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Show Pegylated Interferon Alpha-Associated Optic Neuropathy Kathleen T. Berg, BS, Bruce Nelson, MD, Andrew R. Harrison, MD, Linda K. McLoon, PhD, Michael S. Lee, MD Abstract: A 52-year-old man with chronic hepatitis C presented with painless, bilateral, simultaneous non-arteritic anterior ischemic optic neuropathy (NAION) and peripheral neuropathy. Symptoms began 19 weeks after starting peginterferon alpha-2a. The peripheral neuro-pathy and vision of the right eye improved, but the vision of the left eye worsened after stopping interferon. We identified 23 additional cases of NAION during interferon alpha therapy. At least 12 of these patients suffered bilateral NAION. Patients lost vision 1-40 weeks after initiating therapy. Of 21 eyes that had documented initial and follow-up acuities, 8 improved, 1 worsened, and the rest remained stable. One patient had a painful peripheral neuropathy. Treatment with interferon alpha may result in NAION. Discontinuation of therapy deserves consider-ation after weighing individual risks and benefits. Journal of Neuro-Ophthalmology 2010;30:117-122 doi: 10.1097/WNO.0b013e3181d8e4af 2010 by North American Neuro-Ophthalmology Society Iterferon alpha is a complex glycoprotein with anti-proliferative, antiviral, and immunomodulatory activity (1). Pegylated interferons have a covalently attached 40 kDa branched chain polyethylene glycol moiety, which improves drug absorption and prolongs the half-life from 4 to 22-60 hours (2), allowing for less frequent injections and improved patient compliance. The 2 forms of pegylated interferon alpha currently approved for the treatment of chronic hepatitis C (CHC) are peginterferon alpha-2a and peginterferon alpha-2b. While peginterferon alpha-2b has a larger volume of distribution and more effective renal clearance than peginterferon alpha-2a (3), studies have found no difference in either the sustained virological response or adverse event incidence between the 2 medi-cations in the treatment of CHC (4). The most common adverse events associated with in-terferon alpha therapy are flu-like symptoms, leukopenia, thrombocytopenia, depression, and thyroid disorders (5). Cases of peripheral neuropathy have also been documented (6-10). Several prospective studies have linked interferon alpha therapy with a high incidence of retinopathy, demonstrated by the presence of cotton wool spots and hemorrhage (11-19), although these changes are often asymptomatic (12,16). Other documented ocular compli-cations of interferon alpha therapy include transient blurred vision (20), increased intraocular pressure (21), neovascular glaucoma (22), retinal detachment (5), and orbital and intraocular hemorrhage leading to enucleation (21,23). Nonarteritic anterior ischemic optic neuropathy (NAION) is a relatively rarely reported complication of interferon alpha therapy (15,24-40). We present a case of NAION following treatment of CHC with peginterferon alpha-2a and review the literature for other documented cases of NAION following interferon alpha therapy. CASE REPORT A 52-year-old man with a history of CHC developed painless progressive vision loss in his right eye. He did not detect visual loss in the left eye. He also noted new onset numbness and tingling in both hands and feet. He denied symptoms suggestive of giant cell arteritis. His medical history included migraine headache, cervical radiculopathy, depression, anxiety disorder, and insomnia. Nineteen weeks prior to ophthalmic evaluation, he began treatment for CHC with peginterferon alpha-2a 180 mg/week and Department of Ophthalmology, University of Minnesota (KTB, ARH, LKM, MSL), Minneapolis, Minnesota; and Merit Care, Fargo, North Dakota. Supported by unrestricted grant from Research to Prevent Blind-ness, New York, NY, and the Minnesota Lions and Lionesses. None of the authors have any financial/conflicting interests to disclose. The sponsor or funding organization had no role in the design or conduct