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Table of Contents    
LETTER TO EDITOR
Year : 2011  |  Volume : 59  |  Issue : 1  |  Page : 141-142

Chronic inflammatory demyelinating polyneuropathy following treatment with peglated interferon α-2a for chronic hepatitis C virus infection


Department of Neurology, China-Japan Union Hospital, Jinlin University, Changchun,130033, China

Date of Submission14-Jan-2011
Date of Decision14-Jan-2011
Date of Acceptance15-Jan-2011
Date of Web Publication18-Feb-2011

Correspondence Address:
Liu Song-yan
Department of Neurology, China-Japan Union Hospital, Jinlin University, Changchun,130033
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.76885

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How to cite this article:
Ying C, Xue-mei H, Yao G, Song-yan L. Chronic inflammatory demyelinating polyneuropathy following treatment with peglated interferon α-2a for chronic hepatitis C virus infection. Neurol India 2011;59:141-2

How to cite this URL:
Ying C, Xue-mei H, Yao G, Song-yan L. Chronic inflammatory demyelinating polyneuropathy following treatment with peglated interferon α-2a for chronic hepatitis C virus infection. Neurol India [serial online] 2011 [cited 2021 Jul 26];59:141-2. Available from: https://www.neurologyindia.com/text.asp?2011/59/1/141/76885


Sir,

The etiopathogenisis of chronic inflammatory demyelinating polyneuropathy (CIDP) is unknown yet. Peglated interferon α-2a is an antiviral biological agent, which is widely used to treat chronic viral hepatitis. Although neurological complications such as myasthenia gravis, axonal neuropathy, and central nervous system demyelination have been reported [1],[2] during interferon-α therapy, CIDP is rarely reported. Here, we report a patient with chronic hepatitis C virus (HCV) infection, who developed CIDP during treatment with Peglated interferon α-2a.

A 47-year-old man, who was a diagnosed case of chronic HCV infection in October 2009, was commenced on Peglated interferon α-2a treatment 180 μg subcutaneously once a week in March 2010. After 2 months of antiviral treatment (in May 2010), he developed numbness and weakness of both lower and upper limbs gradually. He received Vitamin B12 treatment, but with no improvement. He discontinued Peglated treatment in June 2010, but his neurological symptoms deteriorated gradually. He presented to us with motor weakness (4/5 grade) of all the four limbs. Deep tendon reflexes were absent. Both hands were dry and rough and hand nails were fragile. Hypoesthesia was noted in the outer part of the lower legs. Cerebrospinal fluid (CSF) was clear, with normal pressure (120 mmH 2 O), 3 leukocytes/mm 3 , normal glucose (4.2 mmol/L) and chloride (120 mmol/L), and elevated protein (2.0 g/L). Nerve conduction studies revealed reduced conduction velocity in both the median nerves, conduction block in both median nerves and left ulnar nerves, prolonged F-wave latency in left ulnar nerve, reduced F-wave frequency in both ulnar nerves, and no H reflex in left tibial nerve [Table 1],[Table 2],[Table 3]. Clinical features, electrodiagnostic studies, and CSF findings supported the diagnosis of CIDP. [3] He was started on intravenous 10 mg/day Dexamethasone treatment for 7 days, followed by 50 mg/day oral prednisone. He did not show any improvement with this treatment for 2 weeks. He was started on intravenous immunoglobulin (0.4 g/kg for 5 days), with which he showed marked improvement in his muscle power over the next 2 weeks. The patient was discharged with nearly normal muscle power.
Table 1: Motor nerve conduction studies

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Table 2: Sensory nerve conduction studies

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Table 3: H-reflex

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This patient had CIDP and the possible etiology could be the following: HCV infection related, Peglated treatment complication, and Peglated triggered CIDP. Interferon α-2a is a broad-spectrum antiviral agent. The common side effects include fever flu-like symptom, myelosuppression and autoimmune diseases such as thyroiditis, thrombocytolytic, rheumatoid symptoms, systemic lupus erythematosus, type I diabetes.[4],[5],[6],[7],[8] These symptoms subside following the withdrawal of the medicine. Neurological complications such as myasthenia gravis, autonomic neuropathy sensory neuropathy, chronic inflammatory demyelinating neuropathy (CIDP) and acute inflammatory demyelinating neuropathy (AIDP) are rare. Two cases of AIDP have been reported in association with peglated interferon α-2a therapy for chronic hepatitis B and C virus infection.[9],[10] Makoto Hirotai [11] reported one case of chronic HCV infection, who developed weakness and numbness of all the four limbs during treatment with Peglated.

