Published online Apr 6, 2024. doi: 10.12998/wjcc.v12.i10.1766
Peer-review started: September 16, 2023
First decision: December 5, 2023
Revised: December 17, 2023
Accepted: March 18, 2024
Article in press: March 18, 2024
Published online: April 6, 2024
Processing time: 199 Days and 1.8 Hours
Hepatitis B rarely leads to demyelinating neuropathy, despite peripheral neuro
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.
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 asso
Core Tip: We report an exceptional case of demyelinating neuropathy in an individual with hepatitis B virus (HBV) infection, emphasizing the importance for clinicians to consistently take this into account when making a diagnosis. The underlying disease process and mechanisms of peripheral neuropathy following HBV infection are still unknown. The patient's fa
- Citation: Yan XX, Huang J, Lin J. Demyelinating neuropathy in patients with hepatitis B virus: A case report. World J Clin Cases 2024; 12(10): 1766-1771
- URL: https://www.wjgnet.com/2307-8960/full/v12/i10/1766.htm
- DOI: https://dx.doi.org/10.12998/wjcc.v12.i10.1766
In 2015, the World Health Organization estimated that there were approximately 257 million individuals suffering from chronic hepatitis B (CHB), a liver disease characterized by long-term inflammation, due to continuous infection with the hepatitis B virus (HBV)[1]. The Western Pacific and African regions accounted for 68% of these individuals. Approximately 650000 individuals across the globe succumb annually due to CHB-related complications, including cirrhosis and hepatocellular carcinoma[2,3]. Currently, there are around 70 million individuals in China who have contracted HBV, and approximately 20 to 30 million of them are CHB patients[3], which poses a significant burden on both the families of these patients and the society as a whole. Extrahepatic manifestations, such as serum sickness-like syndrome, polyarthritis, polyarteritis nodosa (PAN), glomerulonephritis, cryoglobulinemia, and various neurological disorders, are occasionally observed in addition to the common manifestations of the affected liver, such as icteric hepatitis, ascites, cirrhosis, and liver cancer[4]. In this article, we describe an elderly gentleman who exhibited demyelinating neuropathy as the initial indication of HBV infection. Treatment with antiviral therapy and intravenous immunoglobulin (IVIG) led to a re
A previously healthy 64-year-old man was referred the Department of Neurology at our hospital after presenting with numbness and weakness five months previously.
The patient initially noticed numbness in the lower legs and on the ventral side of the fingertips that gradually progressed upwards to the wrists and ankles on both sides. In addition to numbness, he also experienced soreness and swelling of the muscles. He attended the local hospital for treatment and underwent cervical and lumbar magnetic resonance imaging, which revealed normal cervical and lumbar spine parameters. He was given methyl cobalamin tablets, but this treatment was ineffective. One month ago, he felt weak and was no longer able to walk independently. In the previous week, the patient began to experience nocturnal lower limb twitching, which occurred several times each night.
The patient had no previous medical history.
The patient had no related family history.
During the neurological examination, it was observed that the proximal muscle strength was 4/5 and distal muscle strength was 4/5 in the limbs. Additionally, his muscle tone was low and the bilateral brachial biceps, triceps, knee, and Achilles tendon reflexes were all decreased. The distal limbs showed the greatest decrease in temperature and pain perception, and both lower limbs exhibited a negative Babinski sign. No evidence of altered consciousness, linguistic impairment, or cranial nerve paralysis was present.
Laboratory findings revealed normal routine blood counts, liver function, kidney function, and blood sugar. The level of Vitamin B12 was within the normal range. An increase of 4 mm/h in erythrocyte sedimentation rate was noted. There was no evidence of anti-nuclear, anti-DNA, anti-Ro antibody, anti-La antibody, or anti-neutrophil cytoplasmic antibodies (ANCAs), which include proteinase 3 (PR3)-ANCAs and myeloperoxidase (MPO)-ANCAs, and there were no detectable serum cryoglobulins. Immunoelectrophoretic results were negative. Urine levels were as follows: κ light chain < 7.28 mg/L, λ light chain < 4.00 mg/L, and κ/λ light chain ratio 1.82. Hepatitis B surface antigen (HBsAg), hepatitis B core antibody, and hepatitis B e antibody were positive. Test results for hepatitis B surface antibody (HBsAb) and envelope antigen (HBeAg) were negative. Blood HBV DNA level was 6.14E+02 IU/mL. According to cerebrospinal fluid analysis, white blood cell concentration was 2 × 106/L, red blood cell concentration was 0 × 109/L, glucose concentration was 3.61 mmol/L, and protein concentration was 465.78 mg/L. The patient did not have antibodies against human immunodeficiency virus, rubella virus, Campylobacter jejuni, Treponema pallidum, Epstein-Barr virus, herpes simplex virus, and ganglioside (GD1a, GQ1b, GM1, and GM2).
