Search Results (117)

Objective: To evaluate fetal pulmonary artery hemodynamics (PAAT, PAET, PATET) in pregnancies complicated by intrahepatic cholestasis of pregnancy (ICP) and to investigate their association with the aspartate aminotransferase-to-platelet ratio index (APRI). Methods: In this prospective study, 64 ICP cases and 64 healthy pregnancies are included. Doppler measurements of the fetal main pulmonary artery, umbilical artery (UAPI), and middle cerebral artery (MCAPI) were performed by a single operator, and all biochemical analyses were conducted in the same laboratory. APRI was calculated using the standard formula. Results: Doppler evaluation demonstrated significantly higher PAAT, PAET, PATET, UAPI, and MCAPI values in the ICP group (all p < 0.05). AST, ALT, and APRI levels were markedly elevated in ICP pregnancies (all p < 0.001). No significant correlation was observed between PATET and APRI (p = 0.368) or fasting bile acid levels (FBA) (p = 0.116), whereas APRI showed a weak positive correlation with FBA (r = 0.308; p = 0.013). Doppler parameters and APRI values did not differ significantly according to cholestasis severity (10–39/≥40/≥100 μmol/L; all p > 0.05). Conclusions: In ICP, fetal pulmonary artery Doppler indices (PAAT, PAET, PATET) and fetoplacental Doppler parameters are increased; the elevation in PATET is consistent with lower—rather than higher—fetal pulmonary vascular resistance, potentially reflecting accelerated fetal lung maturation or a hemodynamic adaptation to ICP-related physiological perturbations. Despite elevated APRI levels, these biochemical changes do not parallel fetal hemodynamic indicators. These findings suggest that fetal hemodynamic effects in ICP may be independent of biochemical disease severity. PATET is best conceptualized as a hemodynamic monitoring variable complementing bile acid assessment in fetal surveillance, not as a standalone screening or prognostic tool. Full article

Wilson’s disease (WD) is an autosomal recessive disorder of copper metabolism caused by ATP7B mutations, characterized by hepatic copper accumulation and multisystem involvement. Several rare inherited and acquired conditions can closely mimic WD, posing diagnostic challenges and the risk of inappropriate therapy. By examining neuroimaging patterns and distinguishing between diagnostic criteria, this narrative review provides a comprehensive synthesis of WD-mimicking disorders, emphasizing their molecular mechanisms, clinical phenotypes, and biochemical features. WD-mimicking disorders encompass ATP7A-related neurodegenerations (Menkes disease, occipital horn syndrome, X-linked distal hereditary motor neuropathy), MEDNIK syndrome, Huppke–Brendel syndrome, aceruloplasminemia, congenital disorders of glycosylation, primary familial intrahepatic cholestasis type 3, and acquired copper deficiency syndromes. Mechanisms include systemic copper deficiency, impaired intracellular trafficking, defective ceruloplasmin biosynthesis, secondary hepatic copper accumulation, and abnormal glycosylation. Clinical features range from neurodevelopmental delay, movement disorders, and hepatic dysfunction to dermatologic, hematologic, and connective-tissue abnormalities. Biochemical profiles may overlap with WD, particularly low serum ceruloplasmin and total copper, altered urinary copper excretion, and elevated hepatic copper in some disorders. Neuroimaging and genetic testing provide critical discriminative value. Management is largely supportive, with disease-specific therapies available in selected conditions, such as subcutaneous copper in Menkes disease or monosaccharide supplementation in certain congenital disorders of glycosylation subtypes. Accurate differentiation between WD and WD-mimicking disorders requires careful integration of clinical, biochemical, imaging, and molecular data. Recognition of distinctive features and understanding underlying pathophysiology are essential to avoid misdiagnosis and inappropriate anti-copper therapy, optimize management, and improve patient outcomes. Full article

