Methionine and vitamin B‐complex ameliorate antitubercular drugs‐induced toxicity in exposed patients

Abstract

Tuberculosis therapy utilizes drugs that while effective cause treatment‐related toxicity. Modulation of antitubercular drugs‐induced toxicity by methionine and vitamin B‐complex in patients was evaluated. 285 treatment‐naïve tuberculosis patients at the Chest Clinics of Infectious Diseases Hospital, Yaba and General Hospital, Lagos in Lagos, Nigeria was prospectively recruited and allotted into test (antitubercular medicines, methionine and vitamin B‐complex) and control groups (antitubercular medicines). Data on adverse drug reactions and blood samples were collected at initiation, 2 months and 6 months, and then analyzed. Red blood cells and packed cell volume were significantly higher (P < 0.05) in the test group compared to control at 6 months of therapy. At the end of 2 months, results showed a significant decrease (P < 0.001) in aspartate aminotransferase, alkaline phosphatase, alanine aminotransferase, urea, creatinine and total bilirubin in the test group compared to control. Reduced glutathione and superoxide dismutase were significantly increased (P < 0.001) and malondialdehyde significantly decreased (P < 0.001) in the test versus control groups at the end of 2 and 6 months. Adverse drug reactions were significantly lower (P < 0.001) in the test group (32.4%) compared to control group (56.2%), with 1 death. Hepatotoxicity was significantly higher (P = 0.026) in control (6.9%), compared to test group (0%). Alcohol and cigarette smoking were significantly (P = 0.019 and P = 0.027) associated with the occurrence of adverse drug reactions. Methionine and vitamin B‐complex modulated hepatic, renal, hematological, antioxidant indices and adverse effects in patients administered antitubercular medicines. Such interventions can enhance compliance and better treatment outcomes in tuberculosis patients.

Assessing the protective effect of Crassocephalum vitellinum against Rifampicin- induced hepatotoxicity in Wistar rats

“…Although the mechanism of hepatotoxicity of the drug seems unclear, oxidative stress caused by free radical metabolites of drugs has been strongly linked to this adverse drug reaction and a number of studies have demonstrated the presence of oxidative stress amongst patients with drug induced hepatotoxicity 33 .…”

Oral Combination of Vitamin B1, B6, and B12 Supplementation on CD4+ T Cell and IFN-γ in Pulmonary Tuberculosis Patients with First-Line Opioid agonist therapy

“…Administering vitamins B1, B6, and B12 can increase the number of T lymphocytes and the activity of Natural Killer cells (NK cells), both of which can trigger the release of interferon-gamma (INF-γ). Giving vitamins can reduce the risk of recurrence of tuberculosis by 45 % and reduce the incidence of extrapulmonary tuberculosis (14).…”

Isolated Nodal TBC Reactivation in a Patient with Post-Thrombocythemia Myelofibrosis Treated with Ruxolitinib: Case Report and Review of the Literature

“…Anti-TBC therapies are known for their hematological adverse events, in particular isoniazid-induced anemia, through the superoxide generation and the blockade of heme synthesis [15,16]. Also, ruxolitinib may cause or contribute to anemia in MF.…”