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Combutol (Myambutol)

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Combutol is an antibacterial agent. It works by stopping the growth of TB cells, which results in cell death. Combutol is used for treating tuberculosis (TB) infections of the lung along with other medicines. It may also be used to treat other conditions as determined by your doctor.

Other names for this medication:
Etambutol, Ethambutol, Myambutol, Rifafour, Rimstar

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Moxifloxacin, Streptomycin, Etibi, Rifadin, Rofact, Levaquin, Avelox, Mycobutin

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Also known as:  Myambutol.


Combutol is a prescription medication used to treat tuberculosis (TB). Combutol belongs to a group of drugs called antimycobacterial antibiotics. TB is caused by a certain bacteria. Combutol works by stopping the bacteria from forming a cell wall, which kills the bacteria.

This medication comes in tablet form. It is taken once a day with or without food.

Common side effects of Combutol include loss of appetite, upset stomach, and numbness or tingling in hands and feet.


Combutol is supplied as a tablet to be taken by mouth, usually once daily. This medication can be taken with or without food. Try to take Combutol at the same time every day to get the most benefit. Continue taking Combutol as directed by your doctor. Stopping the medicine too early may cause the infection to be more difficult to treat.

If you take aluminum-containing antacids, take this Combutol at least 4 hours before the antacid.

Take Combutol exactly as prescribed by your doctor. Follow the directions on your prescription label carefully. The dosage must be individualized. The dosage is based on your age, weight, medical condition, and response to treatment.


If you take too much Combutol, call your local Poison Control Center or seek emergency medical attention right away.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Combutol are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Combutol may cause decreased vision clearness, including vision loss. This effect may be related to the dose that you take and how long you take Combutol. It is usually reversible when Combutol is stopped. However, permanent blindness has been reported. Contact your doctor right away if you experience vision changes (eg, decreased vision clearness). Discuss any questions or concerns with your doctor.

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Corynebacterium glutamicum belongs to the mycolic acid-containing actinomycetes, which also include Mycobacterium, Nocardia, and Rhodococcus. The cells of this group possess a cell wall with a thick outer layer composed primarily of mycolic acid, which functions as a permeability barrier. To investigate the mechanism of mycolic acid-containing layer (mycolate layer) formation, we have developed a fluorescence microscopic technique detecting the mycolate layer in situ. The staining specificity of fluorescence-labeled phospholipid analogs was determined by simultaneous staining with the hydrophobic fluorescent dye Nile Red and peptidoglycan-staining fluorescence-conjugated vancomycin. We found that fluorescence-labeled phospholipid analogs preferentially stain the mycolate layer. Using this technique, we observed the effect of the anti-mycobacterial drug ethambutol on C. glutamicum mycolate-layer formation. Ethambutol interfered specifically with mycolate-layer formation on the division planes and cell poles, while the side-wall mycolate layer was not severely affected. This indicates that mycolate-layer formation occurs mainly on division planes and cell poles in C. glutamicum, where the peptidoglycan layer is actively synthesized.

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Gynaecomastia due to anti-tubercular chemotherapy is a rare side effect. Isoniazid causing breast tissue enlargement has been very rarely reported. We report a 60-year old, male patient of Pulmonary Tuberculosis who was started on antituberculous treatment (ATT) with rifampicin (R), isoniazid (H), ethambutol (E) and pyrazinamide (Z) together for initial two months and R, H & E thereon. After five months of initiation of treatment, while receiving RHE, he developed painful bilateral gynaecomastia. Isoniazid was stopped and patient was continued on R & E till completion of the treatment up to nine months. After stopping isoniazid, his breast swelling subsided to some extent and became non-tender. Follow up, at six months, after stopping the course of treatment, patient was asymptomatic except for slight bilateral non-tender breast enlargement.

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The accomplishment of the principles for the prevention of a germ resistance and the development of new principles of treatment and highly effective antituberculotics has led to the fact that nowadays actually each case of tuberculosis may be treated and cured purely internally. This progress in the individual treatment were achieved by recommendations of therapy which are actualized from time to time. The modern treatment consists of a daily application of three effective antituberculotics for two to three months, fellowed by an intermittent application twice a week. The duration of the initial intensive period and the whole time of therapy is determined by the clinical and social state before the beginning and by the combination of drugs. INH, rifampizine, streptomycin and ethambutol form the components of the therapy combinations which at present are to be used no longer than twelve months. The redetection of the special microbiological qualities of the pyrazineamide and their importance for the prevention of relapses introduces the last phase of the development of the therapy of tuberculosis. By its means it is possible to shorten the duration of the treatment to 9 months and less and thus to increase the acceptability and cooperation, to decrease the toxicity and costs.

