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Songtanin B, Chaisrimaneepan N, Mendóza R, Nugent K. Burden, Outcome, and Comorbidities of Extrahepatic Manifestations in Hepatitis B Virus Infections. Viruses 2024; 16:618. [PMID: 38675959 PMCID: PMC11055091 DOI: 10.3390/v16040618] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/16/2024] [Revised: 04/11/2024] [Accepted: 04/13/2024] [Indexed: 04/28/2024] Open
Abstract
Hepatitis B virus (HBV) infections affect approximately 296 million people around the world, and the prevalence of any past or present HBV infection during the years 2015-2018 was as high as 4.3%. Acute HBV infection often presents with nonspecific symptoms and is usually self-limited, but 5% of patients can have persistent infections leading to chronic HBV infection and the risk of turning into chronic HBV infection is significantly higher in babies with vertical transmission (95%). Patients with chronic HBV infection are usually asymptomatic, but 15 to 40% of chronic HBV carriers develop cirrhosis and/or hepatocellular carcinoma. In addition to liver-related disorders, HBV is also associated with several extrahepatic complications, including glomerulonephritis, cryoglobulinemia, neurologic disorders, psychological manifestations, polyarthritis, and dermatologic disorders. Making the diagnosis of HBV can be challenging since patients with chronic infections can remain symptom-free for decades before developing cirrhosis or hepatocellular carcinoma, and patients with acute HBV infection may have only mild, nonspecific symptoms. Therefore, understanding how this virus causes extrahepatic complications can help clinicians consider this possibility in patients with diverse symptom presentations. The pathophysiology of these extrahepatic disorders likely involves immune-related tissue injury following immune complex formation and inflammatory cascades. In some cases, direct viral infection of extrahepatic tissue may cause a clinical syndrome. Currently, the American Association for the Study of Liver Diseases recommends treatment of chronic HBV infections with interferon therapy and/or nucleos(t)ide analogs, and this treatment has been reported to improve some extrahepatic disorders in some patients with chronic HBV infection. These extrahepatic complications have a significant role in disease outcomes and increase medical costs, morbidity, and mortality. Therefore, understanding the frequency and pathogenesis of these extrahepatic complications provides important information for both specialists and nonspecialists and may help clinicians identify patients at an earlier stage of their infection.
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Affiliation(s)
- Busara Songtanin
- Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA (K.N.)
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Yan XX, Huang J, Lin J. Demyelinating neuropathy in patients with hepatitis B virus: A case report. World J Clin Cases 2024; 12:1766-1771. [PMID: 38660079 PMCID: PMC11036481 DOI: 10.12998/wjcc.v12.i10.1766] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/16/2023] [Revised: 12/17/2023] [Accepted: 03/18/2024] [Indexed: 04/02/2024] Open
Abstract
BACKGROUND Hepatitis B rarely leads to demyelinating neuropathy, despite peripheral neuropathy being the first symptom of hepatitis B infection. CASE SUMMARY A 64-year-old man presented with sensorimotor symptoms in multiple peripheral nerves. Serological testing showed that these symptoms were due to hepatitis B. After undergoing treatment involving intravenous immunoglobulin and an antiviral agent, there was a notable improvement in his symptoms. CONCLUSION Although hepatitis B virus (HBV) infection is known to affect hepatocytes, it is crucial to recognize the range of additional manifestations linked to this infection. The connection between long-term HBV infection and demyelinating neuropathy has seldom been documented; hence, prompt diagnostic and treatment are essential. The patient's positive reaction to immunoglobulin seems to be associated with production of the antigen-antibody immune complex.
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Affiliation(s)
- Xiao-Xiao Yan
- Department of Neurology, The Third Affiliated Hospital of Wenzhou Medical University, Ruian 325000, Zhejiang Province, China
| | - Jin Huang
- Department of Neurology, The Third Affiliated Hospital of Wenzhou Medical University, Ruian 325000, Zhejiang Province, China
| | - Jing Lin
- Department of Neurology, The Third Affiliated Hospital of Wenzhou Medical University, Ruian 325000, Zhejiang Province, China
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Cai L, Liu X, Zhou H, Li J, Zhou D, Hong Z. Case report: Identification of Hepatitis B Virus in the cerebrospinal fluid of neuromyelitis optica spectrum disorders and successful treatment with ofatumumab and inebilizumab. Front Immunol 2024; 15:1351782. [PMID: 38426084 PMCID: PMC10902669 DOI: 10.3389/fimmu.2024.1351782] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2023] [Accepted: 01/24/2024] [Indexed: 03/02/2024] Open
Abstract
Neuromyelitis optica spectrum disorder (NMOSD) is a rare demyelinating disease of the central nervous system primarily affecting the optic nerves, spinal cord, and brainstem. Viral infection may trigger NMOSD. Here, we report the case of a 34-year-old female presenting with a range of symptoms including nausea, vomiting, dysphagia, choking, and fatigue with unsteady gait, diplopia, hearing loss, left-sided facial paralysis, breathing difficulties, and hoarseness of voice. Her HBV DNA concentration, as determined by quantitative PCR analysis, exceeded 5×107 IU/ml in serum and 4.48×102 IU/ml in CSF. Next-generation sequencing of CSF revealed 1,528 HBV sequences in DNA analysis and 6 sequences in RNA analysis. Serum aquaporin-4 antibody (AQP4-Ab) titer was 1:10, and the CSF titer was 1:3.2. Brain magnetic resonance imaging showed high signal intensities in the brain stem, medulla oblongata, and left middle cerebellar peduncle with mild restricted-diffusion. The patient received antiviral and hepatoprotective medications before the high-dose methylprednisolone pulse therapy. However, the patient did not respond well to the first-line treatment. Subsequently, the patient received ofatumumab and inebilizumab. Throughout the follow-up period, there was a gradual improvement in her neurological symptoms, with no reactivation of hepatitis B or deterioration of liver function observed. Thereby, to the best of our knowledge, we report the first case of successful treatment with ofatumumab and inebilizumab in a patient with NMOSD concurrent with HBV infection.
