Best drug treatment for multidrug-resistant and extensively drug-resistant tuberculosis

Caminero, José A.; Sotgiu, Giovanni; Zumla, Alimuddin; Migliori, Giovanni Battista

doi:10.1016/s1473-3099(10)70139-0

Cited by 500 publications

(419 citation statements)

References 60 publications

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“…However the optimal duration of fluoroquinolone-containing regimens is unknown. Combined and prolonged use of levofloxacin and pyrazinamide has been associated with poor gastrointestinal tolerance [103,104].…”

Section: Treatment Of Active Tb In Transplant Recipientsmentioning

confidence: 99%

The risk of tuberculosis in transplant candidates and recipients: a TBNET consensus statement

Bumbăcea

Arend

Eyüboğlu³

et al. 2012

Eur Respir J

232

261

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Tuberculosis (TB) is a possible complication of solid organ and hematopoietic stem cell transplantation. The identification of candidates for preventive chemotherapy is an effective intervention to protect transplant recipients with latent infection with Mycobacterium tuberculosis from progressing to active disease. The best available proxy for diagnosing latent infection with M. tuberculosis is the identification of an adaptive immune response by the tuberculin skin test or an interferon-c based ex vivo assay. Risk assessment in transplant recipients for the development of TB depends on, among other factors, the locally expected underlying prevalence of infection with M. tuberculosis in the target population. In areas of high prevalence, preventive chemotherapy for all transplant recipients may be justified without immunodiagnostic testing while in areas of medium and low prevalence, preventive chemotherapy should only be offered to candidates with positive M. tuberculosis-specific immune responses. The diagnosis of TB in transplant recipients can be challenging. Treatment of TB is often difficult due to substantial interactions between anti-TB drugs and immunosuppressive medications. This management guideline summarises current knowledge on the prevention, diagnosis and treatment of TB related to solid organ and hematopoietic stem cell transplantation and provides an expert consensus on questions where scientific evidence is still lacking. KEYWORDS: Guideline, management, Mycobacterium tuberculosis, transplantation, tuberculosis T uberculosis (TB) is caused by the pathogenic species of the Mycobacterium tuberculosis complex. Only a minority of individuals who develop an adaptive immune response following infection with M. tuberculosis will ever develop TB, with the actual risk depending on the extent to which the host immune system provides a successful or inadequate response [1,2]. Therefore, individuals with impaired immune response, such as solid organ transplant (SOT) and hematopoietic stem cell transplant (HSCT) recipients, are more prone to develop TB than immunocompetent persons. TB in transplant recipients is more frequent compared to the general population (estimates from the last decades state 20-74 times as frequent in SOT [3,4] and twice as frequent in HSCT [5]), and more often fatal (up to 31% in SOT [6] and up to 50% in HSCT recipients [7]), thus adding effectiveness to interventions for its prevention, even in the face of difficulties, with treatment related to adverse drug events and drug-drug interactions. Active TB in transplant recipients can result from latent infection with M. tuberculosis (LTBI) in the transplant candidate or in the donor tissue, or from de novo post-transplant infection. These various scenarios prompt for targeted pre-transplant screening of both recipient and, if possible, donors to allow focused management of recipients selected for preventive intervention in the pre-and/or posttransplant period. The term ''preventive chemotherapy'' is used to denote treatmen...

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Section: Treatment Of Active Tb In Transplant Recipientsmentioning

confidence: 99%

The risk of tuberculosis in transplant candidates and recipients: a TBNET consensus statement

Bumbăcea

Arend

Eyüboğlu³

et al. 2012

Eur Respir J

232

261

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“…10 WHO guidelines for the treatment of drug-resistant tuberculosis in adults are based on evidence from meta-analyses of individual patients' data. 11 However, recommendations for children are based on expert opinion, drawing on data from case series and cohort studies, 12,13 often with small sample sizes. Consequently, variation exists in program matic choices of treatment regimens, with the choice of drugs informed by previous drug exposure and DST results.…”

Section: Introductionmentioning

confidence: 99%

Treatment outcomes for children with multidrug-resistant tuberculosis: a systematic review and meta-analysis

