Antitubercular drugs pdf

Continue Tb treatment is aimed at shortening the clinical course of tuberculosis, preventing complications, preventing the development of delay and/or subsequent recurrences, and reducing the likelihood of transmission of tuberculosis. In patients with laten tuberculosis, the purpose of therapy is to prevent the progression of the disease. View full drug information This is the primary drug selected for use in preventive therapy and for use in active tuberculosis combination therapy. It is also used in combination with Rifapentin for adults and children aged 2 years or older with laten TB as a once-weekly DOT therapy for 12 weeks. Its mechanism of action is not fully understood, but isosiosied can inhibit the synthesis of myclic acid, resulting in disruption of the bacterial cell wall. In patients receiving active TB, 25-50 mg of pyridoxin should be taken orally once a day to prevent peripheral neuropathy. See the full drug information Rifampin is used in co-ed with at least 1 other anti-tuberculosis drug active in TB. Inhibits DNA-dependent RNA polymerase activity in bacterial cells, but not mammalian cells. Cross resistance may occur. In most susceptible cases, the patient undergoes 6 months of treatment. Treatment lasts for 9 months if the patient's sputum herniation results are positive after 2 months of treatment. View full drug information This is an analogue of nicotinamide pirazine, which is bacteriostatic or bactericidal against M tuberculosis, depending on the concentration of the drug reached at the site of infection. The mechanism of action of pyrazinamide is unknown. Inject the drug into the initial 2 months of a 6-month or longer treatment regimen with drug-sensitive TB. Treat drug-resistant TB with personalized treatments. View the complete drug information on Ethambutol diffuse actively growing mycobacterial cells (eg, tuberculosis bacillus). This impairs cell metabolism by inhibiting the synthesis of 1 or more metabolites, which in turn causes cell death. There's no evidence of cross-resistance. Mycobacterial resistance is common with previous therapy. In such cases, use ethambutol in combination with second-line drugs that have not previously been insansed. Administered every 24 hours until prolonged bacteriological transformation and maximum clinical improvement are observed. Absorption is not significantly changed by food. Adverse effects of ethambutol include optical neuritis, which is usually reversible by discontinuing the drug. During the period when the patient receives a dose of 25 mg/kg per day, a monthly eye test is recommended. View complete drug information on Streptomycin sulfate, aminoglycolyside, used to treat susceptible mycobacterial infections. Use this substance in combination with other antituberculous drugs isoniazide, ethambutol, rifampin). Although the total duration of treatment for tuberculosis is at least 6 months, streptomycin streptomycin it is not commonly used throughout the course of treatment because of toxicity concerns. The drug is recommended if less potentially dangerous therapeutic drugs are ineffective or contraindicated. View the full drug information on Levofloxacin, a second-line antituberculous drug, used in co-rifampin and other antituberculous agents to treat most cases of multidrug-resistant TB (MDR-TB). In a good safety profile, long-term use among fluoroquinolones has made levofloxacin the preferred oral agent for the treatment of MDR-TB caused by organisms resistant to first-line drugs. Levofloxacin triggers the effects of inhibition through bacterial topoimic topoimyrases IV and DNA gyrases, which are necessary for DNA replication, transcription, repair, and recombination. View the full drug information on Moxifloxacin, a second-line antituberculous drug, inhibiting the subunits of DNA gyrases, leading to inhibition of bacterial DNA replication and transcription. Moxifloxacin can be used on MDR-TB by organisms known or suspected to be sensitive to fluoroquinolones, or if the first-line medicinal product cannot be used due to intolerance. View full drug information This substance is used twice a week as part of a multi-drug treatment for 2 months during the intensive phase of TB treatment, and then once a week for 4 months, together with ioniazid or the corresponding active ingredient in susceptible organisms. The medicine is indicated as treatment once a week for adults and children aged 2 years or older with laten TB combined with iszolaziazide. Rifapentin inhibits DNA-dependent RNA polymerase in susceptible strains of M tuberculosis organisms. It should not be used to treat active tuberculosis after 2 months of treatment with HIV infection or positive tb cultures. See the full drug information, etionamide is a second-line drug that is bacteriostatic or bactericidal against M tuberculosis, depending on the concentration of the drug reached at the site of infection. It is recommended if treatment with first-line drugs (isoniazid, rifampin) is unsuccessful. Etionamide can be used to treat any form of active tuberculosis. However, it should only be used with other effective tuberculosis drugs. See the full drug information amikacin is a second-line drug used to treat patients with MDR-TB or those who do not tolerate first-line therapies. This agent irreversibly binds to the 30S subunit of bacterial ribosomes, blocking the detection step of protein synthesis and causing growth inhibition. View the complete drug information on Cycloserine, a second-line TB drug, inhibiting cell wall synthesis of susceptible strains of gram-positive and gram-negative bacteria and M tuberculosis. This Structural analogue d-alanine, which antagonizes the role of D-alanine in bacterial cell wall synthesis, inhibits growth. Like all antituberculosis drugs, cicloserin is With other effective TB drugs and not the only therapeutic agent, look at the complete drug information Capreomycin, which is taken from Streptomyces capreolus, is a second-line drug used in co-ed with other antituberculous agents in lung infections caused by creomin-sensitive strains of M tuberculosis. Creomicin is used only if first-line agents (e.g. isoliazida, rifampin) have been ineffective or cannot be used due to toxicity or the presence of resistant tuberculosis bacilluses. See full drug information This is an ansamycin antibiotic derived from rifamycin S. Rifabutin inhibits DNA-dependent RNA polymerase, preventing chain initiation. It is used in TB to treat individuals with specific HIV drugs when rifampin is contraindicated (most protease inhibitors). View the complete drug information clofazimine inhibits mycobacterial growth, binding preferably to mycobacterial DNA. It has antimicrobial properties, but its mechanism of action is unknown. It is rarely used to treat MDR-TB. As with any drug for TB, clofazimine is always used in other antituberculous agents. Clofazimine is only available on a patient basis, doctors who submit a test for a new drug (IND) application to the U.S. Food and Drug Administration (FDA). View full drug information This is a bacteriostatic agent that is useful as a second line agent against M tuberculosis. This is the most commonly used MDR-TB, or if treatment with ioniazid or rifampin is not possible. It inhibits the development of bacterial resistance against streptomycin and isolesisida. This substance should be administered with other anti-tuberculosis drugs. View the full drug information on Bedaquiline as a diarylquinoline that inhibits mycobacterial adenosine 5'-triphosphate (ATP) synthase, an enzyme essential for the generation of energy in Mycobacterium tuberculosis. 24 weeks of multidrug therapy (at least 4 other antitubercular medicines) in adults and adolescents aged 5 years and older with pulmonary MDR-TB. Therapy with bedaquiline is reserved if no effective treatment regimen can be provided by other means. It is not recommended for the treatment of latening, extrapulmonary or drug-sensitive tuberculosis. View the full drug information on Nitroimidazooxazine, which kills actively reproducing M tuberculosis by inhibiting myoic acid biosynthesis, thereby blocking cell wall production. As part of combination treatment with bedaquiline and linezolide, it is indicated for the treatment of pulmonary, widely drug-resistant TB (XDR-TB) or treatment-intolerant or unresponsive MDR-TB in adults. Delamanid is a dihydro-nitroimidazooxazole derivative. It works by inhibiting the synthesis of the mycobacterial cell wall. The WHO's treatment of drug-resistant tuberculosis 2019 as an imitator, requires that delamanid be included in the treatment of MDR/rifampin-resistant patients older >3 years of age during longer treatment. Treatment of tuberculosisDifferent pharmaceutical tuberculosis treatments and their measuresSpecialInfected diseases[edit wikidata] Treatment of tuberculosis refers to the medical treatment of infectious disease tuberculosis (TB). The standard short course of treatment for TB is isosiazide (along with pyridoxatic phosphate, peripheral neuropathy caused by isoisiazide, rifampicin (also known as rifampin in the United States), pyrazinamide and ethambutol for two months, followed by isoiazide and rifampicin alone for another four months. The patient is considered free of live bacteria after six months. In laten tuberculosis, the standard treatment alone is a combination of 6-9 months of daily ioniazid or three months per week (12 doses in total) of isiazida/rifapentin. [1] [2] [3] If the body is known to be completely sensitive, treatment is treated with ioniazid, rifampicin and pyrazinamid for two months, followed by ioniazid and rifampicin for four months. Ethambutol does not need to be used. [not checked] Drug First Line Tuberculosis Drugs Drugs 3 letter 1 letter 1 letter Ethambutol EMB E Isoniazid INH H Pyrazinamide PZA Z Rifampicin R Streptomycin STM S Second-line tuberculosis drugs Ciprofloxacin CIP (none) Moxifloxacin MXF (none) p- aminosalicylic acid PAS P First line All first-line anti-tuberculosis drug names have a semi-standard three-letter and one-letter abbreviation: ethambutol EMB or E, isoniazid INH or H, pyrazinamide PZA or Z, rifampicin RMP or R, streptomycin SM or S. First-line anti-tuberculosis drug names are often remembered for their mnemonic RIPE, referring to the use of rifamycin (such as rifampin), isazide, pyrazinamid, and ethambutol. U.S. practice uses abbreviations and names that have not been called internationally: rifampicin is called rifampin and abbreviated RIF; streptomycin abbreviated as STM. Other abbreviations have also been widely used (e.g. RIF, RFP and RMP are widely used for rifampicin, and combination treatment regimens have markings such as IRPE, HRZE, RIPE and IREP, which are different cononies or close synonyms, depending on dosage regimens), but for clarity, the semi- standardized abbreviations used above are used in the rest of the article. In this system, supported by the World Health Organization (WHO), RIPE is the RHZE. (Both have mnemonic potential as they are named after tuberculosis tubercles (small tubers) and the tubers can mature and be rhizomes.) Medications are similarly shortened in a semi-standardized way. The drugs are listed in their one-letter abbreviation (in the order above, which is roughly the order of introduction into clinical practice). The prefix indicates that the treatment be given for a period of 1 month; the subscript indicates a periodic