of this research. Address correspondence to Michael S. Lee, 420 Delaware St. SE, MMC 493, Minneapolis, MN 55455; E-mail: mikelee@umn.edu Berg et al: J Neuro-Ophthalmol 2010; 30: 117-122 117 Original Contribution Copyright © North American Neuro-ophthalmology Society.Unauthorized reproduction of this article is prohibited. ribavirin 1000 mg/day. Other medications included filgrastim, albuterol, eletriptan hydrobromide, hydromor-phone, fluticasone and salmeterol, bupropion, clonazepam, omeprazole, zolpidem, prochlorperazine, and tizanidine. Two days later, examination revealed vision of 20/25 in each eye. Pupils were 3 mm bilaterally with a right relative afferent pupillary defect (RAPD). The patient correctly identified all of the Ishihara color plates with each eye. Fundus examination demonstrated bilateral optic disc edema (Fig. 1) with a normal appearance to each retina. Fundus photographs from 2003 revealed a cup-to-disc ratio of 0.1:0.2. Visual field testing demonstrated inferior field loss in the right eye and no abnormality in the left eye (Fig. 2). Contrast-enhanced MRI of the brain and orbits showed no optic nerve or intracranial abnormalities. Lumbar pun-cture demonstrated a normal opening pressure, with normal protein and glucose levels; no white blood cells; and 32 red blood cells. Hemogram showed mild pancytopenia with a white blood cell count of 1800 cells per microliter, platelet count of 110 000 cells per microliter, and hemoglobin of 13 g/dL. A comprehensive metabolic panel showed no abnormalities. Antinuclear antibody, angiotensin-convert-ing enzyme, rapid plasma regain, and neuromyelitis optica (NMO) IgG testing were all negative. Both peginterferon alpha-2a and ribavirin were dis-continued. The patient received intravenous solumedrol 500 mg followed by oral prednisone 40 mg, which was tapered over the next 8 days. When examined 4 weeks later, he reported a 4-day decline in vision in his previously asymptomatic left eye and some improvement in his right eye. Visual acuity was 20/20 in the right eye and 20/60 in the left eye. He saw 8/8 Ishihara color plates with the right eye and 3/8 with the left eye, and there was no evidence of a RAPD. The right optic nerve showed early segmental atrophy while the left optic nerve swelling had worsened. Visual field testing demonstrated slight progression of the inferior arcuate scotoma in the right eye and a new defect in the left eye (Fig. 3). The patient noted almost complete resolution of his paresthesias. DISCUSSION Our patient suffered bilateral simultaneous NAION in the setting of peginterferon alpha-2a treatment. Spontaneous, bilateral, simultaneous NAION is rare and typically sug-gests a systemic disorder or toxicity. While it is conceivable that the interferon therapy was unrelated, this seems un-likely since this case has similar findings to previous reports. In addition, our patient had bilateral paresthesias of the hands and feet, a known side effect of pegylated interferon alpha. With discontinuation of therapy, he noted near total resolution of this symptom, strongly suggestive of a systemic toxic effect of his interferon therapy. We are aware of 23 additional cases of NAION in the setting of interferon alpha therapy (Table 1). Eleven pa-tients experienced bilateral NAION. One probable case of NAION following interferon alpha-2b therapy for CHC (45) and one following interferon alpha-2a therapy for acute hepatitis C (47) were omitted from this compilation be-cause the abstracts were not available in English. All other reported patients suffered visual loss between 1 and 40 weeks after initiating therapy. Thirteen cases received combination therapy with ribavirin and interferon alpha. Of these 13 patients, 6 experienced bilateral visual loss. Four patients suffered NAION while taking interferon alpha-2a and 7 while taking interferon alpha-2b. Eleven reports only described treatment as ‘‘interferon alpha'' therapy. Of these 11 patients, 4 experienced bilateral optic nerve involvement. There