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• W2020182606 abstract "Neurological and sensorineural side effects from tacrolimus (TAC) and Cyclosporine A (CsA) are well documented. Hearing impairment from calcineurin inhibitors has been reported in both adult and pediatric liver transplant (LT) patients. Acute onset of hearing loss is seldom reported. A 61-year-old male patient underwent LT for end-stage liver disease related to hepatitis C virus with hepatocellular carcinoma. Ten weeks after liver transplant, the patient presented with tinnitus and acute onset of bilateral hearing loss confirmed with audiogram. Evaluation of the patient excluded infectious etiologies or drug toxicity other than TAC. Although serum TAC levels were therapeutic, TAC was discontinued and the patient's hearing loss recovered. Audiogram testing confirmed these findings. Calcineurin inhibitors (CI) currently constitute the primary immunosuppressant agents for transplant recipients. Tacrolimus (TAC), the most widely prescribed CI in liver transplant (LT) patients, appears to be associated with a higher incidence of neurotoxicity than Cyclosporine A (CsA) [1, 2]. Neurological disorders are among the most common symptoms in liver recipients, which commonly cause encephalopathy and peripheral neuropathy [3-6]. Calcineurin-associated ototoxicity has been reported in other organ transplant recipients and in most reported cases of hearing impairment, an association is found with high serum levels of CIs [7, 8]. In contrast to progressive slow hearing impairment, acute onset of profound hearing loss is rare [9, 10]. Synergistic ototoxicity with CI and antibiotics such as aminoglycosides, glycopeptides, erythromycin and diuretics must be considered, in particular in children [11, 12]. We report on an adult liver recipient who experienced CI-associated acute onset of bilateral hearing loss 10 weeks post-transplant, without other exacerbating factors and despite TAC level being within therapeutic range. A 61-year-old male underwent LT in July 2004 for end-stage liver disease related to hepatitis C virus and hepatocellular carcinoma. The patient had a history of depression, which was treated with bupropion (Wellbutrin SR) pre- and post-LT. Immunosuppression consisted of TAC twice daily, mycophenol mofetil (MMF) 1 g b.i.d., and corticosteroids. When TAC was therapeutic (serum trough levels of 8–12 ng/ml), MMF was discontinued per protocol for hepatocellular carcinoma, and corticosteroids were tapered off over the first 4 months following LT. The early post-transplant course was complicated by a biliary stricture that required stent placement, with eventual resolution of stricture. The patient was discharged from postoperative outpatient clinic at day 22 without significant clinical issues. After 10 weeks LT, the patient complained of new onset of symptoms of increased tremors, dizziness, light-headedness, tinnitus and decreased hearing. The patient described confused thinking, and recent loss of short-term memory. He denied headache or vertigo symptoms. There was no history of ear, nose or throat disorders and he denied fevers, otalgia, nor did he present with other signs of infection elsewhere. There was no exposure to over-the-counter drugs or any new medications. Both external auditory canals showed no abnormalities. Romberg sign was negative. At the onset of his symptoms, the serum TAC level was 10.9 ng/ml. Other laboratory tests results were within normal ranges with transaminases mildly elevated because of early recurrence of hepatitis C. Magnetic resonance imaging (MRI) of the brain showed mild cerebral/cerebella atrophy and small vessel disease, and no other specific abnormalities were reported. Transplant psychiatry prescribed lorazepam (Ativan, Biovail Pharmaceuticals Inc., NJ, USA), discontinued Wellbutrin and prescribed escitalopram (Lexapro, Forest Pharmaceuticals, MO, USA) for worsening of his depression and increasing anxiety. After 12 weeks LT, the patient was noted to have worsening of tremors, stuttering speech pattern, and profound hearing loss. Serum TAC level was 10.8 ng/ml. The ear, nose and throat (ENT) consult and audiometry showed profound bilateral hearing loss, worse on the left side. The ENT diagnosis was sudden bilateral neurosensory hearing loss with no sign of middle ear disease most likely related to drug toxicity. Tacrolimus was considered the potential cause of acute bilateral hearing loss; therefore, it was discontinued and Sirolimus (Rapamune, Wyeth Laboratories, PA, USA) was initiated. Fourteen days after discontinuing TAC, the patient reported improved hearing and decreased tinnitus symptoms. A repeat