About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
Home Print this page Email this page Users Online: 278

 Table of Contents  
Year : 2016  |  Volume : 16  |  Issue : 1  |  Page : 82-85

Guillain–Barré syndrome following hepatitis E

1 Department of Anaesthesiology, Critical Care Medicine Division, R. G. Kar Medical College, Kolkata, West Bengal, India
2 Department of Anaesthesiology and Critical Care, R. G. Kar Medical College, Kolkata, West Bengal, India
3 Department of Physiology, Burdwan Medical College, Burdwan, West Bengal, India

Date of Web Publication7-Jan-2016

Correspondence Address:
Arunima Chaudhuri
Department of Physiology, Burdwan Medical College, Burdwan - 713 102, West Bengal
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-6308.167756

Rights and Permissions

Guillain–Barré syndrome (GBS) is often triggered by a preceding bacterial or viral infection. A molecular mimicry mechanism is supposed to be involved in the pathogenesis of GBS triggered by infectious agents, although the nature of the shared epitopes has not been characterized in most instances, including that in the case of hepatotropic viruses. We report a case of GBS following acute hepatitis E.

  Abstract in Arabic 

متلازمة جوليان باري التالية لالتهاب الكبد الوبائي E
متلازمة جوليان باري (GBS) غالبا ما تتسبب عن عدوى بكتيرية أو فيروسية .
ويفترض ان آلية المحاكاة الجزيئية أن تشارك في التسبب في GBS النتج من العوامل المعدية على الرغم من عدم تتميز، طبيعة الحواتم المشتركة
في معظم الحالات، بما في ذلك في حالة الفيروسات كبدية التوجه. وفى هذا المقال نعرض حالة GBS اعقبت+ التهاب الكبد الوبائي الحاد E.

Keywords: Guillain–Barré syndrome, hepatitis E, molecular mimicry, viral hepatitis

How to cite this article:
Dasgupta S, Mitra PK, Chaudhuri A, Arijit A. Guillain–Barré syndrome following hepatitis E. Saudi J Sports Med 2016;16:82-5

How to cite this URL:
Dasgupta S, Mitra PK, Chaudhuri A, Arijit A. Guillain–Barré syndrome following hepatitis E. Saudi J Sports Med [serial online] 2016 [cited 2023 Feb 9];16:82-5. Available from: https://www.sjosm.org/text.asp?2016/16/1/82/167756

  Introduction Top

Guillain–Barré syndrome (GBS) is an acute polyradiculoneuropathy (i.e., inflammatory demyelination involves spinal roots and peripheral nerves) presenting, in its classical form, as a rapidly evolving symmetric and ascending motor paralysis with hypotonia and are flexia accompanied by an aleukocytic cerebrospinal fluid (CSF) with elevated protein level. In over two-third of cases, an infection precedes the onset of neuropathy by 1–3 week.[1],[2],[3],[4] The current hypothesis is in the favor of immunological reaction due to hypersensitivity, (molecular mimicry) allergen directed against myelin sheath. Cytomegalovirus and Epstein–Barr virus, measles, Campylobacter jejuni, human immunodeficiency virus (HIV), account for a large proportion of virus-triggered cases. Hepatitis E is a frequent cause of acute hepatitis in Asia, the Middle East, North Africa, and South or Central America.[1],[2],[3],[4],[5],[6] There are also few reports linking acute hepatitis E with GBS.[7],[8]

  Case Report Top

A 33-year-old male presented with jaundice for 30 days and rapidly developing ascending weakness involving lower limbs, upper limbs for 7 days, weakness in respiratory muscle, hoarseness, difficulty in deglutition for last 4 days. There was a history of urinary retention for 7 days for which he was catheterized. He had a fever for 5–10 days before jaundice started and a new episode of fever for 2–3 days before presenting to this institution. He was known alcoholic and chronic smoker. There was no history of trauma, blood transfusion, needle injury, vaccination, or drug intake.

