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Increased risk of sudden sensorineural hearing loss in patients with hepatitis virus infection

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ABSTRACT

The etiology of sudden sensorineural hearing loss (SSNHL) remains unclear. Possible causes of SSNHL include vascular diseases, viral infection, and autoimmune disorders. Therefore, we investigated whether hepatitis virus infection is correlated with the risk of SSNHL. Using data from the Taiwan Longitudinal Health Insurance Database, we conducted a retrospective matched-cohort study to compare patients diagnosed with hepatitis B or C virus (HBV/HCV) infections from January 1, 2000, to December 31, 2010, (N = 170,942) with frequency-matched controls (N = 512,826) at a ratio of 1:3 by sex, age, and index year. We followed each patient until the end of 2010 and evaluated the incidence of SSNHL. At the end of the follow-up period, 647 (0.38%, 647/170,942) patients developed SSNHL in the HBV/HCV group compared with 978 (0.19%, 978/512,826) in the control groups, with a statistical significance of P < 0.001 (using the log-rank test). The incidence rate ratio of SSNHL was 5.743-fold higher in the HBV/HCV group than in the control group (283.17 vs. 49.31 per 100,000 person-years, P < 0.001). The risk of SSNHL increased with HBV/HCV infection, and an adjusted hazard ratio of 5.103 (95% CI, 4.585–5.678) was determined using Cox proportional hazards regression. This study contributes to the awareness of the increased risk of SSNHL in HBV/HCV-infected populations. Our findings suggest that an underlying viral infection contributes to the development of SSNHL.

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Kaplan–Meier curves for the cumulative risk of SSNHL among patients aged ≥20 years with HBV/HCV infection (stratified by HBV or HCV alone, using the log-rank test).
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pone.0175266.g002: Kaplan–Meier curves for the cumulative risk of SSNHL among patients aged ≥20 years with HBV/HCV infection (stratified by HBV or HCV alone, using the log-rank test).

Mentions: The cumulative incidence curve for SSNHL in the total HBV/HCV infection cohort was significantly higher than that for the comparison cohort, after adjustment for age, sex, and comorbidities (Fig 2, log-rank test; P < 0.001). In the patients with HBV/HCV infections, the risk of SSNHL increased progressively with the duration of follow-up, rather than with being limited to the immediate days after a diagnosis of HBV/HCV infection. In the subgroups of HBV and HCV infection, the same trend was independently revealed (Fig 2).


Increased risk of sudden sensorineural hearing loss in patients with hepatitis virus infection
Kaplan–Meier curves for the cumulative risk of SSNHL among patients aged ≥20 years with HBV/HCV infection (stratified by HBV or HCV alone, using the log-rank test).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5383281&req=5

pone.0175266.g002: Kaplan–Meier curves for the cumulative risk of SSNHL among patients aged ≥20 years with HBV/HCV infection (stratified by HBV or HCV alone, using the log-rank test).
Mentions: The cumulative incidence curve for SSNHL in the total HBV/HCV infection cohort was significantly higher than that for the comparison cohort, after adjustment for age, sex, and comorbidities (Fig 2, log-rank test; P < 0.001). In the patients with HBV/HCV infections, the risk of SSNHL increased progressively with the duration of follow-up, rather than with being limited to the immediate days after a diagnosis of HBV/HCV infection. In the subgroups of HBV and HCV infection, the same trend was independently revealed (Fig 2).

View Article: PubMed Central - PubMed

ABSTRACT

The etiology of sudden sensorineural hearing loss (SSNHL) remains unclear. Possible causes of SSNHL include vascular diseases, viral infection, and autoimmune disorders. Therefore, we investigated whether hepatitis virus infection is correlated with the risk of SSNHL. Using data from the Taiwan Longitudinal Health Insurance Database, we conducted a retrospective matched-cohort study to compare patients diagnosed with hepatitis B or C virus (HBV/HCV) infections from January 1, 2000, to December 31, 2010, (N = 170,942) with frequency-matched controls (N = 512,826) at a ratio of 1:3 by sex, age, and index year. We followed each patient until the end of 2010 and evaluated the incidence of SSNHL. At the end of the follow-up period, 647 (0.38%, 647/170,942) patients developed SSNHL in the HBV/HCV group compared with 978 (0.19%, 978/512,826) in the control groups, with a statistical significance of P &lt; 0.001 (using the log-rank test). The incidence rate ratio of SSNHL was 5.743-fold higher in the HBV/HCV group than in the control group (283.17 vs. 49.31 per 100,000 person-years, P &lt; 0.001). The risk of SSNHL increased with HBV/HCV infection, and an adjusted hazard ratio of 5.103 (95% CI, 4.585&ndash;5.678) was determined using Cox proportional hazards regression. This study contributes to the awareness of the increased risk of SSNHL in HBV/HCV-infected populations. Our findings suggest that an underlying viral infection contributes to the development of SSNHL.

No MeSH data available.


Related in: MedlinePlus