broadcast (i.e. 3 means three times a week) and subscript means daily dosing. Most treatments have an initial high intensity phase, followed by a continuation phase (also known as a consolidation phase or liquidation phase): first the high intensity phase, then the continuation phase, the two phases are separated by a slash. So 2HREZ/4HR3 means isoniazide, rifampicin, ethambutol, pyrazinamide for two months a day, followed by four months of isoniazide and rifampicin three times a week. In the U.S. only, streptomycin is not considered a first-line drug ats/IDSA/CDC because of its high resistance. [4] The WHO did not make such a recommendation. [summons required] Second line Second-line medicines (WHO groups 2, 3 and 4) are used only for the treatment of diseases resistant to first-line therapy (i.e. widely drug-resistant tuberculosis (XDR-TB) or multidrug-resistant tuberculosis (MDR-TB). [5] [6] The drug can be classified as a second-line replacement in the front line for one of three possible reasons: it may be less effective than first-line drugs (e.g. p-aminosalicylic acid); or toxic side effects (e.g. cycloserine); may be effective, but in many developing countries (e.g. fluoroquinololes): aminoglycosides (WHO Group 2): e.g. amikacin (AMK), canamycin (KM); polypeptides (WHO group 2): e.g. creomycin, viomycin, enviomycin; fluoroquinoles (WHO Group 3): e.g. ciprofloxacin (CIP), levofloxacin, moxifloxacin (MXF); thioamide (WHO Group 4): e.g. etionamid, prothionamide cycloserine (WHO Group 4) terizildon (WHO Group 5) Third row This section does not cite any sources. Please help improve this section by providing quotes from trusted sources. Sourceless material can be attacked and removed. (August 2019) (Information on how and when to remove this template message) Third-line medicines (WHO Group 5) contain medicines that may be useful but have dubious or unproven efficacy: rifabutin macrolides: e.g. clarithromycin (CLR); linezolid (LZD); tioacetazone (T); tioridazine; arginine; Vitamin D; bedaquiline. These medicines are listed here because they are not very effective (e.g. clarithromycin) or because their effectiveness has not been proven (e.g. linezolid, R207910). Rifabutin is effective, but it is not on the WHO list because it is practically expensive for most developing countries. [medical subpoena required] Standard regimen Justification and evidence of the standard regimen for the treatment of pulmonary tuberculosis, see the main article pathophysiology Tuberculosis has been treated with combination therapy for more than fifty years. Medicines are not used alone (except laten TB or chemo prophylaxis), and regimens using only one drug result in rapid development of resistance and treatment insufficiency. [7] [8] Tuberculosis the rationale for the use of medicines for the treatment of the drug is based on a simple probability. In contrast to individual medicines, apprentices well-known: 1 mutation for every 107 cell divisions to emb, 1 for every 108 dividing data for STM and INH, and 1 for every 1010 divisions for RMP. [9] Patients with extensive pulmonary tuberculosis have approximately 1,012 bacteria in their bodies and are likely to contain approximately 105 EMB-resistant bacteria, 104 STM-resistant bacteria, 104 INH-resistant bacteria, and 10² RMP- resistant bacteria. Resistance mutations appear spontaneously and independently, so the chances of both INH and RMP carrying spontaneously resistant bacteria are 1 in 108 to × in 1010 = 1 in 1018, and the chance of carrying spontaneously resistant bacteria with all four drugs is 1,0033. This is, of course, an excessive simplification, but a useful way to explain combination therapy. There are other theoretical reasons for supporting combination therapy. Different drugs are in order of different modes of action. INH bacteriocidal against replicating bacteria. EMB bacteriostatic is used in TB treatment at low doses, but at higher, bactericidal doses. RMP has a bacterioid and sterilizing effect. PZA is only weakly bactericidal, but it is very effective against bacteria found in the acidic environment, inside macrophagi or in the area of acute inflammation. [medical subpoena required] All tb treatments used were 18 months or longer until rifampicin was available. In 1953, the standard UK order was 3SPH/15PH or 3SPH/15SH2. Between 1965 and 1970, EMB replaced PAS. RMP was started in 1968 to treat tuberculosis, and a BTS study in the 1970s showed that 2HRE/7HR was effective. In 1984, a BTS study showed that 2HRZ/4HR was effective,[10] with a relapse rate of less than 3% after two years. [11] In 1995, by recognising that inh resistance had increased, the British Thoracic Society recommended that EMB or STM be added to the treatment: 2HREZ/4HR or 2SHRZ/4HR,[12] which are currently recommended treatment regimens. The WHO also recommends a six-month continuation phase of HR if the patient still has a positive culture after 2 months of treatment (approximately 15% of patients with fully sensitive tuberculosis) and extensive bilateral cavitation at the beginning of treatment. [medical subpoena required] Monitoring, DOTS, and DOTS-Plus DOTS report On Directly Observed Treatment, Short Term, and a Great Plank of the World Health Organization (WHO) Global Plan to Stop TB. The DOTS Strategy focuses on five main action points. The first element of DOTS is the creation of enhanced sustainable financial services and the establishment of a short- and long-term plan by the government to eradicate tuberculosis. The World Health Organisation is helping to encourage mobilised funding to reduce poverty standards that prevent tuberculosis. A second element is case detection, which includes the improving bacteriological laboratory tests and communication between labs and doctors and patients. Case detection means that laboratories for the detection and testing of bacteriology are accurate and communicative to doctors and patients. The third strategy is standard treatment and support for patients. The purpose of the guidelines for compliance with appropriate treatment is to provide medicines that help eliminate tuberculosis and subsequent screenings in order to ensure that tuberculosis is not a deterrent to the patient's life. There are many cultural barriers as many patients continue to work in unhealthy living conditions or don't have enough money to pay for their treatments. There is also a need for programmes that provide scholarships and incentives for citizens to seek treatment. The fourth element of the DOTS approach is to have a management program that provides sustainable long-term care for reliable antibiotics. Finally, the fifth component is the recording and monitoring of treatment plans to ensure that the DOTS approach is effective. The DOTS approach is not only designed to structure tuberculosis programs, but also to ensure that citizens diagnosed with tuberculosis adhere to protocols that prevent future bacterial infections. [13] These include a government commitment to control TB, diagnosis based on sputum smear microscopic examinations performed on patients who actively report TB symptoms, direct observation of short-term chemotherapy treatments, a definite supply of medications, and standardized reporting and record-keeping cases and treatment results. [14] The WHO advises that all patients with tuberculosis should observe at least the first two months (and preferably the whole) of treatment: this means that an independent observer monitors patients ingesting anti-TB therapy. An independent observer is often not a health care worker and can be a shopkeeper, tribal elder, or similar leader in that society. DOTS is administered at intermittent dosing (three times a week or 2HREZ/4HR3). Twice weekly dosing is effective[15], but the World Health Organisation (WHO) is not recommended as there is no margin of error (if accidentally skipping once a week results in dosing once a week, which is ineffective). [medical subpoena required] The success rate of properly executed DOTS treatment exceeds 95% and prevents the development of additional multi-resistant strains of tuberculosis. Dots administration reduces recurrent possibilities for tuberculosis, resulting in a reduction in unsuccessful treatments. This is partly due to the fact that areas without a DOTS strategy tend to provide lower quality care [14] Areas with DOTS help reduce the number of patients seeking help from other facilities where they are treated with unknown treatments, resulting in unknown results. [16] However, if the DOTS DOTS not implemented or incorrectly positive results are unlikely. In order for the programme to work effectively and accurately, healthcare providers must be fully involved,[14] links must be established between public and private professionals, health services must be accessible to all,[16] and global support should be provided to countries that are trying to achieve their tuberculosis prevention and treatment goals. [17] Some researchers suggest that since the DOTS framework is so successful in treating tuberculosis in sub-Saharan Africa, DOTS should be extended to include non-communicable diseases such as diabetes, hypertension, and epilepsy. [18] DOTS-Plus Strategy The WHO expanded the DOTS programme in 1998 to manage MDR-TB (the so-called DOTS-Plus). [19] The implementation of DOTS-Plus requires the capacity to carry out drug sensitivity tests (not routinely available even in developed countries) and the availability of second-line drugs, in addition to all requirements for DOTS. Dots- Plus is therefore much more resource-expensive than DOTS and requires much greater commitment for countries who want to implement it. Community engagement is a new approach that is initiated together with dots personalised treatment. By providing a community of health workers to support patients and the hospital faculty, the DOTS-plus model also includes psychological structural support treatments to help accommodate patients to ensure treatment is completed. The total duration of treatment with the new strategy is 18-24 months. [20] For DOTS-Plus, monthly monitoring is recommended until the cultures are negative, but not for DOTS. If cultures are positive or symptoms are not resolved after three months of treatment, the patient should be reassessed for drug-resistant illness or non-compliance with medication. If cultures do not turn negative despite three months of therapy, some doctors may consider taking the patient to the hospital to closely monitor the therapy. Extra-pulmonary tuberculosis tuberculosis does not affect the lungs is called extra-pulmonary tuberculosis. Cns disease is explicitly excluded from this classification. Recommendation of the United Kingdom and the World Health Organisation (WHO) 2HREZ/4HR; Recommendation of the United States 2HREZ/7HR. There is good evidence from randomised controlled studies that the six-month treatment in tuberculosis[21] and spinal tuberculosis[22][23][23][24] is the same as nine months of treatment; therefore, the evidence does not support the US recommendation. [medical subpoena required] Patients with tb lymphadenitis 25% worsen during treatment before improving, and this usually happens in the first few months of treatment. [summons required] A few weeks after starting treatment, lymph nodes are often and previously solid lymph nodes may soften and develop into tuberculosis cervical lymph nodes. This should not be interpreted as a failure