Colomba, C.

Mazzola, G.

Rubino, R.

Siracusa, L.

TITONE LANZA DI SCALEA, L.

COLOMBA, Claudia

TITONE LANZA DI SCALEA, Lucina

Rubino, R

Siracusa, L

Mazzola, G

Archivio istituzionale della ricerca - Università di Palermo

J Antimicrob Chemother 2012doi:10.1093/jac/dkr398Advance Access publication 29 September 2011Rhabdomyolysis associated with theco-administration of daptomycin andpegylated interferon a-2b and ribavirinin a patient with hepatitis CClaudia Colomba1*, Raffaella Rubino1, Lucia Siracusa1,Giovanni Mazzola2 and Lucina Titone11Dipartimento di Scienze per la promozione della salute—Sezionedi Malattie infettive, Universita` di Palermo, Via del Vespro,129 - 90127 Palermo, Italy; 2Dipartimento di Patologie Emergenti,Clinica delle Malattie Infettive, Azienda Ospedaliera UniversitariaPoliclinico “Paolo Giaccone”, Via del Vespro, 129 - 90127 Palermo,Italy*Corresponding author. Tel: +39-91-6554054; Fax: +39-91-6554050;E-mail: claudia.colomba@libero.itKeywords: adverse reactions, lipopeptide antibiotics, myopathySir,Rhabdomyolysis is a rare adverse effect reported with daptomy-cin use. Here we report the first case of creatinine phosphokinase(CPK) elevation with rhabdomyolysis developing during theco-administration of daptomycin and pegylated interferon a-2band ribavirin.We describe the case of a patient with a history of intravenousdrug abuse and hepatitis C admitted to our division because offever and pain in the right gluteal region.The patient’s general condition was poor, but his physicalexamination was unremarkable, except for the presence of aright gluteal abscess. The patient had been taking pegylatedinterferon a-2b and ribavirin for 5 months without reportingside effects. On admission, liver function tests were withinnormal limits, serum CPK level was slightly elevated (518 U/L;normal values 39–308 U/L), lactate dehydrogenase (LDH) was580 U/L (normal values 240–480 U/L), serum creatinine was1.6 mg/dL and estimated CLCR was 124.8 mL/min. The whiteblood cell (WBC) count showed neutrophil leucocytosis (WBC11580 cells/mm3, 87.1% neutrophils) and a low platelet count(72000 cells/mm3). All other laboratory findings were withinnormal limits. Hepatitis C virus (HCV) RNA viral load wasundetectable. Blood cultures were performed.The patient was started on empirical antibiotic therapy withlevofloxacin (750 mg once daily intravenously) and piperacillin/tazobactam (4.5 g every 6 h intravenously). Due to lack ofimprovement of symptoms and fever after 48 h, levofloxacinwas switched to daptomycin (500 mg daily intravenously). Thesecond dose was administered, by mistake, 4 h before it shouldhave been. Five days after admission, after only two doses ofdaptomycin, the patient suddenly complained of weakness anddiffuse aches in the proximal thighs and arms. Serum CPKlevels were very high (12933 U/L) and further elevations inaspartate aminotransferase (AST) and alanine aminotransferase(ALT), 371 and 67 IU/L, respectively, were also noted. A urinedrug screen was performed to rule out damage related to illicitsubstance use, and the results were negative. Blood cultureswere positive for methicillin-resistant Staphylococcus aureus(MRSA). Suspecting daptomycin-induced rhabdomyolysis, treat-ment was switched to linezolid (600 mg twice daily intrave-nously) and meropenem (1 g every 8 h intravenously). Thepatient was hydrated (2 L/day) to preserve renal function, andthis was strictly monitored throughout the course; urinalysiswas positive for myoglobin. Although daptomycin had beeninterrupted, CPK levels and AST/ALT levels continued to increasefor 5 days after and on the sixth day the CPK level was 45257 U/L,LDH was 6892 U/L and AST/ALT was 980/107 IU/L. The CPK levelslowly decreased 10 days after discontinuation of daptomycin.Daptomycin is a lipopeptide antibiotic approved for the treat-ment of complicated skin and soft-tissue infections caused bysusceptible Gram-positive strains, including MRSA andvancomycin-susceptible Enterococcus faecalis. Daptomycin hasalso been approved for S. aureus bloodstream infection and forthe treatment of right-sided endocarditis caused by methicillin-susceptible S. aureus and MRSA. The main side effect is skeletalmuscle toxicity. In clinical trials, 2.8% of subjects experiencedelevations in CPK level, and 0.2% of the study populationreported myopathy.1 This condition is favoured in obesity, dia-betes mellitus, chronic