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Shannon P. Pryor, MD; Gail J. Demmler, MD; Anne C. Madeo, MS; Yandan Yang, PhD; Chris K. Zalewski, MA; Carmen C. Brewer, PhD; John A. Butman, MD, PhD; Karen B. Fowler, DrPH; Andrew J. Griffith, MD, PhD

Arch Otolaryngol Head Neck Surg. 2005;131:388-392.

Objective  To determine whether congenital cytomegalovirus (CMV) infection is an etiologic factor in the pathogenesis of enlarged vestibular aqueducts (EVA).

Design  Two different cohort studies.

Subjects  The study population comprised 19 subjects with a history of congenital CMV infection and sensorineural hearing loss (cohort 1); 39 subjects with nonsyndromic EVA and their unaffected mothers (cohort 2); and 16 control subjects with EVA associated with Pendred syndrome and bi-allelic mutations of the SLC26A4 gene and their unaffected mothers.

Results  In cohort 1, we detected EVA in 0 of 19 subjects with congenital CMV infection and sensorineural hearing loss. In cohort 2, anti-CMV serologic profiles were consistent with possible congenital CMV infection in 10 (26%) of 39 subjects with nonsyndromic EVA and 6 (38%) of 16 control subjects with Pendred syndrome (P = .52). These seroprevalence rates are similar to those expected in the general population (40%).

Conclusion  In spite of their auditory phenotypic similarities, congenital CMV infection is not a significant factor in the etiology of EVA.

Author Affiliations: Hearing Section (Drs Pryor, Brewer, and Griffith, Ms Madeo, and Mr Zalewski), Section on Gene Structure and Function (Drs Yang and Griffith), and Office of the Clinical Director (Dr Pryor), National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Md; Department of Pediatrics, Baylor College of Medicine, Houston, Tex (Dr Demmler); Diagnostic Radiology Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda (Dr Butman); and Departments of Pediatrics, Epidemiology, and Maternal and Child Health, University of Alabama at Birmingham (Dr Fowler).

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