of therapy and is a common reason why patients (and their doctors) unnecessarily panic. With patience, two to three months into treatment, the lymph nodes begin to shrink again, and re-circulating or rebiopsy of the lymph nodes is unnecessary: if repeated microbiological tests are prescribed, they show the continued presence of viable bacteria with the same sensitivity pattern, which further increases confusion: doctors inexperienced in the treatment of tuberculosis often add second-line drugs in the belief that treatment does not work. In these situations, all that's necessary is reinsured. Steroids can be useful in solving swelling, especially if painful but unnecessary. Additional antibiotics are unnecessary and the treatment regimen does not need to be prolonged. [summons required] There is no evidence that 6 months of treatment is not appropriate for the treatment of abdominal tuberculosis and there is no additional benefit for the prevention of relapse during 9 months of treatment. However, more large-scale studies are needed to confirm the above conclusion. [25] Tuberculosis of the central nervous system Tuberculosis can affect the central nervous system (meninges, brain or spinal cord), in which case it is called TB meningitis, TB cerebritis and TB myelitis; the standard treatment is 12 months of drugs (2HREZ/10HR) and steroid binding. [medical subpoena required] Diagnosis is difficult, since csf culture is positive in less than half of cases, so most of the cases are treated only on clinical suspicion. csf's PCR does not significantly improve microbiological yield; the culture remains the most sensitive method and at least 5 ml (preferably 20 ml) of CSF should be sent for analysis. Tb cerebritis (or tuberculosis of the brain) can require a brain biopsy to make a diagnosis, since CSF is usually normal: this is not always available, and even if it is, some clinicians discuss whether it is appropriate to expose the patient to such an invasive and potentially dangerous procedure when examining anti-TB therapy gives the same answer; probably the only cause of brain biopsy when drug-resistant TB is suspected. [medical subpoena required] A shorter duration of treatment (e.g. six months) may be sufficient to treat tuberculosis meningitis, but no clinical trials have been considered. The CSF treated for TB meningitis is often abnormal even for 12 months; [26] the degree of resolution of the disorder is not correlating with clinical development or outcome,[27] and does not indicate an extension or repetition of treatment; re- sampling of CSF by lumbar function to assess the progress of treatment although tb meningitis and TB cerebritis are classified together, the experience of many clinicians is that their progression and response to treatment are not the same. TB meningitis usually responds well to treatment, but TB cerebritis can require longer treatment (up to two years), and steroid runoff is often prolonged (up to six months). Unlike TB meningitis, TB cerebritis is often required by repeated CT or MRI imaging of the brain to monitor progress. [medical subpoena required] Tuberculosis of the central nervous system may be secondary to blood-borne spread: therefore, some experts are calling for routine sampling of CSF in patients with miliary Tuberculosis. [28] Anti-TB drugs that are most useful for the treatment of central nervous system tuberculosis: INH (CSF penetration 100%) RMP (10-20%) EMB (only 25-50% inflamed meninges) PZA (100%) STM (only 20% inflamed meninges) LZD (20%) Cycloserine (80-100%) Etionamide (100%) PAS (10-50%) (inflamed meninges only) The use of steroids is routine for TB meningitis (see section below). From a poorly designed study, there is evidence that aspirin may be useful,[29] but further work is needed before it can be routinely recommended. [30] Steroids The usefulness of corticosteroids (e.g. prednisole or dexametazone) in the treatment of TB has been demonstrated for TB meningitis and TB pericarditis. The dose of TB meningitis decreased over six weeks (for those who prefer a more accurate dose, Thwaites et al., 2004[31]) over a six-week period. The dose of pericarditis prednisolon 60 mg daily taper down to four to eight weeks. [medical subpoena required] Steroids can be a temporary benefit for pleura and TB, and TB in children: Pleura treatment: prednisolon 20 to 40 mg per day taper off over 4-8 weeks extremely advanced TB: 40 to 60 mg daily taper off over 4 to 8 weeks TB in children: 2-5 mg/kg/day for a week, 1 mg/kg/day for the next week and then taper off for more than 5 weeks Steroids may benefit from hashenitis, miliary disease, tuberculosis osteomyelitis, TB osteomyelitis, laryngeal TB, lymphadenitis and urogenital disease, but the evidence is scarce, and routine use of steroids is not recommended. In these patients, steroid treatment should be considered on a case-by-case basis by the attending physician. [32] The long-term effect of pleural tuberculosis on lung function is unknown. Therefore, this effect should first be quantified before the need for further clinical trials of corticosteroids treated with pleural TB is assessed. [33] Thalidomide may be beneficial for TB meningitis and has been used in cases where patients have not responded to steroid treatment. [34] Patients who take the treatment irregularly and unreliablely treatment, there is a significant risk of treatment failure, relapse and drug-resistant tuberculosis. There are many reasons why patients do not take their medications. The symptoms of Tuberculosis often go away within a few weeks of starting TB treatment, and many patients then lose the motivation to continue taking the medication. Regular follow-up is important to check compliance and identify patients' problems with medicines. Patients should be told about the importance of taking the tablets regularly, as well as the importance of ending treatment, since relapse or drug resistance develops otherwise. One of the main complaints is the extent of the tablets. The main offender is PZA (the tablet is the size of a horse's tablet). PZA syrup can be offered as a substitute, or if the size of the tablets is really a problem and liquid preparations are not available, then PZA can be completely abandoned. If PZA is omitted, the patient should be warned that this will result in a significant increase in the duration of treatment (details of the treatment regimen leaving PZA are given below). The other complaint is that the drugs should be taken on an empty heart to facilitate their absorption. This can be difficult for patients to follow (for example, shift workers who eat meals at unreareareal times) and can mean the patient wakes up an hour earlier than normal everyday just to take medication. The rules are actually less stringent than many doctors and pharmacists think: the question is whether RMP absorption decreases when taken with fat, but is not affected by carbohydrates, protein,[35] or antacids. [36] This way, the patient can actually consume his medications with food if the food does not contain fat or oil (e.g. a cup of black coffee or toast with and without jam). [37] Taking medications with food also helps to alleviate the nausea of many patients when taking the medicines on an empty heart. The effect of food on the absorption of INH is unclear: absorption with food[38][39] was reduced in two studies, but one study showed no difference. [40] Food has little effect on the absorption of PZA and EMB, which is probably not clinically important. [41] [42] Testing of ioniazid and rifampicin levels in urine is also possible to check compliance. The interpretation of urine analysis is based on the fact that isosiazide has a longer half-life than rifampicin: a urine positive patient of isoazide and rifampicin patient is likely to be completely compliant with isoniazid, only the patient took his medication in the few days before the appointment of the clinic, but has not yet taken a dose on that day. Urine positive for rifampicin only patients missed out on taking the drug in previous days, but did not take it just before going to the clinic. both isoiazide and rifampicin patients were urine negative and the drug was not taken for several days countries where doctors are not able to (e.g. in the UK), some say that urine testing only results in a useless confrontation with patients and does not help increase compliance. In countries where legal measures can be taken to force patients to take medication (e.g. the USA), urine testing can be a useful complement to ensuring compliance. RMP colours urine and all bodily secretions (tears, sweat, etc.) in orange-pink, and this can be a useful substitute if urine testing is not available (although this color fades about six to eight hours after each dose). In a study examining cases of extra-pulmonary tuberculosis (EPTB), researchers at the University of the Philippines found that the similarity of EPTB symptoms to other diseases results in delayed identification of the disease and delayed insurance of the drug. This ultimately contributes to an increase in the mortality rate and incidence rate of EPTB. [43] The World Health Organization (WHO) recommends prescribing fixed doses of combined medicines in order to improve adhere to treatment and possibly reduce prescribing errors by reducing the number of pills to be taken by humans. A Cochrane review published in 2016 found moderate-quality evidence that there is likely little or no difference between fixed-dose combined drugs compared to single-drug drugs. [44] Treatment adherence strategies as mentioned above, non-compliance with anti-tuberculin treatment can lead to treatment failure or drug-resistant tuberculosis. Therefore, general treatment strategies should be focused on promoting the continence of adherence. WHO and the Centers for Disease Control and Prevention (CDC) propose a multifaceted patient-centered care approach. [45] [46] Public health and private sector professionals can help to comply with tuberculosis treatment by enabling patients to be active partners in their own treatment decisions; improving the patient's knowledge and understanding of tuberculosis, treatment and potential spread; and discussing expected transient and long-term outcomes with patients. [45] The CDC also recommends the use of incentives and licensers. [45] Incentives are monetary rewards for healthy behaviour (e.g. transport or food vouchers), while eliminating economic burdens on access to health care[47] (e.g. groupings, medical visits, after-hours medical visits or home visits). However, more research is needed to determine whether incentives and licensers have a significant impact on the long-term to comply with the treatment of the child. [47] It is believed that smartphones can improve compliance. [48] Individuals with tuberculosis can also benefit from emotional support from peers and survivors. Advocacy organizations and patient support groups like STOP TB, TB Alert, Treatment Action Group (TAG) and others are working to connect tb survivors. Adverse effects A the effects of individual anti-TB drugs, please read the individual articles of each drug. The relative incidence of the main adverse effects was carefully described:[49] INH 0.49/ 100 patient months RMP 0.43 EMB 0.07 PZA 1.48 Each drug 2.47 This is an 8.6% risk that all patients should change their drug therapy during standard short-term treatment (2HREZ/4HR). People identified as being most