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PubMed1972

Treatment of chronic drug-resistant pulmonary tuberculosis with rifampin and ethambutol.

Twenty patients with chronic pulmonary tuberculosis completed eight months of rifampin-ethambutol treatment. Half the patients received daily 600 mg. rifampin and 25 mg./kg. ethambutol for the first two months and subsequently 15 mg./kg. The others received the same dosage of ethambutol and 450 mg. rifampin daily. The average time of sputum conversion was seven weeks and 11 weeks in the two groups respectively. The patients tolerated these drug regimens well.Rifampin blood levels and urinary excretion were studied monthly during the therapy. They indicated that after a short period of treatment the elimination of this drug became faster owing to increased excretion of rifampin, and particularly of its desacetyl metabolite, in the bile. Liver damage resulted in a slower excretion rate. Rifampin should be taken on an empty stomach because simultaneous food intake reduces the peak blood concentration.

Administration, Oral↗
PubMed1981

Ethambutol-induced lichenoid eruption.

The tuberculostatic drug ethambutol is an infrequent skin offender. A lichenoid skin eruption restricted to the light-exposed areas in a 67-year-old male was proved by withdrawal and challenge to be caused by ethambutol. Patch tests with ethambutol 0.1%, 0.5% and 1% in watery solution were negative.

Aged↗
PubMed1995

Ethambutol-induced pulmonary infiltrates with eosinophilia and skin involvement.

A 67 year old woman presented with miliary tuberculosis. She was treated with streptomycin, isoniazid, rifampicin, ethambutol and pyrazinamide. However, she developed rifampicin-induced thrombocytopenia after 6 weeks of treatment, and skin rash, blood eosinophilia and pulmonary infiltrates after 8 weeks of therapy. The latter was found to be ethambutol related. Additional evidence, including blood and sputum eosinophilia and the rapidity of its response to corticosteroid, suggested that the pulmonary infiltrates might also be eosinophilic in nature. To the best of our knowledge, this constitutes the first report of such adverse drug reaction, induced by ethambutol.

Aged↗
PubMed1994

Toxic optic neuropathy associated with ethambutol: implications for current therapy.

BACKGROUND: Aside from the direct ocular manifestations of tuberculosis, significant vision loss can occur during treatment with agents that have potential ocular toxicities. Many thoracic specialists and eye care physicians consider these effects rare and readily reversible. With the alarming increase in incidence of tuberculosis in the United States over the past several years a review of anti-tuberculosis medications and their potential side effects is warranted. METHODS: A patient who developed dramatic, permanent vision loss after a 9-month course of treatment with ethambutol and isoniazid for pulmonary tuberculosis is presented. The medical and ophthalmic literature was reviewed for current use of these medications as well as for the reported incidence of visual side effects. RESULTS: Ethambutol, and to a lesser extent isoniazid, are both implicated in the development of visually related side effects. There is documentation of ocular toxicity with ethambutol when administered at dosages generally pronounced as being safe. Controversy as to what constitutes a safe and effective dose of these medications still exists. CONCLUSIONS: Any patient undergoing medical treatment for tuberculosis requires proper education concerning potential drug side effects. Routine ophthalmic observation for the development of optic neuropathy is strongly recommended for patients with significant risk factors that could increase the chance of side effects and those on longer treatment courses. Baseline and follow-up examinations should include: Snellen acuity, Farnsworth D-15 color testing, automated threshold perimetry and optic nerve head photography.

Blindness↗
PubMed1997

[Optic nerve damage caused by administration of ethambutol].

We considered the influence of ethambutol therapy for lung TBC on the visual function of patients. Cases of toxic optic neuropathy caused by ethambutol therapy in patients hospitalized in the Ophthalmic Clinic in Rijeka within 5 years were presented. Results of the treatment of toxic optic neuropathy caused by ethambutol are influenced by risk factors such as: diabetes mellitus, renal insufficiency, alcoholism and in our opinion, atherosclerosis and very old age.

