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Toxins in Neuro-Ophthalmology
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Although advances in the field of oncology is a boon to cancer patients, the spectrum of toxicity of the chemotherapeutic agents is also worrisome. Ocular toxic effects related to the use of cytarabine include corneal epithelial toxicity and hemorrhagic conjunctivitis [48]. Methotrexate has also been noted to cause macular edema [49]. Daunorubicin inhibits proliferative vitreoretinopathy changes after surgery for retinal detachment and glaucoma filtering surgeries due to its antifibroblast action [50–52]. However, it can cause retinal toxicity with high intraocular doses. Cisplatin has been reported to cause delayed optic neuritis. Etoposide causes central retinal artery occlusion secondary to thrombosis when given intra-arterially. It exerts synergistic effect with cisplatin and causes retinal toxicities. Bleomycin causes cortical blindness with concurrent usage with cisplatin.
Chemotherapy in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Nucleoside analogs, including cytarabine and gemcitabine, exhibit their antineoplastic properties by causing incorporation of either the drug or its metabolite into DNA and terminating replication. Cytarabine is indicated in the treatment of multiple types of leukemias, as well as in leptomeningeal carcinomatosis. The compound has been associated with otic and auditory canal anomalies, digital anomalies, lobster claw hand, and lower limb defects (70,71). Unlike most other chemotherapies, cytarabine has been associated with in utero fetal death, when given in the later trimesters, and should be avoided in pregnancy altogether, when alternative agents are available (72).
Antimetabolites
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
In the UK, cytarabine is recommended by NICE for the induction of remission in acute myeloblastic leukemia and for the treatment of lymphomatous meningitis, a complication of lymphoma in which tumor cells have spread from the original (primary) tumor to the meninges. A liposomal cytarabine–daunorubicin combination formulation (VyxeosTM) is also available and recommended by NICE as an option for therapy-related untreated acute myeloid leukemia or acute myeloid leukemia with myelodysplasia-related changes.
Personalized approaches for treatment-naïve mantle cell lymphoma
Published in Expert Review of Hematology, 2023
Other studies have evaluated the use of intensive cytarabine-containing regimens in a non-randomized setting. In the LyMa trial, which was a randomized trial of rituximab maintenance (to be discussed later), patients received R-DHA with clinician’s choice of either cisplatin (P), carboplatin (C), or oxaliplatin (X). On analysis by platinum agent given, 4 year PFS was 87%, and OS 92%, for R-DHAX, vs 65% and 76% for R-DHAP and R-DHAC, respectively [35]. This may be related to increased tolerability, allowing more efficient delivery of the chemoimmunotherapy regimen – 36% of patients treated with cisplatin changed to another platinum agent due to toxicity, while only 1/76 and 1/38 patients in carboplatin and oxaliplatin arms, respectively, changed platinum treatment. While lack of randomization limits comparison, these findings suggest that R-DHAX may be a preferred option over R-DHAP or R-DHAC, particularly in patients where the ability to tolerate intensive chemotherapy containing cisplatin may be limited.
Outcomes of juvenile myelomonocytic leukemia patients after sequential therapy with cytarabine and 6-mercaptopurine
Published in Pediatric Hematology and Oncology, 2020
Abdul Wajid M, Aditya Kumar Gupta, Gargi Das, Debasish Sahoo, Jagdish Prasad Meena, Rachna Seth
Allogenic HSCT is the only curative option for JMML. In the absence of an allogenic HSCT many children succumb within a year of diagnosis.7 There is limited data on optimum therapy for control of disease prior to HSCT. A number of chemotherapeutic drugs either as single agents or in combinations, and differentiation inducing agents have been tested to control manifestations of JMML (like hepatosplenomegaly, thrombocytopenia and pulmonary infiltration) and to improve outcomes. Common regimens include oral 6-mercaptopurine, as monotherapy or sometimes combined with the differentiating agent cis-retinoic acid.14,16 Low-dose intravenous cytarabine administration has also been used; but as a single agent low dose cytarabine is ineffective in inducing remission.18,19 Some authors have also reported transient responses with interferon-alpha,15,18,20 while others did not demonstrate any benefit.21–23 Bergstraesser et al, in a retrospective analysis observed that single agent 6-mercaptopurine or 6-thioguanine resulted in higher response rate with respect to WBC counts. Combination therapy of these drugs with low dose cytarabine gave the best responses with regard to decrease in spleen size.14 Lilleyman et al, observed control of disease in 3 children treated with sequential therapy with subcutaneous cytarabine and oral 6-mercaptopurine.13
Fetal hydrops – a review and a clinical approach to identifying the cause
Published in Expert Opinion on Orphan Drugs, 2020
Esther Dempsey, Tessa Homfray, John M Simpson, Steve Jeffery, Sahar Mansour, Pia Ostergaard
Individuals with trisomy 21 (Down syndrome) are at increased risk of myeloproliferative disorders throughout life [54] . A transient, abnormal myelopoesis (TAM) is recognized to affect approximately 10-15% of infants with trisomy 21 [55]. The trisomy 21 is responsible for an initial dysmegakaryopoesis and, with an acquired GATA1 truncating mutation, control of clonal proliferation of blasts cells is lost [56]. The result is a transient abnormal myelopoesis with up to 30% developing into myeloid leukemia, by the age of 4 years, after acquisition of additional oncogenic driver mutations [57]. In a study by Tamblyn et al, of 31 cases of prenatally diagnosed TAM, 79.5% had hepatosplenomegaly and 30.8% had fetal hydrops. In the 33% of cases with both fetal hydrops and hepatomegaly the fetal or early neonatal mortality was 92% (54% with fetal hydrops alone) [58]. Thus fetal hydrops is a poor prognostic sign as the survival rate for postnatally detected cases is in the region of 70% with most babies undergoing spontaneous resolution of the abnormal myelopoiesis [55,59]. A recent report shows promising results for in-utero treatment with exchange transfusions and low dose cytarabine [60].