Severe Guillain-Barré syndrome associated with chronic active hepatitis C and mixed cryoglobulinemia: a case report.
Chronic hepatitis C
Extra-hepatic manifestations
Guillain-Barre syndrome
Hepatitis C virus
Mixed cryoglobulinemia
Journal
BMC infectious diseases
ISSN: 1471-2334
Titre abrégé: BMC Infect Dis
Pays: England
ID NLM: 100968551
Informations de publication
Date de publication:
17 Jul 2019
17 Jul 2019
Historique:
received:
01
11
2018
accepted:
11
07
2019
entrez:
19
7
2019
pubmed:
19
7
2019
medline:
23
10
2019
Statut:
epublish
Résumé
We describe a case of severe Guillain-Barre syndrome (GBS) associated with chronic active hepatitis C and mixed cryoglobulinemia (MC). To our knowledge, this association between GBS and hepatitis C virus (HCV) infection has been rarely reported. A 56-year-old man developed symmetrical muscle weakness in all extremities, areflexia and sensorial disorder followed by acute respiratory failure associated with chronic active hepatitis C, which was confirmed by the presence of anti-HCV antibodies in the serum and persistence of HCV RNA viral load for more than 6 months. Chronic hepatitis C was further complicated by type 3 MC. Electromyography showed peripheral nerve injury (mainly in axon). A severe acute motor sensory axonal neuropathy (AMSAN) was diagnosed. After treatment with intravenous immunoglobulin and plasma exchange followed by antiviral therapy by direct-acting antiviral agent, patient showed progressive recovery and was transferred 3 months after his first admission to a rehabilitation center. Our case reported a severe GBS associated with HCV infection and MC. EMG classified for the first time the subtype of GBS (severe AMSAN) correlated with severe clinical form. HCV infection should be screened in high-risk patients to prevent silent progression of the chronic hepatitis C and its potentially severe extra-hepatic manifestations.
Sections du résumé
BACKGROUND
BACKGROUND
We describe a case of severe Guillain-Barre syndrome (GBS) associated with chronic active hepatitis C and mixed cryoglobulinemia (MC). To our knowledge, this association between GBS and hepatitis C virus (HCV) infection has been rarely reported.
CASE PRESENTATION
METHODS
A 56-year-old man developed symmetrical muscle weakness in all extremities, areflexia and sensorial disorder followed by acute respiratory failure associated with chronic active hepatitis C, which was confirmed by the presence of anti-HCV antibodies in the serum and persistence of HCV RNA viral load for more than 6 months. Chronic hepatitis C was further complicated by type 3 MC. Electromyography showed peripheral nerve injury (mainly in axon). A severe acute motor sensory axonal neuropathy (AMSAN) was diagnosed. After treatment with intravenous immunoglobulin and plasma exchange followed by antiviral therapy by direct-acting antiviral agent, patient showed progressive recovery and was transferred 3 months after his first admission to a rehabilitation center.
CONCLUSIONS
CONCLUSIONS
Our case reported a severe GBS associated with HCV infection and MC. EMG classified for the first time the subtype of GBS (severe AMSAN) correlated with severe clinical form. HCV infection should be screened in high-risk patients to prevent silent progression of the chronic hepatitis C and its potentially severe extra-hepatic manifestations.
Identifiants
pubmed: 31315560
doi: 10.1186/s12879-019-4278-7
pii: 10.1186/s12879-019-4278-7
pmc: PMC6637463
doi:
Substances chimiques
Antiviral Agents
0
Immunoglobulins, Intravenous
0
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
636Références
Presse Med. 2001 Apr 21;30(15):739
pubmed: 11360742
J Neurol Neurosurg Psychiatry. 2006 May;77(5):626-9
pubmed: 16464900
World J Gastroenterol. 2008 Jan 14;14(2):318-21
pubmed: 18186575
Dtsch Med Wochenschr. 1990 Mar 9;115(10):372-7
pubmed: 2107069
World J Hepatol. 2010 Apr 27;2(4):162-6
pubmed: 21160989
Autoimmun Rev. 2011 Jun;10(8):444-54
pubmed: 21303705
Expert Opin Pharmacother. 2011 Jul;12(10):1551-60
pubmed: 21473704
Clin Neurophysiol. 2012 Aug;123(8):1487-95
pubmed: 22480600
Brain. 2014 Jan;137(Pt 1):33-43
pubmed: 24163275
Nat Rev Neurol. 2014 Aug;10(8):469-82
pubmed: 25023340
Nat Rev Neurol. 2014 Sep;10(9):537-44
pubmed: 25072194
J Hepatol. 2014 Nov;61(1 Suppl):S58-68
pubmed: 25443346
Dig Liver Dis. 2014 Dec 15;46 Suppl 5:S165-73
pubmed: 25458776
Cochrane Database Syst Rev. 2014 Dec 20;(12):CD010404
pubmed: 25525951
World J Gastroenterol. 2015 Feb 28;21(8):2269-80
pubmed: 25741133
Gastroenterol Clin North Am. 2015 Dec;44(4):699-716
pubmed: 26600215
Lancet. 2016 Apr 9;387(10027):1531-1539
pubmed: 26948433
Lancet. 2016 Aug 13;388(10045):717-27
pubmed: 26948435
World J Hepatol. 2016 Apr 28;8(12):545-56
pubmed: 27134702
Clin Microbiol Infect. 2016 Oct;22(10):833-838
pubmed: 27521803
Autoimmun Rev. 2016 Dec;15(12):1145-1160
pubmed: 27640316
J Hepatol. 2017 Jun;66(6):1282-1299
pubmed: 28219772
Clin Liver Dis. 2017 Aug;21(3):535-542
pubmed: 28689591
J Med Virol. 1987 Mar;21(3):207-16
pubmed: 2881973
Arch Neurol. 1987 Apr;44(4):438-42
pubmed: 3030246
Gastroenterol Clin Biol. 1995 May;19(5):551
pubmed: 7590017
Brain. 1995 Jun;118 ( Pt 3):597-605
pubmed: 7600081
Neurology. 1993 Oct;43(10):2143
pubmed: 8413983
Liver. 1998 Feb;18(1):49-51
pubmed: 9548267
Ann Neurol. 1998 Nov;44(5):780-8
pubmed: 9818934