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The overall prevalence of DR TB was 86 (6.6%) with an increase from 23 (5.6%) patients pre-2010 to 63 (7%) post-2010 (P = 0.40). Nine (10.4%) patients were diagnosed on the basis of contact with a parent with DR TB. Overall fluoroquinolone resistance increased from 9 (39.1%) pre-2010 to 59 (93.7%) post-2010 (P = 0.0001): moxifloxacin resistance increased from 2 (8.7%) to 29 (46%) (P = 0.0018) and ofloxacin resistance increased from 7 (30.4%) to 30 (47.6%) (P = 0.14). Ethionamide resistance also increased from 6 (26.1%) to 31 (49.2%) (P = 0.04), aminoglycoside resistance was one (4.3%) pre-2010 and 12 (19%) post-2010 (P = 0.17) and resistance remained virtually the same for both amikacin [0 pre-2010 and 6 (9.5%) after 2010] and kanamycin [one (4.3%) pre- and 6 (9.5%) post-2010]. Of the first-line drugs, resistance remained the same for isoniazid [23 (100%) to 61 (96.8%)], rifampicin [22 (95.7%) to 51 (80.9%),P = 0.17], pyrazinamide [15 (65.2%) to 35 (55.6%), P = 0.47], ethambutol [14 (60.9%) to 38 (60.3%), P = 1.00] and streptomycin [19 (82.6%) to 50 (79.4%), P = 1.00]. Resistance to PAS remained unchanged [2 (8.7%) to 5 (7.9%), P = 1.00].

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We report a rare case in a female infant (age, 3.5 months) with primary immunodeficiency (IFN-γ/IL-12 pathway defect) who presented with suppurative lymphadenitis after Mycobacterium bovis BCG vaccination. The strain of M. bovis BCG identified was found to be resistant to isoniazid and rifampin. The patient was treated with a special pharmacological regimen involving isoniazid (in a limited, strategic manner), ethambutol, streptomycin, and IFN-γ, after which there was complete resolution of the lesions.

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This is a one-year laboratory-based study. Specimens from suspected new TB patients sent to the TB laboratory of the Department of Medical Microbiology, University College Hospital Ibadan, Nigeria from May 1, 2005 to April 27, 2006 were processed and analyzed. The specimens were stained with Ziehl-Neelsen (Z-N) reagents and cultured on Lowenstein-Jensen medium, incubated at 37 degrees C for 6-8 weeks. Isolates were confirmed as MDR-TB by Z-N reactions and biochemical methods. Drug susceptibility to streptomycin, ethambutol, rifampicin and isoniazid was done using Bactec 460 TB radiometric method.

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We described enlargement of intrathoracic diffuse large B-cell lymphoma (DLBCL) during treatment of pulmonary tuberculosis in a 78-year-old man. The patient had previously undergone treatment for pulmonary tuberculosis about 50 years ago and showed disease recurrence in 2010. Although after tuberculosis treatment with the standard chemotherapy regimen of isoniazid, rifampicin, ethambutol, and pyrazinamide, we observed a clear resolution of the main X-ray shadows, a nodular shadow in the right upper lung field was observed to have increased in size. After evaluation by transbronchial biopsy of the upper right lung lobe, we diagnosed DLBCL with subepithelial infiltration of an airway. This is a rare case of coexistence of active pulmonary tuberculosis and intrathoracic DLBCL.

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The role of the serine/threonine kinase PknH in the physiology and virulence of Mycobacterium tuberculosis was assessed by the construction of a pknH deletion mutant. Deletion of the pknH gene did not affect sensitivity to the antimycobacterial drug ethambutol, although it was previously thought to be involved in regulating expression of emb genes encoding arabinosyl transferases, the targets of ethambutol. Nevertheless, transcription analyses revealed that genes associated with mycobacterial cell wall component synthesis, such as emb and ini operons, are downstream substrates of the PknH signaling cascade. In vitro survival studies revealed that a mutant with a deletion of the pknH gene displayed increased resistance to acidified nitrite stress, suggesting that nitric oxide is one of the potential environmental triggers for PknH activation. The effect of pknH deletion on mycobacterial virulence was investigated in BALB/c mice. In this model, the DeltapknH mutant was found to survive and replicate to a higher bacillary load in mouse organs than its parental strain and the pknH-complemented strain. In contrast, another closely related kinase mutant, the DeltapknE mutant, obtained from the same parental strain, was not affected in its virulence phenotype. Infection of THP-1 cells or in vitro growth studies in 7H9 medium did not reveal a significant in vitro growth advantage phenotype for the DeltapknH mutant. In conclusion, we propose that the serine/threonine kinase PknH plays a role in regulating bacillary load in mouse organs to facilitate adaptation to the host environment, possibly by enabling a regulated chronic infection by M. tuberculosis.

