Neurol Sci DOI 10.1007/s10072-014-1854-x
LETTER TO THE EDITOR
Guillain–Barre´ syndrome and encephalitis/encephalopathy associated with acute severe hepatitis E infection Xiujuan Wu • Kangding Liu • Hong-Liang Zhang
Received: 28 April 2014 / Accepted: 4 June 2014 Ó Springer-Verlag Italia 2014
Dear Editor, We read the case report by Chen and colleagues [1] with great interest. They diagnosed acute severe hepatitis E virus (HEV) infection associated Guillain–Barre´ syndrome (GBS) and encephalitis/encephalopathy in a 64-year-old male based on clinical manifestations, laboratory investigations, and electrophysiological findings [1]. However, resembling diseases like critical illness polyneuropathy (CIP) and/or critical illness myopathy (CIM) could not seemingly be ruled out as per their presented information. CIP and CIM, which may occur in isolation or concomitantly, are common complications of patients with severe illnesses, especially for those with acute respiratory response syndrome, sepsis, systemic inflammatory response syndrome and multiple organ failure who are admitted to the intensive care units [2]. The manifestations of CIP/CIM including symmetric and flaccid weakness of the limbs resemble those of GBS [3]. GBS is clinically characterized by albumino-cytologic dissociation in the cerebrospinal fluid (CSF) which contributes to the differential diagnosis between GBS and CIP/CIM. However, other factors that may result in the increased level of proteins in CSF remain yet to be taken into consideration, such as intracranial infection [2]. Moreover, serum creatine kinase level, electrophysiology investigations, anti-ganglioside antibody test and nerve/muscle biopsy may provide discriminative information between GBS and CIP/CIM [2, 3].
In this case, the acute severe HEV infection responsible for his jaundice and tender hepatomegaly was confirmed by the positivity for anti-HEV immunoglobulin (Ig) M in the serum. It has been reported that patients with HEV infection could be complicated with several neurological disorders, among which the first and dominant clinical picture is peripheral nerve involvement with incompletely clear mechanisms [4]. The CSF profile in the case characterized by the increased level of proteins alongside with pleocytosis served as supporting evidence for GBS. Nevertheless, it is noteworthy that the mild high signals in bilateral hippocampus revealed by brain magnetic resonance imaging might contribute to the increased protein in CSF as well. An increase of CSF proteins is frequently seen in encephalitis or encephalopathy. The positivity of anti-GM2 IgM antibodies, which is more frequent in GBS secondary to cytomegalovirus (CMV) infection, has actually been found not only in non-GBS patients with acute CMV infection [5], but also in many other disorders, including chronic motor neuropathy, amyotrophic lateral sclerosislike disorder following ganglioside therapy and chronic demyelinating neuropathy with sensory ataxia [6]. In summary, although the electrophysiology examination revealed decreased conduction velocity suggestive of demyelinating changes in the peripheral nerves, the diagnosis of GBS should be cautious without excluding resembling diseases; muscle and nerve biopsy might be most helpful for differentiation.
X. Wu K. Liu H.-L. Zhang (&) Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Xinmin Street 71#, Changchun 130021, China e-mail: [email protected]; [email protected]
Acknowledgments The work was supported by grants from Young Scholars Program of Norman Bethune Health Science Center of Jilin University (No. 2013205035), Young Scholars Program of the First Hospital of Jilin University (No. JDYY42013003), the Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry, and the National Natural Science Foundation of China (No. 81241147).
