With reference to Kee and Hwang's article entitled ‘Optical coherence tomography in a patient with tobacco-amblyopia’, I doubt whether the presented case of optic neuropathy could be appropriately named ‘tobacco amblyopia’.
In the last two centuries it has been believed that tobacco consumption might result in toxic neuropathy called ‘tobacco amblyopia’.1 Tobacco neuropathy has been supposed to originate from excessive cigar and pipe smoking (or tobacco chewing or snuffing) rather than from cigarette smoking.1 Presently, this disorder is less frequent. Some even argue that ‘tobacco amblyopia’ does not exist. Nevertheless, some data collected during the twentieth century should be considered with regard to this problem.
Firstly, paradoxically, in spite of the explosion of cigarette smoking during the twentieth century, the number of tobacco amblyopia cases significantly decreased. The discussion related to this phenomenon can be found elsewhere.2
Secondly, it was shown that optic neuropathy in excessive alcohol consumers—called ‘alcohol amblyopia’ previously or often ‘tobacco-alcohol amblyopia’ _ is in fact just ‘nutritional optic neuropathy’ related to deficiencies of vitamin B and foliate acid.3 In different studies, it was shown that a supplementation diet improves the prognosis even without tobacco abstinence.4
Thirdly, it was proposed and documented that some cases of ‘tobacco amblyopia’ were in fact Leber's hereditary optic neuropathies (LHON) and, possibly, which is less understood, epidemic optic neuropathies in Tanzania, Cuba, or Nigeria.5
The patient presented in the article had probably some major nutritional deficiencies, although there was no description of tests for vitamin B12 or foliate acid in serum, etc, which could confirm this diagnosis. The LHON and other epidemic causes of optic neuropathy are probably very unlikely in this case. Thus, in my opinion, the patient should be diagnosed as having nutritional optic neuropathy.
I believe that the term ‘tobacco optic neuropathy’ should be reserved only for such cases, where the other—that is nutritional, genetic, as well as toxic or infectious—causes can be excluded. There is also one more argument against using the name ‘tobacco amblyopia’, neither is it caused by tobacco itself (it might be an additional or accompanying factor), nor is it real amblyopia.
Dunphy EB . Alcohol and tobacco amblyopia: a historical survey. Am J Ophthalmol 1969; 68: 569–578.
Grzybowski A . Rozwój badań wp ływu tytoniu na narzaąd wzroku w ostatnich 200 latach (The development of research on the effect of tobacco consumption on the visual organ over the last 200 years). Przeglaąd Lekarski (Med Rev) 2005; 62 (10): 1167–1170.
Heaton JM, McCormick AJA, Freeman AG . Tobacco amblyopia: a clinical manifestation of vitamin B12 deficiency. Lancet 1958; 2: 286–290.
Victor M . Tobacco-alcohol amblyopia. A critique of current concepts of this disorder, with special reference to the role of nutritional deficiency in its causation. Arch Ophthalmol 1963; 70 (3): 313.
Cullom ME, Heher KL, Miller NR, Savino PJ, Johns DR . Leber's hereditary optic neuropathy masquerading as tobacco-alcohol amblyopia. Arch Ophthalmol 1993; 111: 1482–1485.
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Grzybowski, A. Tobacco amblyopia: does it really exist?. Eye 21, 1448–1449 (2007). https://doi.org/10.1038/sj.eye.6702950
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