Inviting an author to review:
Find an author and click ‘Invite to review selected article’ near their name.
Search for authorsSearch for similar articles
3
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Moxifloxacin concentration correlate with QTc interval in rifampicin-resistant tuberculosis patients on shorter treatment regimens

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Drug-resistant tuberculosis (DR-TB) continues to be a global threat. Moxifloxacin is one of the components of the shorter treatment regimen which is suspected to increase the risk of QT prolongation, although it is also likely to be the most effective against DR-TB. A study to evaluate the correlation between the concentration of moxifloxacin and QTc interval in RR-TB patients who received shorter regimens is needed.

          Methods

          This was an observational study in 2 groups of RR-TB patients on shorter treatment regimens (intensive phase and continuation phase), contain moxifloxacin with body weight-adjusted dose. Blood samples were collected at 2 h after taking the 48th-hour dose and 1 h before taking the 72nd-hour dose.

          Results

          Forty-five RR-TB patients were included in this study. At 2 h after taking the 48th-hour dose, the mean of QTc interval in intensive phase and continuation phase was 444.38 ms vs. 467.94 ms, p = 0.026, while mean of moxifloxacin concentration in intensive phase and continuation phase was 4.3 µg/mL vs. 4.61 µg/mL, p = 0.686). At 1 h before taking the 72nd-hour dose, both moxifloxacin concentration and QTc interval in intensive phase and continuation showed no significant difference with p-value of 0.610 and 0.325, respectively. At 2 h after taking the 48th-dose, moxifloxacin concentration did not correlate with QTc interval, both in intensive phase (p = 0.576) and in continuation phase (p = 0.691). At 1 h before taking the 72nd-hour dose, moxifloxacin concentration also did not correlate with QTc interval in intensive phase (p = 0.531) and continuation phase (p = 0.209).

          Conclusions

          Our study found that moxifloxacin concentration did not correlate with QTc interval, which indicates the safe use of moxifloxacin on QTc interval. In addition to close monitoring of QTc interval, the clinicians should also consider other variables which potentially increase risk for QTc prolongation in DR-TB patients who received shorter treatment regimens.

          Related collections

          Most cited references25

          • Record: found
          • Abstract: found
          • Article: not found

          Drug-induced QT interval prolongation: mechanisms and clinical management.

          The prolonged QT interval is both widely seen and associated with the potentially deadly rhythm, Torsades de Pointes (TdP). While it can occur spontaneously in the congenital form, there is a wide array of drugs that have been implicated in the prolongation of the QT interval. Some of these drugs have either been restricted or withdrawn from the market due to the increased incidence of fatal polymorphic ventricular tachycardia. The list of drugs that cause QT prolongation continues to grow, and an updated list of specific drugs that prolong the QT interval can be found at www.qtdrugs.org. This review focuses on the mechanism of drug-induced QT prolongation, risk factors for TdP, culprit drugs, prevention and monitoring of prolonged drug-induced QT prolongation and treatment strategies.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Drug-induced Inhibition and Trafficking Disruption of ion Channels: Pathogenesis of QT Abnormalities and Drug-induced Fatal Arrhythmias

