Evidence map›Paper›PMID 42683731›Full record

ArticleThe South African journal of communication disorders = Die Suid-Afrikaanse tydskrif vir Kommunikasieafwykings2026

Genetic susceptibility to aminoglycoside cochleotoxicity in South African multidrug-resistant and rifampicin-resistant tuberculosis patients.

Nazanin Ghafari, Lebogang Ramma, Richard Court, Noluthando Manyisa, Helen McIlleron, Lucretia Petersen

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In one paragraph

Article in The South African journal of communication disorders = Die Suid-Afrikaanse tydskrif vir Kommunikasieafwykings, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Nazanin GhafariDepartment of Health and Rehabilitation Sciences, Faculty of Health Sciences, University of Cape Town, Cape Town. nazanin.ghafari@uct.ac.za.
Lebogang Ramma
Richard Court
Noluthando Manyisa
Helen McIlleron
Lucretia Petersen

Funding

Pharmacometric optimization of second line drugs for MDR tuberculosis treatmentR01AI116155 · NIAID · UNIVERSITY OF CAPE TOWN · PI GUMBO, TAWANDA, MCILLERON, HELEN · 2015 to 2019
$1.7M
NIAID NIH HHS R01 AI116155
6 · The paper itself

Abstract

backgroundSouth Africa has a high burden of multidrug-resistant tuberculosis (MDR-TB) and rifampicin-resistant tuberculosis (RR-TB). At the time of this study, kanamycin formed part of the South African MDR/RR-TB treatment regimen. Although treatment has shifted towards shorter all-oral regimens, aminoglycoside-related ototoxicity remains clinically relevant.

objectivesThis study investigated the association between two mitochondrial variants, m.15312TC (I189T in MT-CYB [mitochondrially encoded cytochrome b]) and m.10114TC (I19T in MT-ND3 [mitochondrially encoded NADH]), and susceptibility to cochleotoxicity in South African patients receiving kanamycin-based MDR/RR-TB treatment.

methodA prospective cohort study was conducted in Cape Town, South Africa. Hearing thresholds from 0.25 kHz to 16 kHz were monitored at baseline and at 4 weeks, 8 weeks and 12 weeks after treatment initiation. Cochleotoxicity was defined using the American Speech-Language-Hearing Association's significant threshold shift criteria. Mitochondrial variants were identified using polymerase chain reaction and Sanger sequencing. Fisher's exact tests were used to explore associations between variants and cochleotoxicity.

resultsHearing data were analysed for 102 participants. Cochleotoxicity developed in 84 participants (82.4%). The m.15312TC variant was detected in three of 78 successfully sequenced participants, and m.10114TC in four of 80. All variant carriers had cochleotoxicity. Statistically significant associations were not demonstrated for m.15312TC (p = 1.000) or m.10114TC (p = 1.000).

conclusionThe variants were observed only among participants who developed cochleotoxicity, but no statistically significant associations were observed. The findings are exploratory and require validation before clinical screening.Contribution: This study supports future genetic-susceptibility research in African aminoglycoside-exposed populations.

Indexed as

AminoglycosidesAntitubercular AgentsKanamycinOtotoxicityTuberculosis, Multidrug-ResistantAdultFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedProspective StudiesRifampinSouth AfricaAminoglycosidesAntitubercular AgentsKanamycinRifampinaminoglycosidescochleotoxicitykanamycinmitochondrial variantsmultidrug-resistant tuberculosisototoxicityrifampicin-resistant tuberculosisultra-high-frequency audiometry

Identifiers

PMID42683731
PMCPMC13543263

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.