Tuberculosis
Dinesh Kumar Jain in Homeopathy, 2022
Supporters of Ayurveda, homeopathy, and other nonscientific methods of treatment are actually responsible for many deaths of noneducated citizens specially villagers. Poor people and people from villages take Ayurveda and homeopathy and suffer a lot. Many people die or become disabled. Preventable diseases are spreading dangerously in India. I know many people who were taking Ayurvedic or homeopathic treatment for tuberculosis ultimately died. Many people first take medical treatment for one or two months, then start homeopathy or Ayurveda. Tuberculosis treatment should be taken 6–12 months continuously for complete treatment. Otherwise, the tuberculosis of these patients becomes resistant, and then it is not possible to treat them. Such foolishness is responsible for spreading many diseases like malaria and tuberculosis. “The emergence of drug resistant strains of microorganisms or parasites is promoted by treatments that do not result in cure” (Park, 1997, p. 265).
Tuberculosis in Childhood and Pregnancy
Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies in Clinical Tuberculosis, 2020
In mothers who are continued on tuberculosis treatment following the delivery of the infant, questions arise regarding the safety of breastfeeding while the mother is receiving antituberculosis drugs. Snider and Powell showed that a breastfeeding infant would receive no more than 20% of the usual therapeutic dosage of isoniazid and less than 11% for other antituberculosis drugs.234 Potential toxic effects of drugs delivered via breast milk have not been reported. However, because pyridoxine deficiency in the neonate can cause seizures, and breast milk contains relatively low levels of pyridoxine, the infant whose breastfeeding mother is taking isoniazid should receive supplemental pyridoxine. This is often administered in the form of an infant multi-vitamin.235
Respiratory Diseases
Vincenzo Berghella in Maternal-Fetal Evidence Based Guidelines, 2022
Tuberculosis treatment is not altered by pregnancy. Although latent TB treatment may be deferred to the postpartum period, there is no defensible argument for deferring treatment of active disease during pregnancy. Pregnant women who are untreated pose an infection risk to the population at large as well as to their own infants. To guide treatment, sputum samples for smear microscopy and culture should be obtained at monthly intervals until two consecutive negative months are observed.
Treatment of spinal tuberculosis in rabbits using bovine serum albumin nanoparticles loaded with isoniazid and rifampicin
Published in Neurological Research, 2022
Rong Ma, Jianqun Zhang, Zhen Chen, He Ma, Xiaoyin Liu, Simin Liang, Peng Wu, Zhaohui Ge
Anti-tuberculosis chemotherapy is the foundation and core of tuberculosis treatment. However, the commonly used anti-tuberculosis drugs are associated with many adverse effects, including liver, kidney, and nervous system damage. Due to the long treatment period of conventional anti-tuberculosis drugs and their short half-life, patient compliance is poor, which is likely to cause treatment failure. Based on this, we used modern nanotechnology to successfully construct intravenous isoniazid (Isoniazid, INH) and rifampicin (Rifampicin, RFP) bovine albumin nanoparticles [1]. The drug-loaded nanoparticles have a small particle size, with an average of 60.5 ± 4.6 nm. The in vitro drug release studies and rabbit in vivo pharmacokinetic studies [2] revealed that the prepared INH and RFP bovine albumin nanoparticles have good in vitro properties. Due to the slow-release characteristics of anti-tuberculosis drugs in the body, these nanoparticles also have the advantages of strong bone tissue targeting abilities and long sustained-release time. To investigate the efficacy of INH and RFP bovine albumin nanoparticles, we established a New Zealand white rabbit spinal tuberculosis model, used the drug-loaded nanoparticles to treat the model and observed its efficacy.
Advances in the pharmacological management of bacterial peritonitis
Published in Expert Opinion on Pharmacotherapy, 2021
Daniel Pörner, Sibylle Von Vietinghoff, Jacob Nattermann, Christian P Strassburg, Philipp Lutz
Peritonitis has been reported as the sixth most frequent, extrapulmonary manifestation of tuberculosis in the United States [84]. It is usually caused by hematogenic dissemination of mycobacteria. The course of disease is subacute with a nonspecific clinical presentation. Ascites is present in up to 73% of the cases [85]. An increased risk for tuberculous peritonitis has been described for patients with ESRD [86], (alcoholic) cirrhosis [87] and HIV/AIDS [88]. Indicators of potential tuberculous peritonitis are lymphocytic instead of neutrophilic leukocytosis in the ascites, high albumin concentration and elevated levels of adenosine deaminase in the ascites. Usually, detection of mycobacterial nucleic acid, positive cultures or typical histological findings are required for a final diagnosis of tuberculous peritonitis but may be difficult to achieve without laparoscopy [89–91]. Tuberculous peritonitis should be considered as differential diagnosis in cases of culture-negative peritonitis which does not resolve by standard treatment [47]. However, pursuit of this differential diagnosis involves a high degree of suspicion. Tuberculostatic therapy follows the current recommendations for treatment of tuberculosis. For uncomplicated tuberculosis, treatment consists of oral application of isoniazid, rifampicin, pyrazinamide and ethambutol for two months followed by administration of isoniazid and rifampicin for another four months [92].
Corticosteroids as an adjunct to tuberculosis therapy
Published in Expert Review of Respiratory Medicine, 2018
Charlotte Schutz, Angharad G Davis, Bianca Sossen, Rachel P-J Lai, Mpiko Ntsekhe, Yolande XR Harley, Robert J Wilkinson
Globally pulmonary tuberculosis contributes an estimated 81% of all reported tuberculosis cases [1]. The proportion extrapulmonary varies by age, location, HIV-1 status and ascertainment (Table 1). The inflammatory immune response elicited by tuberculosis is responsible for much of the associated structural lung damage and subsequent functional impairment. Use of adjuvant anti-inflammatory agents such as corticosteroids for the treatment of pulmonary tuberculosis has been researched since the 1960s. Adverse pharmacokinetic interactions with tuberculosis treatment and corticosteroid-related side-effects have been areas of concern. Two systematic reviews have been conducted on adjunctive corticosteroid therapy in pulmonary tuberculosis, with contradictory conclusions. A systematic review published in 2003 included 11 RCTs and found that corticosteroids were safe and provide early and sustained benefit as determined by clinical and radiological features of pulmonary tuberculosis in selected patients with advanced disease. However, mortality was not assessed and conclusions were based on findings of small studies only two of which included rifampicin in treatment regimens [4]. A more recent Cochrane review updated the findings of this 2003 systematic review by inclusion of 18 trials (including the 11 trials from the 2003 review). The conclusion on this occasion was that there was no high-quality evidence of benefit in the context of contemporary antimicrobial treatment of tuberculosis, due to lack of large clinical trials using rifampicin in the treatment regimen [5].
Related Knowledge Centers
- Ethambutol
- Hepatotoxicity
- Isoniazid
- Pyridoxal Phosphate
- Rifampicin
- Streptomycin
- Tuberculosis
- Peripheral Neuropathy
- Pyrazinamide
- Latent Tuberculosis