Reactivation of hepatitis C virus caused by steroid monotherapy for sudden deafness.

Hepatitis C virus (HCV) reactivation has been reported to be caused due to several anticancer drugs and immunosuppressive agents; however, HCV reactivation after steroid monotherapy has rarely been reported. Here, we report the case of a 65-year-old Japanese man with HCV infection who developed HCV reactivation after the administration of prednisolone (PSL) for 6 days for sudden deafness. In the patient history, the positivity for anti-HCV antibody was observed, but serum level of HCV RNA was not measured. Two months after PSL administration, the patient experienced an alanine aminotransferase (ALT) flare and the serum level of HCV RNA was observed to be 6.2 log IU/mL; then, the patient was admitted to our hospital for hepatitis treatment. Based on the clinical course and laboratory findings, the patient was diagnosed with HCV reactivation. Although the ALT levels decreased spontaneously during follow-up, they did not drop to normal range; subsequently, sofosbuvir and ledipasvir treatments were started. A sustained virological response 24 weeks after the end of treatment was achieved. This case study suggests that HCV reactivation with hepatitis flare can occur even after a steroid monotherapy, and doctors should pay attention to HCV reactivation when administering PSL for patients with HCV infection.

Bilateral, Sequential Sudden Hearing Loss in a Patient With Multiple COVID-19 Infections and Potential Implications on Subsequent Cochlear Implant Performance.

Viruses are often implicated as a cause of sensorineural hearing loss (SNHL), particularly sudden cases, including COVID-19. Determining the viral mechanism that leads to hearing loss is necessary for its future prevention and treatment. The 47-year-old woman who is the subject of this case study presented with sudden SNHL following multiple infections of COVID-19. Following a trial of a contralateral routing of sound device, she received a right cochlear implant (CI). Following a period of high performance, additional cases of COVID-19 infection and device failure issues resulted in the explant/reimplant of 1 ear and implantation of the contralateral ear. Despite extensive rehabilitation after these events, the patient continues to experience difficulties in speech understanding, not reaching her initial high levels of right ear performance. Further research is needed to determine the implications of COVID-19 as it relates to SNHL. This case study aimed to highlight the course of treatment and provide insight into the impact of COVID-19 on sudden hearing loss and its relationship to CI performance.

Can isolated sudden sensorineural hearing loss (SSNHL) and idiopathic acute facial paralysis (Bell's palsy) be symptoms of COVID-19?

OBJECTIVES: The symptoms of COVID-19 at the time of presentation mainly include fever, cough, respiratory distress and myalgia. On the other hand, as neurological symptoms, disruption of taste and smell and cerebrovascular pathologies are well-known, whereas other neurological symptoms and signs are being newly recognized. Sudden-onset sensorineural hearing loss (SSNHL) and idiopathic acute facial paralysis (Bell's palsy) are otologic emergencies that are frequently encountered by otorhinolaryngology specialists. Although there are many articles describing SSNHL and Bell's palsy in the literature, the literature describing their relationship to COVID-19 is limited. In our study, we aimed to present the neuro-otologic relationship of SSNHL and Bell's palsy with COVID-19. MATERIAL AND METHODS: The pretreatment real-time oronasopharyngeal PCR tests, COVID-19 symptomatology and COVID-19 infection statuses of patients who presented to our clinic with isolated SSNHL and Bell's palsy between April 2020 and April 2021 were questioned, and the data of the patients were collected. Throughout their treatment, the patients were followed-up in terms of COVID-19 infection. This is a prospective study. Moreover, to observe the change in the incidence, the data of patients visiting between January 2019 and January 2020 were also collected. The data of the patients were statistically analyzed using SPSS. RESULTS: The study included a total of 177 patients. The SSNHL group consisted of 91 patients, and the Bell's palsy group consisted of 86 patients. Neither group showed a statistically significant difference in comparison to the year without the pandemic in terms of the patient numbers (incidence), sex, age, morbidity, response to treatment or social habits. There was a statistically significant difference in age only in the Bell's palsy group, but this difference was not medically significant. CONCLUSION: As a result of our study, we did not observe a relationship between COVID-19 and cases of SSNHL and Bell's palsy. It is recommended to apply standard otologic treatment to isolated SSNHL and Bell's palsy patients whose association with COVID-19 is not determined.