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Affiliation(s)
- Linjun Cai
- Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China
| | - Xu Liu
- Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China
| | - Hongyu Zhou
- Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China
| | - Jinmei Li
- Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China
| | - Dong Zhou
- Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China
- Institute of Brain Science and Brain-inspired Technology of West China Hospital, Sichuan University, Chengdu, Sichuan, China
| | - Zhen Hong
- Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China
- Institute of Brain Science and Brain-inspired Technology of West China Hospital, Sichuan University, Chengdu, Sichuan, China
- Department of Neurology, Chengdu Shangjin Nanfu Hospital, Chengdu, Sichuan, China
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Huang CC, Wu KL, Liu JS, Chang YY. Autonomic impairment in treatment-naive patients with chronic hepatitis B and C infections. Auton Neurosci 2022; 238:102928. [PMID: 35021146 DOI: 10.1016/j.autneu.2021.102928] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/11/2021] [Revised: 11/16/2021] [Accepted: 12/10/2021] [Indexed: 10/19/2022]
Abstract
BACKGROUND Peripheral neuropathy is not an uncommon manifestation in patients with chronic hepatitis. The role of cryoglobulin (CG) in neuropathy in patients with chronic hepatitis remains controversial. There is limited information about the autonomic neuropathy in chronic hepatitis. This study aimed to evaluate autonomic function in treatment-naive patients with chronic hepatitis B or hepatitis C infection and to elucidate the association between autonomic neuropathy and CG in these patients. METHODS A total of 29 treatment-naive patients with chronic, yet mild degrees of hepatitis B or C infection were evaluated for autonomic function, including those in the sympathetic sudomotor, cardiovagal, and adrenergic domains, to compare with the control subjects. The autonomic impairment was graded using the Composite Autonomic Scoring Scale. Then, association analyses between autonomic parameters/scores and CG were performed. RESULTS Patients with chronic hepatitis B or C infection had significantly worse autonomic function than control subjects, especially in the sudomotor and cardiovagal domains. The autonomic manifestations in cases with and without CG were similar. There was no significant difference in autonomic dysfunction between patients with hepatitis B and C infections. CONCLUSION The study demonstrated that autonomic neuropathy was not uncommon in patients with chronic hepatitis B or C infection. There was no association between autonomic neuropathy and CG.
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Affiliation(s)
- Chih-Cheng Huang
- Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Kaohsiung, Taiwan
| | - Keng-Liang Wu
- Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Kaohsiung, Taiwan
| | - Jia-Shou Liu
- Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Kaohsiung, Taiwan
| | - Yung-Yee Chang
- Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Kaohsiung, Taiwan.
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Wei J, Duan S. Severe Guillain-Barré syndrome associated with chronic hepatitis B: A case report and literature review. Medicine (Baltimore) 2021; 100:e27989. [PMID: 35049206 PMCID: PMC9191321 DOI: 10.1097/md.0000000000027989] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/17/2021] [Revised: 10/29/2021] [Accepted: 11/11/2021] [Indexed: 01/01/2023] Open
Abstract
RATIONALE Guillain-Barré syndrome (GBS) is a postinfectious autoimmune peripheral neuropathy characterized by acute paralysis of the limbs. Clinically, extrahepatic manifestations of neurologic involvement in chronic hepatitis B (CHB) are uncommon. Little attention has been paid to the relationship between GBS and CHB viral infection. PATIENT CONCERNS We presented a severe case of a 34-year-old man with general fatigue, anorexia, jaundice, numbness, and even muscle atrophy in the limbs, and respiratory failure during an acute exacerbation of CHB. DIAGNOSES Serological liver enzymes test confirmed an acute exacerbation of CHB. Nerve conduction studies revealed the features of acute motor and sensory axonal neuropathy combined with acute inflammatory demyelinating polyneuropathy, and cerebrospinal fluid analysis showed albuminocytologic dissociation. Clinical manifestations and the test results were consistent with a diagnosis of severe CHB-related GBS. INTERVENTIONS He was treated with mechanical ventilation, 2 courses of intravenous immunoglobulin, antichronic hepatitis B drugs therapy supplemented by hepatoprotection, acupuncture and rehabilitation. OUTCOMES After 29 days of hospitalization, his neurological condition improved. At a 6-month follow-up visit, he was able to walk with the support of another person. LESSONS The acute exacerbation of CHB may be a potential predisposing factor for the onset of GBS. This case is a reminder to clinicians that during the acute exacerbation of CHB, patients with neurological symptoms in the limbs should be considered for potential CHB-related GBS.
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LoRusso S. Infections of the Peripheral Nervous System. Continuum (Minneap Minn) 2021; 27:921-942. [PMID: 34623098 DOI: 10.1212/con.0000000000000981] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022]
Abstract
PURPOSE OF REVIEW This article describes infections that affect the peripheral nervous system, including their clinical features, differential diagnoses, and treatments. RECENT FINDINGS Rates of pyomyositis have increased recently in the United States, possibly because of an increase in risk factors such as IV drug use, obesity, and diabetes. Other peripheral nervous system infections, such as diphtheria, have become more common in older patients secondary to a lack of revaccination or waning immunity. Although recommended treatment regimens for most infections remain unchanged over recent years, debate over the ideal dosing and route of administration continues for some infections such as tetanus and leprosy (Hansen disease). SUMMARY Infections of the peripheral nervous system are varied in terms of the type of infection, localization, and potential treatment. Nerve conduction studies and EMG can help determine localization, which is key to determining an initial differential diagnosis. It is important to recognize infections quickly to minimize diagnostic delays that could lead to patient morbidity and mortality.