at risk of major adverse side effects in this study were: age >60, women, HIV-positive patients, and Asians. It can be extremely difficult to identify which drug is responsible, which side effect, but the relative frequency of each side effect is known. [50] Infrastructural medicinal products are given in descending order of frequency: Thrombocytopenia: Rifampicin (RMP) Neuropathy: Ioniazid (INH) Vertigo: Streptomycin (STM) Hepatitis: Pyrazinamide (PZA), RMP, INH rash: PZA, RMP, Ethambutol (EMB) Thrombocytopenia are caused only by RMP and do not need to be subjected to test transmission. Treatment regimens that leave the RMP are discussed below. More details can be found on rifampicin. The most common cause of neuropathy is INH. Peripheral neuropathy of INH is always pure sensory neuropathy, and finding the motor component of peripheral neuropathy should always ask for an alternative cause. After peripheral neuropathy occurs, INH should be stopped and pyridoxin administered at a dose of 50 mg three times a day. After neuropathy occurs, the addition of high doses of piridoxin to treatment does not stop the progression of neuropathy. Patients who are at risk of peripheral neuropathy for other causes (diabetes, alcoholism, kidney failure, malnutrition, pregnancy, etc.) should receive 10 mg daily at the beginning of treatment. Please refer to the entry on isoniazid for other neurological side effects of INH. Rashes most often occur due to PZA, but they can occur with any TB drug. Test dosage using the same regimen as detailed below for hepatitis may be necessary to determine which drug is responsible. Itching of RMP often causes itching without rash during the first two weeks of treatment: treatment should not be stopped, and the patient should be informed that the itch usually disappears on its own. Short courses of calming antihistamines such as chlorfeniramin may be useful for relieving itching. Fever during treatment may be due to a number of causes. This can occur as a natural effect of tuberculosis (in this case, it should be resolved within three weeks of the start of treatment). Fever can be a result of drug resistance (but in this case the body must be resistant to two or more drugs). Fever may be caused by an extraadded infection or further diagnosis (patients with tuberculosis not influenza and other diseases during treatment). In some patients, fever because of the drug allergy. The clinician should also take into account the possibility that the diagnosis of tuberculosis is wrong. If the patient has been on treatment for more than two weeks, and if the fever initially settles, then come back, it is reasonable to stop taking all TB medications for 72 hours. If the fever persists despite the shutdown of all tb drugs, then the fever is not due to the drugs. If the fever disappears from the treatment, then the drugs should be tested individually to determine the cause. The same scheme can be used for drug-induced hepatitis (see below) for investigational treatment. The drug most often involved in causing drug fever RMP: details are given about the entry rifampicin. Drug-induced hepatitis Drug-induced hepatitis, tb treatment, death rate is about 5%. [51] Three medicines can cause hepatitis: PZA, INH and RMP (with decreasing frequency). [1] [52] These three causes cannot be distinguished solely by signs and symptoms. Test giving should be carried out to determine which drug is responsible (this is discussed in detail below). Liver function tests (LFT) should be checked at the beginning of treatment, but if normal, do not need to be re-checked; the patient should only be warned about the symptoms of hepatitis. Some clinicians insist on regular monitoring of LFT during treatment, and in this case the studies should be carried out only two weeks after the start of treatment and then every two months thereafter, unless any problems are detected. An increase in the level of bilirubin is expected with RMP treatment (excretion of RMP blocks bilirubin) and usually ceases after 10 days (production of liver energy increases to compensate). Isolated heights of bilirubin can be safely ignored. Increases in liver transzaminase (ALT and AST) are common during the first three weeks of treatment. If the patient is asymptomatic and the height is not excessive, then no action should be taken; some experts suggest that the permitted limit should be reduced by four times, but there is no evidence to support this number beyond any other number. Some experts believe that treatment should be stopped only if jaundice becomes clinically apparent. If clinically significant hepatitis occurs during treatment with Tuberculosis, then all drugs should be stopped until liver transaminase returns to normal. If the patient is so sick that TB treatment cannot be stopped, then STM and EMB should be given until liver transaminase returns to normal (these two drugs are not associated with hepatitis). Fulminant hepatitis can occur during TB treatment, but fortunately it is rare; liver transplantation may be necessary and death will occur. The drug-induced hepatitis test dos should be re-introduced separately. This outpatient treatment and should be carried out under close observation. The nurse must be a nurse. taking the patient's heart rate and blood pressure at intervals of 15 minutes for at least four hours after each test dose (most problems occur within six hours of the test dose, if at all). Patients can be very suddenly unwell, and access to intensive care should be available. Medicines should be administered in this order: Day 1: INH 1/3 or 1/4 dose 2. RMP in full dose 7. Therefore, article 4(2) is replaced by the following: If the patient completes nine days of study giving, it is reasonable to assume that PZA is caused by hepatitis and no PZA test donation should be performed. The reason for the use of the order of use for the testing of drugs is that the two most important drugs for the treatment of TB are INH and RMP, so they are tested first: PZA is the most likely drug to cause hepatitis and is also the easiest to leave. EMB is useful when the sensitivity pattern of the TB body is not known and can be oused if the body is known to be sensitive to INH. Below are the treatments that skip each standard medication. The order in which medicines are examined may vary according to the following considerations: The most useful drugs (INH and RMP) should be examined first, because the lack of these drugs in the treatment regimen seriously impairs its effectiveness. The medicines that cause the most reaction should be tested as soon as possible (and probably not at all). This avoids the re-publication of patients with a medicine for which they have already (possibly) had a dangerous side effect. A similar system can be applied to other adverse effects (such as fever and rash), using similar principles. Dysbiosis caused by HRZE antibiotic treatment leads to a change in the microbiome structure of the intestine both in mice [53] and in humans during and after treatment. [54] It is not currently known what long-term effects this dysbiosis has on systemic immunity. Differences in standard treatment have evidence supporting certain variations in the standard regimen for the treatment of pulmonary TB. Patients with sputum culture who are smear-negative at the beginning of treatment, are only well with 4 months of treatment (this has not been validated in HIV-positive patients); the sputum culture-negative patients do well only after 3 months of treatment (probably because some of these patients have never had Tuberculosis at all). [55] It is not wise to treat patients for only three or four months, but all tuberculosis and it may be reassuring to know that sometimes retreatment is unnecessary. Elderly patients who have had a large number of pills can be offered 9HR, skipping PZA, which is the most bulky part of the treatment. It may not always be necessary to treat with four drugs from the beginning. Examples include close contact with a patient known to have a strain of fully sensitive tuberculosis: in this case, it is acceptable to use 2HRZ/4HR (emb and STM oesculate) in the hope that their strain will also be INH sensitive. In fact, it was previously the recommended standard regimen in many countries until the early 1990s, when iszoliazida resistance rates increased. TB affecting the brain or spinal cord (meningitis, encephalitis, etc.) is currently being treated with 2HREZ/10HR (12 months of treatment in total), but there is no evidence that it is better than 2HREZ/4HR. [quote required] There is no difference in relapse rates between those who are 6 months or longer. However, more well-designed studies are needed to answer this question. [56] Orders that leave isoleziid asoniazid resistance account for 6.9% of isolates in the United Kingdom (2010). [57] It is the most common type of resistance worldwide, so the current recommendation for hrez is at the beginning of treatment until sensitivity is known. It is useful to know about the current reported outbreaks (such as the current outbreak of INH-resistant tuberculosis in London)[reference required]. If patients are found to be infected with an isoniazide-resistant strain of TB after 2 months of HREZ, then it is necessary to change the RE for another 10 months, and the same thing if the patient is intolerant isoniazide (although 2REZ/7RE may be acceptable if the patient is well supervised). The U.S. recommendation is 6RZE with the possibility of adding a quinolon like moxifloxacin. The level of evidence for all of these orders is poor, and few recommend one over the other. Rifampicin has a prevalence of rifampicin (RMP) resistance of 1.4% in the United Kingdom. [57] It is rare for TB strains to be resistant to RMP without resisting INH,[58] which means that rifampicin resistance usually also means resistance to INH (i.e. MDR-TB). However, RMP intolerance is not uncommon (the most common cause of stopping rifampicin is hepatitis or thrombocytopaenia, the most common cause of stopping rifampicin). Rifampicin is also the most expensive of the first-line drugs, and in the poorest countries, orders that leave rifampicin are therefore often used. Rifampicin is the most potent sterilizing drug available for the treatment of tuberculosis, and any treatment regimen that skips rifampicin is significantly longer than standard treatment. Uk recommendation 18HE or 12HEZ. U.S. Recommendation 9-12HEZ, addition of quinolol (e.g. MXF). MXF). abandonment of pza-pyrazinamid is a common cause of rash, hepatitis and painful arthralgia in HREZ treatment and can be safely stopped in patients who are intolerant to it. Isolated PZA resistance is not common in M. tuberculosis, but M. bovis is congenital resistant to PZA. PZA is not crucial in the treatment of fully sensitive tuberculosis and its main value is to shorten the total duration of treatment from nine months to six. An alternative treatment is 2HRE/7HR, for which there is excellent clinical trial evidence. [59] [10] [60] [61] The 1994 US CDC Guidelines on Tuberculosis[62] erroneously refer to Slutkin[61] as evidence that that the nine-month treatment, which uses only ioniazid and rifampicin, is acceptable, but almost all of the patients in the study received ethambutol in the first two to three months (although this is not evident from the extract of the article). This error was remedied by the 2003 guidelines. [63] This treatment (2HRE/7HR) is