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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2012  |  Volume : 23  |  Issue : 1  |  Page : 139-142
A rare complication of pegylated interferon Alfa 2a in a hepatitis C-positive patient on maintenance hemodialysis

1 Department of Nephrology, St. John's Medical College Hospital, Bangalore, India
2 Department of Neurology, St. John's Medical College Hospital, Bangalore, India

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Date of Web Publication3-Jan-2012

How to cite this article:
Satish R, Gokulnath, Mathew T. A rare complication of pegylated interferon Alfa 2a in a hepatitis C-positive patient on maintenance hemodialysis. Saudi J Kidney Dis Transpl 2012;23:139-42

How to cite this URL:
Satish R, Gokulnath, Mathew T. A rare complication of pegylated interferon Alfa 2a in a hepatitis C-positive patient on maintenance hemodialysis. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2020 Oct 24];23:139-42. Available from: https://www.sjkdt.org/text.asp?2012/23/1/139/91322
To the Editor,

A high prevalence of hepatitis C virus (HCV) infection has been reported among hemodialysis patients. Risk factors such as the number of blood transfusions or duration on hemodialysis have been identified. [1] The combination of pegylated interferon (Peg IFN) and ribavarin has been shown to be effective treatment for chronic hepatitis C. However, in hemodialysis patients, ribavarin is not used due to the high incidence of hemolysis. [2] Peg IFN is the treatment of choice in this population. The common side-effects of Peg IFN are flu-like symptoms, depression, irritability, nervousness, insomnia and, at times, suicidal tendency. [2],[3] Less common side-effects include hematopoietic suppressions, development or exacerbation of autoimmune disease such as thyroid dysfunction, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosis and myasthenia gravis. [3] Neurological complications are rare. Only a few publications have been reported on IFN-related polyneuropathy, including sensory neuropathy. [4] Some rare complications like acute inflammatory demyelinating polyneuropathy (AIDP) and chronic inflammatory demyelinating polyneuropathy (CIDP) have been reported in case reports earlier. [5],[6] Here, we present the case of a severe AIDP that developed at three weeks of Peg IFN therapy.

A 58-year-old female with long-standing hypertension for the last 15 years and diagnosed chronic kidney disease for four years had become dialysis dependent for the last two years at a different center elsewhere. She was on erythropoietin for anemia of CKD. She was detected to have hepatitis C infection four months earlier. Anti-HCV antibody by third-generation enzyme-linked immunosorbent assay (ELISA) was positive. HCV RNA quantitative analysis showed viral load of more than 1.22 million copies with genotype 3. Her liver enzymes were reported as normal. She was started on Peg IFN alfa 2a therapy by our gastroenterologist. She used to have flu-like symptoms with IFN therapy and was uncomfortable taking it. During the second week of IFN therapy, she complained of weakness and difficulty in walking. A week later, she developed fever with chills and cough with expectoration, and her weakness increased and she complained of weakness of both upper limbs as well.

On examination, her vitals were stable, but she was febrile. Respiratory system examination showed right infrascapular coarse crepitations. Cardiovascular and abdominal examinations were normal. Neurological examination revealed that she had musle power 3/5 only in all four limbs with absent reflexes and bilateral equivocal plantars. Sensory examination was normal, but she was complaining of parasthesia. There was no bladder or bowel involvement. She was admitted in the ICU with provisional diagnosis of left basal pneumonia with Guillain Barre Syndrome (GBS). Her preliminary investigations revealed neutrophilic leukocytosis, serum creatinine of 6.8 mg/dL and normal serum electrolytes. X-ray chest showed left infrascapular patch suggestive of pneumonia. Cerebrospinal fluid (CSF) exam showed albuminocytological dissociation. Her collagen work-up was negative. She was started on broad-spectrum antibiotics pending cultures and was continued on hemodialysis as required. Her electro-nuero-myographic (ENMG) test was deferred due to overall poor general condition. The neurologist opined to start IVIG/plasmapheresis. In view of pneumonia, IVIG/plasmapheresis was withheld initially. The patient, after three days of antibiotics, continued to have fever; hence, CT thorax was done. This showed left base pneumonia and also multiple small mediastinal lymph node (LN) and bronchoalveolar lavage (BAL) with transbronchial mediastinal LN biopsy was done. The BAL was negative for bacterial culture, AFB stain and malignancy. Blood and urine cultures showed no growth. With antibiotic, her fever improved and IVIG was given 0.4 mg/kg BW for five days. Her weakness improved and she was able to walk a few steps. However, two days later, suddenly, her weakness worsened and she developed respiratory distress. She was put on a ventilator, but the patient rapidly deteriorated and a day later, died (investigations depicted in [Table 1] and [Table 2].
Table 1: Routine investigations.

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Table 2: Special investigations and imaging.