Objective: This study aimed to evaluate maternal serum afamin levels in women with intrahepatic cholestasis of pregnancy (ICP), examine their relationship with fasting bile acid concentrations, and assess their association with perinatal outcomes. Methods: This prospective case-–control study included 80 singleton pregnancies followed at a tertiary perinatology center between October 2025 and March 2026. Forty women with ICP, defined by pruritus and fasting bile acids > 10 μmol/L, were compared with 40 healthy pregnant controls. Women with ICP were further stratified according to fasting bile acid levels as <40 and ≥40 μmol/L. Maternal serum afamin concentrations were measured using a commercially available enzyme-linked immunosorbent assay (ELISA) kit. Maternal characteristics, liver biochemistry, fetal biometric and Doppler parameters as well as obstetric and neonatal outcomes were compared. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic performance of afamin for ICP, and logistic regression analysis was used to assess its association with ICP. Results: Baseline maternal characteristics were comparable between groups. Maternal serum afamin levels were significantly higher in the ICP group than in controls (6.18 ± 4.24 vs. 3.98 ± 1.95 ng/mL, p = 0.004). Afamin correlated positively with fasting bile acids (r = 0.372, p = 0.018), but not with transaminases, gestational age at delivery, birth weight, or neonatal outcomes. In logistic regression, afamin was independently associated with ICP (adjusted odds ratio [aOR] 1.260; 95% confidence interval [CI] 1.059–1.500; p = 0.009). ROC analysis showed poor discrimination for ICP (area under the curve [AUC] 0.634, 95% CI 0.51–0.76, p = 0.039), whereas afamin did not discriminate between subgroups defined by fasting bile acid levels (<40 vs. ≥40 μmol/L). The optimal cut-off value of 4.93 ng/mL predicted ICP with 55% sensitivity, 67.5% specificity, a positive likelihood ratio of 1.69, and a negative likelihood ratio of 0.67. Conclusions: Maternal serum afamin levels are elevated in ICP and show a modest association with fasting bile acid burden. Its discriminatory performance is limited, and it does not reliably distinguish patients defined by a ≥40 μmol/L threshold. These findings suggest that afamin reflects the maternal response to cholestasis rather than disease severity and may serve as a complementary biomarker. Full article

Pediatric (neonatal and infantile) jaundice resulting from underlying cholestasis (caused by conjugated hyperbilirubinemia) is always pathological and requires prompt evaluation. Pediatric cholestasis can be caused by medical or surgical factors and, if left untreated, can lead to irreversible liver damage. Timely recognition of pediatric cholestasis and identification of the underlying etiology are paramount to improve outcomes. The broad spectrum of causes potentially underlying pediatric cholestasis requires a multidisciplinary diagnostic approach, and each aspect must be interpreted in the concomitant clinical picture. A liver biopsy is one component of a complex diagnostic puzzle. However, interpreting a liver biopsy performed on a newborn/infant with conjugated/direct hyperbilirubinemia can be a challenging task, as these biopsies are rarely encountered in general hospitals. The aim of this review is to provide a practical and simplified approach to pediatric cholestasis with examples of real clinical cases we have encountered and discuss key features, both histological and clinical, that can help narrow the differential diagnosis and identify treatable causes. Full article

Background/Objectives: To compare the maternal, fetal, and neonatal outcomes of pregnancies undergoing amniocentesis with those undergoing non-invasive prenatal testing (NIPT), within a cohort of women with comparable clinical indications, aiming to evaluate differences in adverse outcomes in a risk-indicated population. Methods: In this retrospective cohort study, pregnancy outcomes of 2044 pregnant women who underwent amniocentesis and 7668 pregnant women who underwent NIPT were evaluated using single-center data. The analysis was restricted to pregnancies with normal/reportable test results and without structural or genetic anomalies. Pregnancy loss outcomes were evaluated in the full cohort, while perinatal outcomes were analyzed among cases with available delivery data (377 amniocentesis and 2063 NIPT cases). Pregnancy and perinatal outcomes, including miscarriage, intrauterine fetal demise (IUD), preterm birth (PTB), pregnancy-induced hypertensive diseases (PIHDs), gestational diabetes mellitus (GDM), intrahepatic cholestasis of pregnancy (ICP), low birth weight (LBW), small for gestational age (SGA), and low APGAR scores (<7), were evaluated. Multivariate logistic regression analysis was performed to adjust for potential confounding factors, and adjusted odds ratios (aORs) with 95% confidence intervals (CIs) were reported. Results: Amniocentesis was associated with a significantly higher risk of an adverse outcome compared to NIPT in this risk-indicated cohort. The likelihood of miscarriage was significantly higher in the amniocentesis group (aOR: 1.91, 95% CI: 1.17–3.14, p = 0.025), as was the risk of IUD (aOR: 4.10, 95% CI: 2.05–8.20, p < 0.001). PTB risk was also increased (aOR: 1.96, 95% CI: 1.53–2.51, p < 0.001). LBW was significantly more prevalent in the amniocentesis group (aOR: 7.73, 95% CI: 5.40–11.05, p < 0.001), and the likelihood of delivering a SGA neonate was also increased (aOR: 1.45, 95% CI: 1.02–2.06, p = 0.040). A 1st-minute APGAR score < 7 was also more frequent in the amniocentesis group (aOR: 1.51, 95% CI: 1.06–2.16, p = 0.022), although the association with 5th-minute APGAR scores < 7 did not reach statistical significance (aOR: 1.45, 95% CI: 0.83–2.52, p = 0.193). Overall, the risk of composite maternal and perinatal adverse outcomes (aOR: 1.77, 95% CI: 1.41–2.22, p < 0.001) as well as composite fetal and neonatal adverse outcomes (aOR: 1.97, 95% CI: 1.50–2.58, p < 0.001) was significantly higher in the amniocentesis group compared to the NIPT group. No significant association was observed for PIHD, GDM, or ICP. Conclusions: Our findings showed that, apart from fetal loss, amniocentesis may be associated with adverse perinatal outcomes such as PTB, LBW, SGA and low APGAR scores. Full article

