Abstract
Background
Atorvastatin is widely prescribed for hyperlipidemia and is generally well tolerated. Auditory adverse effects are rarely reported, and statin-associated sensorineural hearing loss (SNHL) remains poorly characterized.
Case presentation
A 45-year-old Ethiopian woman developed bilateral tinnitus followed by progressive, symmetric bilateral SNHL 3 weeks after starting atorvastatin 40 mg daily. She had no other ototoxic risk factors. Pure-tone audiometry confirmed bilateral moderate SNHL. Given the temporal association and exclusion of alternatives, atorvastatin was discontinued. One week later, audiometry showed improvement to mild hearing loss, and at a 1-month follow-up, thresholds normalized with complete symptom resolution. She was subsequently switched to rosuvastatin 20 mg daily, with no recurrence at a 6-month follow-up.
Conclusion
This case demonstrates that atorvastatin-associated SNHL can be reversible when recognized early. Prompt identification of new auditory symptoms and timely discontinuation of the offending medication may prevent permanent hearing impairment.
Keywords: Atorvastatin, Sensorineural hearing loss, Ototoxicity, Statin adverse effects, Reversible hearing loss, Case report
Highlights
Atorvastatin, a commonly prescribed statin, can cause bilateral sensorineural hearing loss.
This case demonstrates that the hearing loss is reversible if the drug is discontinued early.
Tinnitus was a key accompanying symptom that resolved after cessation.
The temporal relationship (onset 3 weeks after initiation, recovery 1 month after cessation) supports a causal link.
Clinicians should consider statin-induced ototoxicity in patients presenting with new-onset hearing loss.
Background
Sensorineural hearing loss (SNHL) results from damage to the cochlear hair cells or the auditory nerve and is distinct from conductive hearing loss. A variety of factors have been identified as contributors to SNHL, including advancing age, noise exposure, chemical agents, ototoxic medications, trauma, and systemic medical conditions, such as autoimmune diseases and infections [1]. Statins are a class of drugs commonly used for treating hyperlipidemia and preventing heart attack and stroke [2]. HMG-CoA reductase inhibitors, commonly known as statins, are widely prescribed globally for the management of hyperlipidemia to lower blood cholesterol levels and prevent atherosclerotic and ischemic complications [3, 4].
Auditory adverse effects associated with statin therapy are exceedingly rare, with only isolated case reports documented in the literature. Several statins, including atorvastatin, simvastatin, and rosuvastatin, have been sporadically linked to tinnitus and hearing loss, though a clear causal relationship has not been firmly established for most [5]. Atorvastatin, in particular, has been the subject of the few published reports of confirmed sensorineural hearing loss. Tinnitus related to medication use may be overlooked or dismissed by patients, potentially allowing progression to permanent hearing impairment if the offending drug is not stopped in a timely manner. The most frequently reported adverse effects of atorvastatin include joint pain, diarrhea, nasopharyngitis, extremity pain, and urinary tract infections [6]. Documenting reversible cases is critical to raise clinician awareness, facilitate early recognition, and prevent irreversible auditory damage through timely intervention. This case highlights reversible atorvastatin-associated SNHL, emphasizing the importance of early recognition and drug discontinuation to prevent permanent auditory damage.
Case presentation
A 45-year-old Ethiopian woman presented to the otolaryngology clinic with bilateral hearing reduction and tinnitus of 3 weeks’ duration. Hearing loss was gradual in onset, symmetric, and progressive. She denied associated vertigo, otalgia, or otorrhea.
She had a 10-year history of type 2 diabetes mellitus, which was well controlled on metformin 500 mg orally once daily. Six months prior to presentation, she was diagnosed with hyperlipidemia and initiated on atorvastatin 40 mg orally once daily. She had no previous history of hearing impairment, chronic ear disease, significant noise exposure, head trauma, or use of other known ototoxic medications.
Approximately 3 weeks after starting atorvastatin, she began to notice bilateral hearing difficulty, which gradually worsened over time. There was no history of recent upper respiratory tract infection, febrile illness, or other systemic symptoms preceding the onset of hearing loss.
On physical examination, otoscopy revealed clear external auditory canals and intact, normal-appearing tympanic membranes bilaterally. Tuning fork tests demonstrated bilateral Rinne Positive (bone conduction < air conduction) and Weber lateralization to the left. Neurological and vestibular examinations were unremarkable, with no focal deficits.