The patient underwent brain and whole spine magnetic resonance imaging, and no abnormalities were found.
The patient was further evaluated via electroneuromyography, which revealed multiple peripheral neuropathies, suggesting the occurrence of motor and sensory demyelination (Table 1). We suggested that he undergo muscle biopsy for a clear diagnosis, but unfortunately, he refused.
Latency (ms) | Amplitude (mv) | Conduction velocity (m/s) | |
R-Ulnar nerve (m) | |||
Wrist – ADM | 3.65 | 7.3 | |
Bl. elbow – wrist | 9.38 | 6.4 | 33.5 |
Ab. elbow – Bl elbow | 10.7 | 5.9 | 78 |
R-Median (m) | |||
Wrist – APB | 3.92 | 5.2 | |
Elbow – Wrist | 12 | 4.8 | 33.4 |
R-Tibial (m) | |||
Ankle – Abd hal | 5.9 | 4.9 | |
Popliteal fossa – Ankle | 17.1 | 3.0 | 32.9 |
R-Peroneal (m) | |||
Ankle – EDB | 7.22 | 3.3 | |
Bl. Fib. head – Ankle | 18.2 | 2.5 | 24.8 |
Ab. Fib. head - Bl. Fib. head | 20.3 | 2.5 | 45.2 |
R-Ulnar nerve (s) | |||
Wrist – Digit V | 2.15 | 4.7 | 48.8 |
Median (s) | |||
Wrist – Digit II | 2.37 | 18.1 | 48.5 |
Superficial peroneal (s) | |||
Lower leg – Ankle | 2.14 | 6.1 | 51.4 |
Sural (s) | |||
Mid lower leg – Lat alleolus | 2.42 | 6.2 | 42.1 |
Suspected demyelinating neuropathy related to HBV based on the above findings.
Following the diagnosis of demyelinating neuropathy related to hepatitis B, our initial course of action was to administer lamivudine. To prevent persistence and replication of the virus, the IVIG dose of 400 mg/kg was given for 5 d, as corti
The patient’s weakness and numbness improved three weeks after treatment.
Around 20% of individuals infected with HBV display extrahepatic symptoms, with 5% experiencing neurological conditions such as peripheral neuropathy and myopathy[6]. In acute or chronic hepatitis, especially when peripheral nerve damage occurs in the advanced stage, after excluding other causes of peripheral nerve damage caused mainly by demyelination, the remaining conditions are classified as hepatic neuropathy. Chronic hepatitis is accompanied by peripheral neuropathy, and the main manifestations are abnormal sensation, weakness, significant decline or disappearance of the tendon reflex, and muscle atrophy. In addition, unilateral or bilateral nerves may be involved, and sphincter dysfunction and meningeal stimulation signs can also appear. There have been reports of different forms of peripheral neuropathy related to HBV, including Guillain-Barré syndrome; PAN; non-PAN vasculitis neuropathy; and chronic neuropathy syndromes, such as chronic polyneuropathy/polyradiculoneuropathy, mononeuritis multiplex, and chronic relapsing demyelinating polyneuropathy[6]. Distinct clinical and pathogenic variances exist among the various genotypes of HBV, potentially leading to diverse clinical presentations, treatment responses, and long-term prognoses based on the viral genotype/subtype. Clinical variations between subcategories and genetic types at different levels of extrahepatic manifestation are becoming more apparent, as indicated by growing evidence[7]. Guillain–Barré syndrome is the most common peripheral neuropathy associated with this viral disease[8,9]. Other polyneuropathies have been reported in CHB, although they are less common than Guillain–Barré syndrome. Multiple peripheral mononeuropathies are even rarer than previously mentioned[9]. Tsukada et al[10] reported the initial instance of demyelinating poly
Patients infected with HBV display demyelinating neuropathy as described in our patient. The fundamental disease process and functioning of peripheral neuropathy after HBV infection remain unclear. Additionally, the positive effect of immunoglobulin suggests the potential existence of chronic neuropathy triggered by the immune system.
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Specialty type: Neurosciences
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