The Effects of Pyridoxine on Retinal Nerve Fiber Layer in Tuberculous Treatment

Year 2019, Volume: 21 Issue: 2, 84 - 89, 30.08.2019

Hüseyin Fındık , Aziz Gümüş , Murat Okutucu Murat Gökhan Aslan Hacı Koç , Feyzahan Uzun

https://doi.org/10.18678/dtfd.515313

Abstract

Aim: Ethambutol and isoniazid, two of the main drugs used in the treatment of tuberculosis, can lead to optic neuropathy. Optical coherence tomography (OCT) is a non-invasive, repeatable, high resolution imaging technique used in the diagnosis and follow-up of optic nerve diseases. The purpose of this study was to investigate the effect of pyridoxine added to antituberculous therapy on retinal nerve fiber layer (RNFL) thickness and the effectiveness of OCT in the early diagnosis and monitoring of optic neuropathy.

Material and Methods: Twenty four patients diagnosed with pulmonary or non-pulmonary tuberculosis were included in the study. Patients divided into two groups. One group received antituberculous therapy alone, and the other group received 50 mg pyridoxine in addition to antituberculous therapy. RNFL thickness in both eyes was measured using OCT before treatment and 2-month after treatment.

Results: The change in the second month of treatment according to baseline in terms of average RNFL thicknesses in the right eyes, showed a statistically significant difference between the groups using and not using pyridoxine (p=0,038). However, there was no significant difference in the left eyes in terms of RNFL thickness in any of the quadrants between the groups.

Conclusion: Despite a decrease in RNFL thickness in patients receiving antituberculous therapy alone, no change in RNFL thickness occurred in patients receiving pyridoxine in addition to antituberculous therapy. We think that early ototoxicity can be detected with RNFL thickness measurement using OCT in asymptomatic patients and that the addition of pyridoxine to antituberculous therapy prevents ototoxicity.

Keywords

isoniazid, optical coherence tomography, retinal nerve fiber layer thickness

Piridoksinin Tüberküloz Tedavisinde Retina Sinir Lifi Tabakası Üzerindeki Etkileri

Abstract

Amaç: Tüberküloz tedavisinde kullanılan başlıca ilaçlardan ikisi olan etambutol ve izoniazid, optik nöropatiye yol açabilir. Optikal kohorens tomografi (OCT), optik sinir hastalıklarının tanı ve takibinde kullanılan noninvaziv, tekrarlanabilir, yüksek çözünürlüklü bir görüntüleme yöntemidir. Bu çalışmanın amacı, antitüberküloz tedavi ile birlikte verilen piridoksinin, retinal sinir lifi tabakası (RNFL) kalınlığı üzerindeki etkisini ve OCT’nin, optik nöropatinin erken tanı ve takibindeki etkinliğini araştırmaktır.

Gereç ve Yöntemler: Çalışmaya pulmoner veya pulmoner olmayan tüberküloz tanısı alan yirmi dört hasta dahil edildi. Hastalar iki gruba ayrıldı. Bir gruba sadece antitüberküloz tedavi uygulandı, diğer gruba ise antitüberküloz tedaviye ek olarak 50 mg piridoksin verildi. Her iki gözde de RNFL kalınlığı tedaviye başlamadan önce ve tedaviye başladıktan 2 ay sonra OCT cihazı kullanılarak ölçüldü.

Bulgular: Sağ gözlerde ortalama RNFL kalınlıkları bakımından başlangıca göre tedavinin 2. ayındaki değişim, piridoksin kullanan ve kullanmayan gruplar arasında istatistiksel olarak anlamlı bir farklılık göstermekteydi (p=0.038). Bununla birlikte, olguların sol gözlerinde ise gruplar arasında hiçbir kadranda RNFL kalınlıkları açısından anlamlı bir farklılık bulunmadı.

Sonuç: Sadece antitüberküloz tedavi alan hastalarda RNFL kalınlığında bir azalma olmasına rağmen, antitüberküloz tedaviye ek olarak piridoksin de alan hastalarda RNFL kalınlığında herhangi bir değişiklik olmadı. Asemptomatik hastalarda OCT cihazı kullanılarak yapılan RNFL kalınlık ölçümü ile erken ototoksisitenin saptanabileceğini ve antitüberküloz tedaviye piridoksin eklenmesinin ototoksisiteyi önlediğini düşünüyoruz.