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Neurol Sci
References 1. Chen XD, Zhou YT, Zhou JJ et al (2014) Guillain–Barre´ syndrome and encephalitis/encephalopathy of a rare case of Northern China acute severe hepatitis E infection. Neurol Sci (Epub ahead of print) 2. Zhou CK, Wu LM, Ni FM et al (2014) Critical illness polyneuropathy and myopathy: a systematic review. Neural Regen Res 9:101–110 3. Hermans G, De Jonghe B, Bruyninckx F et al (2008) Clinical review: critical illness polyneuropathy and myopathy. Crit Care 12:238
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4. Kamar N, Bendall RP, Peron JM et al (2011) Hepatitis E virus and neurologic disorders. Emerg Infect Dis 17:173–179 5. Irie S, Saito T, Nakamura K et al (1996) Association of anti-GM2 antibodies in Guillain–Barre´ syndrome with acute cytomegalovirus infection. J Neuroimmunol 68:19–26 6. Odaka M, Yuki N (2003) Antibodies to GM2 ganglioside in neurological disorders. Intern Med 42:220–221
LETTER TO THE EDITOR
Guillain–Barre´ syndrome and encephalitis/encephalopathy associated with acute severe hepatitis E infection Xiujuan Wu • Kangding Liu • Hong-Liang Zhang
Received: 28 April 2014 / Accepted: 4 June 2014 Ó Springer-Verlag Italia 2014
Dear Editor, We read the case report by Chen and colleagues [1] with great interest. They diagnosed acute severe hepatitis E virus (HEV) infection associated Guillain–Barre´ syndrome (GBS) and encephalitis/encephalopathy in a 64-year-old male based on clinical manifestations, laboratory investigations, and electrophysiological findings [1]. However, resembling diseases like critical illness polyneuropathy (CIP) and/or critical illness myopathy (CIM) could not seemingly be ruled out as per their presented information. CIP and CIM, which may occur in isolation or concomitantly, are common complications of patients with severe illnesses, especially for those with acute respiratory response syndrome, sepsis, systemic inflammatory response syndrome and multiple organ failure who are admitted to the intensive care units [2]. The manifestations of CIP/CIM including symmetric and flaccid weakness of the limbs resemble those of GBS [3]. GBS is clinically characterized by albumino-cytologic dissociation in the cerebrospinal fluid (CSF) which contributes to the differential diagnosis between GBS and CIP/CIM. However, other factors that may result in the increased level of proteins in CSF remain yet to be taken into consideration, such as intracranial infection [2]. Moreover, serum creatine kinase level, electrophysiology investigations, anti-ganglioside antibody test and nerve/muscle biopsy may provide discriminative information between GBS and CIP/CIM [2, 3].
In this case, the acute severe HEV infection responsible for his jaundice and tender hepatomegaly was confirmed by the positivity for anti-HEV immunoglobulin (Ig) M in the serum. It has been reported that patients with HEV infection could be complicated with several neurological disorders, among which the first and dominant clinical picture is peripheral nerve involvement with incompletely clear mechanisms [4]. The CSF profile in the case characterized by the increased level of proteins alongside with pleocytosis served as supporting evidence for GBS. Nevertheless, it is noteworthy that the mild high signals in bilateral hippocampus revealed by brain magnetic resonance imaging might contribute to the increased protein in CSF as well. An increase of CSF proteins is frequently seen in encephalitis or encephalopathy. The positivity of anti-GM2 IgM antibodies, which is more frequent in GBS secondary to cytomegalovirus (CMV) infection, has actually been found not only in non-GBS patients with acute CMV infection [5], but also in many other disorders, including chronic motor neuropathy, amyotrophic lateral sclerosislike disorder following ganglioside therapy and chronic demyelinating neuropathy with sensory ataxia [6]. In summary, although the electrophysiology examination revealed decreased conduction velocity suggestive of demyelinating changes in the peripheral nerves, the diagnosis of GBS should be cautious without excluding resembling diseases; muscle and nerve biopsy might be most helpful for differentiation.
X. Wu K. Liu H.-L. Zhang (&) Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Xinmin Street 71#, Changchun 130021, China e-mail: [email protected]; [email protected]
Acknowledgments The work was supported by grants from Young Scholars Program of Norman Bethune Health Science Center of Jilin University (No. 2013205035), Young Scholars Program of the First Hospital of Jilin University (No. JDYY42013003), the Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry, and the National Natural Science Foundation of China (No. 81241147).
123
Neurol Sci
References 1. Chen XD, Zhou YT, Zhou JJ et al (2014) Guillain–Barre´ syndrome and encephalitis/encephalopathy of a rare case of Northern China acute severe hepatitis E infection. Neurol Sci (Epub ahead of print) 2. Zhou CK, Wu LM, Ni FM et al (2014) Critical illness polyneuropathy and myopathy: a systematic review. Neural Regen Res 9:101–110 3. Hermans G, De Jonghe B, Bruyninckx F et al (2008) Clinical review: critical illness polyneuropathy and myopathy. Crit Care 12:238
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4. Kamar N, Bendall RP, Peron JM et al (2011) Hepatitis E virus and neurologic disorders. Emerg Infect Dis 17:173–179 5. Irie S, Saito T, Nakamura K et al (1996) Association of anti-GM2 antibodies in Guillain–Barre´ syndrome with acute cytomegalovirus infection. J Neuroimmunol 68:19–26 6. Odaka M, Yuki N (2003) Antibodies to GM2 ganglioside in neurological disorders. Intern Med 42:220–221