a first-line treatment for M. bovis, as M. bovis is organically resistant to pyrazinamid. Orders that leave ethambutol EMB intolerance or resistance are rare. If the patient is indeed infected with intolerant or emb-resistant TB, 2HRZ/4HR is an acceptable treatment. [64] The main motivator for the enlisting of the EMB in the first two months should be motivated by the increasing rate of INH resistance. Tuberculosis and other conditions Liver disease People with alcoholic liver disease are at increased risk of tuberculosis. The incidence of tuberculosis peritonitis is particularly high in patients with cirrhosis of the liver. [medical subpoena required] There are roughly two treatment categories: A) Cirrhostics patients are essentially normal baseline liver function studies (Childs of Cirrhosis). Such patients can be treated with a standard 4 drug regimen for 2 months, followed by 2 drugs for the remaining 4 months (full 6 months of treatment). B) Cirrhotic patients changed baseline liver function studies (Childs B&C). According to WHO guidelines 2010: depending on the severity of the disease and the degree of decompensation, the following treatment can be used by changing the number of hepatotoxic drugs. One or two hepatotoxic medicines can be used for moderate to severe diseases (e.g. Childs B cirrhosis), while hepatotoxic medicines can be completely avoided in decompensated Child C cirrhosis. • Two hepatotoxic medicines - 9 months of isoniazid, rifampin and ethambutol (until or if isoniazid sensitivity is not documented) - 2 months Of Isoniazid, Rifampin, Ethambutol and Streptomycin followed by 6 months isoniazid and Rifampin • A hepatotoxic medicine - 2 months Isoniazid, Ethambutol & Streptomycin followed by 10 months Ioniazid and Ethambutol • No hepatotoxic medicine - 18-24 months Patients with ethambutol and Quinoolonma liver disease should be regularly monitored for liver function tests for TB in TB Drug-induent hepatitis is discussed in a separate section above. Pregnancy Pregnancy itself is not a risk factor for TB. Rifampicin reduces the effectiveness of hormonal contraception, so during the treatment of tuberculosis, additional precautions should be taken for contraception. During pregnancy, untreated tuberculosis is associated with an increased risk of miscarriage and the main foetal abnormality, as well as the treatment of pregnant women. U.S. guidelines recommend leaving PZA when treating tuberculosis during pregnancy; uk and WHO guidelines do not make such a recommendation and PZA is commonly used during pregnancy. There is a great deal of experience in the treatment of pregnant women with tuberculosis and the toxic effect of PZA has never been found during pregnancy. High doses of RMP (much higher than humans) cause neural tube defects in animals, but no such effect has ever been found in humans. There may be an increased risk of hepatitis during pregnancy and puerperium. Until tuberculosis treatment is complete, it is advisable to advise all women of childbearing age to avoid becoming pregnant. Aminoglycosides (STM, kreomycin, amikacin) should be used with caution during pregnancy because they may cause deafness in the unborn child. The treating physician should consider the benefits of treatment for the mother against possible harm to the baby and good results have been reported in children whose mothers have been treated with aminoglycaside. [65] Experience in Peru has shown that MDR-TB treatment is not a reason to recommend termination of pregnancy and that good results are possible. [66] Patients with kidney disease had a 10-30-closely increased risk of developing tuberculosis. Where appropriate, patients receiving immunosuppressive medicinal products or receiving transplant treatment should be considered for the treatment of latening tuberculosis. Aminoglycosides (STM, capreomisin and amikacin) should be avoided in patients with mild or severe kidney disease, as there is a risk of increased damage to the kidneys. If the use of aminoglycoides cannot be prevented (e.g. in the treatment of drug-resistant TB), serum levels should be closely monitored and the patient should be warned to report side effects (in particular deafness). If a person has end-stage kidney disease and there is no useful residual kidney function, then aminoglycoides can be used, but only if the level of the drug can be easily measured (often only the level of ottacin can be measured). With mild kidney damage, it is not necessary to change the administration of any of the other medicines routinely used to treat tuberculosis. In severe chronic kidney disease (GFR<30), the dose of EMB should be reduced by half (or completely avoided). The PZA dose is 20 mg/kg/day (UK recommendation) or three quarters of the normal dose (US recommendation), but not many published available to support this. In patients receiving dialysis during 2HRZ/4HR treatment, medicines should be in the initial high intensity phase. In the continuation phase, the drugs should be administered at the end of all hemodialysis treatments and should not be administered at doses on non-dialysis days. In HIV-infected patients, HIV treatment should be postponed until the end of treatment with tuberculosis, if possible. The current UK guideline (provided by the British HIV Federation) on CD4 counts more than 200 delays in treatment until the six-month Tuberculosis treatment is completed. CD4 number 100-200-delay treatment until the initial two-month intensive phase of therapy with a total CD4 count of less than 100 in the situation is unclear, and patients should be involved in clinical trials investigating this issue. There is evidence that if these patients are treated by both tuberculosis and HIV specialists, the results will not be harmed for either disease. [67] If HIV treatment is to be started during tuberculosis, an HIV specialist should be advised. In general, there is no significant interaction with NRTSs. Nevirapine should not be used with rifampicin. Efavirenz can be used, but the dose used depends on the patient's body weight (600 mg per day if his body weight is less than 50 kg; 800 mg per day if his body weight exceeds 50 kg). Efavirenz levels should be checked early after starting treatment (unfortunately this is not a service routinely offered in the US, but it is readily available in the UK). Protease inhibitors should be avoided, if at all possible: patients treated with rifamycins and protease inhibitors are at increased risk of failure or relapse of treatment. [68] The World Health Organization (WHO) warns against the use of tioacetazone in HIV patients, as there is a 23% risk of potentially fatal dermatitis. [69] [70] Study Caprisa 003 (SAPiT) found that mortality in patients undergoing antiretroviral treatment during tuberculosis treatment was 56% lower than in patients starting after the end of TB treatment (risk ratio 0.44 (95% CI: 0.25-0.79); p =0.003). Epilepsy INH may be associated with an increased risk of seizures. Piridoxin 10 mg per day should be given to all patients with epilepsy taking INH. There is no evidence that INH causes seizures in non-epileptic patients. Anti-tuberculosis treatment involves a number of drug interactions with anti-epileptic drugs, and the level of the drug in the serum should be closely monitored. There are serious interactions between rifampicin and carbamazepine, rifampicin and phenytoin, as well as rifampicin and sodium valproate. Always seek advice from a pharmacist. Drug Resistance Main Articles: Multi-Drug-Resistant Tuberculosis and Widely Drug-Resistant Tuberculosis Definitions Multi-Drug Resistant Tuberculosis (MDR-TB) Definitions tb, which is resistant to at least inh and RMP. They are multi-resistant isolates against any other combination of anti-TB drugs, but INH and RMP are not classified as MDR-TB. As of October 2006, it has been widely tuberculosis (XDR-TB) is defined as MDR-TB, which is resistant to quinololes and any of the canamycin, creomicin or ottacin. [71] The old case definition of XDR-TB is MDR-TB, which consists of three or more of the six classes of second-line drugs. [72] This definition should no longer be used, but because it is referred to in many older publications. The management principles of MDR-TB and XDR-TB are the same. The main difference is that XDR-TB has a much higher mortality rate than MDR-TB, as the number of effective treatment options decreases. [72] XDR-TB epidemiology is not currently well studied, but it is believed that XDR-TB does not spread easily in healthy populations, but is capable of inflicting epidemics in populations that are already infected with HIV and are therefore more susceptible to Tuberculosis infection. [73] Epidemiology of Drug-Resistant Tuberculosis This article does not necessarily reflect the encyclopedic tone used on Wikipedia. See Wikipedia's guide to writing better articles for suggestions. (June 2018) (Information on how and when to remove this template message) A 1997 survey of 35 countries found that about a third of the countries surveyed had rates above 2%. The highest rates were in the former Soviet Union, the Baltic States, Argentina, India and China, and were linked to weak or unsuccessful national tuberculosis control programmes. Similarly, the emergence of high rates of MDR-TB in New York in the early 1990s was associated with the dismantling of public health programs under the Reagan administration. [74] Paul Farmer points out that the more expensive the treatment, the harder it is for poor countries. The farmer sees this as a denial of fundamental human rights. Africa's low quality treatment is partly because many African cultures lack the concept of time essential to the agenda of administration. [76] MDR-TB may develop during the treatment of fully sensitive tuberculosis, and this is always the result of patients not administering a dose or not complete treatment. Fortunately, MDR-TB strains seem to be less suitable and less transferable. For many years it has been known that INH-resistant tuberculosis is less viruen in guinea pigs, and according to epidemiological evidence, MDR TB strains naturally do not dominate. A Los Angeles study found that only 6% of cases of MDR-TB were grouped together. This should not be a reason for complacency: it should be remembered that the mortality rate of MDR-TB is similar to lung cancer. It should also be noted that people who have weakened immune systems (because of diseases like HIV or because of medications) are more prone to taking TB. Children represent susceptible populations with increasing MDR and XDR-TB ratios. As the diagnosis of paediatric patients is difficult, the large number of cases is not report it. Pediatric XDR-TB Cases most countries, including the United States. [77] In 2006, an outbreak of XDR-TB south Africa was first reported in 53 patients at a rural hospital in Kwazulu-Natal, where all but one died. [73] What was particularly worrying was that the average survival from sputum collection to death was only 16 days and that the majority of patients had never received tuberculosis treatment before. This is the first outbreak for which the abbreviation XDR-TB was used, although tb strains that met the current definition were identified retroactively,[78][79] the largest group of connected cases ever found. Since the first report in September 2006[80], cases have already been reported in most provinces in South Africa. As of March 16, 2007, 314 