Aged↗
PubMed1996

Early bactericidal activity of ethambutol, pyrazinamide and the fixed combination of isoniazid, rifampicin and pyrazinamide (Rifater) in patients with pulmonary tuberculosis.

The early bactericidal activity (EBA) of ethambutol, pyrazinamide and the fixed combination of isoniazid, rifampicin and pyrazinamide (Rifater: Mer National) was evaluated in patients with pulmonary tuberculosis who were sputum-positive on microscopy for acid-fast bacilli. Twenty-eight patients (mean age 33 years and weight 51 kg on average; range 40-59 kg) were studied. The fall in viable counts of Mycobacterium tuberculosis in sputum collections during the 2 days following the start of treatment was estimated from counts of colony-forming units (CFUs) of M. tuberculosis per ml of sputum cultured on selective 7H10 agar medium. The EBA for ethambutol determined in 9 patients was 0.245 +/- 0.046, log10 CFU/ml sputum/day, that for pyrazinamide was 0.003 +/- 0.014 log10 CFU/ml sputum/day and that for Rifater 0.558 +/- 0.054 log10 CFU/ml sputum/day. The results obtained are similar to those reported in a previous study of the first 2 days of treatment, but in smaller numbers of patients, and confirm the moderate EBA of ethambutol while pyrazinamide is again shown to have very little EBA. Rifater has a marked EBA which may be due mainly to the action of isoniazid. This methodology may be valuable in the rapid evaluation of the bactericidal activity of new antituberculosis agents and the comparison of different dose sizes of agents of the same class.

Adolescent↗
PubMed1963

EFFECT OF ETHAMBUTOL ON CYTOLOGY OF MYCOBACTERIUM SMEGMATIS.

Gale, Glen R. (Veterans Administration Hospital, Durham, N.C.) and Helen H. McLain. Effect of ethambutol on cytology of Mycobacterium smegmatis. J. Bacteriol. 86:749-756. 1963.-Electron microscopy showed the effects of the antimycobacterial drug, ethambutol [d-2,2'-(ethylenediimino)-di-1-butanol], on the cytology of Mycobacterium smegmatis. After 10 hr of exposure to the drug, cells no longer contained material which, in control cells, was closely associated with cellular division, possibly genetic substance. No marked changes were observed in other cellular structures. It was concluded that the drug may block one or more steps in the synthesis of pentose nucleic acid or deoxypentose nucleic acid, ultimately causing cessation of cellular division and loss of viability. These cytological findings were compatible with results of other investigators on the mode of action of this drug.

Antitubercular Agents↗
PubMed1983

Visual evoked potentials in the detection of subclinical optic toxic effects secondary to ethambutol.

In 14 patients with tuberculosis treated with ethambutol hydrochloride, pattern-reversal visual evoked potentials (VEPs) were recorded to monocular, whole-field stimulation before the commencement of treatment and one month and three months subsequently. In six subjects, the VEPs showed changes in the latency and amplitude of the P100 component at the one- or three-month interval. In three cases, the VEP changes reversed after cessation of treatment. In five of the six cases, changes were not associated with a change in visual function, as measured by clinical neuro-ophthalmologic examination. Our findings confirm the usefulness of VEPs in the detection of subclinical optic nerve disease and suggest their use in routine monitoring of ocular function in patients treated with ethambutol.

Adolescent↗
PubMed2001

Detection of embB codon 306 mutations in ethambutol resistant Mycobacterium tuberculosis directly from sputum samples: a low-cost, rapid approach.

Substitutions of codon 306 in the gene embB are the most common mutations found in ethambutol resistant Mycobacterium tuberculosis. The characterization of these mutations has been hampered by the need for prior cultivation of the mycobacteria, or the need for DNA sequencing, or both. Here, we describe a simple and culture-independent technique to detect embB codon 306 mutations directly from sputum samples, requiring little more than a PCR machine and a simple agarose minigel. There is no need for labelled probes or DNA sequencing. In a preliminary test of feasibility, interpretable results were obtained from 21 of 24 selected sputum samples, 12 of which were determined to contain ethambutol resistant M. tuberculosis after culture. All of six samples with embB codon 306 mutations were correctly identified. Although an exact validation of this technique is beyond the scope of this technical report, we conclude from well-known embB codon 306 mutation prevalence figures that approximately one half of EMB resistant cases could already be predicted within 2 working days, with little equipment or hands-on time needed, instead of weeks required for conventional resistance testing.