Keywords

izoniazid, optikal koherens tomografi, retina sinir lifi tabakası kalınlığı

References

• Ditah IC, Reacher M, Palmer C, Watson JM, Innes J, Kruijshaar ME, et al. Monitoring tuberculosis treatment outcome: analysis of national surveillance data from a clinical perspective. Thorax. 2008;63(5):440-6.
• Fekih L, Boussoffara L, Fenniche S, Abdelghaffar H, Megdiche ML. Neuropsychiatric side effects of antituberculosis agents. Rev Med Liege. 2011;66(2):82-5.
• Kass I, Mandel W, Cohen H, Dressler SH. Isoniazid as a cause of optic neuritis and atrophy. J Am Med Assoc. 1957;164(16):1740-3.
• Keeping JA, Searle CW. Optic neuritis following isoniazid therapy. The Lancet. 1955;266(6884):278.
• Fetterhoff KI, Holmes CX, Martın GE. Hazards of isoniazid therapy in epileptics; report of one case. Am Rev Tuberc. 1952;66(4):501.
• Biehl JP, Vilter RW. Effect of isoniazid on vitamin B6 metabolism; its possible significance in producing isoniazid neuritis. Proc Soc Exp Biol Med. 1954;85(3):389-92.
• Preziosi P. Isoniazid: metabolic aspects and toxicological correlates. Curr Drug Metab. 2007;8(8):839-51.
• Vilter RW, Mueller JF, Glazer HS, Jarrold T, Abraham J, Thompson C, et al. The effect of vitamin B6 deficiency induced by desoxypyridoxine in human beings. J Lab Clin Med. 1953;42(3):335-57.
• García-Martín E, Pueyo V, Fernández J, Almárcegui C, Dolz I, Martín J, et al. Atrophy of the retinal nerve fibre layer in multiple sclerosis patients. Prospective study with two years follow-up. Arch Soc Esp Oftalmol. 2010;85(5):179-86.
• Inzelberg R, Ramirez JA, Nisipeanu P, Ophir A. Retinal nerve fiber layer thinning in Parkinson disease. Vision Res. 2004;44(24):2793-7.
• Cikmazkara I, Ugurlu SK. Peripapillary retinal nerve fiber layer thickness in patients with iron deficiency anemia. Indian J Ophthalmol. 2016;64(3):201-5.
• Martinez J, de Letona L, Theodoropoulos DS. Optic neuropathy in vitamin B12 deficiency. Lancet. 1998;352(9122):146-7.
• Jaffe GJ, Caprioli J. Optical coherence tomography to detect and manage retinal disease and glaucoma. Am J Ophthalmol. 2004;137(1):156-69.
• Biehl JP, Nimitz HJ. Studies on the use of high dose of isoniazid. I. Toxicity studies. Am Rev Tuberc. 1954;70(3):430-41.
• Bravo R, Cornejo-Bravo JM, Ramos-Ibarra MA, Estrada-Guzmán JD, Morales-Arango O, Reyes-Báez R, et al. Genotype and phenotype of NAT2 and the occurrence of adverse drug reactions in Mexican individuals to an isoniazid-based prophylactic chemotherapy for tuberculosis. Mol Med Rep. 2008;1(6):875-9.
• Evans DA, Manley KA, McKusick VA. Genetic control of isoniazid metabolism in man. Br Med J. 1960;2(5197):485-91.
• Kinzig-Schippers M, Tomalik-Scharte D, Jetter A, Scheidel B, Jakob V, Rodamer M, et al. Should we use N-acetyltransferase type 2 genotyping to personalize isoniazid doses? Antimicrob Agents Chemother. 2005;49(5):1733-8.
• Parkin DP, Vandenplas S, Botha FJ, Vandenplas ML, Seifart HI, van Helden PD, et al. Trimodality of isoniazid elimination: phenotype and genotype in patients with tuberculosis. Am J Respir Crit Care Med. 1997;155(5):1717-22.
