Abstract
Methotrexate (MTX) is the most widely used drug in cancer chemotherapy and is considered to be the first-line drug for the treatment of a number of rheumatic and non-rheumatic disorders. The pulmonary toxicity, hepatotoxicity of MTX are two of its major side effects. Other toxicities such as endocrinological toxicity, GI toxicity, cutaneous toxicity, hematological toxicity, fatal malfunction or loss, and malignancy can also occur, but at a significantly lower rate of prevalence. This review aims to provide a comprehensive understanding of the molecular mechanisms of methotrexate toxic effects and Lastly, we discussed the management of this toxicity.
Highlights
4-amino-10-methylfolic acid, referred to as Initially, MTX was utilised as an anti-tumour agent
It can be utilised as an anchor agent in individuals who have had an insufficient reaction to MTX, together with additional characteristic or biological disease-modifying anti-rheumatic drugs (DMARDS) in order to enhance disease control [11,12]
In its capacity as an antagonist to folic acid, MTX inhibits the function of enzymes reliant on folate, and the manufacture of purine and pyrimidine essential for the generation of nuclear material that is rapidly replicated within tumour cell lines [14]
Summary
1.1 Overview of Methotrexate employed for the therapy of a spectrum of neoplastic and non-neoplastic pathologies [1]. 4-amino-10-methylfolic acid, referred to as Initially, MTX was utilised as an anti-tumour agent. MTX can be employed as the initial drug of choice in individuals who have not previously received DMARDs [10]. Attention has been drawn to the possible adverse incidents associated with MTX as they reflect the main reason for its cessation [15,16] It is widely utilised in the treatment of a range of autoimmune and inflammatory disorders, there is still drug toxicity associated with low dose MTX. The pathways underlying the toxic consequences of MTX have not been fully delineated Some effects, such as diminished cell counts, digestive issues and oral inflammation are related to folic acid lack; complementary folic acid or folinic acid may resolve such manifestations [19]. A more in-depth comprehension of MTX’s molecular mechanisms may aid in clarifying numerous toxicities related to MTX [14]
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