Cholestasis encompasses a broad spectrum of hepatobiliary disorders characterized by impaired bile formation or flow. Historically classified based on clinical onset and severity, the landscape of cholestatic liver disease has been revolutionized by the advent of high-throughput genomic technologies. This review elucidates the critical role of genetics in redefining the pathophysiology, diagnosis, and management of cholestasis, framing pediatric Progressive Familial Intrahepatic Cholestasis (PFIC) and Adult-Onset Cholestatic Disease (AOCD) as a continuous phenotypic spectrum. We discuss the expansion of the molecular nosology to include 13 distinct PFIC types, highlighting how defects in canalicular transporters, tight junctions, and nuclear receptors underpin clinical heterogeneity. Furthermore, we examine the paradigm shift in the diagnostic flowchart, where Next-Generation Sequencing (NGS) has largely superseded liver biopsy for etiological definition. Finally, we address the therapeutic implications of this molecular precision, demonstrating how specific genotypes dictate eligibility for novel targeted therapies, such as IBAT inhibitors, marking the transition from supportive care to personalized medicine. Full article

Urticaria is a mast cell-mediated disorder commonly encountered in women of reproductive age, making its interaction with pregnancy clinically relevant. Gestation induces profound hormonal and immunologic adaptations—including shifts between Th1/Th17 and Th2/Treg responses and sustained exposure to sex steroids and placental hormones—that can modulate mast cell reactivity. As a result, chronic urticaria (CU) shows heterogeneous behavior during pregnancy: approximately half of patients improve, one third worsen, and the remainder remain stable. Pregnancy also presents several urticaria-like dermatoses, notably polymorphic eruption of pregnancy (PEP/PUPPP), atopic eruption of pregnancy (AEP) and pemphigoid gestationis (PG), as well as rare hormone-induced hypersensitivity reactions. Additionally, systemic disorders such as intrahepatic cholestasis of pregnancy (ICP), chronic kidney disease–associated pruritus and urticarial vasculitis may mimic urticaria but differ markedly in prognosis, maternal–fetal risk and management. Given this complexity, accurate diagnosis requires integration of temporal pattern, lesion morphology and duration, distribution, systemic features and targeted investigations, as outlined in the diagnostic algorithm proposed. Most pregnancy-specific eruptions are benign, whereas PG, ICP and urticarial vasculitis warrant prompt recognition due to potential fetal implications. Management of CU in pregnancy generally follows standard guidelines, with second-generation H1-antihistamines as first-line therapy and omalizumab reserved for severe refractory cases. Full article