The pathogenesis of CIDP is not fully understood; dendritic cells (DCs) probably play an important role in the pathogenesis of CIDP. DCs are antigen-presenting cells (APCs) which play a critical role in the regulation of the adaptive immune response. DCs are unique APCs and only DCs have the ability to induce a primary immune response in resting naïve T lymphocytes. Studies by Salomon et al. [12] suggested that autoimmune diabetes-prone diabetes mouse, deficient in B7-2 costimulation, was protected from developing diabetes but developed spontaneous autoimmune peripheral polyneuropathy. The spontaneous autoimmune peripheral polyneuropathy in these mice had many similarities to CIDP in humans. Press et al. [13] reported the presence of antigen-loaded DCs in the CSF of patients with CIDP. Probably these antigen-loaded DCs then may enter CSF-draining lymphatic vessels and travel to regional lymph nodes, where matured DCs interact with T and B cells to induce and modulate myelin-reactive T and B cell responses, whereas interferon-α could promote maturity of peripheral blood monocyte-derived DCs. [14] These findings suggest that interferon-α probably activates T and B cells via DCs, resulting in CIDP.

In conclusion, though rare, interferon-α treatment may cause CIDP. Since interferon-α is widely used for the treatment of chronic hepatitis C and B virus infections, physicians should be aware of the side effect so that an early diagnosis and treatment can be initiated.

 
 ╗ References Top

1.Konoshi T. A case of myasthenia gravis which developed myaesthenic crisis after alpha-interferon therapy for chronic hepatitis C. Rinsho Shinkeigaku 1996;36:980-5.  Back to cited text no. 1
    
2.Höftberger R, Garzuly F, Dienes HP, Grubits J, Rohonyi B, Fischer G, et al. Fulminant central nervous system demyelination associated with interferon-a therapy and hepatitis C virus infection. Mult Scler 2007;13:1100-6.  Back to cited text no. 2
    
3.Research criteria for diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP). Report from an Ad Hoc Subcommittee of the American Academy of Neurology AIDS Task Force. Neurology 1991;41:617-8.  Back to cited text no. 3
    
4.Russo MW, Fried MW. Side effects of therapy for chronic hepatitis C. Gastroenterology 2003;124:1711-9.  Back to cited text no. 4
    
5.Tosti A, Misciali C, Bardazzi F, Fanti PA, Varotti C. Telogen effluvium due to recombinant interferon alpha-2b. Dermatology 1992;184:124-5.  Back to cited text no. 5
    
6.Formann E, Stauber R, Denk DM, Jessner W, Zollner G, Munda-Steindl P, et al. Sudden hearing loss in patients with chronic hepatitis C treated with peglated interferon/ribavirin. Am J Gastroenterol 2004;99:873-7.  Back to cited text no. 6
    
7.Kawano T, Shigehira M, Uto H, Nakama T, Kato J, Hayashi K, et al. Retinal complications during interferon therapy for chronic hepatitis C. Am J Gastroenterol 1996;91:309-13.  Back to cited text no. 7
    
8.Meriggioli MN, Rowin J. Chronic inflammatory demyelinating polyneuropathy after treatment with interferon-alpha. Muscle Nerve 2000;23:433-5.  Back to cited text no. 8
    
9.Khiani V, Kelly T, Shibli A, Jensen D, Mohanty SR. Acute inflammatory demyelinating polyneuropathy associated with pegylated interferona-2a therpaty for chronic hepatitis C virus infection. World J Gastroenterology 2008;14:318-21.  Back to cited text no. 9
    
10.Boz C, Ozmenoglu M, Aktoz G, Velioglu S, Alioglu Z. Guillain-Barre syndrome during treatment with interferon a for hepatitis B. J Clin Neurosci 2004;11:523-5.  Back to cited text no. 10
    
11.Hirotani M, Nakano H, Ura S, Yoshida K, Niino M, Yabe I, et al. Chronic inflammatory demyelinating polyneuropathy after treatment with interferon-a. Intern Med 2009;48:373-5.  Back to cited text no. 11
    
12.Salomon B, Rhee L, Bour-Jordan H, Hsin H, Montag A, Soliven B, et al. Development of spontaneous autoimmune peripheral polyneuropathy in B7-2-deficient NOD mice. J Exp Med 2001;194:677-84.  Back to cited text no. 12
    
13.Press R, Nennesmo I, Kouwenhoven M, Huang YM, Link H, Pashenkov M. Dendritic cells in the cerebrospinal fluid and peripheral nerves in Guillain-Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy. J Neuroimmunol 2005;159:165-76.  Back to cited text no. 13
    
14.Radvanyi LG, Banerjee A, Weir M, Messner H. Low levels of interferon-alpha induce CD86 (B7.2) expression and accelerates dendritic cell maturation from human peripheral blood mononuclear cells. Scand J Immunol 1999;50:499-509.  Back to cited text no. 14
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]

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