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Babatin MA, AlJohani A. Demyelinating polyneuropathy associated with chronic inactive hepatitis B infection. BMJ Case Rep 2021; 14:14/3/e237070. [PMID: 33766960 PMCID: PMC7996366 DOI: 10.1136/bcr-2020-237070] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/04/2022] Open
Abstract
This is a case report of a 42-year-old female patient with chronic inactive hepatitis B virus (HBV) infection who presented with relapsing chronic inflammatory demyelinating polyneuropathy (CIDP). Her initial attack was of acute onset (ie, acute CIDP) resembling Guillain-Barré syndrome that responded well to intravenous immunoglobulin (IVIG) therapy. The second episode was chronic and refractory to IVIG. She was managed with plasma exchange, long-term corticosteroids, immunosuppressants and HBV antiviral therapy. She showed both clinical and electromyographic improvement, with no recurrence after 2 years of follow-up.
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Nugraha ES, Huang I, Supriyadi R, Girawan D, Bestari MB. Successful Nucleoside Analog and Corticosteroid Therapy for Chronic Inflammatory Demyelinating Polyneuropathy in a Patient With Hepatitis B Virus Liver Cirrhosis. ACG Case Rep J 2021; 8:e00519. [PMID: 33457438 PMCID: PMC7808564 DOI: 10.14309/crj.0000000000000519] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/20/2020] [Accepted: 09/04/2020] [Indexed: 11/17/2022] Open
Abstract
Here, we describe the case of a 44-year-old man with chronic hepatitis B virus (HBV) infection, who was admitted with progressive muscle weakness and paresthesia in all extremities. He showed slight icterus. Positive HBV e-antigen test, significant HBV-deoxyribonucleic acid load, hypoalbuminemia, hyperbilirubinemia, mild ascites, and demyelinating peripheral axonal lesions in both sensory and motor nerves led to the diagnosis of Child-Pugh class B HBV cirrhosis with chronic inflammatory demyelinating polyneuropathy. Oral lamivudine, intravenous steroids, calcium, and vitamin D therapy led to a significant recovery of muscle strength within 6 weeks and a gradual return to normal after 24 weeks.
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Affiliation(s)
- Eka Surya Nugraha
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, Hasan Sadikin General Hospital, Universitas Padjadjaran, Bandung, Indonesia
| | - Ian Huang
- Department of Internal Medicine, Hasan Sadikin General Hospital, Universitas Padjadjaran, Bandung, Indonesia
| | - Rudi Supriyadi
- Department of Internal Medicine, Hasan Sadikin General Hospital, Universitas Padjadjaran, Bandung, Indonesia
| | - Dolvy Girawan
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, Hasan Sadikin General Hospital, Universitas Padjadjaran, Bandung, Indonesia
| | - Muhammad Begawan Bestari
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, Hasan Sadikin General Hospital, Universitas Padjadjaran, Bandung, Indonesia
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Paccoud O, Surgers L, Lacombe K. [Hepatitis B virus infection: Natural history, clinical manifestations and therapeutic approach]. Rev Med Interne 2019; 40:590-598. [PMID: 30982550 DOI: 10.1016/j.revmed.2019.03.333] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/03/2019] [Revised: 03/16/2019] [Accepted: 03/23/2019] [Indexed: 12/15/2022]
Abstract
Chronic hepatitis B infection remains a major public-health problem, with approximately 260 million world-wide cases of infection. Recent advances in the understanding of the natural history of chronic hepatitis B infection have led to progress in the care of infected patients. Sustained viral suppression is now possible for a majority of treated patients and is associated with a decrease in the morbidity and mortality attributable to cirrhosis and hepatocellular carcinoma. Complete cure is however not yet possible, due to the long-term persistence of viral DNA in hepatocytes of treated patients. Assessing the risk of viral reactivation in patients receiving immunosuppressive therapy is an increasingly frequent situation in clinical practice and its management is guided by both the patient's serological status and the potency of the immunosuppressive regimen. This review aims to present the clinical and biological presentations of chronic hepatitis B infection, the modalities of antiviral treatment, and how to assess the risk of viral reactivation in patients receiving immunosuppressive therapy.
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Affiliation(s)
- O Paccoud
- Service des maladies infectieuses et tropicales, hôpital Saint-Antoine, AP-HP, 75012 Paris, France
| | - L Surgers
- Service des maladies infectieuses et tropicales, hôpital Saint-Antoine, AP-HP, 75012 Paris, France; Sorbonne université, CIMI équipe 13, Inserm U1135, 75005 Paris, France
| | - K Lacombe
- Service des maladies infectieuses et tropicales, hôpital Saint-Antoine, AP-HP, 75012 Paris, France; Sorbonne université, Inserm UMR-S1136, IPLESP, 75005 Paris, France.
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10
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Pronier C, Guyader D, Jézequel C, Tattevin P, Thibault V. Contribution of quantitative viral markers to document hepatitis B virus compartmentalization in cerebrospinal fluid during hepatitis B with neuropathies. J Neurovirol 2018; 24:769-772. [PMID: 30097971 PMCID: PMC6280805 DOI: 10.1007/s13365-018-0662-0] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/11/2018] [Revised: 06/18/2018] [Accepted: 07/03/2018] [Indexed: 11/26/2022]
Abstract
Extrahepatic manifestations linked to hepatitis B Virus (HBV) are usually indirect consequences of immune-mediated mechanisms triggered by the virus replication. Strong evidence of brain HBV replication is missing and direct involvement of HBV in nervous system symptoms has been rarely reported. We report two cases of neurological manifestations contemporary to HBV infection. In both cases, HBV-DNA and HBsAg could be quantified in the cerebrospinal fluid (CSF) at relatively high levels. Differential quantification of HBsAg and HBV viral load both in CSF and in blood as well as phylogenic studies on HBV genomic sequences obtained from blood and CSF provided strong arguments for central nervous system viral replication in both cases. Direct causality of HBV replication in the central nervous system in these clinical situations is certainly not demonstrated but these findings could expand the list of hepatitis viruses possibly involved in neurological disorders. Further studies should be promoted to better document possible HBV replication in the brain tissues and its consequences.