The patient was conscious, alert, co-operative, oriented, febrile, normotensive (mean arterial pressure 70 mmHg), having tachycardia, tachypnea along with mild jaundice. Chest examination revealed that equal vesicular breath sound bilaterally, heart sound were audible without added adventitious sounds. On clinical examination of central nervous system gag reflex was absent; patient was not able to close the eyes; there was no sensory involvement; planter reflex response was flexor on right and absent on left; abdominal reflex was normal; deep tendon reflexes responses in upper limbs were less as compared to lower limbs (low > upper); muscle power grade 0/5 in low limbs and 2/5 in upper limbs, hypotonic muscles, single breath count 10; lower motor neuron lesion of 7th, 9th, and 10th cranial nerve. There was no history of blurring of vision. Weakness more in thigh and arm compared to leg and forearm. All sensory functions including touch, temperature and vibration were intact and there was no sign of meningeal irritation. Indirect ophthalmoscopy showed no papilledema. CSF study showed colorless, clear fluid without coagulum, total count 4/cc (all were lymphocytes), Gram-stain, c/s, and Ziehl–Neelsen stain negative, glucose – 71 mg/dl, protein – 429 mg/dl, and adenosine deaminase – 1.6 u/L. Nerve conduction study (NCS) in the present case was suggestive of acute motor sensory axonal neuropathy (AMSAN) subtype of GBS.

Arterial blood gas showed PaCO2 – 60, chest X-ray showed elevated diaphragm bilaterally. Ultrasonography revealed hepatomegaly suggestive of acute hepatitis. He was intubated and ventilated in assist-control mode ventilation mode. The routine investigation, LFT, MP, DA, dengue immunoglobulin M (IgM), NS1, platelet sent. DTS taken for Gram-stain/s, Ziehl–Neelsen stain and fungal stain, acid fast bacillus, blood c/s for aerobic and anaerobic growth, urine c/s sent on the 1st day of admission in our institution. He was put on invasive lines (central venous catheter, radial artery), intravenous immunoglobulin started and continued for 5 days. He had hemodynamic instability during the course of therapy initially required nitroglycerine infusion and later required noradrenalin infusion. Liver enzymes were elevated: Aspartate aminotransferase–1776 U/L, alanine aminotransferase – 1076 U/L, and γ-glutamyltransferase of 94 IU/alkaline phosphatase – 339 U/L. Serum bilirubin – 5.7 g/dl. IgM antibody against hepatitis E virus (HEV) was positive in serum and markers for hepatitis A, B, C, and D were absent. ELISA for HIV was negative. Later, he also required amlodipine and metoprolol. Blood c/s, urine culture sensitivity (c/s), DTS, MP, and DA was negative in spite of that he had intermittent fever persisting without rise in total leukocyte count (TLC) or C-reactive protein (CRP). An elective tracheotomy was done after 7 days and gradually weaned over next 14 days. Total duration in ventilator was 19 days. Last 2 days, he was in T-piece. He had episodes of continuous fever spikes with hypotension and altered sensorium and features of hepatic encephalopathy managed with fluids and noradrenalin. Serum ammonia, TLC, CRP, routine blood, urine, and DTS sent for culture sensitivity and diagnosed as ventilator associated pneumonia with high TLC and CRP count, which was managed with culture directed antibiotics. Limb and chest physiotherapy was started from day 1 and eye pads were used to prevent exposure keratitis. He was able to walk with assistances after 21 days and sent him to physical medicine department for rehabilitation. His fever also subsided and liver enzymes are normalized within 7 days, and discharged from ward after 4 days with the advice of physiotherapy.

  Discussion Top

GBS is a disease of peripheral nervous system, which is caused by the aberrant immune response, directed against some components of peripheral nerves.[2] The targeted antigens may be gangliosides present on the plasma membrane of the cell (e.g. GM-1 and GD-1a), Schwann cell neurons (nerve growth cone region). There are four common subtypes based on clinical and neurophysiological studies: Acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy, AMSAN, and Millar Fisher's syndrome.[1],[3] NCS in the present case was suggestive of AMSAN subtype.

