Effects of NSAIDs on the Inner Ear: Possible Involvement in Cochlear Protection

Hoshino, Tetsuya; Tabuchi, Keiji; Hara, Akira

doi:10.3390/ph3051286

Cited by 22 publications

(24 citation statements)

References 75 publications

(87 reference statements)

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“…Non‐steroidal anti‐inflammatory drugs (NSAIDs) form the mainstay of treatment in AS and spondyloarthritis. NSAIDs have been shown to be both ototoxic and protective for cochlear injury . Since patients usually have high intake of NSAIDs, we postulated that NSAIDs could be the cause of the observed sensory neural HL.…”

Section: Introductionmentioning

confidence: 94%

Hearing loss in ankylosing spondylitis

et al. 2019

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Aim: Several studies have described sensorineural deafness in ankylosing spondylitis (AS) patients while conductive hearing loss has been reported to be rare. In our study we have studied the prevalence of hearing loss (HL) among AS patients and its association with non-steroidal anti-inflammatory drug (NSAID) intake. Methods:We studied 100 AS patients and 40 controls. HL was defined as pure-tone thresholds greater than 20 dB (decibel) in at least two frequencies of the audiogram.Severity of HL was defined as given by World Health Organization. Clinical details and cumulative NSAID doses were noted.Results: Ninety-six of the 100 patients were male with mean age of 32 ± 12 years and mean duration of illness of 8.2 ± 6 years. Median Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI), Bath Ankylosing Spondylitis Metrology Index (BASMI) and cumulative NSAID dose were 3.5 ± 2.2, 2.75 ± 2, 3.7 ± 2.6 and 1202 ± 1290, respectively. Of the 48 with HL, 28 patients had bilateral HL. Twenty-nine patients had pure conductive HL while 16 had mixed HL (components of both sensory and conductive) and 3 had pure sensorineural HL. HL was mild in 38 patients, and moderate to severe in 10 patients. The presence of HL was associated with higher age (P ≤ 0.05). Conductive HL was at low frequency (0.25, 0.5, 1 kHz) in 70% of cases. Sensorineural HL was at high frequency (4, 8 kHz) in 75% of cases. There was no association of HL with disease parameters such as BASMI, BASDI, BASFI or cumulative NSAID dose.Conclusion: HL is common in AS. Conductive HL is more common than sensorineural HL. It is usually mild and occurs at low frequencies. K E Y W O R D Sanalgesics, ankylosing spondylitis, NSAIDs

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Section: Introductionmentioning

confidence: 94%

Hearing loss in ankylosing spondylitis

et al. 2019

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“…Although these agents are often useful to treat infectious or neoplastic lesions and to alleviate the patients' symptoms, their incorrect usage may cause serious problems. Those included are gastric mucosal injury, renal function impairment, allergic reactions, ototoxicity, and cardio-vascular complications [78]. Regarding ototoxicity induced by NSAIDs, tinnitus is often the first subjective symptom, and mild to moderate hearing loss, usually reversible, subsequently tends to occur.…”

Section: Nsaidsmentioning

confidence: 99%

“…Based on recent evidence from both evoked potentials and neuron-pair synchrony measures, it is unlikely that tinnitus is the expression of a set of independently firing neurons, and is more likely the result of a pathologically increased synchrony between sets of neurons [103]. Thus, in addition to the impairment of outer hair cells, changes in the excitability of auditory peripheral or central neurons may be the cause of the otological side effects of salicylate [78].…”

Section: Mechanism Of Nsaid Ototoxicitymentioning

confidence: 99%

Ototoxicity: Mechanisms of Cochlear Impairment and its Prevention

Tabuchi¹,

Nishimura²,

Nakamagoe³

et al. 2011

CMC

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Aminoglycosides, cisplatin, and non-steroidal anti-inflammatory drugs (NSAIDs) are widely used pharmacological agents. There is a possibility, however, that the use of these agents may induce transient or permanent hearing loss and tinnitus as side effects. Recent animal studies have clarified mechanisms leading to the ototoxicity induced by these agents, at least in part. The permanent hearing loss caused by aminoglycosides and cisplatin is suggested to be predominantly associated with the apoptotic death of outer hair cells. Both drugs generate reactive oxygen species (ROS) in the inner ear. ROS can activate cell-death pathways such as the c-Jun Nterminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) pathways, which in turn, induce hair cell apoptosis. On the other hand, the abuse of NSAIDs may transiently cause tinnitus and mild to moderate hearing loss. NSAIDs impair the active process of the outer hair cells and affect peripheral and central auditory neurons. Conversely, recent reports clarified that NSAIDs are potential therapeutic agents against cochlear injuries. In this review, recent findings from animal studies regarding the ototoxicity induced by aminoglycosides, cisplatin, and NSAIDs are summarized. Their ototoxic mechanisms are focused on.

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“…In general, the mechanism is thought to be an idiosyncratic reaction (immunologic or metabolic) rather than an intrinsic toxicity of the agent. Although hepatotoxicity has been attributed to the entire therapeutic class of NSAIDs, the rates and types of injury often vary within and between chemical classes [54]. We thought that the mild hepatic histological lesion which represented by central VC, perivascular lymphocytic infiltration with necrosis of hepatocyte cords in G 3 mice (exposed to meloxicam) is not enough to being hepatotoxic.…”

Section: Al-rekabimentioning

confidence: 99%

Chronic Interaction Between Metformin and Meloxicam in Mice

Al-Rekabi

2019

Asian J Pharm Clin Res

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Objective: This study is performed for investigation the chronic interaction between metformin and meloxicam from toxicological view. Methods: Lethal dose 50 after chronic exposure assessed in mice by up and down method. Their interaction analyzed by isobolographic analysis indicated that both medicines exhibited synergism. Assessment of the effects of repeated chronic dosing for 3 months of both medicines also performed on mice. Medicines in question administered orally as therapeutic doses of metformin 14 mg/kg. Body weight (BW) (G1), meloxicam 0.2 mg/kg.BW (G2), and combination of both medicines (G3) while G4 assigned control and dosed DW. Results: Both G1 and G3 showed significant p˂0.05 decrease in blood glucose and serum cholesterol levels. Meloxicam group (G3) showed statistically significant p˂0.05 increase in triglycerides and alanine aminotransferase (ALT), and aspartate aminotransferase (AST), while group of combination showed statistically significant p≤0.05 decrease in both ALT and AST. Blood urea nitrogen, uric acid, and serum creatinine showed statistically significant p˂0.05 increase in group of meloxicam but decrease in G3 and no changes in G1. Histopathological changes included variable lesions in kidney such as swelling and necrosis in renal tubules of metformin group, cortical vacuolar degeneration in renal tubules, and deterioration of most glomeruli in G2, while G3 showed generalized cortical necrosis of renal tubules and interstitial nephritis. Liver lesions included central venous congestion (VC) and perivascular lymphocytic infiltration and marked necrosis in both groups of metformin and meloxicam, while there were severe VC and necrosis of hepatocytes in group of combination. Conclusion: Metformin administration with meloxicam may have beneficial important through preventing many deleterious effects of meloxicam after long-standing administration, but adjusting dosing regimen study might be recommended.

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Effects of NSAIDs on the Inner Ear: Possible Involvement in Cochlear Protection

Cited by 22 publications

References 75 publications

Hearing loss in ankylosing spondylitis

Hearing loss in ankylosing spondylitis

Ototoxicity: Mechanisms of Cochlear Impairment and its Prevention

Chronic Interaction Between Metformin and Meloxicam in Mice

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