renal failure, bacterial sepsis, electrolyteabnormalities and concomitant treatment with statins(3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors).2Few cases of daptomycin-induced rhabdomyolysis have beendescribed in the literature.2,3 Only two reports described patientswith early onset rhabdomyolysis related to daptomycin use.4Here, we report the second case of onset after only two dosesof daptomycin, with a CPK level of 45257 U/L. To our knowledge,this is the first case of daptomycin-induced rhabdomyolysis in apatient receiving pegylated interferon a-2b and ribavirin forHCV-related hepatitis. Interferon a-2b, but not ribavirin, hasbeen associated with rhabdomyolysis.5 Our patient already hadincreased CPK levels at presentation, but had never had anysign or symptom of myopathy, suggesting that hepatitis Ctherapy had been well tolerated. Thus, daptomycin was adminis-tered despite increased CPK levels. We believe that a prominentrole in daptomycin toxicity was played by the short intervalbetween the two doses (by mistake); according to theliterature, dosing frequency seems to have a more direct effectupon skeletal muscle than peak plasma concentration.6,7 Ourpatient also had MRSA bacteraemia. Bacterial sepsis has beenassociated with the development of rhabdomyolysis, and inthis case it may have functioned as a predisposing factor.In conclusion, given the temporal relationship between dap-tomycin initiation and elevation in CPK level, we identified dapto-mycin as the main cause of the patient’s myopathy. Therefore,we recommend close monitoring of CPK and symptoms of myo-pathy in all patients started on this drug. Moreover, we think thatthe concomitant use of pegylated interferon a-2b most likelyinduced the adverse activity of daptomycin. It may be advisable,given the limited experience, to interrupt therapy with interferonduring daptomycin treatment.FundingThis study was carried out as part of our routine work.Research letters249Downloaded from https://academic.oup.com/jac/article-abstract/67/1/249/723106/Rhabdomyolysis-associated-with-the-coby Massimo Denaro useron 17 September 2017Transparency declarationsNone to declare.References1 Package insert. Cubicin (Daptomycin) Injection. Lexington, MA: CubistPharmaceuticals, November 2010.2 Odero RO, Cleveland KO, Gelfand MS. Rhabdomyolysis and acute renalfailure associated with the co-administration of daptomycin and anHMG-CoA reductase inhibitor. J Antimicrob Chemother 2009; 63:1299–300.3 Kazory A, Dibadj K, Weiner ID. Rhabdomyolysis and acute renal failurein a patient treated with daptomycin. J Antimicrob Chemother 2006; 57:578–9.4 Patel SJ, Samo TC, Suki WN. Early-onset rhabdomyolysis related todaptomycin use. Int J Antimicrob Agents 2007; 30: 472–4.5 Gabrielli M, Santarelli L, Serricchio M et al. Acute reversiblerhabdomyolysis during interferon alpha 2B therapy for hepatitis C. Am JGastoenterology 2003; 98: 940.6 Echevarria K, Datta P, Cadena J et al. Severe myopathy and possiblehepatotoxicity related to daptomycin. J Antimicrob Chemother 2005;55: 599–600.7 Papadopoulos S, Ball AM, Liewer SE et al. Rhabdomyolysis duringtherapy with daptomycin. Clin Infect Dis 2006; 42: e108–110.J Antimicrob Chemother 2012doi:10.1093/jac/dkr435Advance Access publication 23 October 2011Unexpected atazanavir-associatedbiliary lithiasis in an HIV-infectedpatientEve Courbon1, Franc¸ois Laylavoix2, Cathia Soulie´3,Christine Le Beller4, Vincent Calvez3, Christine Katlama2and Gilles Peytavin1*1Clinical Pharmacokinetic Department, APHP, Bichat-ClaudeBernard Hospital and EA449 Paris 7 University, Paris, France;2Infectious Diseases Department, APHP Pitie´-Salpeˆtrie`re Hospitaland INSERM U 943, Paris, France; 3Virology Department, APHP,Pitie´-Salpeˆtrie`re Hospital and INSERM U 943, Paris, France;4Pharmacovigilance Centre, Universite´ Paris Descartes, APHP,European Georges Pompidou Hospital, Paris, France*Corresponding author. Tel: +33-1-40-25-80-15; Fax: +33-1-42-63-58-25; E-mail: gilles.peytavin@bch.aphp.frKeywords: atazanavir, gallstones, biliary lithiasis, HIVSir,Atazanavir is a widely used protease inhibitor with a favourablepharmacokinetic profile, allowing once-daily dosing with orwithout ritonavir boosting. It is both a substrate and a competi-tive inhibitor of cytochrome P450 3A4 and also a competitiveinhibitor of the bilirubin-conjugating enzyme UDP glucuronyltransferase 1A1. Atazanavir