Improvement of Bell’s palsy associated with resolution of acute hepatitis B infection

A 61-year-old man was admitted to the emergency department with facial asymmetry. He had no history of systemic disease or drug usage. Neurologic examination showed no forehead motion, incomplete eye closure and slight mouth movement on the left side. The House– Brackmann score was grade V. General physical examination was normal. Liver tests were abnormal: alanine aminotransferase (ALT) was 888 IU/L, aspartate aminotransferase (AST) 558 IU/L, total bilirubin 1.47 mg/dL, and direct bilirubin 0.59 mg/dL. Because of elevated liver enzymes more than ten times the upper limit of the normal range, serologic markers for viral hepatitis were ordered. The hepatitis B surface antigen (HBs-Ag), hepatitis B e-antigen (HBe-Ag) and hepatitis B core antibody IgM [HBc-Ab (IgM)] were positive, hepatitis B surface antibody (HBs-Ab) negative, hepatitis B virus (HBV)-DNA was 1,748,540 copies/mL. The patient was diagnosed with acute hepatitis B. Because of acute hepatitis B infection, he was followed up without steroid therapy by both gastroenterology and otolaryngology departments. Four months later, control laboratory analysis revealed that ALT was 36 IU/L, AST, 32 IU/L; anti-HBs, positive; Hbs-Ag and HBV-DNA, negative. House–Brackmann scale improved to grade 0. Bell’s palsy is an acute, unilateral, peripheral facial nerve paralysis. Its cause is unknown. Possible etiologies include infections (herpetic, Lyme disease, syphilis, Epstein–Barr viral infection, HIV infection), inflammation, and microvascular disease (diabetes mellitus and hypertension) [1, 2]. HBV is a noncytopathic, hepatotropic virus that settles primarily in liver. It has also been seen to establish persistent infections in many other human organs. Host– virus interactions are involved in viral clearance and disease pathogenesis. Surface antigen–antibody complexes occur during HBV infection, immune complexes also are important in the pathogenesis of extrahepatic manifestations of HBV. These manifestations are characterized by severe damage of blood vessels (for example, polyarteritis nodosa, some forms of chronic glomerulonephritis, and infantile papular acrodermatitis). Neurological disorders including peripheral neuropathy and Guillain–Barre syndrome were also described in the course of HBV infection or after HBV vaccination [3]. There are few reports which suggest an association between cranial nerve paralysis and hepatitis viruses in the literature [2, 4]. Nerve damage due to immune complexes has been blamed for the pathology [1]. In our case, improvement of Bell’s palsy after the achievement of virus clearance supports the association between HBV and immunopathogenesis of the disease. Benefit of steroid therapy in Bell’s palsy has been evidenced [5]. However, steroid treatment may lead to the development of chronic hepatitis in patients with acute hepatitis B infection by suppressing the host immune system. Thus, we did not give the steroid treatment to our patient. Because of growing evidence for the association of Bell’s palsy with viral hepatitis and the adverse effect of steroids on the course of hepatitis, we recommend investigating serologic markers for viral hepatitis, even in the absence of overt liver dysfunction. & Sebahat Basyigit sbuyuktemiz@yahoo.com