cases were reported, with 215 deaths. [81] It is clear that the spread of this strain of tuberculosis is closely linked to the high prevalence of HIV and poor control of infections; in other countries where XDR-TB strains were produced, drug resistance stemmed from mismaning of cases or poor patient compliance with medication, rather than being transmitted from person to person. [82] This strain of TB does not respond to the drugs currently available in South Africa for first- or second-line treatment. It is now clear that the problem has been around for much longer than health department officials have suggested and is much more extensive. [83] 2006[84] Serious thought was placed on isolation procedures, which may deny the human rights of certain patients but may be necessary to prevent the further spread of this strain of tuberculosis. [85] Treatment of MDR-TB The treatment and prognosis of MDR-TB is much more similar to cancer than infection. This mortality rate is up to 80%, which depends on a number of factors, including how many drugs the body is resistant to (the less the better), how many medications are given to the patient (patients treated with five or more drugs better), whether an injectable drug is given or not (to be given in the first three months at least) , the expertise and experience of the doctor responsible, How to cooperate with the patient in the treatment (treatment is laborious and long and requires perseverance and determination on the part of the patient), regardless of whether the patient is HIV positive or not (HIV co-infection is associated with increased mortality). Treatment courses are at least 18 months, and last years; surgery, although the mortality rate remains high despite optimal treatment. That said, good results are still possible. Treatment cures of at least 18 months and directly observed components can increase recovery rates to 69%. [86] [87] MDR-TB treatment should be carried out by a doctor. treatment of MDR-TB. Mortality and morbidity in patients treated in non-specialised centres increased significantly compared to patients treated in specialised centres. In addition to obvious risks (i.e. known exposure in a patient with MDR-TB), the risk factors for MDR-TB include male, HIV infection, previous incarceration, failed TB treatment, failure to respond to standard TB treatment, and relapse following standard TB treatment. Most people with MDR-TB are unable to access treatment as Paul Farmer describes it as an outcome deficiency. The majority of people have gotten the MDR-TB to live in resource-poor settings and refuse treatment because international organizations have refused to make the technologies available to countries who cannot afford to pay for treatment, the reason being that second line drugs are expensive, which is why treatment methods for MDR-TB are not sustainable in impoverished nations. Paul Farmer argues that this is a social injustice and we cannot allow people to die simply because they face conditions where they cannot afford effective therapy. [76] Treatment of MDR-TB should be based on a sensitivity study: such patients cannot be treated without this information. If the patient is treated with suspected MDR-TB, the patient should be started with SHREZ+MXF+cycloserine until the laboratory sensitivity test is complete. In some countries, the rpoB gene probe is available, which serves as a useful marker for MDR-TB, as isolated RMP resistance is rare (unless patients have a history of treating only rifampicin). [88] If the results of the gene probe (rpoB) are known to be positive, it is reasonable to skip RMP and use SHEZ+MXF+cycloserine. Despite the suspicion of MDR-TB, the reason for maintaining the patient on INH is that INH is so strong in the treatment of tuberculosis that it is foolish to miss it until there is microbiological evidence that it is ineffective. Probes for ioniazid resistance (katG[89] and mabA-inhA[90]) are also available, but these are less widely available. If the sensitivity is known and the isolate is resistant to both INH and RMP, five medicinal products should be selected in the following order (based on known sensitivity): aminoglycoside (e.g. amiacin, canamycin) or polypeptide antibiotic (e.g. capreomisin) PZA EMB fluoroquinololons: moxifloxacin is preferred (ciprofloxacin can no longer be used[91]); rifabutin cycloserine a tioamide: prothionamide or etionamide PAS a macrolide: e.g. clarithromycin linezolid high-dose INH (if low resistance) interferon-γ[92] tioridazine meropenem and clavulanic acid[93][94] Medicines are closer to the top of the list as they are more effective and less toxic; drugs are placed closer to the bottom of the list, less effective or toxic, toxic, harder to come by. Resistance to a drug in a class usually means resistance to any drug in that class, but a notable exception is rifabutin: rifampicin resistance does not always mean rifabutin resistance and the laboratory should be asked to test it. It is possible to use only one drug within each class of drugs. If it is difficult to find five drugs that need to be treated, then the clinician may ask for a search for a high level of INH resistance. If the strain has only low inh resistance (0.2 mg/l INH resistance but 1.0 mg/l INH sensitive), high doses of INH may be used as part of the treatment. When counting drugs, PZA and interferon are considered zero; That is, when adding pza to a four-drug treatment, you can also choose another drug to take five. There should be no more than one injection (STM, capreomycin or amikacin), as the toxic effect of these medicines is an additive: if possible, aminoglycoide should be administered for at least three months a day (and perhaps three times a week). Ciprofloxacin should not be used to treat tuberculosis if other fluoroquinoles are available. [95] There is no periodic regimen for validated use of MDR-TB, but clinical experience is that injectable drugs five days a week (because no one is available to take the drug at weekends) seem to produce worse results. Directly observed therapy will certainly help to improve the results of MDR-TB and should be considered an integral part of the treatment of MDR-TB. [96] The response to treatment should be achieved by repeated sputum herdings (monthly, if possible). MDR-TB treatment should last at least 18 months and cannot be stopped until the patient has been culture negative for at least nine months. It is not unusual for patients with MDR-TB to be treated for two years or more. Patients with MDR-TB should be isolated as much as possible in rooms with negative pressure. Patients with MDR-TB should not be placed in the same department as immunosuppressive patients (HIV-infected patients or patients taking immunosuppressive medicines). Careful monitoring of adherence to treatment is essential for the treatment of MDR-TB (and some doctors insist on hospitalization, if only for this reason). Some doctors insist that these patients are isolated until the sputum smear is negative, or even culture negative (which can last for several months or even years). Keeping these patients in hospital for weeks (or months) can be practical or physical impossibility, and the final decision depends on the clinical judgement of the doctor treating that patient. The treating physician should make full use of therapeutic drug monitoring (especially for aminoglycasides) in order to avoid both compliance and toxic effects. Some can be useful as a disa file for but for the purpose of counting MDR-TB drugs are considered zero (if there are already four drugs in the treatment, it may be beneficial to add arginine or vitamin D or both, but you still need another drug for the five). arginine, some clinical evidence[97] (peanuts are a good source) vitamin D (some in vitro evidence[98] & see vitamin D and tuberculosis treatment) The drugs listed below have been used in desperation and it is uncertain whether they are effective at all. They are used when it is not possible to find five drugs from the list above. imipenem[99] co-amoxiclav[100][101] clofazimine[102][103][104] prochlorperazine[105] metronidine[105] was produced on 18 December 2012. On December 28, 2011, the U.S. Food and Drug Administration (FDA) approved bedaquilin (marketed as Johnson & Johnson Sirturo) for the treatment of multi-resistant tuberculosis, the first new treatment in 40 years. Sirturo can be used in combination therapy in patients who have not received standard treatment and have no other options. Sirturo is an adenosine triphosphate synthase (ATP synthase) inhibitor. [107] [108] The following medicinal product is experimental compounds which are not commercially available but which can be obtained from the manufacturer as part of a clinical trial or on a compassionate basis. Their effectiveness and safety are not known: Pretomanid[109] (a product developed in partnership with TB Alliance[110]) produced by Novartis(developed in partnership with the TB Alliance) is increasingly evidenced by the role of surgery (lobectomy or pneumonectomy) in the treatment of MDR-TB, although whether this should be done early or late is not yet clearly defined. See Modern Surgical Management in Asia Asia-Pacific Region carries 58% of the burden of global tuberculosis, which includes multi-resistant tuberculosis. [111] South-East Asia is under heavy tuberculosis burdens due to inefficient and inadequate health infrastructures. According to the World Health Organization, many Asian countries have large cases of tuberculosis, but their governments do not invest in new technologies to treat patients. [111] From 2005 to 2009, the Philippines, the IPHO-Maguindanao, a government organization in Maguindanao, Philippines, partnered with Catholic Relief Services (CRS) to increase tuberculosis awareness. CRS implemented a USAID-backed project to fund tuberculosis testing. [112] They also launched an Advocacy, Communication, and Self-Mobilization project that includes workshops to encourage testing in communities. Citizens attending religious sermons were able to spread information about tuberculosis and inform their communities about where to seek treatment and how to adhere to treatment protocols [112] The DOTS-Plus strategy, which aims to local institutions, has successfully conveyed information on the prevention and treatment of tuberculosis. India in 1906, India opened its first air treatment and isolation of tuberculosis patients. However, the World Health Organization reviewed a national program in India that did not have funding and a treatment regimen that would report accurate tuberculosis case management. By 1945, successful immunization screenings had been made for campaigns that helped spread messages about disease prevention. [113] This was around the same time that the World Health Organisation declared tuberculosis a global emergency and recommended that countries adopt the DOTS strategy. Bangladesh, Cambodia, Thailand in Bangladesh, Cambodia and Indonesia, there is a diagnostic treatment for laten tuberculosis in children under 5 years of age. The IGRA approach (Interferon Gamma Release Assay) is used in these countries. IGRA testing and diagnosis are complete blood cell tests where fresh blood samples are mixed with antigens and controls. A person infected with tuberculosis will have interferon gamma in the bloodstream if mixed with the antigen. [114] This is a very accurate but expensive test for patients with