Continuous venovenous hemodiafiltration for hyperlactatemia caused by telbivudine in a patient with chronic hepatitis <scp>B</scp>: A case report and update review

Wang, Yan Hong; Wu, Ben; Liu, Hui

doi:10.1111/1751-2980.12173

Cited by 5 publications

(5 citation statements)

References 14 publications

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“…Although myalgia and elevated blood CPK levels were reported in a higher number of patients in the telbivudine arm, the rates were consistent with the findings reported earlier in the literature[12,15,18,19]. It is recommended that serum CPK levels should be monitored closely during treatment with telbivudine[20]. …”

Section: Discussionsupporting

confidence: 81%

Telbivudinevstenofovir in hepatitis B e antigen-negative chronic hepatitis B patients: OPTIMA roadmap study

Krastev

Petrova

Kotzev

et al. 2016

WJH

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AIMTo make efficacy and safety comparison of telbivudine-raodmap and tenofovir-roadmap in hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB) patients.METHODSThis was the first prospective, randomised, two-arm, open-label, non-inferiority study in HBeAg-negative CHB patients that compared telbivudine and tenofovir administered as per roadmap concept. Patients were treated up to 24 wk and, depending on virologic response, continued the same therapy or received add-on therapy up to 104 wk. Eligible patients received an additional 52 wk of treatment in the extension period (i.e., up to 156 wk). Patients who developed virologic breakthrough (VB) while on monotherapy also received add-on therapy. The primary efficacy endpoint was the rate of patients achieving hepatitis B virus (HBV) DNA < 300 copies/mL at week 52. Secondary efficacy endpoints included the rates of HBV DNA < 300 and < 169 copies/mL, HBV DNA change from baseline, alanine aminotransferase normalisation, hepatitis B surface antigen (HBsAg) loss, HBsAg seroconversion, VB, and emergence of resistance at various timepoints throughout the study. Safety and estimated glomerular filtration rate (eGFR) were also analysed.RESULTSA total of 241 patients were randomised. Non-inferiority of telbivudine arm to tenofovir arm was demonstrated at week 52 (± 7 d window), with over 91% of patients in each treatment arm achieving HBV DNA level < 300 copies/mL. Both arms were similar in terms of key secondary efficacy variables at weeks 104 and 156. The percentage of patients achieving HBV DNA < 300 copies/mL remained high and was similar in the telbivudine and tenofovir arms at both weeks 104 and 156. Over 82% of patients in both arms achieved alanine aminotransferase normalisation at week 52, and this percentage remained high at weeks 104 and 156. Telbivudine treatment progressively reduced serum HBsAg levels from baseline while no change was reported in quantitative HBsAg during therapy with tenofovir. Both treaments showed acceptable safety profiles. The telbivudine arm showed eGFR improvement unlike the tenofovir arm.CONCLUSIONEfficacy was shown for both telbivudine-roadmap and tenofovir-roadmap regimens in HBeAg-negative CHB patients over 156 wk. Telbivudine arm was associated with renal improvement.

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Section: Discussionsupporting

confidence: 81%

Telbivudinevstenofovir in hepatitis B e antigen-negative chronic hepatitis B patients: OPTIMA roadmap study

Krastev

Petrova

Kotzev

et al. 2016

WJH

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“…found that a case with telbivudine-induced lactic acidosis had a history of hypokalemic periodic paralysis, but the relationship between the pre-existence of myopathy and telbivudine treatment was uncertain [ 6 ]. However, like the case of another previous study, our patient also had no heavy exercise or heavy drinking, and had no history of diabetes mellitus [ 18 ]. Thus the risk factors for telbivudine-induced lactic acidosis or MOF are still ambiguous and need to be further explored.…”

Section: Discussionmentioning

confidence: 57%

“…Wang et al . described a patient who developed hyperlactatemia during telbivudine treatment and was successfully treated with continuous venovenous hemodiafiltration [ 18 ]. However, another patient with telbivudine-induced rhabdomyolysis developed acute renal failure and metabolic acidosis by day 18 after admission and, despite hemofiltration, died within 24 hours of developing these symptoms [ 5 ].…”

