Elevated liver enzymes in inflammatory bowel disease: the role and safety of infliximab

Parisi, Ioanna; O’Beirne, James; Rossi, Roberta; Tsochatzis, Emmanuel; Manousou, Pinelopi; Theocharidou, Eleni; Hamilton, Mark; Murray, Charles; Epstein, Owen; Burroughs, Andrew K.

doi:10.1097/meg.0000000000000624

Cited by 23 publications

(25 citation statements)

References 32 publications

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“…Authors did not give details on IBD treatment and the most commonly observed pattern of injury was mild cholestasis. Parisi et al[13] report abnormal ALT in 39.2% and grade 2 increase in 7.9% of 176 patients treated with infliximab. In this study, authors identified several risk factors for liver injury: previous abnormal ALT suggesting a preexisting liver disease, immunomodulatory use and duration of infliximab therapy.…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, our results appear consistent with previous reports showing ALT elevations in roughly the same proportion of cases. It appears, that transient liver injury occurs during induction, but also during maintenance therapy with a thiopurine as well as anti-TNF[13-15]. …”

Section: Discussionmentioning

confidence: 99%

“…In theory, solo infliximab therapy could be more immunogenic than a combination therapy in triggering an immune response. Parisi et al[13] also found that immunomodulatory therapy increased the risk of infliximab induced liver injury. This might be explained by hepatotoxicity of the immunomodulatory therapy itself, but the true reason for this finding is unclear.…”

Section: Discussionmentioning

confidence: 99%

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Drug-induced liver injury in inflammatory bowel disease: 1-year prospective observational study

Koller¹,

Galambosova²,

Filakovska³

et al. 2017

WJG

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AIMTo analyze 1-year liver injury burden in inflammatory bowel disease (IBD) patients.METHODSDuring a 6-mo inclusion period, consecutive IBD cases having a control visit at IBD center were included. Basic demographics, IBD phenotype and IBD treatment were recorded on entry. Aminotransferase (AT) activities of ALT, AST, ALP and gamma-glutamyl transpeptidase (GGT) were measured at baseline, 3 mo prior to study entry and prospectively every 3 mo for 1 year. Liver injury patterns were predefined as: Grade 1 in ALT 1-3 × upper limit of normal (ULN), grade 2 in ALT > 3 × ULN, hepatocellular injury in ALT > 2 × ULN, cholestatic injury in simultaneous GGT and ALP elevation > ULN. Persisting injury was reported when AT elevations were found on > 1 measurement. Risk factors for the patterns of liver injury were identified among demographic parameters, disease phenotype and IBD treatment in univariate and multivariate analysis. Finally, implications for the change in IBD management were evaluated in cases with persisting hepatocellular or cholestatic injury.RESULTSTwo hundred and fifty-one patients were included having 917 ALT and 895 ALP and GGT measurements. Over one year, grade 1 injury was found in 66 (26.3%), grade 2 in 5 (2%) and hepatocellular injury in 16 patients (6.4%). Persisting hepatocellular injury was found in 4 cases. Cholestasis appeared in 11 cases (4.4%) and persisted throughout the entire study period in 1 case. In multivariate analysis, hepatocellular injury was associated with BMI (OR = 1.13, 1.02-1.26), liver steatosis (OR = 10.61, 2.22-50.7), IBD duration (1.07, 1.00-1.15) and solo infliximab (OR = 4.57, 1.33-15.7). Cholestatic liver injury was associated with prior intestinal resection (OR = 32.7, 3.18-335), higher CRP (OR = 1.04, 1.00-1.08) and solo azathioprine (OR = 10.27, 1.46-72.3). In one case with transient hepatocellular injury azathioprine dose was decreased. In 4 cases with persisting hepatocellular injury, fatty liver or alcohol were most likely causes and IBD treatment was pursued without change. In the case with persisting cholestatic injury, no signs of portal hypertension were identified and treatment with infliximab continued.CONCLUSIONLiver injury was frequent, mostly transient and rarely changed management. Infliximab or azathioprine were confirmed as its risk factors indicating the need for regular AT monitoring.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Drug-induced liver injury in inflammatory bowel disease: 1-year prospective observational study

