1.
How to rescue high-dose methotrexate induced nephrotoxicity and literature review about hemodiafiltration?
Yang, YY, Gao, L, Ding, N, Wang, XB, Zhang, LP, Gao, LH, Wang, Z
Pakistan journal of pharmaceutical sciences. 2020;(3):1163-1167
Abstract
Methotrexate (MTX) is a highly renal and liver toxicity drug used in hematological malignancy treatment in children and adults. High-dose methotrexate (HD-MTX) therapy may cause impairment of kidney and decrease the elimination of MTX, at the same time, the serum concentration of MTX increased. Today the treatment for preventing MTX toxicity after renal shutdown is Carboxypeptidase. We report a patient who experienced nephrotoxicity after the HD-MTX infusions during the treatment for non-Hodgkin lymphoma (NHL) and received hemodiafiltration (HDF) with large dose of leucovorin (LV) to treat MTX intoxication. LV is very potent in the prevention of neurotoxicity and administration of LV could protect the normal cells, but the dosage and duration of LV should be according to the MTX concentration. Although a large dose of LV was applied, the patient's condition did not improve. It was found that the HDF with large dose of LV to save the patient and steadily improved the patient's clinical condition.
2.
Fetal methotrexate syndrome: A systematic review of case reports.
Verberne, EA, de Haan, E, van Tintelen, JP, Lindhout, D, van Haelst, MM
Reproductive toxicology (Elmsford, N.Y.). 2019;:125-139
Abstract
Methotrexate is a folic acid antagonist known to be teratogenic in humans. Several cases of congenital malformations after fetal exposure to methotrexate have been published, resulting in the establishment of the 'fetal methotrexate syndrome'. However, it is unclear which congenital anomalies can truly be attributed to methotrexate exposure. The objective of this review is to delineate a consistent phenotype of the fetal methotrexate syndrome. We performed a systematic review that yielded 29 cases of (congenital) anomalies after in utero exposure to methotrexate and compared their malformation pattern to that of children and fetuses with congenital anomalies in general. Statistically significant higher proportions of microcephaly, craniosynostosis, tetralogy of Fallot, pulmonary valve atresia, limb reduction defects and syndactyly were found in the methotrexate group, indicating that these congenital anomalies are truly part of the fetal methotrexate syndrome. These results aid clinicians with diagnosing fetal methotrexate syndrome.
3.
Prolonged response of meningeal carcinomatosis from non-small cell lung cancer to salvage intrathecal etoposide subsequent to failure of first-line methotrexate: a case report and literature review.
Park, MJ
The American journal of case reports. 2015;:224-7
Abstract
BACKGROUND As the incidence of meningeal carcinomatosis (MC) in non-small cell lung cancer (NSCLC) patients has been increasing, MC has recently become an important clinical problem in the management of NSCLC. However, development of new treatments is lacking and a standard treatment guideline is not yet available. Research on salvage intrathecal chemotherapy after failure of first-line treatment for NSCLC patients with MC has rarely been reported in the literature. Here, we report the case of an NSCLC patient with MC who showed durable response to salvage intrathecal etoposide subsequent to failure of first-line methotrexate. CASE REPORT A 58-year-old Asian man with lung adenocarcinoma with bone metastasis presented gait disturbance, diplopia, and progressively increasing headache. The diagnosis of MC was made by brain magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) cytology. After MC progression was suspected during the first-line treatment of intrathecal MTx, intrathecal etoposide was used as a salvage treatment. Brain MRI performed after 2 months of the treatment demonstrated disappearance of enhancing lesions along the ependymal lining of the lateral ventricles. His clinical status markedly improved from Eastern Cooperative Oncology Group performance status of 4 to 2. Stable neurologic status was maintained and CSF cytology remained negative while weekly injection of etoposide was continued for 19 weeks. However, hepatic metastatic lesions persistently progressed despite systemic palliative chemotherapy and the patient died of the disease. CONCLUSIONS To our knowledge, this is the first case report in which intrathecal etoposide was successfully used to treat MC from NSCLC after failure of MTx. This case report might provide preliminary evidence of the feasibility of intrathecal etoposide as salvage intrathecal chemotherapy (ITC). Further clinical trials including larger numbers of patients are necessary to evaluate the role of this ITC regimen for NSCLC patients with MC.