Effect of ursodeoxycholic acid and vitamin E in the prevention of liver injury from methotrexate in pediatric leukemia

Bordbar, Mohammadreza; Shakibazad, Nader; Fattahi, Mohammad Reza; Haghpanah, Sezaneh; Honar, Naser

doi:10.5152/tjg.2018.17521

Cited by 25 publications

(32 citation statements)

References 19 publications

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“…The usage of natural compounds or drugs, nontoxic cytoprotective agents like ursodeoxycholic acid, β-carotene, etc. as adjuvants may play a significant role in decreasing the incidence of side effects of MTX [13,14]. Among various adjuvant agents, vitamin E or alpha-tocopherol has reconstructing and antioxidant effects [15].…”

Section: Introductionmentioning

confidence: 99%

Efficacy of Vitamin E in Methotrexate-Induced Hepatotoxicity in Rheumatoid Arthritis: An Open-Label Case-Control Study

Vaidya¹,

Bhochhibhoya²,

Nakarmi³

2020

International Journal of Rheumatology

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Objective. To examine the efficacy of vitamin E in methotrexate- (MTX-) induced transaminitis in patients with rheumatoid arthritis (RA). Methods. A case-control study was conducted at a tertiary rheumatology center for 12 months. Patients with RA on MTX and deranged aminotransferases were included. Patients with previous liver diseases, baseline transaminitis before methotrexate initiation, alcohol intake, muscle diseases, under hepatotoxic drugs, and aminotransferases>3 times the upper normal limit were excluded. The patients were divided into treatment (vitamin E 400 mg bid for 3 months) and control groups (no vitamin E) using a random number table. The dose of MTX was unaltered. Follow-up was done after 3 and 6 months. Independent t-test was done to compare means of two groups. Paired t-test was done to compare differences in mean. Results. Among 230 patients, 86.5% were female with a mean BMI of 25.9±4.5 kg/m2. In the treatment group, SGPT and SGOT at baseline were 73.1±20.4 and 60.2±24.5 IU/L, respectively; at 3-month follow-up 44.6±34.2 and 38.3±20.8 IU/L, respectively; and at 6-month follow-up 40.4±35.7 and 34.2±21.9 IU/L, respectively. In the control group, SGPT and SGOT at baseline were 63.4±15.1 and 46.8±13.7 IU/L, respectively, and at 3-month follow-up 55.8±45.9 and 45.5±30.9 IU/L, respectively. Significant decrease in the level of aminotransferases was seen in the treatment group (p value < 0.001) and not in the control group (p values 0.161 and 0.728, respectively). The change in levels of SGPT and SGOT from baseline to 3 months of follow-up was statistically significant in between two study groups (p values 0.007 and <0.001, respectively). From the control group, 29 patients were crossed over to vitamin E for the next 3 months. SGPT and SGOT decreased from 97.6±44.1 to 46.1±40.9 and 69.3±34.9 to 29.1±11.6 IU/L, respectively (p values 0.031 and 0.017, respectively). Conclusion. Vitamin E significantly attenuates MTX-induced transaminitis.

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Section: Introductionmentioning

confidence: 99%

Efficacy of Vitamin E in Methotrexate-Induced Hepatotoxicity in Rheumatoid Arthritis: An Open-Label Case-Control Study

Vaidya¹,

Bhochhibhoya²,

Nakarmi³

2020

International Journal of Rheumatology

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“…MTX inhibits enzymatic incorporation of reduced folate into nucleotide synthesis, thus inhibiting DNA synthesis. The inhibition leads to cell cycle S phase arrest and apoptosis (Bordbar, Shakibazad, Fattahi, Haghpanah, & Honar, ). Presently, clinical application is reduced because of its widespread toxicity on delicate organs, including the brain and spinal cord (Celik et al, ; Famurewa et al, ; Uzar et al, ).…”

Section: Introductionmentioning

confidence: 99%

Moringa oleiferaseed oil or virgin coconut oil supplementation abrogates cerebral neurotoxicity induced by antineoplastic agent methotrexate by suppression of oxidative stress and neuro‐inflammation in rats

