Tacrolimus induced hepatotoxicity in a patient with bilateral lung transplant

Sacher, Vikas Y.; Bejarano, P.A.; Pham, Si M.

doi:10.1111/j.1432-2277.2012.01546.x

Cited by 16 publications

(12 citation statements)

References 10 publications

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“…As higher cholestasis parameters in patients with TAC-based immunosuppression were reported before, we interpret this as effects of CNI reduction 37,38. In line with the present publications, a trend to higher liver function parameters in patients receiving TAC was seen; however, statistically significance was not reached 39. However, higher lipid levels in patients with CSA-based immunosuppression were reported before 4,40–42.…”

Section: Discussionsupporting

confidence: 86%

Renal function in heart transplant patients after switch to combined mammalian target of rapamycin inhibitor and calcineurin inhibitor therapy

Helmschrott¹,

Rivinius²,

Brückner³

et al. 2017

DDDT

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BackgroundA calcineurin inhibitor (CNI)-based immunosuppression combined with mammalian target of rapamycin inhibitors (mTORs) seems to be attractive in patients after heart transplantation (HTX) in special clinical situations, for example, in patients with adverse drug effects of prior immunosuppression. Previous studies in patients after HTX detected advantageous effects regarding renal function of a tacrolimus (TAC)-based vs cyclosporine-A (CSA)-based immunosuppression (in combination with mycophenolate mofetil). However, data regarding renal function after HTX in mTOR/CNI patients remain limited.AimPrimary end point of the present study was to analyze renal function in HTX patients 1 year after switch to an mTOR/CNI-based immunosuppression.MethodsData of 80 HTX patients after change to mTOR/CNI-based immunosuppression were retrospectively analyzed. Renal function was assessed by measured serum creatinine and by estimated glomerular filtration rate (eGFR) calculated from Modification of Diet in Renal Disease equation.ResultsTwenty-nine patients received mTOR/CSA-based treatment and 51 patients received mTOR/TAC-based therapy. At time of switch and at 1-year follow-up, serum creatinine and eGFR did not differ significantly between both study groups (all P=not statistically significant). Analysis of variances with repeated measurements detected a similar change of renal function in both study groups.ConclusionThe present study detected no significant differences between both mTOR/CNI study groups, indicating a steady state of renal function in HTX patients after switch of immunosuppressive regimen.

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Section: Discussionsupporting

confidence: 86%

Renal function in heart transplant patients after switch to combined mammalian target of rapamycin inhibitor and calcineurin inhibitor therapy

Helmschrott¹,

Rivinius²,

Brückner³

et al. 2017

DDDT

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“…Cyclosporine was stopped, the patient was started on sirolimus and mycophenolate mofetil, and liver enzymes normalized 3 weeks after stopping cyclosporine. 3 We conclude that cholestatic jaundice in our patient was due to tacrolimus toxicity because even on extensive work-up we could not find out other etiologies of hepatic dysfunction and LFT completely normalized after tacrolimus was stopped.…”

Section: Discussionmentioning

confidence: 60%

“…[1][2][3][4] The incidence of cholestatic syndrome is 5.4% in pediatric liver transplant patients. 1 Tacrolimus-induced veno-occlusive of liver disease has been reported in RTx recipients.…”

Section: Introductionmentioning

confidence: 99%

Tacrolimus-Induced Severe Cholestasis Complicating Renal Transplantation

et al. 2013

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Tacrolimus, a calcineurin inhibitor, is a potent immunosuppressive agent used by a majority of transplanters across the globe. Its adverse effects include nephrotoxicity, neurotoxicity, new onset diabetes after transplant, gastro-intestinal toxicity, hepatotoxicity, and thrombotic microangiopathy. Tacrolimus-induced hepatotoxicity is a very uncommon side effect. We report a case of tacrolimus-induced hepatotoxicity in the form of cholestatic hepatitis a renal transplant recipient. Hepatotoxicity did not decrease after dose reduction; however, normalization of liver enzymes occurred after discontinuing tacrolimus.

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“…3 Sacher et al described a case of tacrolimus-induced hepatotoxicity in a patient with bilateral lung transplant. 2 No other reports on tacrolimus hepatotoxicity may be found in the literature using the PubMed and MedLine databases with keywords: tacrolimus, hepatotoxicity, kidney transplantation, liver, FK-506, sirolimus, everolimus, and/or mTOR.…”

Section: Discussionmentioning

confidence: 99%

“…Although tacrolimus at higher blood concentrations often cause mild elevation of liver chemistries, severe hepatotoxicity is a rare side effect and has been reported only in liver or lung transplant recipients. 2,3 To the best of our knowledge, severe tacrolimus hepatotoxicity has never been described in a renal transplant recipient. We present a case of sirolimus rescue therapy for treatment of tacrolimus-associated hepatotoxicity in a renal transplant recipient.…”

Section: Introductionmentioning

confidence: 96%

Rescue therapy with sirolimus in a renal transplant recipient with tacrolimus-induced hepatotoxicity

et al. 2013

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Calcineurin inhibitors at elevated serum concentrations frequently cause mild elevation of the liver chemistries. Although rare, severe hepatotoxicity is their serious complication. A 54-year-old man with end-stage renal disease due to chronic glomerulonephritis without biopsy received a renal allograft from the deceased donor. Eleven days after transplantation severe liver injury (AST up to 421 IU/L, ALT 1242 IU/L, and GGT 212 IU/L) with the serum bilirubin within the normal range was recorded. Tacrolimus trough level was 5.5 ng/mL. Liver ultrasound and color-Doppler of the portal system were normal. Liver failure completely resolved after withdrawal of the calcineurin inhibitor and switch to sirolimus. After 9 months of follow-up our patient has excellent graft and liver function. Awareness of the possible association of tacrolimus use with hepatotoxicity is important to timely discontinuation of the causative agent, and to introduce sirolimus as the rescue therapy.

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Tacrolimus induced hepatotoxicity in a patient with bilateral lung transplant

Cited by 16 publications

References 10 publications

Renal function in heart transplant patients after switch to combined mammalian target of rapamycin inhibitor and calcineurin inhibitor therapy

Renal function in heart transplant patients after switch to combined mammalian target of rapamycin inhibitor and calcineurin inhibitor therapy

Tacrolimus-Induced Severe Cholestasis Complicating Renal Transplantation

Rescue therapy with sirolimus in a renal transplant recipient with tacrolimus-induced hepatotoxicity

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