Ototoxicity of Ethacrynic Acid: Demonstrated in a Human Temporal Bone

Matz, Gregory J.; Beal, David D.; Krames, Lawrence

doi:10.1001/archotol.1969.00770030154011

Cited by 59 publications

(9 citation statements)

References 3 publications

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“…This is consistent with previous reports of human pathological changes in loop diuretic ototoxicity. Human temporal bone studies of ethacrynic acid ototoxicity have demonstrated edema in the stria vascularis, loss of outer hair cells and cystic changes in the ampullae of the posterior canal and saccule . Arnold et al observed cystic dilations in the stria vascularis and dark cells of the vestibular system in patients with sudden hearing loss and ataxia after furosemide and ethacrynic acid administration .…”

Section: Discussionmentioning

confidence: 99%

“…In human temporal bone studies, cystic changes in the stria vascularis and dark cells of the vestibular organs, and loss of inner and outer hair cells have been observed in cases of ethacrynic acid and ethacrynic acid with concurrent furosemide exposure . Animal studies of furosemide otoxicity have also demonstrated pathological change in the stria vascularis …”

Section: Introductionmentioning

confidence: 99%

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Temporal bone histopathology of furosemide ototoxicity

Santos

Nadol

2017

Laryngoscope Investig Oto

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ObjectivesTo describe the human temporal bone pathology in two patients who incurred furosemide induced ototoxicity.Patients1) A 46‐year‐old woman in acute liver and renal failure treated with high doses of furosemide for anasarca who developed a rapidly progressive severe‐to‐profound asymmetric sensorineural hearing loss. 2) A 65‐year‐old woman with undifferentiated small cell carcinoma of the lung who received intravenous furosemide 1 day prior to death for pulmonary edema.InterventionsRemoval of temporal bones, histologic processing, and light microscopy of temporal bones.Main Outcome MeasuresTemporal bone histopathology and correlation with clinical and audiometric data.ResultsAll three temporal bones demonstrated edema and cystic changes in the stria vascularis. In the first case the furosemide exposure was associated with hearing loss and the pathological changes were more extensive including cystic changes in the Hensen's cells, collapse of Reissner's membrane and the tectorial membrane and diffuse loss of inner and outer hair cells with only modest reduction in the spiral ganglion cell population. In the second case, without attributable hearing loss, there was only modest reduction in hair cell and spiral ganglion cell counts. Pathological changes were not observed in the ampullae of the semicircular canals or epithelium of the saccular or utricular maculae in either case.ConclusionsThe temporal bone pathologic correlate for furosemide‐induced ototoxicity is edema and cystic degeneration of the stria vascularis. The degree of degenerative change appears dose‐dependent. We infer that pathological changes may occur in the absence of a measurable immediate clinical effect.Level of EvidenceNA.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Temporal bone histopathology of furosemide ototoxicity

Santos

Nadol

2017

Laryngoscope Investig Oto

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“…well established for several years, and its toxic effect on human and animal subjects has been documented by numerous studies (1)(2)(3)(4)(5)(6)(7)(8). The recommended therapeutic dose is 1 mg/kg of body weight.…”

Section: Dichloro-4-(2-methylenebutyryl)-phenoxy]acetic Acid Has Beenmentioning

confidence: 99%

Ethacrynic Acid EFFECTS ON THE COCHLEAR POTENTIALS IN NORMAL AND HIGH BLOOD OXYGEN

Prazma¹,

Pecorak²

1975

J. Clin. Invest.

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(Po2), the partial pressure of carbon dioxide (Pco2), and the pH of the blood were measured before EA administration and at the end of the experiment (3 h later) by drawing blood samples from the contralateral carotid artery. Cochlear potentials-endocochlear potential (EP), cochlear microphonics (CM), and action potentials (AP)-were recorded by standard methods from the first turn of the cochlea. Experimental data seem to indicate that elevation of the Po2 to 174-179 mm Hg during relatively high doses of EA treatment prevents the declines in cochlear potentials which were observed in the first and second groups (normal and lower Po.), and preserves active ion transport which is responsible for the generation of cochlear potentials. These data suggest a means by which to reduce the ototoxic effect of EA and possibly indicates a method of treatment for hearing loss which developed after the administration of EA.

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“…Because of the reduced excretion of the drug, the hearing loss occurs in patients with hepatic or renal impairment. Ethacrynic acid has produced a reversible hearing loss in the presence of chronic liver disease (39) and permanent deafness in the presence of both cirrhosis and renal failure (40). In the presence of uremia, the hearing loss is acute in onset, usually transient (41,42,43), and can be initiated by normal oral dosage of the drug (41), although usually large intravenous doses were used.…”

Section: Drug-induced Ototoxicitymentioning

confidence: 99%