Objective: This study aimed to investigate maternal serum fatty acid-binding protein 4 (FABP4) levels in pregnancies complicated by intrahepatic cholestasis of pregnancy (ICP) and to evaluate its diagnostic and prognostic utility for maternal and neonatal outcomes. Methods: This prospective case–control study included 44 women diagnosed with ICP and 44 gestational age-matched healthy pregnant controls between 24 and 41 weeks of gestation. Serum FABP4 concentrations were measured using a quantitative sandwich enzyme-linked immunosorbent assay (ELISA). Demographic, biochemical, and perinatal data were collected prospectively. Group comparisons were performed using the t-test or Mann–Whitney U test, correlations by Pearson or Spearman tests, and diagnostic performance by receiver operating characteristic (ROC) curve analysis. Results: Maternal serum FABP4 levels between 25 and 39 weeks of gestation were significantly higher in the ICP group than in the control group (median 3.60 [Q1–Q3: 3.25–4.20] vs. 2.40 [Q1–Q3: 2.00–2.95] ng/mL; p < 0.001). ROC analysis revealed excellent diagnostic accuracy for ICP (AUC = 0.899; 95% CI: 0.816–0.953; p < 0.001) with an optimal cut-off value of >3.0 ng/mL, yielding 90% sensitivity and 84% specificity. FABP4 correlated inversely with gestational age at delivery in the total cohort (r = −0.430, p < 0.001) but not within the ICP subgroup. In predicting composite neonatal outcomes, FABP4 showed moderate performance (AUC = 0.634, 95% CI: 0.525–0.734, p = 0.032) and limited predictive ability within the ICP group (AUC = 0.535, p = 0.685). Conclusions: Maternal FABP4 levels are significantly elevated in ICP and show high diagnostic accuracy for ICP but have limited prognostic value for neonatal outcomes. FABP4 may represent a novel biomarker reflecting the metabolic–inflammatory interplay underlying the pathophysiology of intrahepatic cholestasis of pregnancy. Full article

Cholestatic diseases in children represent a heterogeneous group of disorders that, with few exceptions, have no cure. For decades, off-label drugs and/or drugs with little evidence of efficacy have been used to treat pruritus or as supportive therapy. In recent years, a family of molecules known as bile acid transporter inhibitors (IBATis) has been developed, with two of these being approved for treating pruritus in progressive familial intrahepatic cholestasis (PFIC) and Alagille syndrome (ALGS). Blocking the ileal reabsorption of bile acids (BAs) lowers serum levels. This contributes to reducing cholestatic pruritus. Such a mechanism of action may also have a potential benefit in other cholestatic diseases and even in the consequences of chronic cholestasis. This is a narrative review of the literature, including the most recent communications, to summarize data on the efficacy and safety of IBATis in the treatment of pruritus in PFIC and ALGS in children, including a description of the latest results from their use in a real-world setting. Reports on off-label use and experiences in adults are also discussed. This review aims to help physicians understand the potential and limitations of these new drugs in the treatment of cholestatic pruritus. Full article

Background/Objectives: Antepartum computerized cardiotocography (cCTG) represents an essential tool for assessing fetal well-being. This study aimed to comparatively evaluate antepartum cCTG-derived indices across high-risk pregnancies to identify distinctive fetal autonomic and reactivity profiles. Methods: A comparative analysis of antepartum cCTG parameters was conducted. The cohort included pregnancies beyond 28 weeks of pregnancy, 169 cases of hypertensive disorders of pregnancy (HDP), 146 of gestational diabetes mellitus (GDM), 86 of intrahepatic cholestasis (ICP), and 87 low-risk pregnancies as controls. Results: Baseline FHR remained within the physiological range across all groups (110–160 bpm; p > 0.05). Dynamic cCTG parameters exhibited clear pathology-dependent alterations. Short-term variability (STV) showed a stepwise decline from controls to ICP and GDM, reaching its lowest values in HDP (mean 1.08 bpm; p < 0.00001), accompanied by an increased proportion of epochs with STV < 1 bpm. Long-term variability suppression (LTV < 5 bpm) was significantly higher in GDM and HDP (p = 0.0077). Acceleration frequency decreased across all pathological groups, with the most pronounced reduction observed in HDP, whereas fetal movements were paradoxically elevated in both GDM and HDP. Total decelerations were more frequent in ICP and HDP; however, repetitive, late, prolonged, and >5 min decelerations remained rare and did not differ significantly between groups. Conclusions: HDP showed the most unfavorable cCTG profiles, consistent with impaired fetal autonomic regulation and chronic subclinical hypoxemia. GDM and ICP had moderate changes, suggesting milder adaptive responses. These findings emphasize the value of quantitative cCTG in differentiating fetal autonomic patterns in high-risk pregnancies and the importance of tailored surveillance strategies. Full article