Rised sudden sensorineural hearing loss during COVID-19 widespread.

BACKGROUND: Sudden sensorineural hearing loss (SSNHL) is commonly encountered in otolaryngologic practice. SARS-CoV-2 infection is typically marked by respiratory symptoms although neurologic manifestations of the disease have also been described. OBJECTIVE: We want to measure the incidence and clinical aspects of persons exhibiting in otolaryngology clinic (OC) with SSNHL during the COVID-19 widespread and in the constant interval of previous year. METHODS: We retrospectively inspected the medical information for admissions to OC in Eskisehir, Turkey, during the COVID-19 widespread to describe the patients SSNHL. Clinical knowledge was saved for each subject and corresponded with that of SSNHL subjects demonstrating in 2019. RESULT: Between 1 April and 30 September 2020, 68 patients admitted to OC for SSNHL; in 2019, there were 41 subjects, for an incidence rate ratio of 8.5 per 100.000 (95% CI 1.02-2.92) for the 2020 cohort. Of the 2020 group, forty-one patients (60.3%) presented with active or recent symptoms consistent with COVID-19 infection, compared with four (9.8%) in 2019 (p < 0.001). Furthermore, subjects in 2020 group were younger (-15.5 years, p = 0.0141) than 2019 group and demonstrated prolonged interim (+1.7 days, p < 0.001) between SSNHL initiation and OC petition. CONCLUSION: We detected increased incidence of SSNHL during the COVID-19 widespread compared to the same interval of the prior year; 60.3% of subjects confronting with SSNHL had signs that were harmonious with COVID-19.

Otolaryngological symptoms in COVID-19.

PURPOSE: The aim of this study was to evaluate the frequency of various otolaryngological symptoms in patients with COVID-19 with regard to age, gender and pneumonia-related thorax CT characteristics. METHODS: This is a retrospective study conducted between March 25, 2020 and April 25, 2020. The anamnesis and medical files of 155 patients who applied to our outpatient COVID-19 clinic were evaluated. Patients with positive PCR tests for COVID-19 who were aged between 18-72 years were divided into groups according to the presence of otolaryngological symptoms. The differences between the two groups were examined. RESULTS: Of the 155 patients, 89 (57.4%) had otolaryngological symptoms. The mean age of the patients was 36.3 ± 8.1 years. Ninety-one (58.7%) patients were female, and 64 (42.2%) were male. Fifty-eight (37.4%) patients had received a clinical diagnosis of viral pneumonia with ground glass findings in tomography. The frequency of otolaryngological symptoms was higher in females than males (p: 0.029). The otolaryngological symptoms were also observed to be more frequent in the 18-30 age group (p: 0.013) compared to other age groups. CONCLUSIONS: Tinnitus, gingivitis, sudden hearing loss, Bell's palsy, and hoarseness can be seen in COVID-19, albeit rarely. Revealing the otolaryngological symptoms of COVID-19, and obtaining more information about the extent of disease will be useful in managing patients and their complaints associated with otolaryngology.

Bilateral Sudden Sensorineural Hearing Loss and Intralabyrinthine Hemorrhage in a Patient With COVID-19.

OBJECTIVE: To describe a case of bilateral sudden sensorineural hearing loss (SSNHL) and intralabyrinthine hemorrhage in a patient with COVID-19. STUDY DESIGN: Clinical capsule report. SETTING: Tertiary academic referral center. PATIENT: An adult woman with bilateral SSNHL, aural fullness, and vertigo with documented SARS-CoV-2 infection (IgG serology testing). INTERVENTIONS: High-dose oral prednisone with taper, intratympanic dexamethasone. MAIN OUTCOME MEASURES: Audiometric testing, MRI of the internal auditory canal with and without contrast. RESULTS: A patient presented with bilateral SSNHL, bilateral aural fullness, and vertigo. Serology testing performed several weeks after onset of symptoms was positive for IgG COVID-19 antibodies. MRI showed bilateral intralabyrinthine hemorrhage (left worse than right) and no tumor. The patient was treated with two courses of high-dose oral prednisone with taper and a left intratympanic dexamethasone injection, resulting in near-resolution of vestibular symptoms, a fluctuating sensorineural hearing loss in the right ear, and a severe to profound mixed hearing loss in the left ear. CONCLUSIONS: COVID-19 may have otologic manifestations including sudden SSNHL, aural fullness, vertigo, and intralabyrinthine hemorrhage.