Ettehad

Schaaf

Seddon

et al. 2012

The Lancet Infectious Diseases

156

115

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“…As is well known, rifampicin is currently by far the best available drug, and is the only one that combines excellent bactericidal, sterilising and resistance preventing activity [7]. Therefore, it is the only drug with the ability to reduce the duration of TB treatment to 9 months (6 months if the other highly…”

mentioning

confidence: 99%

“…The achievable treatment success rate for MDR-TB cases ranges between 62% and 69% using long and poorly tolerated second-line drug regimens [8,9]. These success rates can be achieved despite the absence of R and H in the regimen because we have two other families of drugs with high efficacy against M. tuberculosis: the FQs and the second-line drug injectables (kanamycin, amikacin and capreomycin) [7], both with reproducible and relatively reliable drug susceptibility tests. Therefore, the definition of XDR-TB covers these two families of drugs, which can be tested in the laboratory and whose resistance carries a clearly worse prognosis, with a success rate of just 43.7% as reported in the meta-analysis by JACOBSON et al [10].…”

mentioning

confidence: 99%

Tuberculosis: are we making it incurable?

2013

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@ERSpublications With proper management all TB patients have a chance to be cured; it should never be thought that a TB case is incurable http://ow.ly/ksm5gTuberculosis (TB) is most probably the disease that has caused more damage to the human species throughout its history in terms of number of patients and, above all, death toll. There have been thousands of years spent fighting against Mycobacterium tuberculosis in which the human species could only rely on the efficiency of the immune system [1]. We must recall its importance as, in the pre-antibiotic era, the immune system alone could ensure important achievements such as: 1) only 50% of the people exposed to M. tuberculosis contract the infection [2]); 2) only 10% of those infected progress to active disease; and 3) up to 30% of patients with advanced TB disease heal spontaneously ( fig. 1) [3,4]. In spite of this, the fate of TB patients in the pre-chemotherapy period was very bleak, with a mortality of .50% within 5 years after the onset of disease [3,4]. For centuries, several empirical treatments were attempted to trying to change this fateful prognosis. Additionally, sanatoriums were built throughout the world for many decades ( fig. 2). However, all these interventions were not really effective, and none of them contributed significantly to improve the doom of TB patients [4]. Then, fortunately, their fate changed dramatically with the advent of the antibiotic era. The two decades from the discovery of streptomycin in 1943 to that of rifampicin in 1963 changed a devastating disease into a relatively easy to cure one. Not only were up to 11 different drugs with activity against M. tuberculosis discovered (streptomycin, p-aminosalicylate (PAS), thiacetazone, isoniazid (H), pyrazinamide, cycloserine, kanamycin, ethionamide, ethambutol, capreomycin and rifampicin (R)), but, based on multiple randomised clinical trials, the basic fundamentals of TB treatment were also established [4,5]. Probably the most essential of these was the need to combine at least two to three drugs to which the patient was sensitive, as M. tuberculosis can develop resistance to single drugs.The ability of M. tuberculosis to develop resistances to antibiotics was described in the very first randomised clinical trial conducted with streptomycin and published in 1948 [6]. The first great lesson learnt from early randomised clinical trials was that using TB drugs in monotherapy, or in poor combinations, would lead to the selection of resistance to these drugs [5]. Thus, as a result of the misuse of the available drugs, monoresistant TB started to develop, followed by poly-resistant TB (resistance to two or more drugs), multi-drug resistant (MDR)-TB (resistance to at least H+R), and extensively-drug resistant (XDR)-TB (defined as MDR-TB plus resistance to at least one fluoroquinolone (FQ) and one second-line injectable drug). The need for definitions beyond XDR-TB is a currently an issue of debate.The definitions in the field of anti-TB drug resistance should be based on two main fact...

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Best drug treatment for multidrug-resistant and extensively drug-resistant tuberculosis

Cited by 500 publications

References 60 publications

The risk of tuberculosis in transplant candidates and recipients: a TBNET consensus statement

The risk of tuberculosis in transplant candidates and recipients: a TBNET consensus statement

Treatment outcomes for children with multidrug-resistant tuberculosis: a systematic review and meta-analysis

Tuberculosis: are we making it incurable?

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