Section: Discussionmentioning

confidence: 99%

Rhabdomyolysis, lactic acidosis, and multiple organ failure during telbivudine treatment for hepatitis B: a case report and review of the literature

et al. 2017

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BackgroundTelbivudine can cause severe side effects, including myositis, neuritis, rhabdomyolysis, and lactic acidosis. However, reported cases of telbivudine leading to multiple organ failure are rare. Here, we report a case of telbivudine-induced severe polymyositis, lactic acidosis, and multiple organ failure.Case presentationA 30-year-old Chinese man with hepatitis B virus infection received antiviral treatment with 600 mg of telbivudine daily for more than 11 months. He developed progressive weakness and myalgia, and subsequently experienced palpitations, chest tightness, lethargy, hypotension, and hypoxemia. Blood tests showed markedly elevated levels of alanine aminotransferase (955 U/L), aspartate aminotransferase (1375 U/L), blood urea nitrogen (14.9 mmol/L), creatine kinase (peak at 8050 U/L), and blood lactate (>20.0 mmol/L). His symptoms improved after continuous renal replacement therapy and short-term methylprednisolone treatment. Hyperbaric oxygen therapy, physical therapy, and rehabilitation for more than 2 months led to recovery of muscle strength to the normal range.ConclusionsWe conclude that continuous renal replacement and steroid therapies play key roles in stabilizing telbivudine-induced severe rhabdomyolysis, lactic acidosis, and multiple organ failure. Hyperbaric oxygen, physical therapy, and rehabilitation may aid in functional recovery after the acute phase of lactic acidosis and organ failure.

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“…Dasabuvir-ombitasvir-paritaprevirritonavir (3), 36 sulfamethoxazoletrimethoprim (3), 31,37,38 telbivudine (2) 39,40 Entecavir (7), 41 linezolid (19), [21][22][23][42][43][44][45][46][47][48][49][50] ribavirin-sofosbuvir (5) 51…”

Section: Discussionunclassified

Medication‐Induced Hyperlactatemia and Lactic Acidosis: A Systematic Review of the Literature

2019

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Hyperlactatemia and lactic acidosis are two syndromes that are associated with morbidity and mortality. Medication-induced hyperlactatemia and lactic acidosis are diagnoses of exclusion and have the potential to be overlooked. The purposes of this systematic review are to identify published reports of medication-induced lactate level elevations to aid clinicians in diagnosing and comprehending the underlying mechanism of this rare adverse drug effect and to provide management strategies. The PubMed database was searched for case reports, case series, retrospective studies, and prospective studies describing cases of medication-induced lactate level elevation, including lactic acidosis and hyperlactatemia, published between January 1950 and June 2017. A standardized search strategy was used, and the articles identified underwent two rounds of independent evaluation by two reviewers to assess for inclusion. Articles were included if they described at least one patient older than 12 years with hyperlactatemia or lactic acidosis caused by a medication with United States Food and Drug Administration (FDA) approval and if alternative etiologies for an elevated lactate level were ruled out. Metformin and nucleoside/nucleotide reverse transcriptase inhibitors were excluded since the pathophysiology and incidence of lactic acidosis have been well established for these agents. Overall, 1918 articles were identified, and 101 met inclusion criteria. A total of 286 patients experienced medication-induced lactate level elevations, from which 59 unique medications were identified. The most commonly identified agents were epinephrine and albuterol. Medication-induced lactate level elevation was classified as lactic acidosis (64.0%), hyperlactatemia (31.1%), or not specified (4.9%). The doses ingested included FDA-labeled doses (86%), intentional overdoses (10.8%), or prescribed doses exceeding the FDA-labeled dose (3.1%). Medications were continued without a change (40.8%), were permanently discontinued (34.4%), were continued with a dosage reduction (11.6%), or were initially withheld then resumed after lactate level normalized (2.9%); medication management for the remaining 10.0% was not reported. Forty-six patients died (16%). Six deaths were attributed by treating clinicians to be secondary to medication-induced lactic acidosis. Management strategies were heterogeneous, and treatment included supportive care, exogenous bicarbonate therapy, medication specific antidotes, and decontamination strategies. Unexplained lactate level elevations should prompt clinicians to assess for medication-induced lactate level elevations. Pharmacists are members of the health care team that are well positioned to serve as experts in the diagnosis and management of medication-induced lactate level elevations. KEY WORDS adverse drug reactions, hyperlactatemia, systematic review, lactate, lactic acidosis. (Pharmacotherapy 2019;39(9):946-963)

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Continuous venovenous hemodiafiltration for hyperlactatemia caused by telbivudine in a patient with chronic hepatitis B: A case report and update review

Cited by 5 publications

References 14 publications

Telbivudinevstenofovir in hepatitis B e antigen-negative chronic hepatitis B patients: OPTIMA roadmap study

Telbivudinevstenofovir in hepatitis B e antigen-negative chronic hepatitis B patients: OPTIMA roadmap study

Rhabdomyolysis, lactic acidosis, and multiple organ failure during telbivudine treatment for hepatitis B: a case report and review of the literature

Medication‐Induced Hyperlactatemia and Lactic Acidosis: A Systematic Review of the Literature

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