was one documented case of NAION following therapy with natural (nonrecombinant) interferon alpha. Of the 17 cases that provided follow-up information, 9 described improvement in signs and symptoms following cessation of interferon alpha, and one showed symptomatic improvement without the withdrawal of therapy. One pa-tient developed painful polyneuropathy in addition to NAION (37). How interferon causes NAION is currently unknown. Sugano et al (44) studied patients who developed retinopathy while taking interferon alpha (49). They discovered abnor-mally high levels of circulating activated plasma complement FIG. 1. Bilateral optic disc edema is present with a flame hemorrhage (arrow) on the left eye. Original Contribution 118 Berg et al: J Neuro-Ophthalmol 2010; 30: 117-122 Copyright © North American Neuro-ophthalmology Society.Unauthorized reproduction of this article is prohibited. 5 (C5a), an intravascular aggregator of granulocytes. High C5a levels may disrupt blood flow in the retinal circulation, leading to retinal capillary infarction, cotton wool spot for-mation, and hemorrhage (48,49). Guyer et al (16) proposed that therapy with interferon alpha may cause autoantibody formation and immune complex deposition, with resultant lymphocyte infiltration and inflammation of vessels, leading to retinal ischemia. Nishiwaki et al (50) used a rat model to demonstrate that interferon alpha causes leukocyte activation and adherence to vascular endothelium. The mechanisms proposed for interferon alpha-associated retinopathy could also underlie the development of NAION, with involvement of the posterior ciliary arterial circulation, leading to optic nerve ischemia (26). It is unlikely that the coadministration of ribavirin contributes directly to the development of NAION, as the only known ocular complication of ribavirin therapy is conjunctivitis. Presumably, this occurs from topical irrita-tion of the conjunctiva, as conjunctivitis only follows aerosol administration (51). Hepatitis C virus (HCV) has been linked to various immunologic abnormalities, including cryoglobulinemia, arteritis, and thrombocytopenia (52). It appears unlikely that the virus itself was the cause of NAION in our patient, as there was no evidence of systemic vasculitis. While our patient did have thrombocytopenia, Hayasaka et al (13) found no association between thrombocytopenia and ocular complications in patients with CHC receiving interferon therapy. Additionally, development of NAION due directly to HCV infection is extremely rare, with only 2 cases documented (53,54). Our patient had a preexisting small cup-to-disc ratio, a proposed risk factor in the development of NAION (42). One previous report of unilateral NAION associated with pegylated interferon noted a small optic disc in the fellow eye with crowding and absence of cupping (32). Two other cases of bilateral NAION documented absence of physio-logic cupping in the fellow eye prior to second eye in-volvement (26). It is conceivable that a small cup-to-disc ratio may increase the risk of NAION in patients receiving interferon alpha. Based on the evidence from our patient, as well as from the compiled case reports, we propose that the association between interferon alpha therapy and the development of NAION is ‘‘possible,'' based on the World Health Orga-nization criteria for establishing causality in adverse drug reactions (Table 2) (http://www.who-umc.org/DynPage. aspx?id=22682). The visual changes consistent with FIG. 2. Initial visual fields show an inferior arcuate defect in the right eye and a normal result in the left eye. FIG. 3. Four weeks later, visual fields reveal slight progression of field loss in the right eye and an inferior altitudinal defect with central involvement in the left eye. Original Contribution Berg et al: J Neuro-Ophthalmol 2010; 30: 117-122 119 Copyright © North American Neuro-ophthalmology Society.Unauthorized reproduction of this article is prohibited. TABLE 1. Previously reported cases of NAION