Herpes zoster does not increase the risk of sudden sensory neural hearing loss: a longitudinal follow-up study using a national sample cohort.

Objective: This study aimed to investigate the risk of sudden sensorineural hearing loss (SSNHL) in Herpes zoster patients from a representative population cohort.Design: A longitudinal follow-up studyStudy sample: Data were obtained from the Korean National Health Insurance Service-National Sample Cohort for the period from 2002 to 2013. We matched 61,702 subjects in the Herpes zoster group with subjects in a control group (246,808 subjects with no history of Herpes zoster) based on demographic factors (age, sex, income, and region of residence) and medical history (diabetes, dyslipidemia, and hypertension). The crude (simple) and adjusted hazard ratios (HRs) for Herpes zoster with SSNHL were analysed using the Cox-proportional hazard model.Results: Only 0.5% (338/61,364) of the Herpes zoster group and 0.7% (1664/245,144) of the control group showed SSNHL. The Herpes zoster group did not exhibit a higher rate of SSNHL (adjusted HR = 0.81, 95% CI = 0.72-0.91, p < 0.001) than the control group. In subgroup analyses, no age subgroups showed a significant risk of SSNHL in the Herpes zoster group.Conclusions: After adjusting for confounding factors, the risk of SSNHL did not increase in the Herpes zoster group compared with the control group.

Sudden bilateral sensorineural hearing loss in a patient immunocompromised by the human immunodeficiency virus.

It is known that in less than a third of patients presenting sudden hearing loss, the disorder can be attributed to viral infection, trauma, neoplasms, and vascular and autoimmune diseases. However, the role of the HIV in the onset of this disease has not yet been well described. A 46-year-old female, in an immunosuppression state induced by HIV infection, presented with sudden bilateral hearing loss, with no improvement despite treatment. Several mechanisms were reported by which the virus could induce damage to the auditory pathway. However, little is known regarding the prevention and treatment of this morbidity.

Sudden bilateral sensorineural hearing loss in a patient immunocompromised by the human immunodeficiency virus

Abstract It is known that in less than a third of patients presenting sudden hearing loss, the disorder can be attributed to viral infection, trauma, neoplasms, and vascular and autoimmune diseases. However, the role of the HIV in the onset of this disease has not yet been well described. A 46-year-old female, in an immunosuppression state induced by HIV infection, presented with sudden bilateral hearing loss, with no improvement despite treatment. Several mechanisms were reported by which the virus could induce damage to the auditory pathway. However, little is known regarding the prevention and treatment of this morbidity.

Anti-mumps IgM antibody positive rate with sudden sensorineural hearing loss using second-generation enzyme immunoassay: A retrospective, multi-institutional investigation in Hokkaido, Japan.

OBJECTIVE: Although elevated anti-mumps IgM antibody levels were reported in 5.7%-7.2% of Japanese patients with sudden sensorineural hearing loss (SSNHL), there were several reports of false-positive cases, such as the continually IgM positive case and the IgM positive case in normal adults. To improve specificity, the new enzyme immuno assay (EIA) anti-mumps IgM antibody measurement kit was introduced in December 2009. This study re-examined the frequency of anti-mumps IgM antibody test positivity with SSNHL using the new measurement kit and compared the results with those from a previous report that used old kit. METHODS: This is a retrospective multi-institutional study involving patients diagnosed with SSNHL who exhibited the anti-mumps IgM antibody. We compared the positive rate of anti-mumps IgM antibody and the annual average number of mumps cases per sentinel in Hokkaido between the patients in the present study and patients previously evaluated. RESULTS: Overall, 100 patients with SSNHL were enrolled. One case (1.0%) was positive for anti-mumps IgM antibody. Of the 69 patients evaluated in the previous study, 5 cases (7.2%) were positive for anti-mumps IgM antibody. The positive rate of the anti-mumps IgM antibody in the present cases was significantly lower than that previously reported (p=0.042). The annual average number of mumps cases per sentinel in Hokkaido of the present and previous surveillance period was 34.47 and 42.77, respectively; no significant difference was seen in these data (p=0.4519). CONCLUSION: The present study revealed that 1.0% of SSNHL was positive for the anti-mumps IgM antibody using the new EIA-IgM measurement kit. After the introduction of the new EIA-IgM measurement kit, anti-mumps IgM antibody positive rate with SSNHL significantly decreased, indicating that the proportion of asymptomatic mumps among etiology of SSNHL may be lower than those previously reported.

