Ocular toxicity of ethambutol.

Department of Ophthalmology, Hong Kong Sanatorium and Hospital, Happy Valley, Hong Kong.
Hong Kong medical journal = Xianggang yi xue za zhi / Hong Kong Academy of Medicine 03/2006; 12(1):56-60.
Source: PubMed

ABSTRACT To review the literature on ocular toxicity of ethambutol--its background, clinical presentation, toxicity characteristics, management, monitoring, and preventive measures.
Literature search of Medline from 1962 to May 2005.
All related literature in English using the search formula: (ethambutol OR myambutol) AND (eye* OR ophthal* OR ocular) AND (adverse OR toxic).
All information was collected and analysed by authors.
Ethambutol hydrochloride is a commonly used first-line anti-tuberculous agent. Although rare, ocular toxicity in the form of optic neuritis (most commonly retrobulbar neuritis) has been well documented since its first use in the 1960s. Classically described as dose- and duration-related and reversible on therapy discontinuation, reversibility of optic neuritis remains controversial. International guidelines on prevention and early detection of ethambutol-induced ocular toxicity have been published. Nonetheless, opinion of the clinical effectiveness of regular vision tests to enable early detection of toxicity is divided.
The course of ethambutol-induced ocular toxicity is unpredictable. Measures to ensure a high level of awareness in medical staff and patients of this potential adverse effect appear to be the best current preventive method. Classified by the World Health Organization as a place with an intermediate tuberculosis burden and good health infrastructure, Hong Kong is in a good position to examine the unanswered questions about ethambutol-induced ocular toxicity.

1 Bookmark
  • [Show abstract] [Hide abstract]
    ABSTRACT: Autosomal dominant optic atrophy is an inherited optic neuropathy manifesting with variable penetrance and expressivity. Other genetic and environmental factors are postulated to contribute to more marked visual loss in some affected individuals. Optic neuropathy is also a known adverse effect of ethambutol therapy for tuberculosis. This case report demonstrates an atypical presentation of ethambutol toxicity, with progressive profound loss of vision despite drug cessation. A subsequent diagnosis of autosomal dominant optic atrophy was made when the proband's sons presented with mild visual disturbances and color vision defects, confirmed with electrophysiology and OPA1 gene mutational analysis. This case emphasizes the importance of avoiding potentially neurotoxic therapy in predisposed individuals and the influence of environmental factors in patients with inherited optic neuropathies.
    Survey of Ophthalmology 07/2010; 55(4):378-85. · 2.86 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although the development of multiple sclerosis (MS) after idiopathic optic neuritis (ON) is well known, MS following ethambutol-induced ON is not widely recognized. We hypothesize the possible association between ethambutol-induced ON and MS based on empirical data of six patients with ethambutol-induced ON who progressed to MS. Whether there is a genuine link between ethambutol-induced ON and MS is unresolved, but our observations do raise the possibility. It is difficult to speculate on the mechanism for such a link, because the etiology of MS itself is unknown. It is possible that ethambutol or its metabolites induce an autoimmune response, through molecular mimicry or other phenomena, cross-reacting with central nervous system (CNS) myelin.
    Medical Hypotheses 12/2010; 75(6):679-80. · 1.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: : There is a group of optic neuropathies of either genetic or acquired origin characterized by similar clinical manifestations with preferential involvement of the papillomacular bundle (PMB). PMB fibers are most susceptible to injury as they are small, unmyelinated, and have high-energy demands. These optic neuropathies share a presumed common pathophysiology of mitochondrial dysfunction. : A variety of medications cause optic neuropathy by interfering with mitochondrial function. The evidence linking these therapeutic agents as a cause of mitochondrial optic neuropathy (MON) is well established in some and less certain in others. The differential diagnosis includes other optic nerve disorders producing bilateral, symmetric visual loss, including certain nutritional deficiencies, toxins, and genetic diseases. : Ethambutol, chloramphenicol, linezolid, erythromycin, streptomycin, and antiretroviral drugs can cause drug-related MON. In many cases, drug toxicity is dose and duration dependent, and discontinuation of the drug in a timely manner can lead to significant visual recovery. : Mitochondrial optic neuropathies are increasingly recognized as a spectrum of conditions that reach a similar end point by compromising a common pathway of mitochondrial dysfunction. Clinicians should be aware of drugs that can cause a MON. Prompt recognition of this association is critical in preventing irreversible, profound visual loss.
    Journal of neuro-ophthalmology: the official journal of the North American Neuro-Ophthalmology Society 06/2013; 33(2):172-8. · 1.09 Impact Factor


Available from