Background: Progressive familial intrahepatic cholestasis (PFIC) describes a group of genetically heterogeneous disorders. Several mutations in the ATP-Binding Cassette Subfamily B Member 4 (ABCB4) gene have been confirmed to cause reduced phosphatidylcholine levels in bile, leading to a deficiency of biliary vesicles and instability of mixed in micelles. The disease spectrum ranges from PFIC type 3 (PFIC3) to milder conditions. Herein, we present a rare case of PFIC3 in a young woman, emphasizing the importance of early detection and management. Methods: The patient was diagnosed using next-generation sequencing, with genetic testing and analysis performed by the Chengdu Hua Chuang Testing Institute. Variant pathogenicity was evaluated according to the American College of Medical Genetics and Genomics guidelines and classified into five categories: pathogenic, likely pathogenic, uncertain significance, likely benign, and benign. Nomenclature was assigned following the Human Genome Variation Society standards. Results: Contrast-enhanced abdominal computed tomography demonstrated liver cirrhosis with marked splenomegaly. Histological examination of liver biopsy specimens using hematoxylin and eosin and Masson staining further confirmed cirrhotic changes. Genetic testing was subsequently performed and revealed a likely pathogenic variant, c.2757T > A (p. Tyr919Ter), in exon 22 of the ABCB4 gene, which was also detected in the patient’s mother but absent in her father. Finally, PFIC3 was diagnosed. Following initiation of ursodeoxycholic acid therapy, the patient showed moderate improvement in liver function tests, underscoring a clinical case with therapeutic implications. Conclusions: Molecular genetic analyses of ABCB4 are essential for the accurate diagnosis of PFIC3. Clinicians should consider cholestatic liver diseases, particularly PFIC, as a differential diagnosis in cases of liver cirrhosis with unknown etiology, especially in young patients who lack prior symptoms or a family history of liver disease. Full article

Variants of the MYO5B gene, which encodes the molecular motor protein myosin-Vb, have gained prominence as a causative factor in familial intrahepatic cholestasis (FIC). Understanding the disease mechanism is pivotal for therapy development and clinical decision-making. The prevailing theory for the mechanism underlying MYO5B-associated cholestasis implicates faulty trafficking of the ABCB11-encoded bile salt export pump (BSEP) in hepatocytes due to dysfunctional myosin-Vb. This is supported by cell and mouse studies. However, while BSEP localization was abnormal in some patients’ liver biopsies, BSEP appeared normally localized in others, raising questions with regard to the role of BSEP in MYO5B-associated FIC. We present a focused systematic narrative review of all cases of MYO5B variant-associated isolated FIC reported in the MEDLINE database. We assembled a comprehensive patient dataset and assessed clinical features of MYO5B-associated FIC, their relationship with MYO5B genotype, the clinical value and significance of BSEP abnormalities, and the relationship of MYO5B-associated FIC to ABCB11 variant-associated FIC. Our review revealed that aberrant BSEP localization correlated with the absence of one MYO5B allele carrying a truncating nonsense or frameshift variant. Notably, biochemical and clinical parameters including treatment outcome were indistinguishable between patients presenting with normal and aberrant BSEP localization. Further, myosin-Vb and BSEP deficiency-associated FIC patient cohorts showed distinct biochemical and clinical phenotypes, indicating different underlying mechanisms. This suggests that whether or not BSEP localization was abnormal depended on the MYO5B genotype without a predictable effect on clinical parameters and treatment response. Treatment decisions should be guided by clinical parameters rather than by genotype or immunohistochemistry findings. Full article