audiogram 4 weeks after initial testing confirms marked improvement of hearing loss. The patient experienced full recovery of his hearing loss and had not suffered any other episodes after 1 year. Although there are previously documented cases of calcineurin-associated neurotoxicity, this is a unique case study because this patient developed a neurotoxic adverse reaction, despite having therapeutic TAC levels, which is not previously reported. Systemic side effects of CIs include hypertension, renal dysfunction, hyperkalemia, hypomagnesia, hyperglycemia, myocardial hypertrophy, nausea, diarrhea, and neurotoxicity with subtle differences between CsA and TAC [13]. Mild symptoms of tremors, paresthesias, neuralgia, and peripheral neuropathy are common, however, up to 5% of patients are affected by severe symptoms such as seizures, psychoses, hallucinations, or cerebella ataxia [2]. Between 10% and 28% of patients prescribed CsA experience a neurotoxic event. However, the incidence of cardiovascular side effects are more common with CsA, which long-term might have a negative effect blood supply to the brain and sensory organs [1, 2, 8]. Neurotoxic adverse events appear more common in patients receiving TAC with 30–90% of LT recipients experiencing some form of neurologic complications [13, 14]. Special senses can be affected by symptoms of abnormal vision, tinnitus, hearing loss, and altered speech pattern [10]. Liver transplant recipients may have a higher risk for these side effects because of hepatic encephalopathy prior to their LT and frequent exposure to other neurotoxic drugs [3-6]. Additionally, patients with alcoholic liver disease may be more prone to neurotoxicity than patients with other liver diseases [15]. Hearing loss is not common, and acute onset of hearing loss is even less frequent [9, 10]. The exact etiology of how the hearing is affected is unknown. However, there is a known association with CIs. Min et al. [10] described a kidney–pancreas transplant patient who experienced acute onset of hearing loss and tinnitus when TAC levels were >30 ng/dl. Dose reduction contributed to reversal of hearing impairment, and the patient recovered. Marioni et al. [7] reported a renal transplant patient had sensorineural hearing loss with CsA, over a period of 10 months. Dose reduction prevented progression of hearing loss; however, it is unknown if this patient ever fully recovered their hearing. It should be noted that in this particular case, this patient experienced hearing loss about 7 years after their transplant, suggesting a chronic hearing loss. A more recent study on hearing loss in LT patients reports on three patients who experienced sudden deafness related to high levels of CIs, two patients from CsA and one patient from TAC. However, in contrast to our patient, after dose reduction, the patients did not have full recovery of hearing loss [8]. Possibly, early and complete withdrawal of CIs and avoidance of any possible neurotoxic agent might be necessary to achieve full recovery in all cases. Although other causes, such as other drugs or an undiagnosed infection, might have caused or contributed to the hearing loss in our patient, the condition seems highly suspicious for TAC toxicity, as symptoms resolved after discontinuing the CI and switching to Sirolimus [4, 16-18]. Our patient was switched to CsA approximately 2 months after taking Sirolimus because of progressive pancytopenia. The patient had no further neurological symptoms by 1 year follow-up despite reintroduction of a CI. However, CsA was cautiously introduced and trough levels were kept low (100 ng/ml). To summarize, TAC may cause severe hearing loss even at therapeutic levels. In our case, the Naranjo Nomogram reached a score of four points; therefore, the adverse event is considered possible. The exact mechanism or etiology is unknown. Min et al. proposed two potential mechanisms for this adverse event [10]. On the one hand, TAC inhibits calcineurin in the brain and this may be contributed to hearing loss. On the other hand, TAC is related to erythromycin via the macrolide chemical structure. As erythromycin may cause ototoxicity possibly by inhibiting potassium secretion in the inner ear, this also could be a similar mode of action. Notable, the condition may completely reverse by early drug withdrawal – as also shown with macrolides – which emphasizes the importance of early recognition of this rare toxicity." @default.
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• W2020182606 title "Sudden hearing loss associated with tacrolimus in a liver transplant recipient" @default.
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