PubMed · 14472715
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O J MENZEL. 1961. Quantifying auditory handicaps.. https://pubmed.ncbi.nlm.nih.gov/14472715/
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Cosegregation of markers on chromosome 5q12.3-q14.1 with profound congenital deafness in two Pakistani families (PKDF041 and PKDF141) defines a new recessive deafness locus, DFNB49. A maximum two-point lod score of 4.44 and 5.94 at recombination fraction theta=0 was obtained for markers D5S2055 and D5S424 in families PKDF041 and PKDF141, respectively. Haplotype analysis revealed an 11 cM linkage region flanked by markers D5S647 (74.07 cM) and D5S1501 (85.25 cM). Candidate deafness genes in this region include SLC30A5, OCLN, GTF2H2, and BTF3, encoding solute carrier family 30 (zinc transporter) member 5, occludin, RNA polymerase II transcription initiation factor, and basic transcription factor 3, respectively. Sequence analysis of the coding exons of SLC30A5 in DNA samples from two affected individuals of families PKDF041 and PKDF141 revealed no mutation. The mapping of DFNB49 further confirms the heterogeneity underlying autosomal recessive forms of nonsyndromic deafness.
A 52-year-old Korean woman who complained of impaired hearing and tinnitus of the left ear was diagnosed with an aberrant internal carotid artery (ICA) in the middle ear using a temporal bone high resolution CT (HRCT) scan. Upon otoscopic examination, her left eardrum was found to be in contact with a mass in the middle ear cavity. Upon audiometric evaluation, a mild conductive hearing impairment was documented, and a discrepancy in the results of otoacoustic emissions (OAEs) was found for the left ear. This case report studies the aberrant ICA in the middle ear that revealed abnormal OAE findings.
BACKGROUND: Our objectives were to describe the frequency and determine risk factors for hearing deterioration following pediatric stem cell transplantation (SCT). METHODS: In this prospective cohort study, we performed pure tone audiometry and measured otoacoustic emissions (OAE) prior to and following SCT. Worse hearing was considered deterioration in either audiometry or OAE. RESULTS: Between October 2000 and November 2002, 45 informative audiometry or OAE results were obtained. Hearing deteriorated following SCT in 20/45 (44%) of these children. Those with worse hearing following SCT were more likely to have neuroblastoma (odds ratio [OR] 16.0 [95% CI 1.8, 143.2; P = 0.003]), receive carboplatin conditioning (OR 7.7 [95% CI 1.4, 41.9; P = 0.01]), have abnormal baseline hearing (OR 5.1 [95% CI 1.3, 19.5; P = 0.02]), and have higher baseline serum creatinine (OR for every increase of 5 micromol/L of serum creatinine of 1.5 [95% CI 1.03, 2.1; P = 0.03]). CONCLUSION: Many children who undergo SCT will have deterioration in hearing following SCT. A high-risk group of children can be delineated who may benefit from more intensive audiological monitoring following SCT.