Rare genetic diseases (RGDs) affect individuals, families, and healthcare systems worldwide. Population-scale genomic data remain largely restricted to Western cohorts with an estimated 10,000 RGDs. South Asian populations remain underrepresented in molecular, clinical, and genomic databases. This study presents the first preliminary molecular genetic characterization of RGDs in the Punjabi population of Pakistan. Data were collected from the provincial RGD registry at the Punjab Thalassemia and Other Genetic Disorders Prevention and Research Institute (PTGDPRI), Lahore. Families diagnosed using next-generation sequencing (NGS) between 2021 and 2023 were enrolled. Structured questionnaires captured clinical, demographic, and socioeconomic information, and statistical and genetic analyses were performed to assess allele frequencies, and disease distribution. The registry included 167 families with 72 distinct RGDs, with a mean burden of 0.81 ± 0.24 affected children per family. Niemann–Pick disease (NP), progressive familial intrahepatic cholestasis (PFIC), and mucopolysaccharidosis (MPS) were the most common diseases. Consanguinity was observed in 89% of families, 77% of which involved first-cousin marriages, and was significantly associated with RGD incidence. Most families belonged to low-income groups despite high literacy rates, underscoring inequity in healthcare. The primary and secondary variants included 131 variants, including copy number variants (CNVs) and single nucleotide variants (SNVs), annotated as pathogenic, likely pathogenic, or variants of unknown significance (VUS) across 109 genes, including 24 South Asian-enriched variants. This study provides the first genomic and epidemiological overview of RGDs in the Punjabi population. The findings reveal how genetic, socioeconomic, and cultural factors converge to amplify the RGD burden and highlight the need for affordable molecular diagnostics, inclusive genomic databases, and regional genomic surveillance initiatives in South Asia. Full article

Background/Objectives: Intrahepatic cholestasis of pregnancy (ICP) is associated with adverse perinatal outcomes. However, its metabolic consequences on newborns remain inadequately characterized. This study investigated amino acid, carnitine, and acylcarnitine profiles in neonates born to mothers with ICP. Methods: This retrospective study encompassed 299 neonates born to mothers with ICP. For comparative analysis, term infants without additional complications (ICP-term, n = 150) were compared with term controls (n = 150). Capillary blood samples collected at 24–48 h of life as part of newborn screening were analyzed using LC–MS/MS for acylcarnitine and amino acid profiles. Results: The ICP cohort exhibited a high preterm delivery rate (46.2%), with maternal bile acids negatively correlating with gestational age (r = −0.266, p < 0.001). No inborn errors of metabolism were observed. Elevated levels of amino acids (alanine, leucine/isoleucine, valine, tyrosine, arginine, glycine, and ornithine) and specific acylcarnitines (C5, C5-OH, C10:1, and C18:2), along with decreased levels of amino acids (argininosuccinic acid and glutamic acid) and specific acylcarnitines (C3, C5-DC, C6-DC, C14, C14:1, C16, C16:1, and C18:1-OH), were observed in ICP-term neonates (p < 0.05). Receiver operating characteristic curve analysis identified ornithine (area under the curve [AUC] = 0.74) and leucine/isoleucine (AUC = 0.73) as strong discriminators. A multivariable model integrating multiple metabolites achieved high accuracy (AUC = 0.86 ± 0.03). Conclusions: This first comprehensive characterization of neonatal metabolic alterations in ICP reveals amino acid metabolism, fatty acid oxidation, and mitochondrial function disruptions, suggesting fetal adaptation to a cholestatic intrauterine environment. Metabolomic profiling may improve understanding of maternal–fetal interactions and inform strategies for risk stratification and long-term monitoring. Full article

Acute liver injury during pregnancy is rare and predominantly associated with pregnancy-related conditions including acute fatty liver of pregnancy; Hemolysis, Elevated Liver Enzymes and Low Platelets syndrome; intrahepatic cholestasis of pregnancy; and preeclampsia. Drug-induced liver injury (DILI) is a less common and often overlooked cause of acute liver injury in pregnant patients. A literature search on acute liver injury during pregnancy and therapeutic plasma exchange was conducted, revealing the most common causative factors and syndromes. A 39-year-old woman was diagnosed with acute liver injury in the 23rd week of her third pregnancy and, upon extensive differential diagnoses, a suspicion of DILI occurred after the use of methyldopa. Methyldopa, the drug of choice for the treatment of hypertensive disorders of pregnancy, has a high safety profile for the developing fetus and is well tolerated by pregnant women, yet, in susceptible individuals, a hepatotoxic effect may occur. The drug was discontinued and symptomatic treatment with ursodeoxycholic acid and prednisone was implemented with marginal effect. Upon a multidisciplinary joint consultation, plasmapheresis procedures were introduced, granting a significant improvement in the patient’s liver function and enabling the continuation of the pregnancy. Plasmapheresis treatment was safely and effectively used for the first time in the therapeutic process in a pregnant patient with DILI. Interdisciplinary cooperation of specialists with gastroenterology, nephrology, and obstetrics expertise is crucial to achieving a timely diagnosis and begin effective treatment for pregnant patients with acute liver injury. Full article