            Risk of severe and fatal ventricular arrhythmias, presenting as Torsade de Pointes (TdP), is increased in congenital and acquired forms of long QT syndromes (LQTS). Drug-induced inhibition of K+ currents, IKs, IKr, IK1, and/or Ito, delay repolarization, prolong QT, and increase the risk of TdP. Drug-induced interference with IKr is the most common cause of acquired LQTS/TdP. Multiple drugs bind to KNCH2-hERG-K+ channels affecting IKr, including antiarrythmics, antibiotics, antivirals, azole-antifungals, antimalarials, anticancer, antiemetics, prokinetics, antipsychotics, and antidepressants. Azithromycin has been recently added to this list. In addition to direct channel inhibition, some drugs interfere with the traffic of channels from the endoplasmic reticulum to the cell membrane, decreasing mature channel membrane density; e.g., pentamidine, geldalamicin, arsenic trioxide, digoxin, and probucol. Other drugs, such as ketoconazole, fluoxetine, norfluoxetine, citalopram, escitalopram, donepezil, tamoxifen, endoxifen, atazanavir, and roxitromycin, induce both direct channel inhibition and impaired channel trafficking. Although many drugs prolong the QT interval, TdP is a rare event. The following conditions increase the risk of drug-induced TdP: a) Disease states/electrolyte levels (heart failure, structural cardiac disease, bradycardia, hypokalemia); b) Pharmacogenomic variables (presence of congenital LQTS, subclinical ion-channel mutations, history of or having a relative with history of drug-induced long QT/TdP); c) Pharmacodynamic and kinetic factors (high doses, women, elderly, metabolism inhibitors, combining two or more QT prolonging drugs, drugs that prolong the QT and increase QT dispersion, and drugs with multiple actions on ion channels). Because most of these conditions are preventable, careful evaluation of risk factors and increased knowledge of drug use associated with repolarization abnormalities are strongly recommended.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              Long QT Syndrome: An Emerging Role for Inflammation and Immunity

              The long QT syndrome (LQTS), classified as congenital or acquired, is a multi-factorial disorder of myocardial repolarization predisposing to life-threatening ventricular arrhythmias, particularly torsades de pointes. In the latest years, inflammation and immunity have been increasingly recognized as novel factors crucially involved in modulating ventricular repolarization. In the present paper, we critically review the available information on this topic, also analyzing putative mechanisms and potential interplays with the other etiologic factors, either acquired or inherited. Accumulating data indicate inflammatory activation as a potential cause of acquired LQTS. The putative underlying mechanisms are complex but essentially cytokine-mediated, including both direct actions on cardiomyocyte ion channels expression and function, and indirect effects resulting from an increased central nervous system sympathetic drive on the heart. Autoimmunity represents another recently arising cause of acquired LQTS. Indeed, increasing evidence demonstrates that autoantibodies may affect myocardial electric properties by directly cross-reacting with the cardiomyocyte and interfering with specific ion currents as a result of molecular mimicry mechanisms. Intriguingly, recent data suggest that inflammation and immunity may be also involved in modulating the clinical expression of congenital forms of LQTS, possibly triggering or enhancing electrical instability in patients who already are genetically predisposed to arrhythmias. In this view, targeting immuno-inflammatory pathways may in the future represent an attractive therapeutic approach in a number of LQTS patients, thus opening new exciting avenues in antiarrhythmic therapy.
                Bookmark

                Author and article information

                Contributors
                Journal
                J Clin Tuberc Other Mycobact Dis
                J Clin Tuberc Other Mycobact Dis
                Journal of Clinical Tuberculosis and Other Mycobacterial Diseases
                Elsevier
                2405-5794
                06 June 2022
                August 2022
                06 June 2022
                : 28
                : 100320
                Affiliations
                [a ]Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Indonesia
                [b ]Department of Pulmonology and Respiratory Medicine, Faculty of Medicine, Universitas Airlangga, Surabaya, East Java, Indonesia
                [c ]Department of Medical Microbiology, Faculty of Medicine, Universitas Airlangga, Surabaya, East Java, Indonesia
                [d ]Laboratory of Tuberculosis, Institute of Tropical Disease, Universitas Airlangga. Surabaya, Indonesia
                [e ]Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Airlangga, Surabaya, East Java, Indonesia
                [f ]Department of Clinical Pharmacy, Faculty of Pharmacy, Universitas Airlangga, Surabaya, East Java, Indonesia
                Author notes
                [* ]Corresponding author at: Jl. Mayjen Prof. Dr. Moestopo No. 47, Surabaya 60131, Indonesia. nmademertaniasih@ 123456gmail.com
                Article
                S2405-5794(22)00025-0 100320
                10.1016/j.jctube.2022.100320
                9189108
                35706565
                f9d1caf9-f6d7-4b3f-b68d-85be9be0c2a0
                © 2022 The Authors. Published by Elsevier Ltd.

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Categories
                Article

                drug-resistant tuberculosis,shorter treatment regimen,moxifloxacin concentration,qtc interval

                Comments

                Comment on this article