Idiopathic sudden sensorineural hearing loss: vascular or viral?

OBJECTIVE: To demonstrate that sudden sensorineural hearing loss is possibly of viral origin rather than vascular. STUDY DESIGN: The histopathologic morphology in 7 temporal bones with known vascular impairment due to surgical interventions was compared with that of 11 bones with a history of idiopathic sudden sensorineural hearing loss (ISSNHL). Attention was paid to the spiral ligament, stria vascularis, organ of Corti hair cells, tectorial membrane, ganglion cell population, and degree of perilymph fibrosis and the auditory nerve. SETTING: A temporal bone laboratory that has been in operation for more than 50 years and includes a database consisting of clinical and histopathological information that facilitates quantitative and qualitative analysis. SUBJECTS: Eight hundred forty-nine individuals who pledged their temporal bones for scientific study, of which 18 were selected for this study by means of the database criteria of sudden sensorineural hearing loss and postmiddle fossa and retro sigmoid sinus tumor removal or vestibular nerve section. RESULTS: Sudden sensorineural hearing loss bones exhibited no perilymph fibrosis compared with 6 of 7 vascular cases with fibrosis (P ≤ .001), exhibited less loss of ganglion cells (P ≤ .026), exhibited greater survival of spiral ligament (P ≤ .029), and averaged twice the survival of hair cells and more widespread tectorial membrane abnormalities. CONCLUSION: Analysis of human temporal bones from patients with a sudden sensorineural hearing loss does not support a vascular insufficiency but is more suggestive of a viral etiology.

Detection of serum IgA to HSV1 and its diagnostic role in sudden hearing loss.

A viral etiology of sudden hearing loss has been hypothesized by many authors. HSV1 neurotropism and its involvement in sudden hearing loss has implicated HSV1 as one of the most accredited etiological agents. A non-invasive method such as the titration of HSV1-specific IgA was evaluated to determine the role of HSV1 as a possible cause sudden hearing loss. A prospective study was carried out by titration of serum IgA to HSV1 in 93 patients and in a control group of 50 healthy subjects and 35 subjects suffering from recent herpes labialis reactivation. Statistical analysis of the results disclosed that IgA titers to HSV1 higher than 1:80 are suggestive for the association of HSV1 infection and sudden hearing loss. Moreover, acyclovir therapy was effective in 81% of patients who showed high specific IgA titers. Overall, the titration of specific serum IgA to HSV1 can be a useful tool to determine the viral etiology of certain cases of sudden hearing loss. This method is simple to perform and minimally invasive. It can lead to a rapid presumptive diagnosis and to prompt specific therapy, reducing the need for corticosteroids.

Influenza A (H1N1): a rare cause of deafness in two children.

OBJECTIVE: We report deafness occurring as an extremely rare complication of influenza A caused by the H1N1 virus ('swine flu'), in two children. METHODS: Case reports and review of the literature concerning influenza A (H1N1) and acquired viral infection causing deafness. RESULTS: Two children with normal hearing developed bilateral deafness following influenza A (H1N1). The diagnosis was confirmed using polymerase chain reaction. Both patients were treated with oseltamivir. CONCLUSION: Following a review of the literature, these two patients appear to be the first reported cases of bilateral deafness following influenza A (H1N1).

Recent advances in viral inner ear disorders.

PURPOSE OF REVIEW: To highlight the recent advances in the understanding of the diagnosis and management of viral inner ear disorders. Congenital sensorineural hearing loss (cSNHL), sudden sensorineural hearing loss (SSNHL), Ménière's disease, and vestibular neuritis/viral labyrinthitis are discussed. RECENT FINDINGS: Cytomegalovirus infection during pregnancy is an under-recognized cause of hearing loss and central nervous system disease amongst the general population. Prevention of maternal infection and treatment of affected newborns with ganciclovir are promising interventions. Recent evidence in SSNHL patients has resulted in recommendations against viral serology or the use of antivirals. There appears to be an increased risk of SSNHL in patients with comorbid hypertension and diabetes. The viral hypothesis of Ménière's disease remains unproven. In patients with an acute episode of vestibular neuritis, there is presently not sufficient evidence to support the routine use of corticosteroids or antiviral medications. SUMMARY: cSNHL remains the most clearly defined of the viral inner ear disorders. The evidence for viral involvement in SSNHL, Ménière's disease, and vestibular neuritis is indirect and equivocal. This review highlights the recent advancements in the diagnosis and management of these disorders.