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Affiliation(s)
- Charlotte Pronier
- Department of Virology, CHU Pontchaillou, Univ Rennes, INSERM, EHESP, IRSET - UMR_S 1085, Rennes, France
| | - Dominique Guyader
- Deparment of Liver diseases (SMF), Pontchaillou University Hospital, Univ Rennes, UMR 1241, Rennes, France
| | - Caroline Jézequel
- Deparment of Liver diseases (SMF), Pontchaillou University Hospital, Univ Rennes, UMR 1241, Rennes, France
| | - Pierre Tattevin
- Infectious Diseases and Intensive Care Unit, Pontchaillou University Hospital, Rennes, France
| | - Vincent Thibault
- Department of Virology, CHU Pontchaillou, Univ Rennes, INSERM, EHESP, IRSET - UMR_S 1085, Rennes, France.
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Sonavane AD, Saigal S, Kathuria A, Choudhary NS, Saraf N. Guillain-Barré syndrome: rare extra-intestinal manifestation of hepatitis B. Clin J Gastroenterol 2018. [PMID: 29542024 DOI: 10.1007/s12328-018-0847-3] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/25/2022]
Abstract
Extrahepatic syndromes are uncommon manifestations of acute and chronic hepatitis B. The pathogenesis likely involves an aberrant immunologic response to extrahepatic viral proteins. Antiviral therapy reduces the availability of these viral protein antigens and thus halts immune activation. Approximately 1% of all cases of acute inflammatory demyelinating polyneuropathy are associated with hepatitis B. Guillain-Barre syndrome (GBS) is a remarkably clinically diverse disorder with distinctive variants characterised by an immune-mediated attack to components of the peripheral nervous system. In this report, we present a rare case of GBS with chronic hepatitis B that resolved with antiviral and intravenous immunoglobulin therapy.
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Affiliation(s)
- Amey Dilip Sonavane
- Department of Liver Transplantation and Regenerative Medicine, Medanta - the Medicity, 14th Floor, Gurugram, 122001, India.
| | - Sanjiv Saigal
- Department of Liver Transplantation and Regenerative Medicine, Medanta - the Medicity, 14th Floor, Gurugram, 122001, India
| | - Abhishek Kathuria
- Department of Liver Transplantation and Regenerative Medicine, Medanta - the Medicity, 14th Floor, Gurugram, 122001, India
| | - Narendra S Choudhary
- Department of Liver Transplantation and Regenerative Medicine, Medanta - the Medicity, 14th Floor, Gurugram, 122001, India
| | - Neeraj Saraf
- Department of Liver Transplantation and Regenerative Medicine, Medanta - the Medicity, 14th Floor, Gurugram, 122001, India
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Aktas B, Basyigit S, Yılmaz B, Aktürk T, Nazligul Y. Dramatic Improvement of Chronic Inflammatory Demyelinating Polyneuropathy Through Tenofovir Treatment in a Patient Infected with Hepatitis B Virus. J Neuroimmune Pharmacol 2015; 10:191-2. [DOI: 10.1007/s11481-015-9607-z] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/24/2015] [Accepted: 03/25/2015] [Indexed: 11/28/2022]
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Salemi JL, Whiteman VE, August EM, Chandler K, Mbah AK, Salihu HM. Maternal hepatitis B and hepatitis C infection and neonatal neurological outcomes. J Viral Hepat 2014; 21:e144-53. [PMID: 24666386 DOI: 10.1111/jvh.12250] [Citation(s) in RCA: 36] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/30/2013] [Accepted: 01/12/2014] [Indexed: 12/13/2022]
Abstract
To examine the associations between maternal hepatitis B (HBV) and hepatitis C (HCV) infection status and selected infant neurological outcomes diagnosed at birth, we conducted a population-based, retrospective cohort study on singleton live births in Florida from 1998 to 2009. Primary exposures included maternal HBV and HCV monoinfection. The neurological outcomes included brachial plexus injury, cephalhematoma, foetal distress, feeding difficulties, intraventricular h aemorrhage and neonatal seizures. Multivariable logistic regression models were used to generate odds ratios (OR) and 95% confidence intervals (CI) that were adjusted for socio-demographic characteristics, risky behaviours, pregnancy complications and pre-existing medical conditions, and timing of delivery. The risk of an adverse neurological outcome was higher in infants born to mothers with hepatitis viral infection (7.2% for HCV, 5.0% for HBV), compared with infants of hepatitis virus-free mothers (4.2%). After adjusting for potential confounders, women with HBV were twice as likely to have infants who suffered from brachial plexus injury (OR = 2.04, 95% CI = 1.15-3.60), while those with HCV had an elevated odds of having an infant with feeding difficulties (OR: 1.32, 95% CI = 1.06-1.64) and a borderline increased likelihood for neonatal seizures (OR = 1.74, 95% CI = 0.98-3.10). Additionally, HCV+ mothers had a 22% increased odds of having an infant with some type of adverse neurological outcome (OR: 1.22, 95% CI = 1.03-1.44). Our findings add to current understanding of the association between maternal HBV/HCV infections and infant neurological outcomes. Further research evaluating the role of maternal HBV and HCV infections (including viraemia, treatment) on pregnancy outcomes is warranted.