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Polyneuropathy is a rare and infrequent side-effect seen in patients treated with IFN∝. [5] To the best of our knowledge, there is only one reported case of AIDP associated with PEG IFN 2 ∝ therapy for HCV infection. [6] The probable etiology in their patient mentioned is infectious processes or immune-mediated processes. In our patient also, probably, the infectious processes precipitated AIDP. However, immune-mediated cause cannot be ruled out. Immune-mediated AIDP of GBS type has been reported after infection, post vaccination and surgery. This also accounts for a significant portion of demyelinating polyneuropathy. [7] Autoimmune disease can also flare up and cause AIDP. In our patient, serology was negative. CIDP usually includes the clinical deterioration of neurological symptoms for a period of greater than eight weeks, as opposed to AIDP and/or GBS, which usually had deterioration over a period of approximately four weeks or less. [8] Our patient had symptoms within two weeks, and probably worsened with chest infection. Hence, her time course fit AIDP.

A typical presentation of GBS includes a significant motor weakness along with mild to moderate parasthesia. The muscle weakness typically starts on distal muscles of the lower extremities and weakness ascends rapidly, involving the upper extremities. In addition, CSF analysis usually reveals on elevated protein level with normal white blood cell count. Our patient's CSF analysis showed albumino-cytological dissociation suggestive of AIDP. The pathogenesis of AIDP related to Pegasys use is thought to be an acute immune-mediated process similar to GBS. The immune system mistakenly attacks the host's nerve tissue after recognizing a molecular epitope similar to a foreign antigen and results in acute inflammatory neuropathy. [5] Immunomodulation with IVIG therapy or plasmapheresis shows improvement in disease process. [5] Our patient showed improvement and later deteriorated probably due to worsening infection. Vasculitic neuropathy, an autoimmune process, may also occur in association with chronic HCV. Generally, patients may develop a chronic symmetrical axonal sensori-motor peripheral polyneuropathy due to a necrotizing vasculitis. [9] Treatment with IFN may worsen vasculitis neuropathy. In our patient, we did not check the cryoglobin level, but other clinical features of cryoglobunemia were not seen.

In conclusion, the treatment of HCV infection in a hemodialysis patient has come a long way in the recent years. We all are aware of the common side effects of PEG IFN 2 α, but rare complication as in our case can occur. Hence, it is imperative that we are aware of all possible complications of therapy, recognize them early and treat them accordingly.

   References Top

1.Hinrichsen H, Leimenstall G, Stegen G, Schrader H, Folsch UR, Schmidt WE. Prevalence of risk factors of hepatitis C virus infection haemodialysis patients: a multicentre study in 2796 patients. Gut 2002;51(3):429-33.  Back to cited text no. 1
2.Rusco MW, Fried MW. Side effects of therapy of chronic hepatitis C. Gastroenterology 2003; 124:1711-9.  Back to cited text no. 2
3.Anta Funes JA, Mariona Mastero VA, Helano Carranza E. Guillain Barre Syndrome - etiology & pathogenesis. Rev Invest Clin 2002; 54:357-63.  Back to cited text no. 3
4.Ruth Ove SB. An unusual axonal polyneuropathy induced by low dose interferon alfa 2a. Arch Neurol 1997;54:907.  Back to cited text no. 4
5.Marzo M, Tintore M, Fabregues O, Montbanx, Cedina A. Chronic inflammatory demyelinating polyneuropathy during treatment with interferon alfa. J Neurol Neurosurg Psychiatry 1998;65:604-15.  Back to cited text no. 5
6.Khiani V, Kelly T, Shibli A, Jensen D, Mohanty SR. Acute inflammatory demyelinating polyneuropathy associated with pegylated interferon á2a therapy for chronic hepatitis C virus infection. World J Gastroenterol 2008;14 (2):319-21.  Back to cited text no. 6
7.Beers M, Berhow R. Disorders peripheral nervous system. The Merk Manual of Diagnosis & therapy. 18 th Edition White house station, NJ: Merk & Co. Inc. 2006;1887-91.  Back to cited text no. 7
8.Vignani AG, Macedo-de-oliveiro A, Pavan MH, Pedvo MN Concates FI Jr. Hepatitis C virus infection, cryoglobulinemia and peripheral neuropathy. A case report. Bruz J Med Biol Res 2005;38:1729-34.  Back to cited text no. 8
9.Boonyapisit K., Kakiriji B. Severe exacerbation of hepatitis C associated vasculitic neuropathy following treatment with interferon alpha: a case report & literature review. Muscle Nerve 2002;25:909-13.  Back to cited text no. 9

Correspondence Address:
Renuka Satish
Department of Nephrology, St. John's Medical College Hospital, Bangalore
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PMID: 22237239

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  [Table 1], [Table 2]


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