Acute disseminated encephalomyelitis associated with hepatitis B virus reinfection – Consequence or coincidence?

Lazibat, Ines; Brinar, Vesna

doi:10.1016/j.clineuro.2013.09.018

Cited by 7 publications

(7 citation statements)

References 17 publications

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“…Chronic HBV infection can cause persistent hepatic inflammation and cirrhosis. [14] However, neurologic complications of HBV such as acute disseminated encephalomyelitis (ADEM) [15] and Guillain Barré syndrome have also been noticed, which suggests that periphery disease can affect the brain. [16,17] In addition, HBsAg has been identified in the CSF of patients without active liver disease but with positive HBsAg in serum.…”

Section: Discussionmentioning

confidence: 99%

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Relapsing–remitting lesions in a woman with progressive hemifacial atrophy and chronic hepatitis B virus infection

Zhang

Zhu

et al. 2016

Medicine

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Introduction:Progressive hemifacial atrophy (PHA) is a rare disorder characterized by unilateral facial atrophy affecting the skin, subcutaneous tissue, and fat, muscle, and osteocartilagenous structures creating a sunken hemiface appearance.Etiopathogenesis of PHA is poorly understood; no definitive treatment is currently available.Clinical Findings:We report a 41-year-old woman with PHA who showed an uncharacteristic “relapsing–remitting” evolution of brain lesions and was seropositive for hepatitis B virus (HBV). She presented with a history of recurrent tonic-clonic seizures. Magnetic resonance imaging (MRI) showed progressive atrophy and multiple white matter lesions in the left side of the brain. Interestingly, the serial MRI examination (4 MRI scans over a period of 9 years) showed a “relapsing–remitting” pattern of brain lesions akin to that observed in a subtype of multiple sclerosis. Autoimmune-related investigations revealed increased serum levels of immunoglobulin (Ig) G, anti-nuclear antibody (ANA), and γ-IgG. Infection is considered as one of the possible causes of PHA. However, the association of peripheral infection such as HBV infection with PHA has not been reported.Conclusion:Our experience with this case suggests that PHA may have a relapsing–remitting disease course. Autoimmune inflammatory response to chronic HBV infection may have triggered the relapse in this case. This case underlines a novel etiopathogenetic mechanism of PHA.

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Section: Discussionmentioning

confidence: 99%

“…[19,20] The molecular mimicry between HBV DNA and myelin proteins and the subsequent activation of autoimmune inflammatory cells could constitute the other possible underlying mechanisms of neurological injury in this patient. [15,16] …”

Section: Discussionmentioning

confidence: 99%

Relapsing–remitting lesions in a woman with progressive hemifacial atrophy and chronic hepatitis B virus infection

Zhang

Zhu

et al. 2016

Medicine

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“…[4] HBV infection and vaccination are associated with CNS demyelinating diseases, such as ON, transverse myelitis, acute disseminated encephalomyelitis, and multiple sclerosis. [5][6][7][8] Furthermore, previous studies in the US have investigated the incidence of NMOSD postHBV vaccination. [9] Zhao et al [7] found that patients with NMOSD and concomitant CHB infection exhibited severe manifestations.…”

Section: Introductionmentioning

confidence: 99%

Neuromyelitis optica spectrum disorder with active replication of hepatitis B virus and seropositive anti-aquaporin-4 antibody