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Affiliation(s)
- J L Salemi
- Department of Epidemiology and Biostatistics, College of Public Health, University of South Florida, Tampa, FL, USA
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Sellner J, Steiner I. Neurologic complications of hepatic viruses. HANDBOOK OF CLINICAL NEUROLOGY 2014; 123:647-61. [PMID: 25015509 DOI: 10.1016/b978-0-444-53488-0.00031-6] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Affiliation(s)
- Johann Sellner
- Department of Neurology, Christian-Doppler-Klinik, Paracelsus Medical University, Salzburg, Austria; Department of Neurology, Klinikum rechts der Isar, Technische Universität Munich, Germany
| | - Israel Steiner
- Department of Neurology, Rabin Medical Center, Petach Tikva, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
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Mehndiratta M, Pandey S, Nayak R, Saran RK. Acute onset distal symmetrical vasculitic polyneuropathy associated with acute hepatitis B. J Clin Neurosci 2012; 20:331-2. [PMID: 23164826 DOI: 10.1016/j.jocn.2012.03.029] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/06/2012] [Accepted: 03/03/2012] [Indexed: 12/30/2022]
Abstract
Hepatitis B can have varied extrahepatic manifestations involving the skin, renal, haematological and nervous systems. Neurological manifestations in hepatitis B may take the form of Guillain-Barré syndrome and secondary systemic vasculitis-related mononeuritis multiplex. The clinical course of hepatitis B-related, vasculitis-related neuropathy is usually subacute to chronic and clinical evolution is relatively benign. To our knowledge, acute hepatitis B-associated vasculitis manifesting as acute distal symmetric polyneuropathy has not been reported. We report a 60-year-old man who presented with fever, mild hepatomegaly, skin lesions in the form of non-palpable purpura and acute onset distal symmetric sensorimotor polyneuropathy. Serum transaminase levels were raised and viral serological markers revealed acute hepatitis B. The patient remained anicteric throughout his clinical course. Nerve conduction studies showed severe axonal sensorimotor polyneuropathy and histopathological examination of sural nerve biopsy was suggestive of vasculitic neuropathy. The patient was first given a course of intravenous immunoglobulin with the antiviral drug entecavir. The fever subsided after 1 week of treatment. The patient was started on prednisolone in addition to the entecavir, and showed significant improvement in motor power and marked resolution in paresthesia after 2 weeks of treatment. Thus, acute onset distal symmetric sensorimotor polyneuropathy of vasculitic etiology can be a manifestation of acute hepatitis B.
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Affiliation(s)
- Manmohan Mehndiratta
- Department of Neurology, Room 511, Academic Block, GB Pant Hospital, JLN Marg, New Delhi-2 110002, India
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Abstract
Approximately 400 million worldwide are chronically infected with the hepatitis B virus (HBV). During the course of illness, approximately 20% of patients develop disease manifestations outside the liver. Neuropathy develops in approximately 5% of patients with chronic HBV infection and rarely during acute HBV infection. The pathogenesis of the various HBV-associated neuropathy syndromes possibly involves deposition of immune complexes in nerves or blood vessel walls. Direct viral infection of nerves has not been demonstrated. Management entailed supportive care with antiviral and immunomodulatory treatment as clinically indicated. Rare cases of muscle disease, mostly inflammatory myopathy, have been associated with HBV infection. Presumably, HBV-associated antigens trigger immune mechanisms directed against components of muscle tissue. There is no evidence of replicative virus infection of muscle fibers. Management entailed immunomodulatory treatment, occasionally with anti-HBV therapy. Physicians should be aware that HBV infection has the potential to trigger presumed immune-mediated neuromuscular syndromes.
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Stübgen JP. Immune-mediated myelitis associated with hepatitis virus infections. J Neuroimmunol 2011; 239:21-7. [PMID: 21945641 DOI: 10.1016/j.jneuroim.2011.09.001] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/31/2011] [Revised: 07/24/2011] [Accepted: 09/02/2011] [Indexed: 12/14/2022]
Abstract
Virus-induced spinal cord damage results from a cytolytic effect on anterior horn cells or from predominantly cellular immune-mediated damage of long white matter tracts. Infection with the hepatitis virus group, most notably hepatitis C virus, has infrequently been associated with the occurrence of myelitis. The pathogenesis of hepatitis virus-associated myelitis has not been clarified: virus-induced autoimmunity (humoral or cell-mediated, possibly vasculitic) seems the most likely disease mechanism. Limited available information offers no evidence of direct hepatitis virus infection of the spinal cord. Virus neuropenetration may occur after virus-infected mononuclear cells penetrate the blood-brain barrier, but a true neurolytic effect has not been demonstrated. Attacks of acute myelitis usually respond favorably to immunomodulatory therapy. Antiviral therapy plays no confirmed role in the treatment of acute bouts of myelitis, but may limit the relapsing course of HCV-associated myelitis.
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Affiliation(s)
- Joerg-Patrick Stübgen
- Department of Neurology and Neuroscience, Cornell University Medical College/New York Presbyterian Hospital, 525 East 68th Street, New York, NY 10065-4885, USA.
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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 2010; 180:255-7. [PMID: 21063804 DOI: 10.1007/s11845-010-0635-7] [Citation(s) in RCA: 36] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/02/2010] [Accepted: 10/26/2010] [Indexed: 12/25/2022]
Abstract
BACKGROUND Hepatitis E infection is most prevalent in developing countries with poor sanitation, but can also occur apparently sporadically in more developed areas. CASE We here report a second European case of Guillain-Barre syndrome due to hepatitis E infection in association with anti-glycolipid GM2 antibody. INTERPRETATION This is likely to be a specific association involving molecular mimicry, and further European cases can therefore be expected.
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Affiliation(s)
- S Cronin
- Dublin Neurological Institute, Mater Misericordiae University Hospital, 57 Eccles Street, Dublin 7, Ireland
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20
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Nam TS, Lee SH, Park MS, Choi KH, Kim JT, Choi SM, Kim BC, Kim MK, Cho KH. Mononeuropathy multiplex in a patient with chronic active hepatitis B. J Clin Neurol 2010; 6:156-8. [PMID: 20944818 PMCID: PMC2950922 DOI: 10.3988/jcn.2010.6.3.156] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/07/2009] [Revised: 07/10/2009] [Accepted: 07/10/2009] [Indexed: 12/02/2022] Open
Abstract
Background Mononeuropathy multiplex is a rare complication during the course of chronic hepatitis B, despite various neuropathies following acute hepatitis B having been reported previously. Case Report A 30-year-old man presented with sensorimotor symptoms in multiple peripheral nerves. The serological tests for hepatitis were consistent with chronic active hepatitis B. After treatment with oral prednisone combined with an antiviral agent, the sensory and motor symptoms improved and hepatitis B virus replication was reduced. Conclusions We suggest that chronic immune-mediated neuropathy associated with hepatitis B virus infection should be considered in the differential diagnosis of patients with hepatitis B.