technologically complex immunodeficiency. [115] These developing countries have not been able to effectively get rid of tuberculosis, as national health policies have not covered tuberculosis screening and testing. There were also no programmes for educating citizens and training health workers. Without mobilising adequate resources and supporting sustainable government funding, these developing countries have not adequately provided the treatment and resources needed to combat tuberculosis. According to Vietnam, who, Vietnam is the 13th world war. In Vietnam, nearly 400 new tuberculosis and 55 deaths occur every day. [116] In 1989, the Vietnamese Ministry of Health addressed the burden of tuberculosis with the establishment of the National Institute of Tuberculosis and Lung Diseases and implemented the DOTS strategy as a national priority. [116] Vietnam's health service system consists of four different levels: the central level led by the Ministry of Health (MOH), provincial health services, district health services and commune health centers. These departments have worked with the National Institute of Tuberculosis and Lung Diseases to ensure that treatment and prevention plans for long-term tuberculosis reduction are in place. [117] In 2002, Vietnam also implemented a communication plan to provide accurate educational information in order to respond to obstacles or misconceptions about the treatment of tuberculosis. The government has collaborated with the World Health Organization, Center for Disease and Control Prevention, and local medical non-profit such as Friends for International Tuberculosis Relief to give the cause of tuberculosis, sources of infection, how it spreads, symptoms, symptoms, and prevention. The National Tuberculosis Control Program works closely with the primary health care system at the central, provincial, district, and commune levels, which has proven to be an incredibly essential measure of success. [116] Tuberculosis is a non-profit organization in Asia. FIT not only diagnoses patients, but also provides preventive tuberculosis detection in order to pilot a comprehensive patient-centered TB program that aims to stop TB transmission and reduce suffering. The organization focuses on island screening due to high levels of risk and population space. Fit works closely with most of the island's population (roughly 2,022 patients) through search, treatment, prevention and integrative sustainability, and is partnering with the Ho Si Minh City Public Health Association with a pilot that provides active community information, patient-centered care and stakeholder involvement. [118] Located in Ha Noi, the National Institute of Tuberculosis and Lung Diseases is responsible for the management and management of tuberculosis control activities at central level. The Institute shall support the MOH in the development of tuberculosis strategies and in the management of the management and technical guidelines of the system. Provincial-level centers diagnose, treat and treat patients, implement TB policies issued by the NTP, and develop action plans based on guidelines from the Provincial Health Office and the provincial TB audit committees. Districts are able to detect tuberculosis and treat patients. In each district there are doctors specializing in TB, laboratories, and X-ray equipment and either the TB department or the TB infectious diseases department of the district hospital. The district level is responsible for the implementation and supervision of the NTP and for the supervision and management of TB programmes in the municipalities. The municipal level provides treatment, as required by the district level, insans drugs and vaccinates children. In the control of tuberculosis, village health workers play a critically important role in identifying patients with suspected tuberculosis, advising on testing and testing, paying home visits to patients undergoing treatment, and reporting problems at monthly meetings with the CHC. [118] TB Alliance is a South African-based NGO that was discovered in the early 2000s. The NGO is one of the main sources of global tuberculosis research and development of new tuberculosis vaccines. non-profit organisation. [119] In order to promote the development of tuberculosis, the TB Alliance is developing partnerships with private, public, scientific and philanthropic sectors to develop products in under-equipped communities. In 2019, tb alliance became the first non-profit organization to develop and register an anti-TB anti-TB The TB Alliance works closely with the World Health Organization (WHO), the U.S. FDA and the European Medicines Agency (EMA) to support affordable regulatory policies and treatments. FHI 360is is an international tuberculosis non-profit organization funded by USAID to treat and support patients in Myanmar, China and Thailand. The organization has developed an app called DOTsync in order for medical staff to use antibiotics and monitor patients for side effects. This is incredibly essential to eradicate tuberculosis, as it allows health workers to have follow-up screenings with patients to ensure that tuberculosis treatment is effective. Operation ASHAis is a social security nonprofit organization founded in 2006. Operation ASHA in India and Cambodia focuses on improving e-compliance, a monitoring and SMS text messaging system where patients can access medical records with their fingerprints and are reminded daily via text message when to take their medications. [120] According to operation ASHA, the consecutive rate of e-compliance treatment is 85%. Treatment failure Patients who have failed treatment should be distinguished from patients with relapse. Patients who responded to treatment and appeared to have recovered after the course of tuberculosis are not considered treatment errors, but relapse, and are discussed in a separate section below. Patients say they have failed treatment if they do not respond to treatment (cough and sputum production persists throughout the treatment), or just experience a temporary response to treatment (the patient gets better at first, but then worse off, all the while undergoing treatment). It is very rare that patients do not respond to tuberculosis treatment at all (even temporarily), because this means that it is resistance to all medicines in the baseline. Patients who do not receive an answer at all during treatment should first be questioned very carefully about whether they have taken their medications and may even need to be admitted to hospital to monitor their treatment. Blood or urine samples can be taken to check for malabsorption of TB medications. If it can be shown that they are fully compliant with their medications, then the likelihood is very high that they have a different diagnosis (perhaps in addition to the diagnosis of TB). These patients should carefully review their diagnosis and the samples received during the tuberculosis and sensitivity test. Patients who get better and then get worse again should also be asked very closely about compliance with treatment. If adhesion is confirmed, they must be tested for resistant (including MDR-TB), even if a sample has already been obtained for microbiology before starting treatment. Errors in prescribing or issuing patients who do not respond to treatment. Immunosomes are a rare cause of non-response. In a small number of patients, the failure of treatment reflects extreme biological variations and no cause is found. This section does not refer to any source. Please help improve this section by providing quotes from trusted sources. Sourceless material can be attacked and removed. (May 2011) (Information on how and when to remove this template message) Treatment relapse Patients are told to relapse if they improve while on treatment, but fall ill again after discontinuation of treatment. Patients who show only temporary improvement during treatment or who never respond to treatment say they have failed treatment and have been discussed above. There is a small relapse rate associated with all treatment regimens, even if the treatment was taken religiously for 100% compliance (the standard regimen of 2HREZ/4HR has a relapse rate of 2-3% in test conditions). [10] The majority of relapses occur within 6 months of the end of treatment. Patients who are more likely to fall back are those who have taken their medicines in an unreliable and irregular manner. The likelihood of resistance is higher in patients who are in relapse and every effort should be made to get a sample that can be applied to sensitivity. That said, most patients who relapse to do so have a completely sensitive strain, and it is possible that these patients are not relapse, but have been re-infected; these patients can be re-treated with a dosing regimen similar to the previous one (treatment does not need to be added and the duration should no longer be included). WHO recommends 2SHREZ/6HRE if microbiology is not available (most countries where tuberculosis is highly endemic). This treatment regimen is designed to provide optimal treatment for fully sensitive tuberculosis (the most common find in patients with relapse) and to cover the possibility of INH-resistant TB (the most common form of resistance). Due to the lifelong risk of relapse, all patients should be warned of the symptoms of tuberculosis relapse at the end of treatment and strict instructions should be given to return to their doctor if symptoms occur. Public health and health policy in 2010, India reported more cases of tuberculosis than any other country. [121] This is partly due to the serious mismaning of tuberculosis diagnosis and treatment in India's private healthcare sector, which serves around 50% of the population. [121] This is why the private sector is being asked to participate in the state's revised national tuberculosis control programme, which has proved effective in patients receiving healthcare through the government. [121] In addition, a 2013 study by Maurya and her co-author shows that she is under the burden of multi-resistant tuberculosis in India and that studies require a change, monitoring and management. [122] During the COVID-19 pandemic, 80% fewer TB cases were reported daily in India in April 2020, reducing the diagnosis and treatment of tuberculosis. [123] [124] Study of therapy In areas where tuberculosis is highly endemic, it is not unusual to encounter a febrile patient but who do not have a source of infection. The doctor then, after extensive examination ruled out all other diseases, resorted to the examination of social security treatment. [125] Treatment used for at least three weeks in hez; RMP and STM are left out of treatment because they are broad-spectrum antibiotics, while the other three first-line drugs treat only mycobacterial infections. The elation of fever after three weeks of treatment is good evidence of occult TB and the patient should then be changed to conventional TB treatment (2HREZ/4HR). If the fever does not resolve after three weeks of treatment, it is reasonable to conclude that the patient has another cause for his fever. This approach was not recommended by the WHO and most national guidelines. [126] Surgical intervention has played an important role in the treatment of tuberculosis since the 1930s. Historical surgical treatment The first successful treatment of tuberculosis was all surgical. They were based on the observation that the