Pure-tone audiometry demonstrated bilateral moderate sensorineural hearing loss (Fig. 1). Speech discrimination scores were appropriate for the degree of hearing loss. Tympanometry revealed type A curves bilaterally, indicating normal middle ear function.
Fig. 1.
Baseline pure-tone audiogram obtained 3 weeks after atorvastatin initiation, demonstrating bilateral moderate sensorineural hearing loss. A Right ear thresholds; B Left ear thresholds. Key frequencies (250–8000 Hz) show elevation of thresholds to 40–60 dB HL bilaterally, consistent with moderate SNHL
Laboratory investigations showed normal fasting blood glucose levels, as well as normal renal and hepatic function tests. The lipid profile remained abnormal, consistent with her known hyperlipidemia. No metabolic, infectious, or autoimmune abnormalities were identified.
Given the temporal association and exclusion of alternatives, a diagnosis of suspected atorvastatin-induced sensorineural hearing loss was made. Atorvastatin was promptly discontinued in coordination with her primary care physician.
One week after discontinuation, repeat pure-tone audiometry showed improvement of hearing thresholds from moderate to mild bilateral sensorineural hearing loss, and tinnitus had resolved completely (Fig. 2). At the 1-month follow-up, the patient reported complete subjective resolution of hearing symptoms, and repeat audiometry confirmed normalization of bilateral hearing thresholds (Fig. 3). She was subsequently switched to rosuvastatin 20 mg daily, with no recurrence of auditory symptoms at the 6-month follow-up.
Fig. 2.

Pure-tone audiogram obtained 1 week after atorvastatin discontinuation, demonstrating improvement to mild bilateral sensorineural hearing loss. Air-conduction thresholds show improvement of 15–25 dB compared with baseline, with better preservation of low and mid frequencies and mild residual loss predominantly at higher frequencies (4000–8000 Hz)
Fig. 3.

Pure-tone audiogram obtained 1 month after atorvastatin discontinuation, demonstrating normalization of hearing thresholds. All thresholds are within 0–25 dB HL bilaterally across all tested frequencies (250–8000 Hz), confirming complete recovery
Clinical timeline
A chronological summary of the key clinical events is presented in Table 1 to illustrate the temporal relationship between atorvastatin exposure, symptom onset, and recovery following drug discontinuation.
Table 1.
Clinical timeline of events
| Time point | Event | Audiometric finding |
|---|---|---|
| 6 months prior to presentation | Atorvastatin 40 mg daily initiated for hyperlipidemia | Not performed (baseline hearing normal per patient history) |
| 3 weeks after statin initiation | Onset of bilateral tinnitus and progressive hearing loss | Not performed at onset |
| Presentation (3 weeks after symptom onset) | Initial otolaryngology evaluation; atorvastatin discontinued | Figure 1: Bilateral moderate SNHL (thresholds 40–60 dB HL) |
| 1 week after discontinuation | Follow-up visit; tinnitus resolved | Figure 2: Improvement to mild bilateral SNHL (thresholds 25–40 dB HL) |
| 1 month after discontinuation | Follow-up visit; complete subjective resolution | Figure 3: Normalization of bilateral hearing thresholds (0–25 dB HL) |
| 6 months after discontinuation | Final follow-up; no recurrence; switched to rosuvastatin 20 mg daily | Not performed (asymptomatic) |
SNHL: sensorineural hearing loss; dB HL: decibels hearing level
This timeline demonstrates a clear temporal sequence: symptom onset occurred 3 weeks after drug initiation, improvement began within 1 week of discontinuation, and complete recovery was achieved by 1 month. The absence of recurrence at 6 months on an alternative statin further supports the causality.
Discussion
HMG-CoA reductase inhibitors, commonly known as statins, are widely prescribed for the management of hyperlipidemia. They are used globally to lower blood cholesterol levels and to prevent atherosclerotic and ischemic diseases associated with elevated lipid levels [4].