following treatment with interferon alpha-2a, interferon alpha-2b, or natural interferon alpha Patient Age, Gender (reference) Underlying Disease Medication Unilateral vs Bilateral Treatment Duration Prior to NAION Visual Acuity at Presentation Visual Acuity After IFN Cessation 54, Female (37) CHC IFN alpha-2a, ribavirin, and amantadine Bilateral 6 months Unknown Unknown 68, Female (25) CHC IFN alpha-2a and ribavirin Unilateral 3 weeks 20/50 20/30 61, Female (25) CHC IFN alpha-2a and ribavirin Bilateral 8 weeks 20/100 OU 20/25 OU 71, Male (25) CHC IFN alpha-2a and ribavirin Unilateral 7 months 20/100 20/30 64, Male (24) CHC IFN alpha and ribavirin Unilateral 8 months 20/100 Marked improvement Unknown (35) Malignant melanoma IFN alpha Unknown Unknown Unknown Unknown 40, Male (26) RCC IFN alpha Bilateral 3 weeks 20/25 Unknown 51, Male (26) Multiple myeloma IFN alpha Bilateral 1 week 20/20 OD; 20/30 OS 20/20 OD; 20/30 OS 70, Male (34) RCC IFN alpha Unilateral 6 weeks 20/80 20/100 72, Male (34) RCC IFN alpha Unilateral 10 months Counting fingers Did not return to baseline Unknown (40) CHC IFN alpha and ribavirin Unknown Unknown Unknown Unknown 64, Male (38) CHC IFN alpha Unilateral Unknown 20/200 Improved 59, Gender not specified (31) CHC IFN alpha Unknown 8 weeks Unknown Unknown 44, Male (15) CHC IFN alpha Bilateral 10 weeks 20/100 OD; 20/200 OS 20/100 OD; 20/200 OS 61, Male (15) Essential thrombocytosis IFN alpha Bilateral 3 months 20/60 OD; 20/80 OS 20/30 OU 46, Male (30) CHC IFN alpha-2b and ribavirin Bilateral 3 weeks 20/400 OD; 20/100 OS 20/80 OU 51, Male (28) CHC IFN alpha-2b and ribavirin Bilateral 3 months Unknown Unknown 64, Male (29) CHC IFN alpha-2b and ribavirin Bilateral 6 weeks Unknown 20/20 OD; 20/200 OS (both worsened) 60, Male (27) Malignant melanoma IFN alpha-2b Bilateral 23 weeks 20/120 OD; 20/400 OS 20/120 OD; 20/400 OS 46, Male (33) CHC IFN alpha-2b and ribavirin Unilateral Unknown Unknown Improved without treatment cessation 55, Female (39) CHC IFN alpha-2b and ribavirin Bilateral 6 months 20/400 OD; 20/80 OS ,20/400 OD; 20/80 OS 57, Male (32) CHC IFN alpha-2b and ribavirin Unilateral 6 months 20/60 20/20 40, Female (36) CHC Natural IFN alpha Unilateral 2 months 20/30 20/20 CHC, chronic hepatitis C; IFN, interferon; NAION, nonarteritic anterior ischemic optic neuropathy; OD, right eye; OS, left eye; OU, both eyes; pegIFN, pegylated interferon; RCC, renal cell carcinoma. Original Contribution 120 Berg et al: J Neuro-Ophthalmol 2010; 30: 117-122 Copyright © North American Neuro-ophthalmology Society.Unauthorized reproduction of this article is prohibited. NAION occurred within a reasonable time frame following the start of interferon alpha therapy. The cases reviewed could not be clearly linked to the presence of other diseases, underlying risk factors, or other medications. While improvement in visual acuity was noted following discontinuation of interferon alpha in 9 of the 23 cases reported in the literature, a large, randomized, prospective study of patients with NAION showed that 43% of un-treated eyes with vision of 20/64 or worse gained 3 lines or more of vision at a 6-month follow-up (55). It is also unclear whether continuing therapy with interferon alpha results in progressive visual deterioration. The high fre-quency of bilateral NAION in cases linked to interferon alpha therapy suggests that presentation in one eye may place the fellow eye at risk, especially in patients with small cup-to-disc ratio. Further study is warranted to identify whether discontinuing therapy diminishes the likelihood of NAION in the fellow eye. In conclusion, treatment with interferon alpha may lead to the development of NAION. Currently, the decision to continue or discontinue interferon alpha in patients pre-senting with unilateral NAION should be made on a case-by- case basis until proven therapeutic guidelines are established. REFERENCES 1. Baron S, Tyring SK, Fleischmann WR Jr, Coppenhaver DH, Niesel DW, Klimpel GR, Stanton GJ, Hughes TK. The interferons. Mechanisms of action and clinical applications. JAMA. 1991;266:1375-1383. 