Famurewa¹,

Aja

Nwankwo

et al. 2018

J Food Biochem

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Methotrexate (MTX) is an effective antineoplastic drug associated with wide organ toxicity. Accumulating evidence implicates oxidative stress to be a leading underlying mechanism of MTX‐induced neurotoxicity. The study explores antioxidant potential of virgin coconut oil (VCO) or Moringa oleifera seed oil (MOO) in MTX‐induced oxidative stress‐mediated cerebral neurotoxicity and inflammation in rats. Rats treated with VCO or MOO (5 ml/kg bw) for 17 days were administered MTX (20 mg/kg, intraperitoneally) on day 14 only. Cerebral activities of acetylcholinesterase, antioxidant enzymes, lipid peroxidation, reduced glutathione and nitric oxide levels as well as cytokines were evaluated. MTX‐induced neurotoxic alterations were significantly abrogated by MOO and VCO supplementation via inhibition of cholinesterase, oxidative stress, and anti‐inflammatory mechanisms. VCO and MOO showed comparable antioxidant potentials with the standards in DPPH and FRAP assays. VCO and MOO are promising natural oils for modulating MTX neurotoxicity in cancer patients. Practical applications Methotrexate chemotherapy induces neurotoxicity in cancer patients, and this is a source of worry for clinicians. This study reports, for the first time, the beneficial health effects of functional food oils, Moringa oleifera seed oil, and virgin coconut oil against anticancer drug methotrexate‐induced cerebral neurotoxicity. Supplementation of these natural oils may be beneficial in the prevention of cerebral neurotoxic side effect in cancer patients undergoing methotrexate chemotherapy.

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“…In various studies, it has been determined that MTX increases the level of oxidative parameters and reduces the level of antioxidant parameters and it has been stated that hepatotoxicity is due to the increase of ROS (10). In the literature, antioxidants such as methionine, folic acid, and nicotinamide have been used to reduce the side effects of MTX treatment, and these antioxidants have been shown to have protective effects (11)(12)(13)(14)(15)(16)(17). MTX is stored in hepatocytes by forming polyglutamate derivatives from folic acid.…”

Section: Discussionmentioning

confidence: 99%

“…MTX is used in the treatment of many cancers and autoimmune diseases due to its antiproliferative, anti-inflammatory, and immunosuppressive properties (8-13). However, many side effects such as hepatotoxicity, small intestine damage, acute renal failure, and lung infiltration have also been reported (14,15). Although the cause of hepatotoxicity due to MTX has been tried to be explained with several possible mechanisms, the main reason is not yet known.…”

Section: Discussionmentioning

confidence: 99%

Histological changes in methotrexate hepatotoxicity after boron application and evaluation of serum thiol-disulfide balance

Neşelioğlu

Akcan²,

Nakkas³

et al. 2021

Journal of Health Sciences and Medicine

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Aim: Methotrexate, a folic acid antagonist is a chemotherapeutic drug used in the treatment of various inflammatory diseases as well as some cancer types. The purpose of this study; it is the study of the effects of boric acid against the hepatotoxic side effects of methotrexate. Material and Method: Male Wistar albino rats were divided into five groups and each group consisted of six animals. The rats in group 1 were used as a control group. Methotrexate was administered to the rats in group 2 and boric acid to the rats in group 3. While the rats in group 4 were given first methotrexate and then boric acid, the rats in group 5 were administered boric acid first and then methotrexate. Results: Light microscopic examination revealed sinusoidal dilatation, hepatocyte degeneration, vascular congestionthrombosis, and inflammatory infiltration in the livers of rats treated with methotrexate. It was observed that the protective effect of boric acid was more effective than its treatment. In the groups given methotrexate, the level of oxidative stressrelated parameters such as lipid hydroperoxide, MPO and disulfide increased (p<0.05 for all parameters), whereas the level of antioxidant parameters such as native thiol, total thiol and catalase decreased (p<0.05 for all parameters). Conclusion:In this study, the protective effect of boric acid was found to be higher than the therapeutic effect in liver damage caused by methotrexate. Oxidative hepatotoxicity resulting from methotrexate application disrupted the thiol disulfide balance and caused a shift to the oxidation side.

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Effect of ursodeoxycholic acid and vitamin E in the prevention of liver injury from methotrexate in pediatric leukemia

Abstract: ABSTRACT

Cited by 25 publications

References 19 publications

Efficacy of Vitamin E in Methotrexate-Induced Hepatotoxicity in Rheumatoid Arthritis: An Open-Label Case-Control Study

Efficacy of Vitamin E in Methotrexate-Induced Hepatotoxicity in Rheumatoid Arthritis: An Open-Label Case-Control Study

Moringa oleiferaseed oil or virgin coconut oil supplementation abrogates cerebral neurotoxicity induced by antineoplastic agent methotrexate by suppression of oxidative stress and neuro‐inflammation in rats

Histological changes in methotrexate hepatotoxicity after boron application and evaluation of serum thiol-disulfide balance

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