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Affiliation(s)
- Tai Seung Nam
- Department of Neurology, Chonnam National University Hwasun Hospital, Hwasun, Korea
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21
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Abstract
This article focuses on autoimmune manifestations related to the hepatitis B virus (HBV). Although the HBV vaccination has resulted in the decline of the virus, approximately 400 million individuals are infected worldwide. Up to twenty percent of the afflicted may develop extrahepatic manifestations ranging from the severe polyarteritis nodosa to the many, varied, and less severe clinical and biologic forms. Currently, control of the viral infection is mainly based on the use of antiviral drugs (with the current availability of potent agents). Discussion of two hypotheses of the pathophysiology of the virus is followed by descriptions of the general, renal, rheumatologic, neurologic, skin, ophthalmologic, and hematologic manifestations.
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Affiliation(s)
- Patrice Cacoub
- Service de Médecine Interne, AP, HP Pitié-Salpêtrière Hospital Group, 75651 Paris Cedex 13, France.
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22
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Luth S, Birklein F, Schramm C, Herkel J, Hennes E, Muller-Forell W, Galle PR, Lohse AW. Multiplex neuritis in a patient with autoimmune hepatitis: A case report. World J Gastroenterol 2006; 12:5396-8. [PMID: 16981276 PMCID: PMC4088213 DOI: 10.3748/wjg.v12.i33.5396] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
A 37-year old woman presented with a 9-year history of hepatitis of unknown origin and aminotransferases within a 3-fold upper limit of normal. Autoimmune hepatitis (AIH) was diagnosed on the basis of elevated aminotransferases, soluble liver antigen/liver pancreas (SLA/LP) autoantibodies and characteristic histology. Immunosuppressive therapy led to rapid normalization of aminotransferases. Two years later, the patient developed left sided hemisensory deficits under maintenance therapy of prednisolone and azathioprine (AZT). Later she developed right foot drop and paraesthesia in the ulnar innervation territory on both sides. Magnetic resonance imaging (MRI) and cerebral panangiography suggested cerebral vasculitis. Neurological investigation and electromyography disclosed multiplex neuritis (MN) probably due to vasculitis. Consistent with this diagnosis, autoantibodies to extractable nuclear antigens were detectable in serum. Immunosuppression was changed to oral 150 mg cyclophosphamide (CPM0) per day. Prednisolone was increased to 40 mg/d and then gradually tapered to 5 mg. Oral CPM was administered up to a total dose of 40 g and then substituted by 6 times of an intervall infusion therapy of CPM (600 mg/m2). Almost complete motoric remission was achieved after 3 mo of CPM. Sensibility remained reduced in the right peroneal innervation territory. Follow-up of cranial MRI provided stable findings without any new or progressive lesions. This is the first report of multiplex neuritis in a patient with autoimmune hepatitis.
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Affiliation(s)
- S Luth
- Department of Medicine I, University Medical Centre Hamburg-Eppendorf, Martinistr. 52, Hamburg 20246, Germany
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23
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Abstract
BACKGROUND Acute myelopathies represent a heterogeneous group of disorders with distinct etiologies, clinical and radiologic features, and prognoses. Transverse myelitis (TM) is a prototype member of this group in which an immune-mediated process causes neural injury to the spinal cord, resulting in varying degrees of weakness, sensory alterations, and autonomic dysfunction. TM may exist as part of a multifocal CNS disease (eg, MS), multisystemic disease (eg, systemic lupus erythematosus), or as an isolated, idiopathic entity. REVIEW SUMMARY In this article, we summarize recent classification and diagnostic schemes, which provide a framework for the diagnosis and management of patients with acute myelopathy. Additionally, we review the state of current knowledge about the epidemiology, natural history, immunopathogenesis, and treatment strategies for patients with TM. CONCLUSIONS Our understanding of the classification, diagnosis, pathogenesis, and treatment of TM has recently begun to expand dramatically. With more rigorous criteria applied to distinguish acute myelopathies and with an emerging understanding of immunopathogenic events that underlie TM, it may now be possible to effectively initiate treatments in many of these disorders. Through the investigation of TM, we are also gaining a broader appreciation of the mechanisms that lead to autoimmune neurologic diseases in general.
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Affiliation(s)
- Adam I Kaplin
- Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Osler 320, 600 N. Wolfe Street, Baltimore, MD 21287, USA.
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24
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Abstract
Acute transverse myelitis is a group of disorders characterized by focal inflammation of the spinal cord and resultant neural injury. Acute transverse myelitis may be an isolated entity or may occur in the context of multifocal or even multisystemic disease. It is clear that the pathological substrate--injury and dysfunction of neural cells within the spinal cord--may be caused by a variety of immunological mechanisms. For example, in acute transverse myelitis associated with systemic disease (i.e. systemic lupus erythematosus or sarcoidosis), a vasculitic or granulomatous process can often be identified. In idiopathic acute transverse myelitis, there is an intraparenchymal or perivascular cellular influx into the spinal cord, resulting in the breakdown of the blood-brain barrier and variable demyelination and neuronal injury. There are several critical questions that must be answered before we truly understand acute transverse myelitis: (1) What are the various triggers for the inflammatory process that induces neural injury in the spinal cord? (2) What are the cellular and humoral factors that induce this neural injury? and (3) Is there a way to modulate the inflammatory response in order to improve patient outcome? Although much remains to be elucidated about the causes of acute transverse myelitis, tantalizing clues as to the potential immunopathogenic mechanisms in acute transverse myelitis and related inflammatory disorders of the spinal cord have recently emerged. It is the purpose of this review to illustrate recent discoveries that shed light on this topic, relying when necessary on data from related diseases such as acute disseminated encephalomyelitis, Guillain-Barré syndrome and neuromyelitis optica. Developing a further understanding of how the immune system induces neural injury will depend upon confirmation and extension of these findings and will require multicenter collaborative efforts.
