Deafness After Ethacrynic Acid

Ng, Popov; Conley, C.E.; Ing, Todd S.

doi:10.1016/s0140-6736(69)92032-7

Cited by 28 publications

(6 citation statements)

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“…While several studies have reported permanent hearing loss and cochlear hair cell degeneration after a single diuretic treatment possibly due to autolysis and inadequate fixation ( Ng et al., 1969 , Meriwether et al., 1971 , Quick and Hoppe, 1975 , Rifkin et al., 1978 , Gallagher and Jones, 1979 , Akiyoshi, 1981 , Forge and Brown, 1982 ) the vast majority of published articles indicate that a single systemic administration of loop diuretics to experimental animals only induces temporary pathological damage or edema to the stria vascularis and cochlear lateral wall. The characteristic features include damage to the marginal cells and swelling of both the intermediate cells and intrastrial space.…”

Section: Diuretics-induced Reversible Pathological Damage In the Cochmentioning

confidence: 99%

Ototoxic effects and mechanisms of loop diuretics

Ding

et al. 2016

Journal of Otology

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Over the past two decades considerable progress has been made in understanding the ototoxic effects and mechanisms underlying loop diuretics. As typical representative of loop diuretics ethacrynic acid or furosemide only induces temporary hearing loss, but rarely permanent deafness unless applied in severe acute or chronic renal failure or with other ototoxic drugs. Loop diuretic induce unique pathological changes in the cochlea such as formation of edematous spaces in the epithelium of the stria vascularis, which leads to rapid decrease of the endolymphatic potential and eventual loss of the cochlear microphonic potential, summating potential, and compound action potential. Loop diuretics interfere with strial adenylate cyclase and Na+/K+-ATPase and inhibit the Na-K-2Cl cotransporter in the stria vascularis, however recent reports indicate that one of the earliest effects in vivo is to abolish blood flow in the vessels supplying the lateral wall. Since ethacrynic acid does not damage the stria vascularis in vitro, the changes in Na+/K+-ATPase and Na-K-2Cl seen in vivo may be secondary effects results from strial ischemia and anoxia. Recent observations showing that renin is present in pericytes surrounding stria arterioles suggest that diuretics may induce local vasoconstriction by renin secretion and angiotensin formation. The tight junctions in the blood-cochlea barrier prevent toxic molecules and pathogens from entering cochlea, but when diuretics induce a transient ischemia, the barrier is temporarily disrupted allowing the entry of toxic chemicals or pathogens.

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Section: Diuretics-induced Reversible Pathological Damage In the Cochmentioning

confidence: 99%

Ototoxic effects and mechanisms of loop diuretics

Ding

et al. 2016

Journal of Otology

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“…Acute, transient or irreversible hearing loss can occur after intravenous or oral ethacrynic acid (Maher and Schreiner, 1965;Schneider and Becker, 1966;Pillay et al, 1969;Hanzelik and Peppercorn, 1969;Ng et al, 1969;Matz etal., 1969) -at least 26 cases have been reported. Although initially it was thought that this only occurred after high doses and in renal failure, transitory deafness has been reported after standard (50mg) intravenous doses in 2 non-uraemic patients (Meriwether et al, 1971).…”

Section: Ethacrynic Acidmentioning

confidence: 99%

Diuretics

Davies

Wilson

1975

Drugs

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Despite the bewildering number of diuretics available to the physician, these drugs can be divided into 4 main groups, characterised by their site of action on sodium reabsorption in the kidney. Drugs acting on the ascending limb of the loop of Henle have a powerful but short acting diuretic effect; they include frusemide, ethacrynic acid and bumetanide. The benzothiadiazines and related compounds have a moderate diuretic action spread over a longer period, whilst the potassium-sparing diuretics, triamterene, amiloride and spironolactone, have only a weak diuretic effect but a marked ability to diminish urinary potassium excretion. The fourth group is made up of miscellaneous substances which function as vasodilator or osmotic agents. The pathogenesis of oedema formation in heart failure is outlined and a logical approach to treatment suggested. Duiretics are being increasingly used in the treatment of non-oedematous states, in particular hypertension, diabetes insipidus and hypercalciuria; their exact role in pregnancy and acute renal failure remains controversial. Side-effects can be related to their effect on electrolyte excretion and include hypokalaemia, hyponatraemia, hyperkalaemia and hyperuricaemia. The incidence of disturbed carbohydrate tolerance in previously normal individuals is low. Other less common side-effects are also discussed.

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“…The cascade of changes in the previously mentioned potentials affect the complex potentials that depend on them, causing rapid and significant decreases in amplitude [57]. Early scientific reports on the effects of loop diuretics of furosemide and ethacrynic acid have shown permanent degeneration in cochlear cells after a single administration [58][59][60][61][62][63]. However, subsequent studies with animal models have shown that single administration of loop diuretics causes temporary damage or swelling of the stria vascularis and side-wall of the cochlea.…”

Section: Ototoxicity Of Diureticsmentioning

confidence: 99%

Ototoxicity as a Side-Effect of Drugs: Literature Review

Skarżyńska¹,

Król²,

Czajka³

2020

J Hear Sci

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Background:The first reports of drug ototoxicity were documented in the 1940s. Epidemiological data indicate that changes in audiometric image may affect several percent of patients taking ototoxic drugs. Ototoxicity is manifested by hearing loss and/or changes in the vestibular system. Knowledge of mechanisms responsible for ototoxic effects, as well as important physiological parameters of the human body, may be used as a basis for developing guidelines for the pharmacotherapy. The aim of this paper is to draw attention to the scale and nature of adverse effects of ototoxic drugs. Materials and methods:The review of current literature included the databases PubMed, ResearchGate, GoogleScholar, and ScienceDirect. The studies were reviewed in relation to the inclusion criteria and subsequently evaluated for internal and external validity.Results: According to the literature, pharmacotherapy using drugs with documented ototoxic potential may cause hearing loss and changes in the vestibular system. Depending on the drugs used, changes may be reversible or irreversible. Pathological changes involve hair cells in Corti's organ, stria vascularis, and cochlear potentials. The effect of drugs may cause dysfunction in psychophysical and psychosocial development, especially important for the pediatric population. Conclusion:The ototoxicity of drugs is well known as a cause of cochlear hearing loss. Due to the nature of these substances and their use, more extensive monitoring of adverse reactions should be introduced, including in clinical trial protocols.

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Deafness After Ethacrynic Acid

Cited by 28 publications

References 0 publications

Ototoxic effects and mechanisms of loop diuretics

Ototoxic effects and mechanisms of loop diuretics

Diuretics

Ototoxicity as a Side-Effect of Drugs: Literature Review

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