is metabolized and eliminated pri-marily by the liver and its metabolites are excreted in the bile.In healthy subjects, renal elimination of unchanged atazanavirwas only 7% of the administered daily dose. A population phar-macokinetic sub-study, derived from study AI424007 in naivepatients receiving 200, 400 or 500 mg of atazanavir once daily(a clinical Phase III trial of atazanavir efficacy, safety and toler-ability), demonstrated the relationship between plasma exposure(area under the curve and trough plasma concentration) andboth safety (hyperbilirubinaemia) and viral efficacy.1 Renal lithia-sis is a commonly reported side effect of atazanavir, with at least30 cases identified by the FDA between 2002 and 2007.2 Onecase of choledocholithiasis-associated atazanavir in a 47-year-old HIV-infected African female 6 weeks after the initiation ofan atazanavir-containing regimen has been published recently.3Six additional cases of cholelithiasis occurring within months toyears after initiation of atazanavir are recorded in the FrenchNational Pharmacovigilance Database. A cholecystectomy wasperformed in four of these cases and atazanavir was identifiedin biliary stones in two cases. Here we report a new case. Thepatient signed a written informed consent for publication.A 64-year-old HIV-1-infected male who was immunovirologi-cally stable (plasma HIV-1 RNA ,20 copies/mL and CD4 cells525/mm3; CD4 cells¼33% of white blood cells) and showedgood treatment adherence was hospitalized in July 2010 forexploration of a right flank pain experienced for severalmonths. Ultrasonography revealed a huge gallstone (weight13 g, diameter 25 mm), which was subsequently extractedfrom the common bile duct by laparoscopic cholecystectomy.After solubilization of the stone in acid aqueous solvent, thebrown-coloured solution obtained was analysed to determineantiretroviral drug concentrations using ultra-performanceliquid chromatography-mass spectrometry/mass spectrometry.4The atazanavir concentration determined in the gallstone recov-ered from this patient, who had switched from atazanavir/ritona-vir to a darunavir/ritonavir+tenofovir/emtricitabine (300/200 mgonce daily)-containing regimen 1 year previously, was approxi-mately 6.0 mg/g. In the same sample, darunavir and ritonavirconcentrations were 0.9 and 0.13 mg/g, respectively, whileneither tenofovir nor emtricitabine was found. Since 1993, thispatient had received 19 successive antiretroviral regimens,including six protease inhibitors, seven nucleoside reverse tran-scriptase inhibitors and two non-nucleoside reverse transcriptaseinhibitors in combination. He had no history of opportunistic infec-tion, and liver and renal functions were normal. The plasma viralload was undetectable for the last 9 years except for two treat-ment interruptions. Cumulative durations of protease inhibitortherapies were approximately 5 years for indinavir and 5 yearsfor atazanavir. One year after starting unboosted indinavir, thepatient developed a nephrolithiasis that resolved completely onswitching 800 mg of indinavir three times daily to indinavir/ritona-vir (400/100 mg twice daily), leading to a lower indinavir peakplasma concentration and adequate hydration.Follow-up parameters [median (interquartile range; number ofsamples)] collected during the last 41 months were as follows:atazanavir plasma concentration at 24 h, 502 ng/mL (330–631; 8); tenofovir plasma concentration at 24 h, 53 ng/mL(49–68; 8); variability of atazanavir and tenofovir plasma concen-trations at 24 h, 16% and 21%, respectively; estimated glomer-ular filtration rate (according to the Cockcroft–Gault equation),Research letters250Downloaded from https://academic.oup.com/jac/article-abstract/67/1/249/723106/Rhabdomyolysis-associated-with-the-coby Massimo Denaro useron 17 September 2017

Rhabdomyolysis associated with the co-administration of daptomycin and pegylated interferon α-2b and ribavirin in a patient with hepatitis C

https://iris.unipa.it/bitstream/10447/62882/2/Rhabdomyolysis%20associated%20with%20the.pdf

Rhabdomyolysis associated with the co-administration of daptomycin and pegylated interferon \u3b1-2b and ribavirin in a patient with hepatitis C

Rhabdomyolysis associated with the co-administration of daptomycin and pegylated interferon \u3b1-2b and ribavirin in a patient with hepatitis C

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