Koller¹,

Galambosova²,

Filakovska³

et al. 2017

WJG

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“…The anti-TNF α agents, primarily Infliximab, have also been reported to cause drug induced liver injury [18]. However, most of these cases only had mild elevation of liver enzymes, occurring months after initiation of the anti-TNF α agent [18, 19]. Our patient on the other hand had dramatic elevations in her liver enzymes.…”

Section: Discussionmentioning

confidence: 83%

Fulminant Hepatic Failure in a Patient with Crohn’s Disease on Infliximab Possibly Related to Reactivation of Herpes Simplex Virus 2 Infection

Golds

Worobetz

2016

Case Reports in Hepatology

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HSV hepatitis is a rare but often fatal cause of liver failure which tends to affect immunocompromised individuals. Early treatment with Acyclovir has been shown to reduce mortality in HSV hepatitis making recognition of the condition critically important. Here, we present a case of HSV hepatitis in a young woman with Crohn's disease on Prednisone, Azathioprine, and Infliximab. We discuss the clinical presentation of HSV hepatitis as well as the possible causes of hepatitis in a patient on these medications. This case helps demonstrate the importance of early clinical suspicion for HSV in undifferentiated fulminate liver failure. It is also the first reported case of HSV hepatitis in a patient on Infliximab, raising the possibility of HSV reactivation in patients on Infliximab.

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“…The most common form of liver injury related to TNF‐α inhibitors has been shown to be hepatocellular injury with autoantibodies, mostly with positive ANA and some with anti‐smooth muscle antibody, and histologic features consistent with AIH. Development of this pattern of injury has been reported in up to 92% of TNF‐α inhibitor‐induced DILI . Additionally, there seems to be a lack of cross‐reactivity between TNF‐α inhibitors, possibly due to the difference in molecular structure of these agents.…”

Section: Tumor Necrosis Factor Alpha Inhibitorsmentioning

confidence: 99%

Biologic and Checkpoint Inhibitor‐Induced Liver Injury: A Systematic Literature Review

2020

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Biologics are among the most commonly prescribed medications for several chronic inflammatory diseases. Tumor necrosis factor alpha inhibitors, more so than other agents, have been observed to cause drug-induced liver injury. Additionally, because the approval and popularity of checkpoint inhibitors have grown, similar patterns of liver injury have been documented, with a majority of cases describing immune-mediated hepatitis. Although the exact mechanism of injury is unknown, various host and medication characteristics play a role in the outcome of the molecular cascade invoked by biologics. Prognosis is usually favorable with cessation of the offending agent, but cases of acute liver failure requiring liver transplantation have also been observed. Therefore, algorithms have been created to assist clinicians in treating drug-induced autoimmune hepatitis, mostly with corticosteroids. Additionally, case reports have documented successfully rechallenging patients with a different biologic without recurrence of liver injury, but data are limited. Further investigation is warranted regarding the potential for cross-reactivity and mechanism of injury to develop guidelines to aid clinicians in further management of these patients. (Hepatology Communications 2020;4:172-184).

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Elevated liver enzymes in inflammatory bowel disease: the role and safety of infliximab

Cited by 23 publications

References 32 publications

Drug-induced liver injury in inflammatory bowel disease: 1-year prospective observational study

Drug-induced liver injury in inflammatory bowel disease: 1-year prospective observational study

Fulminant Hepatic Failure in a Patient with Crohn’s Disease on Infliximab Possibly Related to Reactivation of Herpes Simplex Virus 2 Infection

Biologic and Checkpoint Inhibitor‐Induced Liver Injury: A Systematic Literature Review

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