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Affiliation(s)
- Douglas A Kerr
- Department of Neurology, School of Medicine, Johns Hopkins University, Pathology 627 C, 6000 N Wolfe Street, Baltimore, MD 21287-6965, USA.
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25
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Chaudhry V, Umapathi T, Ravich WJ. Neuromuscular diseases and disorders of the alimentary system. Muscle Nerve 2002; 25:768-84. [PMID: 12115965 DOI: 10.1002/mus.10089] [Citation(s) in RCA: 17] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
This review outlines the relationship and interaction between neuromuscular diseases and disorders of the alimentary system. Neuromuscular manifestations of gastrointestinal and hepatobiliary diseases are first considered. Such diseases may cause neuromuscular disorders by leading to nutritional deficiency or by more direct mechanisms. The pathogenesis, clinical features, and treatment of these various neuromuscular manifestations are discussed. The impact of disorders of nerve, neuromuscular transmission, and muscle on the alimentary system is then reviewed. The main sequelae are impaired deglutition and gastrointestinal dysmotility. The management of these complications is considered.
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Affiliation(s)
- Vinay Chaudhry
- Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Meyer 6-119, Baltimore, Maryland 21287, USA.
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26
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Caniello M, Baxter P, Lino AMM, Lima LG, Pinto WP. Confluent peripheral multiple mononeuropathy associated to acute hepatitis B: a case report. Rev Inst Med Trop Sao Paulo 2002; 44:171-3. [PMID: 12163912 DOI: 10.1590/s0036-46652002000300011] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/30/2023] Open
Abstract
A thirty three year-old, male patient was admitted at the Hospital of the São Paulo University School of Medicine, at the city of São Paulo, Brazil, with complaint of pains, tingling and decreased sensibility in the right hand for the last four months. This had progressed to the left hand, left foot and right foot, in addition to a difficulty of flexing and stretching in the left foot. Tests were positive for HBeAg, IgM anti-HBc and HBsAg, thus characterizing the condition of acute hepatitis B. The ALT serum level was 15 times above the upper normal limit. Blood glucose, cerebral spinal fluid, antinuclear antibodies (ANA) and anti-HIV and anti-HCV serum tests were either normal or negative. Electroneuromyography disclosed severe peripheral neuropathy with an axon prevalence and signs of denervation; nerve biopsy disclosed intense vasculitis. The diagnosis of multiple confluent mononeuropathy associated to acute hepatitis B was done. This association is not often reported in international literature and its probable cause is the direct action of the hepatitis B virus on the nerves or a vasculitis of the vasa nervorum brought about by deposits of immune complexes.
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27
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Créange A, Temam G, Lefaucheur JP. Lumbosacral acute demyelinating polyneuropathy following hepatitis B vaccination. Autoimmunity 1999; 30:143-6. [PMID: 10520897 DOI: 10.3109/08916939908993848] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022]
Abstract
We report a patient who presented with an acute inflammatory demyelinating polyneuropathy, that followed the second injection of a hepatitis B vaccination, and characterized by motor and sensory deficit restricted to lower limbs and perineum, and persistent bladder dysfunction. The relationship between the preceding event and neurological disease is discussed.
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Affiliation(s)
- A Créange
- Service de Neurologie, Centre Hospitalier Universitaire Henri Mondor, Créteil, France.
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28
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Lange D, Aleksic S, Kassubek J, Vrvic MM, Kist M, Steinbrückner B, Mitova M. Detection of antibodies against Campylobacter jejuni serogroup PEN O:19 purified flagellar protein in a patient with Guillain-Barré syndrome. ZENTRALBLATT FUR BAKTERIOLOGIE : INTERNATIONAL JOURNAL OF MEDICAL MICROBIOLOGY 1999; 289:429-44. [PMID: 10603661 DOI: 10.1016/s0934-8840(99)80083-8] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 10/15/2022]
Abstract
C. jejuni serogroup PEN O:19 was isolated from a stool specimen from a patient with Guillain-Barré syndrome (GBS). Flagellar protein was isolated and purified from reference strain C. jejuni PEN O:19, ATCC 43,446, as well as from a homologous patient strain. Antibodies against flagellar protein were detected by means of immunoblotting, enzyme-linked immunosorbent assay (ELISA) and tube agglutination test. The antibody titres were found to be directly correlated at the beginning and in the recovery phase of GBS. Antibodies of IgG and IgA classes were present from the very onset of the disease as well as 5 months later, but with a lower titre population. However, antibodies of the IgM class were persistent only at the onset of the infection and disappeared during the following 5 months. Our results strongly support the hypothesis that in GBS patients, antiflagellar antibodies are induced during C. jejuni infection and can be used in the diagnosis of C. jejuni-associated GBS.
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Affiliation(s)
- D Lange
- Johnson & Johnson Medical, Norderstedt, Germany.
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29
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Chaudhry V, Corse AM, O'Brian R, Cornblath DR, Klein AS, Thuluvath PJ. Autonomic and peripheral (sensorimotor) neuropathy in chronic liver disease: a clinical and electrophysiologic study. Hepatology 1999; 29:1698-703. [PMID: 10347110 DOI: 10.1002/hep.510290630] [Citation(s) in RCA: 64] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
Peripheral neuropathy has been reported in association with chronic liver disease. However, the precise incidence, severity and characteristics of neuropathy, and the relationship of neuropathy to different etiologies of liver disease have not been defined. In this study, 58 patients with advanced liver disease were evaluated in detail for the presence of neuropathy. Peripheral (sensorimotor) neuropathy was found in 71% and autonomic neuropathy was found in 48% of the patients. Although the majority of patients were asymptomatic, neurological examination showed distal sensory loss to pain, or vibration or distal loss of reflexes in 17 patients (29%). Sensory neuropathy was seen more commonly than motor axonal polyneuropathy on nerve conduction studies. Quantitative sensory testing was frequently abnormal (62%) and cooling thresholds were more affected than vibration thresholds. Overall, the pattern of neuropathy in patients with liver disease conformed to the pattern expected in "dying back" or length-dependent neuropathy. The neuropathy was most severe in patients with advanced hepatic decompensation. Comparison of causes of liver disease showed no significant differences in the severity of neuropathy among the different etiologies. In conclusion, axonal sensory-motor polyneuropathy and autonomic neuropathy are commonly seen in patients with end-stage liver disease of different causes.