2. Bailon P, Palleroni A, Schaffer CA, Spence CA, Spence CL, Fung WJ, Porter JE, Ehrlich GK, Pan W, Xu ZX, Modi MW, Farid A, Berthold W, Graves M. Rational design of a potent, long-lasting form of interferon: a 40 kDa branched polyethylene glycol-conjugated interferon alpha-2a for the treatment of hepatitis C. Bioconjug Chem. 2001;12: 195-202. 3. Berenguer J, Gonzalez-Garcia J, Lopez-Aldeguer J, Von-Wichmann MA, Quereda C, Hernando A, Sanz J, Tural C, Ortega E, Mallolas J, Santos I, Miralles P, Montes ML, Bellon JM, Esteban JH, GESIDA HIV/HCV Cohort. Pegylated interferon {alpha}2a plus ribavirin versus pegylated interferon {alpha}2b plus ribavirin for the treatment of chronic hepatitis C in HIV-infected patients. J Antimicrob Chemother. 2009;63:1256-1263. 4. McHutchison JG, Lawitz EJ, ShiffmanML, Muir AJ, Galler GW, McCone J, Nyberg LM, Lee WM, Ghalib RH, Bacon BR, Davis MN, Mukhopadhyay P, Kuory K, Noviello S, Pedicone LD, Brass CA, Albrecht JK, Sulkowski MS, IDEAL Study Team. Peginterferon alfa-2b or alfa-2a with ribavirin for treatment of hepatitis C infection. N Engl J Med. 2009;361:580-593. 5. Okanoue T, Sakamoto S, Itoh Y, Minami M, Yasui K, Sakamoto M, Nishioji K, Katagishi T, Nakagawa Y, Tada H, Sawa Y, Mizuno M, Kagawa K, Kashima K. Side effects of high-dose interferon therapy for chronic hepatitis C. J Hepatol. 1996;25:283-291. 6. Quattrini A, Comi G, Nemni R, Martinelli V, Villa A, Caimi M, Wrabetz L, Canal N. Axonal neuropathy associated with interferon-alpha treatment for hepatitis C: HLA-DR immunoreactivity in schwann cells. Acta Neuropathol. 1997;94:504-508. 7. Gastineau DA, Habermann TM, Hermann RC. Severe neuropathy associated with low-dose recombinant interferon-alpha. Am J Med. 1989;87:116. 8. Cudillo L, Cantonetti M, Venditti A, Lentini R, Rossini PM, Caramia M, Masi M, Papa G. Peripheral polyneuropathy during treatment with alpha-2 interferon. Haematologica. 1990;75:485-486. 9. La Civita L, Zignego AL, Lombardini F, Monti M, Longombardo G, Pasero G, Ferri C. Exacerbation of peripheral neuropathy during alpha-interferon therapy in a patient with mixed cryoglobulinemia and hepatitis B virus infection. J Rheumatol. 1996;23:1641-1643. 10. Negoro K, Fukusako T, Morimatsu M, Liao CM. Acute axonal polyneuropathy during interferon alpha-2A therapy for chronic hepatitis type C. Muscle Nerve. 1994;17: 1351-1352. 11. Kawano T, Shigehira M, Uto H, Nakama T, Kato J, Hayashi K, Maruyama T, Kuribayashi T, Chuman T, Futami T, Tsubouchi H. Retinal complications during interferon therapy for chronic hepatitis C. Am J Gastroenterol. 1996; 91:309-313. 12. Hayasaka S, Nagaki Y, Matsumoto M, Sato S. Interferon associated retinopathy. Br J Ophthalmol. 1998;82:323-325. 13. Hayasaka S, Fujii M, Yamamoto Y, Noda S, Kurome H, Sasaki M. Retinopathy and subconjunctival haemorrhage in patients with chronic viral hepatitis receiving interferon alfa. Br J Ophthalmol. 1995;79:150-152. 14. Schulman JA, Liang C, Kooragayala LM, King J. Posterior segment complications in patients with hepatitis C treated with interferon and ribavirin. Ophthalmology. 2003;110: 437-442. TABLE 2. World Health Organization causality assessment of suspected adverse drug reactions Certain: A clinical event, including laboratory test abnormality, occurring in a plausible time relationship to drug administration, and which cannot be explained by concurrent disease or other drugs or chemicals. The response to withdrawal of the drug (dechallenge) should be clinically plausible. The event must be definitive pharmacologically or phenomenologically, using a satisfactory rechallenge procedure if necessary. Possible: A clinical event, including laboratory test abnormality, with a reasonable time sequence to administration of the drug but that could also be explained by concurrent disease or other drugs or chemicals. Information on drug withdrawal may be lacking or unclear. Unlikely: A clinical event, including laboratory test