|LETTER TO EDITOR
|Year : 2012 | Volume
| Issue : 1 | Page : 79
Tobacco-alcohol amblyopia: Nonexistent entity
Andrzej Grzybowski1, Martyna Pieniazek2
1 Department of Ophthalmology, Poznan City Hospital, Olsztyn; Department of Chair of Ophthalmology, University of Warmia and Mazury, ul. Zolnierska 14C, Olsztyn, Poland
2 Department of Ophthalmology, Wroclaw Medical University, 213 Borowska St, 50 556 Wroclaw, Poland
|Date of Web Publication||22-Apr-2013|
Department of Ophthalmology, Jozef Strus Poznan City Hospital, 3 Szwajcarska St, 361 285 Poznan
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Grzybowski A, Pieniazek M. Tobacco-alcohol amblyopia: Nonexistent entity. Ind Psychiatry J 2012;21:79
With the reference to a case study done by Prakash et al. entitled "Tobacco-alcohol amblyopia: A rare complication of prolonged alcohol abuse"  we would like to discuss the misleading and thus inappropriate use of term of tobacco-alcohol amblyopia.
As the authors mention, tobacco-alcohol amblyopia was often described prior to II World War.  Later, it was proved by many authors that this condition was due to malnutrition, namely, vitamin B12 and folate acid deficit or tobacco use than alcohol itself.  Already in 1878, Horner noticed that excessive alcohol and tobacco consumption do not lead to ocular deficits unless patient develops "a gastric catarrh or anorexia".  In 1896, De Schweinitz wrote that 'other circumstances (besides alcohol) which favor a deleterious effect of tobacco on vision are malnutrition from any source, chronic gastritis, dyspepsia, mental worry, and particularly insomnia'.  It was subsequently described that the ocular symptoms of so called tobacco-alcohol amblyopia improves or even fully resolves after vitamin B supplementation notwithstanding the tobacco and alcohol intake,  so, in fact were due to nutritional optic neuropathy.
Thus, every case of optic neuropathy in an alcohol abuse patient should primarily be suspected as nutritional optic neuropathy. Examination of vitamin B and folate acid serum concentration, not provided in the presented case, is in such cases of major importance.
The improvement of vision in the case described by Prakash et al. after nutritional supplementation indicates a malnutritional nature of the ocular symptoms, and, in our opinion, should be diagnosed as nutritional optic neuropathy.
The differential diagnosis of the discussed case should also include Leber's hereditary optic neuropathy (LHON), as its clinical picture contains majority of the features of the presented case. LHON often manifests with painless bilateral visual loss with normal fundus of the eye and temporal optic disc pallor, more often in young males. It was shown that tobacco and alcohol consumption act as the triggering factors in LHON mutation carriers. 
Concluding, the presented case was probably a nutritional optic neuropathy, and the term "tobacco-alcohol amblyopia" as inappropriate and misleading should cease to be used in present scientific communications.
| References|| |
|1.||Prakash J, Ryali V, Srivastava K, Bhat PS, Shashikumar R, Singal A. Tobacco-alcohol amblyopia: A rare complication of prolonged alcohol abuse. Ind Psychiatry J 2011;20:66-8. |
|2.||Grzybowski A, Holder GE. Tobacco optic neuropathy (TON)-the historical and present concept of the disease. Acta Ophthalmol 2011;89:495-9. |
|3.||Deschweinitz GE. Toxic amblyopias. Philadelphia: Lea Brothers and Co.; 1896. |
|4.||Carroll FD. Nutritional amblyopia. Arch Ophthal 1966;76:406-11. |
|5.||Sadun AA, La Morgia C, Carelli V. Leber's Hereditary Optic Neuropathy. Curr Treat Options Neurol. 2011;13:109-17. |