No increased risk of sudden sensorineural hearing loss following recent herpes zoster: a nationwide population-based study.

CONCLUSION: There is no increased risk for sudden sensorineural hearing loss (SSNHL) among people who have experienced a recent herpes zoster attack, compared with a matching population. OBJECTIVE: The pathogenesis of SSNHL remains unknown, but viral infection is considered to be one of the main causes. The objective of this case-cohort study was to investigate the frequency and risk for SSNHL following a recent herpes zoster attack in the general population. METHODS: We extracted 313 612 patients with herpes zoster from a nationwide health registry in Taiwan, and also randomly selected 313 612 matched control subjects. Each participant was individually tracked for 2 months from their index ambulatory care visit to identify those who developed SSNHL. Stratified Cox proportional hazard regressions were conducted to analyze the risk of SSNHL for the sampled patients. RESULTS: Of the sample of 627 224 patients, 121 (0.02%) had SSNHL during the 2-month follow-up period, 59 from the study group (0.02% of the herpes zoster patients) and 62 from the comparison group (0.02% of patients without herpes zoster). Regression analysis revealed no increased adjusted hazard of SSNHL during the 2-month follow-up period for patients with herpes zoster as compared to those without (hazard ratio = 0.89, 95% confidence interval (CI) = 0.63-1.28, p = 0.540).

Etiología viral de la hipoacusia sensorioneural súbita: ¿Mito o realidad? / Viral etiology of sensorineural sudden deafness: myth or reality?

Introducción: La hipoacusia sensorioneural súbita (HSNS), es una causa poco frecuente de hipoacusia. La mayoría son consideradas idiopáticas y sólo en el 10 por ciento-15 por ciento puede descubrirse un factor etiológico. Se han propuesto 4 teorías fisiopatológicas: viral, vascular, inmunológica y por ruptura de membranas. La etiología viral es controversial. Objetivo: Investigar la etiología viral como posible causa de HSNS y evaluar su presencia en relación con el pronóstico de recuperación auditiva. Material y método: Estudio descriptivo observacional de 24 meses, de pacientes con cuadro clínico de HSNS y exámenes compatibles. Previo al tratamiento se tomó hisopado y aspirado nasofaríngeo analizados mediante Microarray. Resultados: Se reclutaron 15 pacientes. En 9 se detectó virus respiratorio sincicial (VRS) y simultáneamente cuatro de ellos además otros virus (bocavirus, herpes VI y VII). No se detectaron casos de virus herpes I y II. No se han evidenciado diferencias en la evolución auditiva en el grupo con muestras positivas para virus. Conclusiones: La etiología viral de HSNS permanece en controversia. El 60 por ciento de los pacientes evaluados resultaron positivos, sin embargo, no hubo ningún virus herpes I ó II en las muestras. El VRS aparece como nuevo agente involucrado, aun cuando se encuentra fuera de temporada habitual.

Introduction: Sudden sensorineural hearing loss (SSHL) is a rare cause of hearing loss. Most are considered idiopathic and only 10-15 percent can discover an etiologic factor. Four pathophysiological theories have been proposed: viral, vascular, immunological and rupture of membranes. The viral etiology is controversial and there are reports with varying results. Aim: To investigate the viral etiology as a cause of HSNS and evaluate their presence in relation to the prognosis of hearing recovery. Material and method: descriptive, observational study of 24 months, patients with symptoms and exams compatible SSHL. Before treatment, nasopharyngeal aspirate was taken and then analyzed using Microarray. Results: Were enrolled 15 patients. In 9 was detected a respiratory syncytial virus (RSV) and four of them simultaneously also other viruses (Bocavirus, Herpes VI and VII). There were no cases of Herpes Virus I and II. There were no evidence differences in auditory development in the group with samples positive for virus. Conclusions: The viral etiology of SSHL remains controversial. 60 percent of patients tested were positive, however, there was no Herpes virus I or II in the samples. RSV appears as a new agent involved, even when was out of regular season.

