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Cancer
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Elyce Cardonick, Charlotte Maggen, Puja Patel
Treatment of severe leukocytosis is necessary to reduce maternal risk of stroke hypoxia, deep venous thrombosis (DVT). There are case reports of observation alone during pregnancy in patients without splenomegaly. Leukophoresis can be a temporizing measure to reduce WBC and spleen size if necessary [85]. Tyrosine kinase inhibitors such as imatinib, the newest advance in the treatment of chronic leukemia in non-pregnant adults, has been shown to cause teratogenic effects in rats, including exencephaly or encephalocele and absent or reduced frontal and absent parietal bones. If a pregnant patient newly diagnosed with CML is symptomatic with splenomegaly, with no clinical response to leukapheresis or other medications and is beyond the first trimester, imatinib would be preferred over second generation tyrosine kinase inhibitors such as dasatinib or nilotinib. Reports show imatinib is 95% bound to plasma proteins with a molecular weight of 590 which suggests low placental transfer. Case reports of tyrosine kinase inhibitor imatinib during pregnancy beyond the first trimester have been reassuring with prompt responses in pregnancy [86–89].
Chemotherapy in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Imatinib is a specific inhibitor of a number of tyrosine kinase enzymes and is indicated for the treatment of chronic myelogenous leukemia. It has been associated with a high rate of teratogenicity (108). However, Skoumalova et al. reported on its administration throughout the first trimester of pregnancy, followed by the use of interferon for the remainder of the gestation, with the delivery of a normal and healthy child (108). Neither the drug nor its active metabolite appears to cross the placenta in significant concentrations (109). Nonetheless, Pye et al. reported on the evaluation of 125 pregnancies complicated by the use of imatinib (110). They reported that 3 of the 35 patients who terminated their pregnancies did so because of detected fetal malformations. Of the remaining infants delivered, 12 had malformations, and 3 of them had similar complex malformations including renal and vertebral anomalies.
Respiratory, endocrine, cardiac, and renal topics
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Imatinib is used for the treatment of chronic myeloid leukaemias Philadelphia chromosome (bcr-abl) Positive (Ph+). Its activity is being studied in paediatric Ph+ acute leukaemias. Imatinib is administered orally to the child at doses of 240 mg/m2 during the chronic phase (max dose 400 mg per day) and 340 mg/m2 during the acute phase (max dose 600 mg per day) [4].
Managing women of childbearing age with chronic myeloid leukemia: safety and treatment considerations
Published in Expert Review of Hematology, 2023
HF Robertson, MJ Buckton, JF Apperley
There have, however, been a number of cases in which imatinib has been safely administered later in pregnancy [41,46,47]. Ali et al. provided a case report of a woman successfully treated with imatinib in week 21 of pregnancy. The authors then reviewed the literature and summarized 26 cases of females who were treated with imatinib during pregnancy and concluded that when used after the first-trimester imatinib was safe and effective [39]. Furthermore, Chelysheva reported 15 cases in which imatinib was restarted due to loss of major molecular response (MMR) in the 2nd and 3rd trimester, and showed no birth defects or teratogenicity [48]. This observational evidence has been confirmed by findings that imatinib exhibits limited placental transfer [41,49].
Drugs repurposing for SARS-CoV-2: new insight of COVID-19 druggability
Published in Expert Review of Anti-infective Therapy, 2022
Sujit Kumar Debnath, Monalisha Debnath, Rohit Srivastava, Abdelwahab Omri
Imatinib is a tyrosine kinase receptor inhibitor used in diseases like gastrointestinal stromal tumors and chronic myelogenous leukemia. Unregulated cell growth has been observed in abnormal and constitutive expressed tyrosine kinase. An in-vitro study confirmed that imatinib hindered the early stages of the virus life cycle. However, the inhibitory activity of this drug COVID-19 is debatable due to unpredictable outcomes from preclinical studies [109]. This drug does not impair the virus-host interactions directly. It has been hypothesized that this drug acts on the upregulation of genes involved in virus response. It perhaps also acts as an immunomodulatory that reduce pro-inflammatory cytokines and chemokines. In a randomized clinical trial, imatinib could not reduce the time to discontinue mechanical ventilation, and supplemental oxygen in COVID-19 patients needed supplementary oxygen [110]. C-ABL-1 kinase signaling pathways serve a crucial role in the egress of poxviruses and Ebola viruses. This kinase is signaling equally critical in the replication of MERS-CoV and SARS-CoV. A phase 3 clinical trial is currently underway for hospitalized COVID-19 patients. This trial’s hypothesis is to decrease the SARS-CoV-3 by increasing endosomal pH, interfering with the replication of SARS-CoV-2 and clinical outcome of COVID-19 patients in the intensive care unit.
Tenosynovial giant cell tumors (TGCT): molecular biology, drug targets and non-surgical pharmacological approaches
Published in Expert Opinion on Therapeutic Targets, 2022
Geert Spierenburg, Lizz van der Heijden, Kirsten van Langevelde, Karoly Szuhai, Judith V.G.M. Bovée, Michiel A.J. van de Sande, Hans Gelderblom
Imatinib is an inhibitor of a few tyrosine kinases, including Abelson proto-oncogene (Abl), breakpoint cluster region-Abl (Bcr-Abl) complex, c-Kit proto-oncogene (KIT), platelet-derived growth factor receptor (PDGFR) and CSF1R[75]. Before imatinib was applied in TGCT, this oncogene-targeted therapy was already indicated for patients with chronic myeloid leukemia and gastrointestinal stromal tumors[57]. The effect of imatinib on TGCT was first evaluated in one patient, in which complete remission was observed five months after initiation[57]. After treatment interruption, TGCT relapsed both clinically and radiologically, but diminished again after treatment was resumed. After successful treatment of this single patient, a retrospective study reported the effect of imatinib in 29 patients with advanced or metastatic D-TGCT [57,75]. Imatinib is an oral drug, dosed at 400 mg daily. Imatinib led to an objective response rate (ORR) of 20% according to Response Evaluation Criteria in Solid Tumors (RECIST) and symptomatic/functional improvement in 74% of patients. Although a substantial activity against D-TGCT was observed, the effect was less when compared with GIST and dermatofibrosarcoma protuberans, probably due to a lower activity against CSF1-driven chemotaxis[75]. Six patients had to stop due to toxicity (of which three had grade 3 or 4 toxicities), and four without any apparent medical reason[75].