Only a single case report to date has clearly documented atorvastatin-associated sensorineural hearing loss in humans. Liu et al. [6] described a 32-year-old man who developed progressive, bilateral, mid-frequency sensorineural hearing loss after prolonged atorvastatin use (approximately 18 months), which ultimately proved irreversible despite drug discontinuation. In contrast, the present case demonstrates a reversible form of atorvastatin-associated hearing loss, defined as the complete normalization of hearing thresholds on audiometry and resolution of symptoms following drug discontinuation. This complete recovery occurred within 1 month. This difference highlights the potential role of duration of exposure and timing of intervention in determining auditory outcomes and emphasizes the importance of clinician awareness of this rare but clinically significant adverse effect (Table 2).
Table 2.
Published case reports of atorvastatin-associated SNHL
| Author (Year) | Age/sex | Atorvastatin dose | Time to onset | Audiological findings | Outcome after discontinuation |
|---|---|---|---|---|---|
| Liu et al. [6] | 32/Male | 20 mg daily | ~ 18 months | Bilateral mid-frequency (cookie bite) SNHL with tinnitus | Irreversible hearing loss |
| Dari et al. (Current case) | 45/Female | 40 mg daily | 3 weeks | Bilateral moderate SNHL with tinnitus | Complete recovery within 1 month |
Causality assessment
To strengthen the causal inference, the Naranjo adverse drug reaction probability scale was applied. This validated tool assesses the likelihood that a medication caused an adverse event. Our patient scored 7, indicating a probable adverse drug reaction (Table 3).
Table 3.
Naranjo ADR probability scale assessment
| Question | Yes | No | Do Not Know | Score |
|---|---|---|---|---|
| 1. Previous conclusive reports of this reaction? | + 1 | 0 | 0 | + 1 |
| 2. Did the adverse event appear after the suspected drug was administered? | + 2 | − 1 | 0 | + 2 |
| 3. Did the adverse event improve when the drug was discontinued? | + 1 | 0 | 0 | + 1 |
| 4. Did the adverse event reappear when the drug was readministered? | + 2 | − 1 | 0 | 0 (not performed) |
| 5. Are there alternative causes? | − 1 | + 2 | 0 | + 2 |
| 6. Did the reaction appear after placebo was given? | − 1 | + 1 | 0 | 0 |
| 7. Was the drug detected in blood or other fluids at toxic levels? | + 1 | 0 | 0 | 0 |
| 8. Was the reaction more severe with increased dose? | + 1 | 0 | 0 | 0 |
| 9. Had the patient had a similar reaction to the same or similar drugs in the past? | + 1 | 0 | 0 | 0 |
| 10. Was the adverse event confirmed by objective evidence? | + 1 | 0 | 0 | + 1 |
| Total Score | 7 |
Value shown in bold represent patient-specific score assigned for each criterion and contributed to the final Naranjo score of 7, indicating a probable adverse drug reaction
*Scoring: ≥ 9 = definite; 5–8 = probable; 1–4 = possible; ≤ 0 = doubtful
Establishing a causal link between atorvastatin and the patient's hearing loss relies on several key factors. First, there is a strong temporal relationship: symptoms began 3 weeks after initiating atorvastatin and completely resolved 1 month after discontinuation. Second, there were no alternative explanations: the patient had no history of noise exposure, other ototoxic medication use, or recent infections. Her diabetes was well controlled, and laboratory tests ruled out other systemic causes. While a dose–response relationship was not tested, the use of a standard therapeutic dose (40 mg) and the resolution upon cessation support a pharmacologically induced effect.
Differential diagnoses
Differential diagnoses considered included idiopathic sudden sensorineural hearing loss, diabetic cochleopathy, and autoimmune inner ear disease. Idiopathic sudden SNHL was unlikely given the gradual, symmetric progression over 3 weeks rather than acute onset. Diabetic cochleopathy, a known microvascular complication of long-standing diabetes, typically presents as progressive, bilateral, high-frequency hearing loss developing over years, not weeks. Autoimmune inner ear disease was excluded by the absence of fluctuating hearing loss, systemic autoimmune symptoms, and the lack of response to corticosteroids (which were not administered). Furthermore, the rapid and complete reversal upon drug withdrawal strongly supported an ototoxic medication effect rather than an underlying degenerative or autoimmune process.