Sudden sensorineural hearing loss: an autoimmune disease?

OBJECTIVES: To review our current knowledge of the pathogenesis of sudden sensorineural hearing loss, including viral infection, vascular occlusion and immune system-mediated mechanisms, and to discuss the pathogenesis as it relates to pharmacotherapy. SYSTEMATIC REVIEW METHODOLOGY: Relevant publications on the pathogenesis of sudden sensorineural hearing loss from 1944 to 2010 were analysed. RESULTS AND CONCLUSIONS: Sudden sensorineural hearing loss is defined as hearing loss of 30 dB in three sequential frequencies over 3 days or less. It can be an isolated symptom or the presenting symptom of a systemic disease. The aetiology and pathogenesis remain unknown. Detailed investigation typically reveals a specific cause in about 10% of patients. Proposed theories of causation include viral infections, vascular occlusion and immune system-mediated mechanisms. A variety of therapies have been proposed based on the various proposed aetiologies.

Cochlear implantation in a case of bilateral sensorineural hearing loss due to mumps.

It is well known that unilateral profound sensorineural hearing loss is caused by mumps; however, bilateral deafness is rare. Herein we report a case of bilateral profound hearing loss caused by mumps infection in a four-year-old boy. Labyrinthitis due to the mumps virus was suspected. His verbal understanding was poor, and he completely stopped talking. He was soon fitted with a hearing aid, but it proved insufficient. Thereupon, cochlear implantation was performed on his left ear. Six months after the operation, his speech perception and speech production were improved. In cases of bilateral profound hearing loss due to mumps infection conservative therapy is ineffective; therefore, cochlear implantation is recommended. Vaccine coverage for mumps virus is also strongly recommended in Japan.

Do viruses cause inner ear disturbances?

The association of viral infection to inner ear disease is controversial. Experiments on animals show that several viruses are capable of causing hearing loss, if applied into the perilymph. Some of these have specific affinity to the cellular type of the inner ear, as sensory epithelia and cochlear nerve. Some viruses as adenoviruses and Coxsackie virus B have specific CAR receptors that are identified in different cell types, whereas other act by attaching onto nonspecific cellular surface receptors. Some viruses such as varicella zoster virus (VZV) do not cause disease in rodents. We assessed 273 patients with clinical, serological, neuro-otologic and endoscopic evaluations. Of the 273 patients, 43 served as control subjects. The patients either had Ménière's disease (n = 158), recurrent vertigo of unknown etiology (n = 56), or hearing loss (n = 17). Antibodies against neurotropic and common viruses were evaluated. VZV, influenza B, CBV5 and RSV titers were significantly elevated in patients with inner ear disease when compared with the control group. In analyzing the internal relationship, VZV and influenza B were intercorrelated. We did not find a correlation between hearing loss and viral titers. In conclusion, VZV, Coxsackie virus B5 and influenza B virus may be the main causes of inner ear disorder. The spiral and Scarpa's ganglion are potential sites harboring viral DNA for possible latent infection.

Sudden deafness: is it viral?

A number of theories have been proposed to explain the etiopathogenesis of idiopathic sudden sensorineural hearing loss (ISSHL), including viral infection, vascular occlusion, breaks of labyrinthine membranes, immune-mediated mechanisms and abnormal cellular stress responses within the cochlea. In the present paper, we provide a critical review of the viral hypothesis of ISSHL. The evidence reviewed includes published reports of epidemiological and serological studies, clinical observations and results of antiviral therapy, morphological and histopathological studies, as well as results of animal experiments. The published evidence does not satisfy the majority of the Henle-Koch postulates for viral causation of an infectious disease. Possible explanations as to why these postulates remain unfulfilled are reviewed, and future studies that may provide more insight are described. We also discuss other mechanisms that have been postulated to explain ISSHL. Our review indicates that vascular occlusion, labyrinthine membrane breaks and immune-mediated mechanisms are unlikely to be common causes of ISSHL. Finally, we review our recently proposed theory that abnormal cellular stress responses within the cochlea may be responsible for ISSHL.