Yadav et al. have documented a case of oculomotor palsy associated with hepatitis E.[9]

Santos et al. in 2013 reported case of a patient with HEV genotype 3a infection complicated by GBS in Portugal in December 2012.[10]

Sood et al.[11] reported a case of GBS who presented with are flexic quadriparesis with positive titers of IgM antibodies to HEV and negative titers of antibodies to hepatitis A, B, and C. Nerve conduction showed alteration in nerve conduction velocity and increased F responses while CSF showed increased proteins without cellular response.

In the Netherlands, 5% of patients with GBS were found to have an associated acute HEV infection. The frequency of HEV infections was determined by anti-HEV serology in a cohort of 201 patients with GBS and 201 healthy controls with a similar distribution in age, sex, and year of sampling by van den Berg et al. in 2014. An increased ratio of anti-HEV IgM antibodies was found in 10 patients with GBS (5.0%) compared with 1 healthy control. HEV RNA was detected in blood from 3 of these patients and additionally in feces from 1 patient. Seventy percent of anti-HEV IgM-positive patients had mildly increased liver function tests.[12]

Kamar et al.[13] described 7 cases of HEV-induced neurologic disorders, which occurred in 3 nonimmunocompromised patients with acute HEV infection, in 2 kidney transplant recipients and 1 kidney–pancreas transplant recipient with chronic HEV infection, and in 1 HIV-positive patient with chronic HEV infection. 2 were cases of GBS.

A 60-year-old woman from Toulouse, France, the patient's clinical and laboratory findings were best explained by AIDP (GBS) associated with HEV infection. HEV RNA became undetec[table 1]-month after the initial examination. Her neurologic condition gradually improved over the next 18 months, but residual weakness in her lower limbs remained.

In a 44-year-old man from Toulouse, France, acute autochthonous HEV infection developed 50 months after a kidney transplant. After 33 months of chronic HEV infection, the patient experienced progressive bilateral muscular weakness, difficulty walking, and palmar and plantar dysesthesia without fever. Neurologic examination revealed peripheral nerve involvement (with proximal muscular weakness that affected all limbs) and central nervous system involvement (bilateral pyramidal signs). Electrophysiologic studies showed signs of peripheral demyelinating polyradiculoneuropathy. After 3 months, because the patient had severe ataxia and loss of sphincter control, a neuromuscular biopsy was performed and showed nonspecific signs of neurogenic muscular atrophy but no signs of vasculitis in either muscule or nerve specimens. After another month, decompensated cirrhosis developed, and the patient died of bleeding esophageal varices.

Kamani et al.[14] reported a case of GBS with acute hepatitis E infection. He presented with symmetric are flexic quadriparesis with left infranuclear facial weakness and positive titers to IgM antibodies to HEV (ELISA) though CSF showing albuminocytologic dissociation, but NCSs was not done. Loly et al.[15] also showed a similar association in their patient wherein nerve conduction showed acute demyelinating affection; also serum antiganglioside antibodies to GM-2 IgM were positive. Cronin et al.[16] reported a case wherein they demonstrated antiglycolipid GM-2 antibody in GBS with HEV infection.

Comont et al.[17] reported a case of a 73-year-old man who presented with an acute polyradiculopathy and an acute hepatitis E. Abnormalities in NCS were consistent with demyelination and represented specific findings for classic GBS. Delayed distal latencies, slowed nerve conduction velocities, temporal dispersion of waveforms, conduction block, prolonged F-waves, and prolonged H-reflexes were all findings that supported demyelination.

Tse et al.[18] reported a case with unusual GBS triggered by an atypical microbe, HEV, in a Chinese patient, via a common route of transmission in this locality.

