Recurrent heart failure in pulmonary tuberculosis patients on antitubercular therapy: A case of protector turning predator

Ray, Animesh; Nangia, Vivek; Chatterji, R.; Dalal, Navin; Ray, Ruchismita Satpathy

doi:10.4103/1687-8426.211400

Cited by 8 publications

(6 citation statements)

References 3 publications

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“…Liver toxicity and gastrointestinal reaction were predominant side effects observed during clinical drug use and several cases indicate that isoniazid causes cardiotoxicity [29,30]. In our study, we discovered that isoniazid caused a deficiency in cardiac development via a ROS dependent manner.…”

Section: Discussionmentioning

confidence: 53%

Isoniazid causes heart looping disorder in zebrafish embryos by the induction of oxidative stress

Wang

Wei

et al. 2020

BMC Pharmacol Toxicol

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Background: The cardiotoxicity of isoniazid on zebrafish embryos and its underlying mechanism is unclear. Methods: Here, we exposed zebrafish embryos at 4 h post-fertilization to different levels of isoniazid and recorded the morphology and number of malformed and dead embryos under the microscope. Results: The high concentration of isoniazid group showed more malformed and dead embryos than the low concentration of isoniazid group and control group. The morphology of the heart and its alteration were visualized using transgenic zebrafish (cmlc2: GFP) and confirmed by in situ hybridization. The negative effects of isoniazid on the developing heart were characterized by lower heart rate and more heart looping disorders. Mechanistically, PCR showed decreased expression of heart-specific transcription factors when exposed to isoniazid. Oxidative stress was induced by isoniazid in cardiomyocytes, mediated by decreased activities of catalase and superoxide dismutase, which were rescued by scavengers of reactive oxygen species. Conclusion: In conclusion, this study demonstrated that isoniazid led to heart looping disturbance by the downregulation of cardiac-specific transcription factors and induction of cardiomyocyte apoptosis.

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Section: Discussionmentioning

confidence: 53%

Isoniazid causes heart looping disorder in zebrafish embryos by the induction of oxidative stress

Wang

Wei

et al. 2020

BMC Pharmacol Toxicol

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“…As a first-line anti-tuberculosis drug, isoniazid plays an irreplaceable role in the treatment of tuberculosis [2]. Liver toxicity and gastrointestinal reaction were predominant side effects observed during clinical drug use and several cases indicate that isoniazid causes cardiotoxicity [31,32]. In our study, we discovered that isoniazid caused a deficiency in cardiac development via a ROS dependent manner.…”

Section: Discussionmentioning

confidence: 65%

Isoniazid causes heart looping disorder in zebrafish embryos by the induction of oxidative stress

Wang

Wei

et al. 2020

Preprint

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Background: The cardiotoxicity of isoniazid on zebrafish embryos and its underlying mechanism is unclear. Methods: Here, we exposed zebrafish embryos at 4 hours post-fertilization to different levels of isoniazid and recorded the morphology and number of malformed and dead embryos under the microscope. Results: The high concentration of isoniazid group showed more malformed and dead embryos than the low concentration of isoniazid group and control group. The morphology of the heart and its alteration were visualized using transgenic zebrafish (cmlc2: GFP) and confirmed by in situ hybridization. The negative effects of isoniazid on the developing heart were characterized by lower heart rate and more heart looping disorders. Mechanistically, PCR showed decreased expression of heart-specific transcription factors when exposed to isoniazid. Oxidative stress was induced by isoniazid in cardiomyocytes, mediated by decreased activities of catalase and superoxide dismutase, which were rescued by scavengers of reactive oxygen species. Conclusion: In conclusion, this study demonstrated that isoniazid led to heart looping disturbance by the downregulation of cardiac-specific transcription factors and induction of cardiomyocyte apoptosis.

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“…In conclusion, anti-TBC drugs can rarely cause cardiotoxicity and heart failure; there are a few reports published. None of those adverse events occurred in our case during follow-up [7,8].…”

mentioning

confidence: 51%

Acute pericarditis in a young patient with IgG immunodeficiency

Skowerski¹,

Skowerski²,

Grzywocz³

et al. 2020

aoms

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A 35-year-old female health care worker with IgG deficiency was urgently admitted to our department due to pericardial effusion, which was diagnosed during a follow-up visit in an outpatient clinic. The IgG deficiency was detected over 10 years ago and classified by a hematologist as mild. There was no known history of IgG replacement therapy or chronic or recurrent infections. Two months prior to admission, she had been urgently hospitalized in a cardio-thoracic center due to an episode of cardiac tamponade evacuated with a pericardiocentesis. She had been discharged after 5 days in good condition and remained asymptomatic until a week before admission to our hospital. The pericardial fluid had been sent to diagnostics, but the test results remained unknown. The patient presented fatigue, dyspnea, and heart failure symptoms (New York Heart Association (NYHA) class III). Physical examination revealed tachycardia (heart rate 120 bpm) and hypotension (90/60 mm Hg). The patient denied weight loss, cough, fever, or night chills. Laboratory tests showed anemia (hemoglobin 8.9 mg/dl), elevated C-reactive protein level (CRP 64 mg/dl), no leukocytosis, and elevated CA-125 level (169.3 U/ml, reference < 35 U/ml). In the ECG, sinus rhythm with tachycardia (120 bpm), PR depression in inferior leads (II, III, aVF), and negative T waves in precordial leads (V2-V6) were found. Transthoracic echocardiography (TTE) revealed preserved left ventricular ejection fraction (LVEF, > 60%), pericardial effusion (> 30 mm of fluid), and impaired right ventricular function (right atrium and ventricle were collapsing; Figures 1 A, B). A diagnosis of cardiac tamponade was made, and urgent pericardiocentesis was performed. Over 450 ml of bright yellow, cloudy fluid was evacuated (Figure 1 C). The patient's condition improved significantly. In the angio-CT, hepatomegaly, a tumor in the uterus (defined by the radiologist as a uterine fibroid), and bilateral pleural effusion were described. Rheumatic diseases and HIV infection were excluded. The pericardial fluid's microscopic test revealed Mycobacterium tuberculosis, whereas the pleural fluid's microscopic test for Mycobacterium tuberculosis was negative. Initial anti-tuberculosis treatment was administered, and the patient was transferred to the pulmonology ward for further treatment. The tuberculosis was treated with rifampicin (6 months), pyrazinamide (3 months), ethambutol (3 months), and prednisolone (30 mg daily for 8 weeks) due to pericarditis. Two months after the initiation of TBC treatment, she was urgently admitted to the hospital due to jaundice, which was caused by TBC therapy. The pyrazinamide and rifam

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Recurrent heart failure in pulmonary tuberculosis patients on antitubercular therapy: A case of protector turning predator

Cited by 8 publications

References 3 publications

Isoniazid causes heart looping disorder in zebrafish embryos by the induction of oxidative stress

Isoniazid causes heart looping disorder in zebrafish embryos by the induction of oxidative stress

Isoniazid causes heart looping disorder in zebrafish embryos by the induction of oxidative stress

Acute pericarditis in a young patient with IgG immunodeficiency

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