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Affiliation(s)
- V Chaudhry
- Department of Neurology,The Johns Hopkins University School of Medicine, Baltimore, MD, USA
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30
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Abstract
Since the eradication of polio in most parts of the world, Guillain-Barré syndrome (GBS) has become the most common cause of acute flaccid paralysis. GBS is an autoimmune disorder of the peripheral nervous system characterized by weakness, usually symmetrical, evolving over a period of several days or more. Since laboratories began to isolate Campylobacter species from stool specimens some 20 years ago, there have been many reports of GBS following Campylobacter infection. Only during the past few years has strong evidence supporting this association developed. Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS. Campylobacter is thought to cause this autoimmune disease through a mechanism called molecular mimicry, whereby Campylobacter contains ganglioside-like epitopes in the lipopolysaccharide moiety that elicit autoantibodies reacting with peripheral nerve targets. Campylobacter is associated with several pathologic forms of GBS, including the demyelinating (acute inflammatory demyelinating polyneuropathy) and axonal (acute motor axonal neuropathy) forms. Different strains of Campylobacter as well as host factors likely play an important role in determining who develops GBS as well as the nerve targets for the host immune attack of peripheral nerves. The purpose of this review is to summarize our current knowledge about the clinical, epidemiological, pathogenetic, and laboratory aspects of campylobacter-associated GBS.
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Affiliation(s)
- I Nachamkin
- Department of Pathology & Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA.
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31
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Abstract
A previously unrecognized sequelum of infection with Campylobacter jejuni, a common cause of gastroenteritis, is Guillain-Barré syndrome (GBS). GBS is the most common cause of acute neuromuscular paralysis; 30% to 40% of cases are preceded by C. jejuni infection. Both patient and bacterial characteristics likely play a role in the pathogenesis of C. jejuni-induced GBS. Molecular mimicry between the LPS of some campylobacters and structures present on the gangliosides of the peripheral nerve may explain how this acute infectious diarrheal illness triggers GBS.
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Affiliation(s)
- B M Allos
- Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
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32
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Abstract
Demyelination is a component of several viral diseases of humans. The best known of these are subacute sclerosing panencephalitis (SSPE) and progressive multifocal leukoencephalopathy (PML). There are a number of naturally occurring virus infections of animals that involve demyelination and many of these serve as instructive models for human demyelinating diseases. In addition to the naturally occurring diseases, many viruses have been shown to be capable of producing demyelination in experimental situations. In discussing virus-associated demyelinating disease, the chapter reviews the architecture and functional organization of the CNS and considers what is known of the interaction of viruses with CNS cells. It also discusses the immunology of the CNS that differs in several important aspects from that of the rest of the body. Experimental models of viral-induced demyelination have also been considered. Viruses capable of producing demyelinating disease have no common taxonomic features; they include both DNA and RNA viruses, enveloped and nonenveloped viruses. The chapter attempts to summarize the important factors influencing viral demyelination, their common features, and possible mechanisms.
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Affiliation(s)
- J K Fazakerley
- Department of Pathology, University of Cambridge, England
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Arakawa K, Umezaki H, Noda S, Itoh H. Chronic polyradiculoneuropathy associated with human T-cell lymphotropic virus type I infection. J Neurol Neurosurg Psychiatry 1990; 53:358-9. [PMID: 2341854 PMCID: PMC1014182 DOI: 10.1136/jnnp.53.4.358-a] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
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Cohen JA, Wilborn SL, Rector WG, Golitz LE. Mononeuropathy multiplex associated with acute hepatitis B infection. Muscle Nerve 1990; 13:195-8. [PMID: 2157150 DOI: 10.1002/mus.880130304] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]
Abstract
Immunologic syndromes are associated with hepatitis B viral (HBV) infection. However, mononeuropathy multiplex (MM), a syndrome in which immune factors may play a role, is rare in acute HBV infection. Few cases of MM associated with HBV infection have been reported. We report a case of acute HBV infection in which MM involving the median, ulnar and lateral femoral cutaneous nerves complicated the course of the acute illness. Skin biopsy demonstrated vasculitic changes which may accompany the immunologic factors in HBV infection.
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Affiliation(s)
- J A Cohen
- Department of Medicine, Denver General Hospital, CO 80204-4507
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35
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Lin SM, Ryu SJ, Liaw YF. Guillain-Barré syndrome associated with acute delta hepatitis virus superinfection. J Med Virol 1989; 28:144-5. [PMID: 2754426 DOI: 10.1002/jmv.1890280306] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/02/2023]
Abstract
We describe a patient with the clinical characteristics of Guillain-Barré syndrome, including progressive ascending paresis; cerebrospinal fluid albumino-cytological dissociation; polyphasic small evoked potential, with prolonged latency and slow motor nerve conduction velocity; and active denervation pattern on electromyography, in association with acute delta hepatitis virus superinfection. The patient recovered from Guillain-Barré syndrome but developed chronic active delta hepatitis.
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Affiliation(s)
- S M Lin
- Department of Neurology, Chang Gung Memorial Hospital, Taipei, Taiwan
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36
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Abstract
This report describes six cases of chronic alcoholics affected by Guillain-Barré syndrome. The syndrome was the main clinical feature recorded in the patients. The possibility that alcohol abuse may have relevance in the pathogenesis of the Guillain-Barré syndrome is discussed.
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Affiliation(s)
- L Pastena
- Department of Neurology, University La Sapienza, Rome, Italy
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