In the present case of hepatitis E with GBS there were few features: Bladder involvement; 7th, 9th, and 10th cranial nerve lower motor neuron type palsy; persistent fever in spite of normal TLC, CRP, sterile c/s, and unstable hemodynamics.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Seneviratne U. Guillain-Barré syndrome. Postgrad Med J 2000;76:774-82.  Back to cited text no. 1
Palazzuoli A, Lenzi C, Iovine F, Carrera A, Nuti R. A case of acute heart failure associated with Guillain-Barré syndrome. Neurol Sci 2006;26:447-50.  Back to cited text no. 2
Hughes RA, Cornblath DR. Guillain-Barré syndrome. Lancet 2005;366:1653-66.  Back to cited text no. 3
Murthy JM. Guillain-Barre syndrome following specific viral infections – An appraisal. J Assoc Physicians India 1994;42:27-9.  Back to cited text no. 4
Ono S, Chida K, Takasu T. Guillain-Barré syndrome following fulminant viral hepatitis A. Intern Med 1994;33:799-801.  Back to cited text no. 5
Tsukada N, Koh CS, Inoue A, Yanagisawa N. Demyelinating neuropathy associated with hepatitis B virus infection. Detection of immune complexes composed of hepatitis B virus surface antigen. J Neurol Sci 1987;77:203-16.  Back to cited text no. 6
Khanam RA, Faruq MO, Basunia RA. Guillain-Barré syndrome associated with acute HEV hepatitis. Ibrahim Med Coll J 2008;2:32-4.  Back to cited text no. 7
Kumar R, Bhoi S, Kumar M, Sharma B, Singh BM, Gupta BB, et al. Guillain-Barré syndrome and acute hepatitis E: A rare association. J Indian Acad Clin Med 2002;3:389-91.  Back to cited text no. 8
Yadav KK, Rohatgi A, Sharma SK, Kulshrestha M, Sachdeva S, Pardasani V. Oculomotor palsy associated with hepatitis E infection. J Assoc Physicians India 2002;50:737.  Back to cited text no. 9
Santos L, Mesquita JR, Rocha Pereira N, Lima-Alves C, Serrão R, Figueiredo P, et al. Acute hepatitis E complicated by Guillain-Barre syndrome in Portugal, December 2012 – A case report. Euro Surveill 2013;18. pii: 20563.  Back to cited text no. 10
Sood A, Midha V, Sood N. Guillain-Barré syndrome with acute hepatitis E. Am J Gastroenterol 2000;95:3667-8.  Back to cited text no. 11
van den Berg B, van der Eijk AA, Pas SD, Hunter JG, Madden RG, Tio-Gillen AP, et al. Guillain-Barré syndrome associated with preceding hepatitis E virus infection. Neurology 2014;82:491-7.  Back to cited text no. 12
Kamar N, Bendall RP, Peron JM, Cintas P, Prudhomme L, Mansuy JM, et al. Hepatitis E virus and neurologic disorders. Emerg Infect Dis 2011;17:173-9.  Back to cited text no. 13
Kamani P, Baijal R, Amarapurkar D, Gupte P, Patel N, Kumar P, et al. Guillain-Barre syndrome associated with acute hepatitis E. Indian J Gastroenterol 2005;24:216.  Back to cited text no. 14
Loly JP, Rikir E, Seivert M, Legros E, Defrance P, Belaiche J, et al. Guillain-Barré syndrome following hepatitis E. World J Gastroenterol 2009;15:1645-7.  Back to cited text no. 15
Cronin S, McNicholas R, Kavanagh E, Reid V, O'Rourke K. Anti-glycolipid GM2-positive Guillain-Barre syndrome due to hepatitis E infection. Ir J Med Sci 2011;180:255-7.  Back to cited text no. 16
Comont T, Bonnet D, Sigur N, Gerdelat A, Legrand-Abravanel F, Kamar N, et al. Acute hepatitis E infection associated with Guillain-Barré syndrome in an immunocompetent patient. Rev Med Interne 2014;35:333-6.  Back to cited text no. 17
Tse AC, Cheung RT, Ho SL, Chan KH. Guillain-Barré syndrome associated with acute hepatitis E infection. J Clin Neurosci 2012;19:607-8.  Back to cited text no. 18


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Case Report

 Article Access Statistics
    PDF Downloaded93    
    Comments [Add]    

Recommend this journal