abnormality, with a temporal relationship to drug administration that makes a causal relationship improbable and in which other drugs, chemicals, or underlying disease provide plausible explanations. Conditional/Unclassified: A clinical event, including laboratory test abnormality, reported as an adverse reaction about which more data is essential for a proper assessment or the additional data are under examination Unassessible/Unclassifiable: A report suggesting an adverse reaction, which cannot be judged because information is insufficient or contradictory and which cannot be supplemented or verified. Original Contribution Berg et al: J Neuro-Ophthalmol 2010; 30: 117-122 121 Copyright © North American Neuro-ophthalmology Society.Unauthorized reproduction of this article is prohibited. 15. Vardizer Y, Linhart Y, Loewenstein A, Garzozi H, Mazawi N, Kesler A. Interferon-alpha-associated bilateral simultaneous ischemic optic neuropathy. J Neuroophthalmol. 2003;23: 256-259. 16. Guyer DR, Tiedeman J, Yannuzzi LA, Slakter JS, Parke D, Kelley J, Tang RA, Marmor M, Abrams G, Miller JW. Interferon-associated retinopathy. Arch Ophthalmol. 1993; 111:350-356. 17. Jain K, Lam WC, Waheeb S, Thai Q, Heathcote J. Retinopathy in chronic hepatitis C patients during interferon treatment with ribavirin. Br J Ophthalmol. 2001; 85:1171-1173. 18. Nakamura T, Takahashi H, Koike N, Mitsutaka M, Soda M, Kimu M. Retinopathy during interferon treatment in combination with ribavirin for chronic hepatitis C. Nippon Ganka Gakkai Zasshi. 2005;109:748-752. 19. Neubauer AS, Hoops JP. Interferon-induced retinopathy in asymptomatic cancer patients. Ophthalmology. 2002; 109: 821-822; author reply 822. 20. Ene L, Gehenot M, Horsmans Y, Detry-Morel M, Geubel AP. Transient blurred vision after interferon for chronic hepatitis C. Lancet. 1994;344:827-828. 21. Kuga K, Hasumura S, Nagamori S, Toda G, Kitahara K. Intraocular hemorrhage developing during interferon therapy. Intern Med. 1996;35:15-18. 22. Ayaki M. Development of neovascular glaucoma in the course of interferon alfa therapy for hepatitis type C. Br J Ophthalmol. 1994;78:238. 23. Yamada H, Mizobuchi K, Isogai Y. Acute onset of ocular complications with interferon. Lancet. 1994;343:914. 24. Gupta R, Singh S, Tang R, Blackwell TA, Schiffman JS. Anterior ischemic optic neuropathy caused by interferon alpha therapy. Am J Med. 2002;112:683-684. 25. Kabbaj N, Sentissi S, Mohammadi M, Benaissa A, Amrani N. Anterior ischemic optic neuropathy complicating interferon alpha and ribavirin therapy in patients with chronic hepatitis C. Gastroenterol Clin Biol. 2009;33:115-117. 26. Purvin VA. Anterior ischemic optic neuropathy secondary to interferon alfa. Arch Ophthalmol. 1995;113:1041-1044. 27. Lohmann CP, Kroher G, Bogenrieder T, Spiegel D, Preuner J. Severe loss of vision during adjuvant interferon alfa-2b treatment for malignant melanoma. Lancet. 1999;353:1326. 28. Kirchhoff A, Kirchhoff U, Lafrenz M, Guthoff R. Bilateral AION after the combined therapy of hepatitis C with PEG-interferon alpha2B and ribavirin. Klin Monatsbl Augenheilkd. 2004;221:791-793. 29. Kiuchi K, Kitagawa C, Miyashiro M. Serious loss of vision in bilateral anterior ischemic optic neuropathy caused by interferon. Nippon Ganka Gakkai Zasshi. 2009;113:16-23. 30. Miserachs-Garcia S, Mesa-Toledo E, Arruga-Ginebreda J, Castillo-Campillo L. Ischemic neuroretinopathy associated with use of interferon. Arch Soc Esp Oftalmol. 2005;80: 533-535. 31. Stoffelns BM. Interferon causes ischemic ocular diseases-case studies and review of the literature. Klin Monatsbl Augenheilkd. 2006;223:367-371. 32. Wei YH, Wang IH, Woung LC, Jou JR. Anterior ischemic optic neuropathy associated with pegylated interferon therapy for chronic hepatitis C. Ocul Immunol Inflamm. 2009;17: 191-194. 33. Chan JW. Bilateral non-arteritic ischemic optic neuropathy associated with pegylated interferon for chronic hepatitis C. Eye. 2007;21:877-878. 