Lei

Wang

2021

Medicine

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Rationale: Neuromyelitis optica spectrum disorder (NMOSD) associated with active replication of hepatitis B virus (HBV) is rare. High-dose corticosteroids are the mainstay treatment of NMOSD; however, these may cause reactivation of viral replication in patients with stable HBV which may lead to liver damage. Therefore, care should be placed in corticosteroid use in patients with NMOSD and HBV infection. Patient concerns: Herein, we report the case of a 31-year-old woman with NMOSD and HBV infection who was seropositive for anti-aquaporin-4 antibody. The stable and HBV carrier status of the patient led to the deferment of antiviral and hepatoprotective agents in early treatment. However, liver function impairment was detected during follow-up, with an improvement in the best-corrected visual acuity. Diagnoses: The patient was diagnosed with NMOSD with active replication of HBV and seropositive anti-aquaporin-4 antibody considering the medical history and ancillary examinations. Interventions: To manage NMOSD, intravenous high-dose methylprednisolone (20 mg/kg d) was administered for 5 days which was gradually tapered to oral steroids. However, liver function impairment was observed during follow-up; therefore, anti-HBV drugs (entecavir) and hepatoprotective drugs (bicyclol or polyunsaturated phosphatidylcholine) were administered. Outcomes: A marked improvement was observed in the patient's best-corrected visual acuity after 4 weeks of treatment. However, follow-up examinations revealed liver function damage which necessitated administration of antiviral and hepatoprotective drugs. Liver function normalized after 1 month. Lesson: This case underscores the importance of preventive treatment of liver protection in patients with HBV infection prior to or simultaneous with glucocorticoid therapy and furthermore, there is an urgent need to develop authoritative guidelines regulating corticosteroid use in the treatment of patients with HBV infection.

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“…About 20% of HBV patients develop extrahepatic manifestations [4]. Different studies or case reports showed that HBV infection and vaccination are associated with the onset of CNS demyelinating diseases, such as multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM), optic neuritis (ON), and transverse myelitis (TM) [5][6][7][8][9]. For example, Zhao et al [6] showed that CHB infection may lead to ON worsening [6].…”

Section: Introductionmentioning

confidence: 99%

Comprehensive analysis of patients with neuromyelitis optica spectrum disorder (NMOSD) combined with chronic hepatitis B (CHB) infection and seropositive for anti-aquaporin-4 antibody

Liu

Chen

et al. 2017

Bosn J of Basic Med Sci

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Previous research indicated the association between hepatitis B virus (HBV) infection/vaccination and the onset of demyelinating diseases. However, most of these studies were single case reports, and comprehensive data are still scarce. Here we present a comprehensive analysis of 10 patients with neuromyelitis optica spectrum disorder (NMOSD) combined with chronic hepatitis B (CHB) infection and seropositive for anti-aquaporin-4 antibody (AQP4-Ab). Demographic, clinical, laboratory, neuroimaging, outcome, and follow-up data of the 10 patients were retrospectively analyzed. The median age at the onset of NMOSD was 35 years (range 25-43). Nine patients were female (90%). All patients were positive for HBsAg and had been diagnosed with CHB earlier than with NMOSD. One patient had an autoimmune disease. All patients had normal thyroid function. Paresthesia and visual impairment were the most common clinical symptoms. The cerebrospinal fluid (CSF) parameters (protein and glucose) were normal in 10 cases, whereas slightly higher CSF white blood cell count was detected in 3 patients. The brain and spinal cord magnetic resonance imaging findings were abnormal in 8 patients. All patients were treated with hormone and immunosuppressive therapy, and anti-HBV agents. Patients with detectable serum HBV DNA were more prone to liver damage after receiving high doses of corticosteroids. In 8 patients, the symptoms improved before they were discharged. Two patients with optic neuritis (ON) maintained the symptoms. A month later, 1/8 patient had recurrence of symptoms, and one ON patient progressed to NMO. Overall, the characteristics of NMOSD patients with CHB and seropositive for AQP4-Ab are usually nonspecific. Abnormal liver function test results in NMOSD patients should be a warning of possible CHB infection, and the treatment should be modified accordingly.

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Acute disseminated encephalomyelitis associated with hepatitis B virus reinfection – Consequence or coincidence?

Cited by 7 publications

References 17 publications

Relapsing–remitting lesions in a woman with progressive hemifacial atrophy and chronic hepatitis B virus infection

Relapsing–remitting lesions in a woman with progressive hemifacial atrophy and chronic hepatitis B virus infection

Neuromyelitis optica spectrum disorder with active replication of hepatitis B virus and seropositive anti-aquaporin-4 antibody

Comprehensive analysis of patients with neuromyelitis optica spectrum disorder (NMOSD) combined with chronic hepatitis B (CHB) infection and seropositive for anti-aquaporin-4 antibody

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