Proposed mechanisms
The mechanism by which atorvastatin may lead to hearing loss is not fully understood, but impaired prestin function has been proposed as a possible explanation. Prestin is a motor protein in the cochlea that enables outer hair cells to amplify sound by responding to voltage changes across their membranes. Its activity is optimal around − 60 mV, and alterations in membrane cholesterol can shift the local voltage environment, potentially reducing prestin efficiency and leading to diminished hearing [5].
Statins act by blocking the conversion of 3-hydroxy-3-methylglutaryl–coenzyme A to mevalonate, an essential intermediate in LDL cholesterol synthesis [7]. Mevalonate also serves as a precursor for coenzyme Q10 (CoQ10), an important antioxidant and membrane-stabilizing molecule. As a result, statin therapy reduces products of the mevalonate pathway, which may promote mitochondrial dysfunction and apoptotic changes in cochlear neuronal cells [8]. Schulz et al. reported that, in cultured neuronal cells, statins induce neurite loss by disrupting the synthesis of geranylgeranyl pyrophosphate [9]. Inner ear injury results from multiple mechanisms, including vascular impairment, inflammation, oxidative stress, and apoptosis, suggesting that statins could have a therapeutic role in inner ear disorders. However, evidence in humans is limited, and the effectiveness of statins in treating hearing loss related to inner ear damage remains uncertain [10].
Practical implications for clinicians
This case has several practical implications. First, clinicians prescribing atorvastatin should be aware of the potential, though rare, ototoxic adverse effect. Patients who report new-onset tinnitus or hearing loss should undergo prompt audiometric evaluation. Second, if a causal link is suspected, timely discontinuation of the statin (in consultation with the managing physician) is crucial as this case demonstrates that early intervention can lead to complete reversal. Third, for patients with pre-existing hearing loss, a discussion of the risks and benefits may be warranted. Alternatives such as other statins or non-statin lipid-lowering therapies could be considered though the comparative risk of ototoxicity between different statins remains unknown.
Limitations and generalizability
As a single case report, the findings are not generalizable to the broader population. The patient had well-controlled diabetes, which itself is a risk factor for hearing loss, but the acute onset and resolution with drug withdrawal strongly implicate atorvastatin. The absence of a re-challenge, while ethically appropriate, means we cannot definitively prove causality beyond a reasonable doubt; however, the Naranjo score of 7 supports a probable association. Furthermore, the incidence of hearing loss in patients taking atorvastatin compared to other statins or the general population is not established, and large population-based studies have yielded conflicting results [2, 7]. Therefore, the risk–benefit ratio remains favorable for atorvastatin given its proven cardiovascular benefits, but this case highlights the importance of vigilance for rare adverse effects.
Conclusion
This case demonstrates that atorvastatin-associated sensorineural hearing loss, although rare, can be reversible when identified early. The clear temporal relationship between drug initiation, onset of auditory symptoms, and complete recovery after discontinuation supports a likely causal association. Clinicians should be alert to new-onset hearing loss or tinnitus in patients receiving atorvastatin and consider prompt evaluation and medication review. Early recognition and timely withdrawal of the offending agent may prevent progression to permanent hearing impairment, underscoring the importance of awareness of potential ototoxic effects even with commonly prescribed medications.
Acknowledgements
We would like to express our gratitude to the patient for her cooperation and to the clinical staff who supported this case.
Abbreviations
- SNHL
Sensorineural hearing loss
- HMG-CoA
3-Hydroxy-3-methylglutaryl–coenzyme A
- CoQ10
Coenzyme Q10
- ADR
Adverse drug reaction
Author contributions
Dr. Mohammedsefa Arusi Dari and Dr. Sara Abdulkadir Memhur contributed substantially to the conception, design, drafting of the manuscript, and final approval of the version to be published. Dr. Zelalem Tadesse Wondimu and Dr. Nahom Chernet Assefa contributed to data acquisition, interpretation of data, critical revision of the manuscript, and final approval of the version to be published. All authors reviewed and approved the manuscript.
Funding
Not applicable.
Data availability
Supporting data, including anonymized audiometric records, are available from the corresponding author upon reasonable request.
Declarations
Ethics approval and consent to participate
Ethical approval was not required for this single case report. Written informed consent was obtained from the patient for participation and publication. The consent form is held by the corresponding author and is available for review upon request.
Consent for publication
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
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Data Availability Statement
Supporting data, including anonymized audiometric records, are available from the corresponding author upon reasonable request.

