Frontiers in medicine · 2026
Case Report: Severe persistent transaminitis during pregnancy: a complex differential diagnosis involving suspected toxoplasmosis, possible drug-induced liver injury, and intrahepatic cholestasis.
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Sabonytė-Balšaitienė Živilė, Volochovič Jelena
Аннотация
INTRODUCTION: Severe transaminitis during pregnancy represents a diagnostic challenge because multiple etiologies may coexist. We report a pregnant woman with suspected toxoplasmosis, intrahepatic cholestasis of pregnancy, and possible drug-induced liver injury who developed prolonged severe liver dysfunction despite extensive investigation and treatment.
CASE PRESENTATION: A 33-year-old primigravida was referred at 15 weeks' gestation because of positive Toxoplasma gondii serology and elevated liver enzymes (ALT/AST 460/150 U/L). Despite treatment with spiramycin, later changed to pyrimethamine-based therapy, and ursodeoxycholic acid, liver injury progressed (ALT/AST 1,363/466 U/L). Amniocentesis at 25 weeks showed negative T. gondii PCR. At 27 weeks, liver injury peaked (ALT/AST 1,734/728 U/L); anti-SS-A/Ro52 antibodies were detected, and bile acids subsequently increased to 82.4 μmol/L. Extensive investigations excluded viral hepatitis and did not support autoimmune hepatitis, while serial fetal assessment and amniotic fluid PCR showed no evidence of congenital toxoplasmosis. The clinical picture was considered most consistent with multifactorial liver injury involving possible drug-induced hepatotoxicity and intrahepatic cholestasis of pregnancy in the setting of suspected toxoplasmosis. Labor was induced at 38 weeks. A healthy male infant (3,140 g, Apgar scores 10/10) was delivered vaginally. Three days postpartum, ALT/AST decreased to 90/57 U/L.
CONCLUSION: Severe transaminitis during pregnancy may have a multifactorial etiology, particularly when infectious, pregnancy-specific, medication-related, and immunological findings coexist. This case highlights the importance of careful differential diagnosis and multidisciplinary management when severe hepatocellular injury develops during pregnancy. Close maternal and fetal surveillance enabled the continuation of pregnancy to term, resulting in favorable maternal and neonatal outcomes.
CASE PRESENTATION: A 33-year-old primigravida was referred at 15 weeks' gestation because of positive Toxoplasma gondii serology and elevated liver enzymes (ALT/AST 460/150 U/L). Despite treatment with spiramycin, later changed to pyrimethamine-based therapy, and ursodeoxycholic acid, liver injury progressed (ALT/AST 1,363/466 U/L). Amniocentesis at 25 weeks showed negative T. gondii PCR. At 27 weeks, liver injury peaked (ALT/AST 1,734/728 U/L); anti-SS-A/Ro52 antibodies were detected, and bile acids subsequently increased to 82.4 μmol/L. Extensive investigations excluded viral hepatitis and did not support autoimmune hepatitis, while serial fetal assessment and amniotic fluid PCR showed no evidence of congenital toxoplasmosis. The clinical picture was considered most consistent with multifactorial liver injury involving possible drug-induced hepatotoxicity and intrahepatic cholestasis of pregnancy in the setting of suspected toxoplasmosis. Labor was induced at 38 weeks. A healthy male infant (3,140 g, Apgar scores 10/10) was delivered vaginally. Three days postpartum, ALT/AST decreased to 90/57 U/L.
CONCLUSION: Severe transaminitis during pregnancy may have a multifactorial etiology, particularly when infectious, pregnancy-specific, medication-related, and immunological findings coexist. This case highlights the importance of careful differential diagnosis and multidisciplinary management when severe hepatocellular injury develops during pregnancy. Close maternal and fetal surveillance enabled the continuation of pregnancy to term, resulting in favorable maternal and neonatal outcomes.