34. Rodney AJ, Gombos DS, Pagliaro LC, Tannir NM. Ischemic optic neuropathy associated with low-dose interferon alfa: Report of two cases. Am J Clin Oncol. 2009;32:86-87. 35. Kreutzer K, Bonnekoh B, Franke I, Ulrich J, Gollnick H. Sarcoidosis, myasthenia gravis and anterior ischaemic optic neuropathy: severe side effects of adjuvant interferon-alpha- therapy in malignant melanoma? J Dtsch Dermatol Ges. 2004;2:689-694. 36. Norcia F, Di Maria A, Prandini F, Redaelli C. Natural interferon therapy: optic nerve ischemic damage? Ophthalmologica. 1999;213:339-340. 37. Chrissafidou A, Musch E. Peripheral polyneuropathy and bilateral optic neuropathy during treatment of chronic hepatitis C. Dtsch Med Wochenschr. 2009;134:927-930. 38. Shahidullah AB, Cerulli MA, Berman DH. Interferon may cause retinopathy during hepatitis therapy. Am J Gastroenterol. 1995;90:1543. 39. Sene D, Touitou V, Bodaghi B, Saadoun D, Perlemuter G, Cassooux N, Piette JC, Hoang PL, Cacoub P. Intraocular complications of IFN-alpha and ribavirin therapy in patients with chronic viral hepatitis C. World J Gastroenterol. 2007; 13:3137-3140. 40. Sauer A, Lenoble P, Bader P, Speeg-Schatz C, Bourcier T, Nasica X. Ocular complications of hepatitis C treatment. J Fr Ophtalmol. 2007;30:e20. 41. Kerr NM, Chew SS, Danesh-Meyer HV. Non-arteritic anterior ischaemic optic neuropathy: a review and update. J Clin Neurosci. 2009;16:994-1000. 42. Burde RM. Optic disk risk factors for nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol. 1993;116: 759-764. 43. Miller NR. Anterior ischemic optic neuropathy: Diagnosis and management. Bull N Y Acad Med. 1980;56:643-654. 44. Sugano S, Suzuki T, Watanabe M, Ohe K, Ishii K, Okajima T. Retinal complications and plasma C5a levels during interferon alpha therapy for chronic hepatitis C. Am J Gastroenterol. 1998;93:2441-2444. 45. Gabler B, Kroher G, Bogenrieder T, Spiegel D, Preuner J, Lohmann CP. Severe, bilateral vision loss in malignant melanoma of the skin. Anterior ischemic optic neuropathy with irreversible vision and visual field loss in adjuvant interferon alfa-2b therapy. Ophthalmologe. 2001;98: 672-673. 46. Lessell S. Nonarteritic anterior ischemic optic neuropathy: Enigma variations. Arch Ophthalmol. 1999;117: 386-388. 47. Yaghi C, Baz P, Koussa S, Daniel F, Haddad F, Sayegh R. Ischemic anterior optic neuropathy complicating interferon alpha-2a and ribavirin treatment for acute hepatitis C. Gastroenterol Clin Biol. 2005;29:616-617. 48. Jacobson DM, Vierkant RA, Belongia EA. Nonarteritic anterior ischemic optic neuropathy. A case-control study of potential risk factors. Arch Ophthalmol. 1997;115: 1403-1407. 49. Sugano S, Yanagimoto M, Suzuki T, Sato M, Onmura H, Aizawa H, Makino H. Retinal complications with elevated circulating plasma C5a associated with interferon-alpha therapy for chronic active hepatitis C. Am J Gastroenterol. 1994;89:2054-2056. 50. Nishiwaki H, Ogura Y, Miyamoto K, Matsuda N, Honda Y. Interferon alfa induces leukocyte capillary trapping in rat retinal microcirculation. Arch Ophthalmol. 1996;114: 726-730. 51. Sifton DW, ed. Physicians' Desk Reference, 55th edition.Montvale, NJ: Medical Economics, 2001. 52. Pyrsopoulos NT, Reddy KR. Extrahepatic manifestations of chronic viral hepatitis. Curr Gastroenterol Rep. 2001;3: 71-78. 53. Fodor M, Nagy V, Berta A, Tornai I, Pfliegler G. Hepatitis C virus presumably associated bilateral consecutive anterior ischemic optic neuropathy. Eur J Ophthalmol. 2008;18: 313-315. 54. Sinnreich M, Rossillion B, Landis T, Burkhard PR, Sztajzel R. Bilateral optic ischemic neuropathy related to chronic hepatitis C-associated anticardiolipin antibodies. Eur Neurol. 2003;49:243-245. 55. The Ischemic Optic Neuropathy Decompression Trial Research Group. Optic nerve decompression surgery for nonarteritic anterior ischemic optic neuropathy (NAION) is not effective and may be harmful. JAMA. 1995;273: 625-632. Original Contribution 122 Berg et al: J Neuro-Ophthalmol 2010; 30: 117-122 Copyright © North American Neuro-ophthalmology Society.Unauthorized reproduction of this article is prohibited. |