• Krishnamurthy DV, Selkon JB, Ramachandran K, Devadatta S, Mitchison DA, Radhakrishna S, et al. Effect of pyridoxine on vitamin B6 concentrations and glutamic-oxaloacetic transaminase activity in whole blood of tuberculous patients receiving high-dosage isoniazid. Bull World Health Organ. 1967;36(5):853-70.
• Matar KM, Mayet AY, Ayoola EA, Bawazir SA, Al-Faleh FZ, Al-Wazzan A. Isoniazid acetylation phenotyping in Saudi Arabs. J Clin Pharm Ther. 2004;29(5):443-7.
• Wang PY, Xie SY, Hao Q, Zhang C, Jiang BF. NAT2 polymorphisms and susceptibility to anti-tuberculosis drug-induced liver injury: a meta-analysis. Int J Tuberc Lung Dis. 2012;16(5):589-95.
• Cranswick N, Mulholland K. Isoniazid treatment of children: can genetics help guide treatment? Arch Dis Child. 2005;90(6):551-3.
• Mount FW, Ferebee SH. United States Public Health service cooperative investigation of antimicrobial therapy of tuberculosis, V. Report on thirty-two-week observations on combinations of isoniazid, streptomycin, and para-aminosalicylic acid. Am Rev Tuberc. 1954;70(3):521-6.
• Gammon GC, Burge FW, King G. Neural toxicity in tuberculous patients treated with isoniazid (isonicotinic acid hydrazide). AMA Arch Neurol Psychiatry. 1953;70(1):64-9.
• Höök O. Polyneuritis caused by hydrazide of isonieotinic acid. A report of 7 cases. Acta Med Scand. 1954;147(2):167-74.
• Jones WA, Jones GP. Peripheral neuropathy due to isoniazid report of two cases. Lancet. 1953;1(6770):1073-4.
• Kokkada SB, Barthakur R, Natarajan M, Palaian S, Chhetri AK, Mishra P. Ocular side effects of antitubercular drugs - a focus on prevention, early detection and management. Kathmandu Univ Med J (KUMJ). 2005;3(4):438-41.
• Lubing HN. Peripheral neuropathy in tuberculosis patients treated with isoniazid. Am Rev Tuberc. 1953;68(3):458-61.
• Nair KG. Optic neuritis due to INH complicating tuberculous meningitis. J Assoc Physicians India. 1976;24(4):263-4.
• Carlson HB, Anthony EM, Russell WF Jr, Middlebrook G. Prophylaxis of isoniazid neuropathy with pyridoxine. N Engl J Med. 1956;255(3):119-22.
• Ross RR. Use of pyridoxine hydrochloride to prevent isoniazid toxicity. J Am Med Assoc. 1958;168(3):273-5.
• McCune R, Deuschle K, McDermott W. The delayed appearance of isoniazid antagonism by pyridoxine in vivo. Am Rev Tuberc. 1957;76(6):1100-5.
• Kulkarni HS, Keskar VS, Bavdekar SB, Gabhale Y. Bilateral optic neuritis due to isoniazid (INH). Indian Pediatr. 2010;47(6):533-5.
• Kocabay G, Erelel M, Tutkun IT, Ecder T. Optic neuritis and bitemporal hemianopsia associated with isoniazid treatment in end-stage renal failure. Int J Tuberc Lung Dis. 2006;10(12):1418-9.
• Kim YK, Hwang JM. Serial retinal nerve fiber layer changes in patients with toxic optic neuropathy associated with antituberculosis pharmacotherapy. J Ocul Pharmacol Ther. 2009;25(6):531-5.
• Chai SJ, Foroozan R. Decreased retinal nerve fibre layer thickness detected by optical coherence tomography in patients with ethambutol-induced optic neuropathy. Br J Ophthalmol. 2007;91(7):895-7.
• Azuma J, Ohno M, Kubota R, Yokota S, Nagai T, Tsuyuguchi K, et al. NAT2 genotype guided regimen reduces isoniazid-induced liver injury and early treatment failure in the 6-month four-drug standard treatment of tuberculosis: a randomized controlled trial for pharmacogenetics-based therapy. Eur J Clin Pharmacol. 2013;69(5):1091-101.