Chemistry, Clinical↗
PubMed1987

Fulminant hepatitis during treatment with rifampicin, pyrazinamid and ethambutol.

A 10-year-old girl with cervical tuberculosis was treated with Isoniazid, Rimfampicin and Ethambutol. After 2 weeks of treatment a hepatotoxic reaction developed. Withdrawal of therapy resulted in complete clinical improvement and in normalization of all laboratory measurements. Treatment was restarted with Rifampicin, Pyrazinamid and Ethambutol. Liver enzyme levels were monitored weekly. Seven weeks after this three-drug regiment was started, all therapy was discontinued because of elevated liver enzyme levels. However, the patient died 2 weeks later of progressive fulminant hepatitis.

Cervical Vertebrae↗
PubMed1992

Susceptibility of Mycobacterium kansasii to ethambutol and its combination with rifamycins, ciprofloxacin and isoniazid.

The susceptibility of Mycobacterium kansasii to antibacterial agents alone and in combination was studied. Widespread resistance to ethambutol, ciprofloxacin and isoniazid was found when these drugs were tested separately. However, pronounced antibacterial effects were seen when ethambutol was tested in combination with ciprofloxacin, rifampicin or rifabutin, which corresponded to significantly decreased resistance to these drugs in combination.

Ciprofloxacin↗
PubMed2006

Nucleotide polymorphism associated with ethambutol resistance in clinical isolates of Mycobacterium tuberculosis.

Ethambutol (EMB) is a first-line drug used for antitubercular therapy in combination with other drugs as recommended by World Health Organization DOTS/DOTS-Plus regimens. EMB is also effective in the treatment of opportunistic mycobacterial infections in patients with human immunodeficiency virus. The emb locus has been considered as a drug target for EMB, and substitutions of codon 306 in Mycobacterium tuberculosis gene embB have been shown to be the most frequent and predictive mutations for EMB resistance. The aim of the present study was to detect embB and embC gene mutations in EMB-resistant clinical isolates. A total of 23 isolates of M. tuberculosis from patients with pulmonary tuberculosis were included in the study. Drug sensitivity was tested by proportion method and E-test. All 23 isolates were EMB resistant. Primers to amplify the embB and embC gene were designed, and polymerase chain reaction products were subjected for sequence analysis. H37Rv standard laboratory strain was used as control. Nucleotide sequencing showed that 16 strains had a mutation in the embB gene. The most common mutation observed in the embB gene was at codon 306, followed by mutations at codons 299 and 378 in 4 and 2 isolates, respectively. Novel mutations have been reported at codons 239, 240, 247, 282, 311, 368, 397, 446, 469, and 471. Sequence analysis of the embC gene showed mutation in 8 isolates at codon 270. Novel mutations in embC have been reported at codons 251 and 254. The most common nucleotide polymorphism in our isolates was at codons 306 and 299 in the embB gene and at codon 270 in the embC gene. A mutation at codon 306 was usually associated with high-level ethambutol resistance.

Antitubercular Agents↗
PubMed1986

Ocular toxicity following ethambutol in standard dosage.

We describe a patient who developed rapid irreversible blindness following treatment with ethambutol in the recommended dose of 15 mg/kg body weight which in clinical practice is widely considered to be safe. This case exemplifies the potential risks of ethambutol and re-emphasizes the importance of instructing patients to stop the drug at once if they develop visual symptoms.

Adult↗
PubMed1981

Experimental ethambutol neuropathy in rats. Morphometric and teased-fiber studies.

