma. Her initial platelet count was 1520x10^9/L for which she was on aspirin .Follow-up CBC showed a platelet count of 1609x10^9/L. She was investigated further and there was absence of any cause of essential thrombocytosis. Conclusion:This article to emphasize that Persistent reactive thrombocytosis can occur in a case of peritoneal carcinomatosis after CRS followed by HIPEC.

AMD3100 (Plerixafor), a specific antagonist of CXCR4, is the most potent small molecule non-peptide inhibitor to CXCR4/CXCL12 axis. The chemokine receptor CXCR4 and its ligand CXCL12 (SDF-1) expressed in a variety of tumor cells play an important role in regulating tumor biological behavior. The tumor microenvironment (TME) is the environment around a tumor, comprising blood vessels, immune cells, fibroblasts, signalling molecules and the extracellular matrix which are involved in tumor growth, invasion, metastasis, immune escape and tumor eradication. Although AMD3100 has been intensively investigated in tumor biology, it remains unclear how this treatment regimen modulates immune cells in the TME, which in turn affects the antitumor efficacy of other therapies. In this review, we specifically revisit the evidence from our and others' studies that AMD3100 acts as an immunomodulator to regulate immune responses in the TME and provide the perspective of synergy of AMD3100 with other therapeutics to prevent tumor development, progression, and metastasis.

He was referred to hematology clinic in June 2017 due to persistent symptomatic anemia post chemotherapy. He has no bleeding orifices, eating well no vomiting or diarrhea. His bone marrow examination showed hyper cellular marrow with evidence of erythroid dysplasia and significant ringed sideroblast

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