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combutol drug 2015-04-28

The electroretinograms were normal in 25 patients. Twelve patients had normal electro-oculogram (EOG) findings in both eyes and the remaining 15 patients had abnormal EOG findings in at least one eye. Ten eyes showed supranormal EOG (light/dark (L/D)) ratios of more than 2.33, and 13 eyes had decreased L/D Ciprofloxacin Yeast Infection ratios (< 1.65). The symptom duration was shorter in the supranormal EOG group.

combutol tablet side effects 2015-03-11

The Erythromycin Benzoyl Peroxide Topical Gel Reviews Study C trial, a parallel-group, open-label, noninferiority, randomized controlled trial conducted in 11 sites in Africa, Asia, and Latin America between 2003 and 2008. Patients were 1585 adults with newly diagnosed smear-positive pulmonary tuberculosis.

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A major metropolitan county public health Zithromax Dose Pediatric Pneumonia department.

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The outcome of DOTS in the present study was impressive, and Para Que Sirve Clamoxin Amoxicilina Acido Clavulanico Suspension the programme should be extended to other rural communities; however, more efforts should be made towards the tracing of defaulters.

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A 61-year-old woman presented with decreased vision in her right eye and cystoid macular edema resistant to periocular corticosteroid Ambilan Bid Suspension Oral treatment. There were no other findings.

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Results were generated by three laboratories: the Instituto Adolfo Lutz (IAL) Mycobacteria Reference Laboratory and two IAL Regional Laboratories in Santo André and Sorocaba, São Paulo State, Brazil. One hundred and twenty M. tuberculosis strains were simultaneously tested using NRA and the proportion method (PM), while 117 strains were Fleming 375 Mg tested using both NRA and BACTEC MGIT 960 (M960).

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The authors present a case of multifocal choroiditis and panuveitis secondary to disseminated Klamoks 625mg 15 Tablet Mycobacterium avium complex infection in a patient with human immunodeficiency virus/AIDS.

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To our knowledge this is the first reported case of tuberculous uveitis following treatment with etanercept. This etiology has to be considered in patients taking this drug Flazol Dose who present with intraocular inflammation.

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Little information is available regarding changes in immune status for patients with Mycobacterium avium complex (MAC) lung disease during antibiotic therapy. Serum immunomolecules from 42 patients with MAC lung disease were assayed comparatively using an array-based system according to (i) patients with MAC lung disease at the time of diagnosis versus healthy controls and (ii) alterations after 12 months of antibiotic therapy in the MAC lung disease group. In addition, cytokine analyses were performed to determine whether cytokine responses were associated specifically with the disease phenotype, treatment outcome and aetiological agent. Notably, the serum concentrations of type 1 cytokine-associated molecules, such as CD40L, interferon (IFN)-γ, interleukin (IL)-8 and IL-23, were decreased significantly in patients at the time of diagnosis, suggesting that these molecules may serve as indicators of host susceptibility to MAC disease. Although the overall serum level of T helper type 1 (Th1)-related molecules, such as CD40L and IFN-γ, was restored after treatment, Th17-related cytokines, such as IL-17 and IL-23, were down-regulated significantly at 12 months post-treatment compared to pretreatment. Furthermore, these cytokine patterns differed among patient subgroups. Decreased serum concentrations of IL-17 and/or IL-23 were associated with failure of sputum conversion, the fibrocavitary disease phenotype and M. intracellulare lung disease. Thus, the reciprocal balance between Th1 and Th17 immunity during antibiotic therapy for MAC lung disease is critical for dictating the treatment response. In conclusion, a low level of Th1-related immunomolecules may perpetuate MAC lung disease, and the serum concentrations of Th17-related cytokines can reflect the treatment outcome, disease phenotype and aetiological agent.