Eight rats were given 500 mg/kg body weight of the antituberculous drug ethambutol orally every day for 3 months (group A), and 7 took 150 mg/kg of the drug for 9 months (group B). The sciatic nerves at midthigh level and the posterior tibial nerves at ankle level were studied with morphometric examination and teased-fiber method. The number of myelinated fiber/mm(2) of fascicular area was significantly reduced in both sciatic and posterior tibial nerves of group B. The pattern of frequency distribution of myelinated nerve fiber diameters of both groups was not different from that of the controls. Teased-fiber study revealed that many fibers were undergoing axonal degeneration in both groups A and B. In addition, regenerating fibers after axonal degeneration were observed in group B. These results showed that the predominant pathologic change in ethambutol neuropathy was axonal degeneration and that regeneration was already occurring in the animals taking a small dose of the drug for a long period. The fact that the degree of pathologic change was rather more severe in the sciatic nerve than in the posterior tibial nerve indicated that this was not a "dying-back" neuropathy.

Animals↗
PubMed1981

Sensitivity of opportunist mycobacteria to rifampicin and ethambutol.

A total of 1237 strains of opportunist mycobacteria were tested for sensitivity to rifampicin and ethambutol. Most strains of Mycobacterium kansasii and all strains of M. marinum tested were sensitive to both drugs. A variable pattern was given by M. xenopi strains, but a general resistance was observed with the M. avium--intracellulare--scrofulaceum group. All strains of M. fortuitum and M. chelonei were highly resistant. Scotochromogens were mostly sensitive to ethambutol, but there was variable resistance to rifampicin. These properties may be useful in identification of species. No acquired resistance was found in follow-up cultures from confirmed cases of mycobacterioses, but details of therapy, if any, were not known.

Drug Resistance, Microbial↗
PubMedDate not supplied

Serial pattern evoked potential recording in a case of toxic optic neuropathy due to ethambutol.

Visual evoked potentials (VEPs) were studied in a patient who developed visual impairment during ethambutol treatment. The ERG and the flash VEP were normal at the time of maximal visual loss, whereas pattern reversal VEPs 2 and 5 months after onset revealed evidence of severe bilateral optic nerve involvement, especially affecting macular fibres. Seven months after onset paramacular PNP complexes with a late positivity (scotomatous response) were recorded after pattern reversal and half-field stimulation, suggesting involvement of fibres subserving central vision. At the time when visual acuity was normal there was still electrophysiological evidence of a mild involvement of the anterior visual pathway. The papillomacular bundle seems to be especially involved in ethambutol eye toxicity.

Aged↗
PubMed1986

Amikacin, ethambutol, and rifampin for treatment of disseminated Mycobacterium avium-intracellulare infections in patients with acquired immune deficiency syndrome.

Synergistic combinations of achievable serum levels of amikacin, rifampin, and ethambutol were tested for their ability to inhibit growth of Mycobacterium avium-intracellulare strains isolated from seven patients with acquired immune deficiency syndrome. Even when the isolates were very resistant to the individual antimicrobial agents in vitro, growth was completely inhibited by all combinations of the three agents tested. Four of the patients treated with a combined regimen of amikacin, rifampin, and ethambutol showed clinical improvement. Synergistic antimicrobial susceptibility tests seem to more accurately represent the efficacy of combined regimens used to treat these extremely resistant mycobacteria than do conventional susceptibility determinations with individual antimicrobial agents.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Ethambutol in tuberculosis.

Ethambutol gained rapid acceptance as a substitute for PAS in tuberculosis therapy because of improved patient tolerance and convenience of administration. Ocular toxicity was recognized early on but was thought to be a problem only at higher dosages. There have, however, been a number of reports of serious visual impairment on conventional dosage, with permanent blindness in some cases, and painfully slow recovery in others. The precise mechanism for the optic neuritis is not clear, and toxicity is difficult to predict in the individual patient. Ethambutol appears to contribute only marginally to modern short course regimens and should be replaced with a less toxic agent.

Blindness↗