healed tuberculosis cavities were all closed. Surgical treatment was therefore aimed at closing open cavities in order to stimulate healing. These procedures were all used in the pre-antibiotic era. There is a myth that surgeons believed that the goal was to deprive the body of oxygen: however, it was well known that the body survives anaerobic conditions. Although these procedures can be regarded as barbaric in the 21st century, they are not the same as those of the 21st century. Recurrent or persistent pneumothorax The simplest and earliest procedure was to introduce air into the pleural space to collapse the affected lungs and thus the open cavity. Pneumothorax was always in spontaneous resolution and the procedure had to be repeated every few weeks. Phrenic nerve crush the phrenic nerve (which supplies the diaphragm) is cut or crushed to permanently paralyze the diaphragm on that side. The paralyzed membrane then rises up and the lungs on that side collapse, leaving a closing cavity. Thoracoplasty When the cavity was located at the tip of the lung, thoracoplasty can be performed. They broke six or eight ribs and pushed it into the thoracic cavity to collapse the lungs. It was a distorting operation, but it avoided the need for repeated procedures. Osteoplastic thoracoplasty (a variant of extrapleural thoracoplasty) at the Novosibirsk TB Research Institute (Russia) in the last 50 years in patients with complicated cavitary forms of tuberculosis, in whom resection of the lungs is contra-ed. [127] Plombage Plombage reduced the need for a disfiguring operation. This involves inserting porcelain balls into the thoracic cavity to collapse the lungs underneath. Surgical resections of infected lungs were rarely attempted in the 1930s and 1940s due to extremely high perioperative death rates. [128] Modern surgical treatment In modern times, surgical treatment for tuberculosis is limited to the treatment of multi-resistant tuberculosis. A patient with MDR-TB who continues to culture positive after several months of treatment may be referred to as lobectomy or pneumonectomy with the aim of cutting out the infected tissue. The optimal timing of the operation has not yet been determined, and the operation still provides significant morbidity. [129] [130] [131] [132] [133] [134] [135] [136] [137] The center has the most experience in the U.S. at the National Jewish Medical and Research Center in Denver, Colorado. [132] Between 1983 and 2000, 172 patients had 180 surgeries; of these were 98 were lobectomies and 82 were pneumonectomies. 3.3% of operational deaths are reported and a further 6.8% die after surgery; 12% experienced significant morbidity (especially extreme shortness of breath). Of the 91 patients who culture positive before surgery, only 4 had culture positive after surgery. Some complications of treated tuberculosis, such as recurrent hemoptysis, destroyed or bronchiectasic lung and empyema (a collection of pus in the pleural cavity), can also indicate surgical therapy. [136] With extrapulmonary TB, surgery is often required to make a diagnosis (instead of the effect of a cure): surgical exciation of lymph nodes, drainage abscesses, tissue biopsy, etc. are all examples of this. Samples taken for the TB culture must be sent to the laboratory in a sterile container without an additive (even water or salt water) and must arrive at the laboratory as soon as possible. If liquid culture facilities are available, samples from sterile sites can be introduced directly following the procedure: this can improve yields. In the spine with tuberculosis, surgery indicates spinal instability (if extensive bony destruction) or if the spinal cord is threatened. Therapeutic drainage of tuberculosis abscesses or collections is routinely not recommended and is eliminated with appropriate treatment. With TB meningitis, hydrocephalus is a possible complication and may require the insertion of ventricular shunnel or duct. Nutrition It is well known that malnutrition is a strong risk factor for tuberculosis malaise,[138] that tuberculosis is in itself a risk factor for malnutrition[139][140] and that malnourished patients with Tuberculosis (BMI less than 18.5) are still the right increased risk of death. [141] Knowledge of the association Malnutrition and tuberculosis are prevalent in some cultures and can reduce diagnostic delay and improve treatment adherence. [142] Although the blood levels of some micronuts may be low in people starting treatment for active tuberculosis, a review of Cochrane 35 concluded that there is insufficient research to determine whether routine provision of free food or energy supplements improves the results of tuberculosis treatment. However, dietary supplementation is likely to improve weight gain in certain settings. [143] The epidemiological lack of vitamin D and tuberculosis is a risk factor for tuberculosis[144] and appears to be that vitamin D deficiency impairs the body's ability to fight tuberculosis,[145] but there is no clinical evidence that the treatment of vitamin D deficiency prevents tuberculosis,[146] although the available evidence is that this should be done. The decrease in vitamin D levels may explain African-Americans' increased sensitivity to tuberculosis,[147] and may also explain why light therapy is effective for lupus vulgaris (tuberculosis of the skin) (a finding that won Niels Finsen's Nobel Prize in 1903), as skin exposed to sunlight naturally produces more vitamin D. Treatment of tuberculosis seems to reduce levels of vitamin D alone[149][150] and does not appear to be a problem in clinical practice. [151] [152] [153] Genetic differences in the West African vitamin D receptor,[154] affecting the tendency to tuberculosis in gujarati[155] and Chinese[156] populations, however, no data are available in any population showing replacement of vitamin D (i.e. people with vitamin D levels of tav) having any effect on Tuberculosis. [summons required] Vitamin D and tuberculosis treatment Vitamin D for vitamin D patients who are vitamin D deficient may be useful to some patients. If taken as a group, it appears that supplementation with vitamin D is not beneficial, if sputum culture conversion is as the end point,[157][158] and thus vitamin D supplements for TB patients who have normal vitamin D levels do not provide any benefit in terms of TB. [159] Vitamin TaqI has a vitamin D receptor tt genotype and some vitamin D-deficient patients with vitamin D supplementation seem to accelerate the transformation of sputum culture. [157] Studies on vitamin D do not exist using the outcome of the gold standard for relapse, so the true benefit of vitamin D is currently unknown. In the mid-19th century, the addition of vitamin D appears to enhance the ability of monocytes and macrophases to destroy M. tuberculosis in vitro[98][164][165][166][147][167] to mitigate the potentially harmful effects of the human immune system. [168] Other arginine has some clinical evidence[97] as an adjuvant. Mycobacterium vaccae is used by Anhui Zhifei Longcom Biologic Pharmacy Co., Ltd. Injectable Vaccae(TM) [169] and Immunitor LLC. [170] [171] Laten tuberculosis Additional information: Laten tb Treatment of laten tuberculosis infection (LTBI) is essential to control tuberculosis and eliminate tuberculosis by reducing the risk that tuberculosis infection will lead to the development of the disease. Preventive therapy and chemo prophylaxis have been used for decades and are preferred in the UK because it involves giving medication to people who are not active in disease and are currently doing well, the reason for treatment is primarily to prevent people from going wrong. Latening tuberculosis treatment is beneficial in the U.S., because the drug does not actually prevent infection: it prevents an existing silent infection from becoming active. The feeling in the U.S. is that the treatment of LTBI promotes a broader implementation by persuading people to receive treatment for the disease. There is no convincing reason to favour one term over another. It is essential that the assessment of the exclusion of ACTIVE Tuberculosis is carried out before the start of treatment with LTBI. The treatment of LTBI to a person with active tuberculosis is a serious mistake: tuberculosis is not properly treated and there is a risk of developing drug-resistant strains of tuberculosis. A number of treatment regimens are available: 9H-Isoniazid for 9 months is the gold standard, and 93% effective. 6H-Isoniazid for 6 months might be adopted by a local TB program based on price-effectiveness and patient license. This regimen is currently recommended for routine use in the UK. U.S. guidance excludes this treatment from the use of children or individuals with radiological evidence of previous tuberculosis (old fibrotic lesions). (69% effective) 6-9H2– The two treatment regimens above are an alternative when administered with direct-observed treatment (DOT). 4R-Rifampicin is an alternative for 4 months for those who are unable to take ioniazid or who have been known to be exposed to ioniazid-resistant TB. 3HR- Isoniazide and rifampicin may be given for 3 months. 2RZ– 2-month treatment with rifampicin and pyrazinamide is no longer recommended for the treatment of LTBI, as drug-induced hepatitis and death have increased significantly. [172] [173] 3RPT/INH - 3-month (12-dose) weekly doses of rifapentin and ioniazid. [1] [2] Evidence of treatment effectiveness: The 2000 Cochran review, which included 11 double-blind randomised control studies and 73,375 patients who and 12 months of isolazziad (INH) treatment for latening tuberculosis. HIV-positive and current or earlier excluded in the case of tuberculosis. The main result was a relative risk of developing active tuberculosis over two years or more in patients treated with INH over a period of two years or more, with a relative risk of developing active tuberculosis of 0.40 (95% condinate interval (CI) 0.31-0.52), 6 to 12 months of treatment (RR 0.44.95% CI 0.27-0.73 for six months and 0.38.95% CI 0.28-0.50 for 12 months). [174] A systematic review published by the Cochrane Collaboration in 2013 to compare Rifamycins (monotheraphy and combination therapy) with INH monotheraphy as an alternative to preventing active TB in HIV-negative populations. The evidence suggested that shorter Rifampicin systems (3 or 4 months) experienced higher treatment rates and fewer adverse events compared to INH. However, the overall quality of the quality criteria was low or medium. [175] Another meta-analysis came to a similar conclusion, namely that treatment regimens containing rifamycin for 3 months or more prevented tuberculosis reactivation with a better profile. [176] Research based on animal[177] and clinical trials[178] suggesting that moxifloxacin-containing treatment may be as effective for up to four months as conventional treatment six months ago. [179] Bayer is currently a II.[180] Encouraging, Bayer also promised that if the studies were successful, Bayer would make moxifloxacin affordable and accessible in countries where it was needed. [summons required] Another approach to anti-TB drug development, which does not rely on antibiotics, consists of targeting NAD+ synthase, an essential enzyme for tuberculosis bacteria, but not humans. [181] Low-level laser therapy for tuberculosis treatment is not supported by reliable evidence. 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