Epstein-Barr virus infection usually presents as infectious mononucleosis with fever, pharyngitis, and lymphadenopathy, while cholestatic jaundice is a rare manifestation. We report a 36-year-old man who presented with progressive jaundice, pruritus, and dark-coloured urine with deranged liver function tests showing a cholestatic pattern. Evaluation revealed atypical lymphocytosis and positive EBV IgM serology after exclusion of biliary obstruction and other common causes of hepatitis. The patient improved with supportive treatment alone. This case highlights the importance of considering EBV infection in the differential diagnosis of cholestatic jaundice.

Clostridioides difficile infection (CDI) typically presents with diarrhea in elderly or antibiotic-exposed patients. We report a 40-year-old immunocompetent man with alcohol use disorder who presented with abdominal pain and jaundice, rapidly progressing to refractory constipation and colonic dilation (14.7 cm) mimicking acute colonic pseudo-obstruction. Conservative management including bowel regimens and neostigmine (generally contraindicated in suspected toxic megacolon) were attempted. Colonoscopic decompression revealed cecal pseudomembranes whereas rest of colon was grossly normal. Stool testing showed discordant results that is, negative toxin enzyme immunoassay but positive stool polymerase chain reaction (Nucleic Acid Amplification Testing), supporting CDI in appropriate clinical context. Despite appropriate broad-spectrum antibiotics and emergent subtotal colectomy for fulminant disease with ischemic changes, he developed septic shock and multiorgan failure. This atypical, fulminant CDI presentation without diarrhea, initially mimicking acute colonic pseudo-obstruction, with isolated cecum and ileum involvement, underscores diagnostic pitfalls and need for early polymerase chain reaction/endoscopy in unexplained megacolon.

Severe neonatal thrombocytopenia is a formidable complication of maternal immune thrombocytopenic purpura (ITP). We report the case of a male newborn, preterm at 32 weeks of gestation, presenting on day 4 of life with jaundice and severe cutaneous hemorrhagic syndrome. The maternal history was significant for severe ITP requiring splenectomy. The initial assessment showed a significant drop in platelets, with a count of 6,000/mm[3], even though the bone marrow aspirate appeared normal. Treatment included corticosteroids, platelet transfusions, polyvalent immunoglobulins, and phototherapy. This approach led to a gradual improvement, and the platelet count returned to normal within three months. This case highlights the association between the severity of maternal ITP and the risk of severe neonatal thrombocytopenia. It also emphasizes the importance of a thorough, team-based treatment plan that combines treatments to relieve symptoms with immunomodulatory therapies.

BACKGROUND Stasis within the biliary limb of the Roux loop is rarely reported after successful Kasai portoenterostomy (KPE) for biliary atresia (BA). CASE REPORT This retrospective report describes 2 children (cases 1 and 2, aged 47 and 42 months) who underwent KPE for type 3 BA at 33 and 54 days of life, respectively, with postoperative jaundice clearance at 3 months (total bilirubin levels of 15 and 6 μmol/L, respectively). Both children experienced frequent episodes of cholangitis (5 episodes each within 3 months and 1 month post-KPE, respectively); they presented with fever and elevated liver enzymes. Hepatobiliary scintigraphy demonstrated prompt hepatic uptake and excretion, with extrahepatic stasis in the Roux loop. Laparotomy (at 4 and 19 months of age, respectively) confirmed dense adhesions and bowel dilatation in the biliary limb in case 1, and at the T-junction of the enteroenterostomy of the Roux loop in case 2. Adhesiolysis, resection of the dilated bowel, and restoration of bowel continuity resulted in improved liver function, with cholangitis resolution during 33 months of follow-up in case 1 and 3 episodes of cholangitis over 23 months in case 2. CONCLUSIONS Evaluation of recurrent cholangitis after successful KPE for BA may reveal bile stasis in the Roux limb. However, further studies are required to clarify any association or causal relationship before general recommendations can be made regarding surgical exploration to relieve biliary stasis and reduce the risk of cholangitis.

Objective: To investigate the clinical characteristics and gene mutation status of progressive familial intrahepatic cholestasis caused by a ubiquitin-specific peptidase 53 (USP53) gene mutation (USP53-FIC) in a family. Methods: A female infant patient with USP53-FIC and her family who presented to the Department of Gastroenterology, Children's Hospital Affiliated with Zhengzhou University, in May 2025 with a one-month history of jaundice and yellow urine, which worsened over a one-week period of ecchymosis, were selected as the study subjects. Peripheral blood samples were collected from the patient, her parents, and her elder brother for whole-exome sequencing of the family, followed by Sanger sequencing for validation. Results: The patient was a 5-month-23-day-old female presenting primarily with jaundice of the skin and sclera, dark urine, and skin ecchymosis. Liver function tests indicated cholestasis, normal gamma-glutamyl transferase, and abnormal coagulation function. Whole-exome sequencing of the family revealed a compound heterozygous variant of c.1558C>T and c.829dup in the USP53 gene, inherited from her mother and father, respectively. Sanger sequencing confirmed that the patient's older brother carried the same variants. The c.1558C>T was previously reported as a pathogenic variant, while c.829dup was previously unreported. PVS1 + PM2_Supporting + PM3 was reported as a pathogenic variant according to the American Society for Medical Genetics and Genomics variant rating guidelines. Conclusion: The compound heterozygous variant c.1558C>T and c.829dup in the USP53 gene are the genetic cause of this USP53-FIC in a family. USP53-FIC should be suspected for infants who suddenly develop cholestasis accompanied by coagulation disorders but normal gamma-glutamyl transferase levels. Genetic testing is helpful in clarifying the diagnosis and guiding treatment. The c.829dup variant enriches the variant spectrum of the USP53 gene.

Maternal thyroid hormone homeostasis during early gestation is fundamental for fetal growth and development, yet the specific clinical implications of the ratio between free triiodothyronine and free thyroxine, a marker of peripheral deiodinase activity and metabolic status, remain insufficiently explored regarding newborn health.

Jaundice, a condition characterized by elevated circulating bilirubin generated by biliverdin reductase A (BVRA), is protective against malaria. Beyond its oxidoreductase activity, BVRA acts as a protein kinase and transcriptional regulator. To probe the protective effect of BVRA oxidoreductase activity, we generated mice harboring G17A and E97A missense mutations in its NAD(P)H-binding and reductase motifs, respectively. BVRA oxidoreductase activity was reduced by ∼95% and ∼80%-90% in Blvra [G17A] and Blvra [E97A] vs. wild-type (Blvra [WT]) mice, respectively. Plasmodium chabaudi chabaudi AS (Pcc) infection was lethal in Blvra [G17A] and Blvra [E97A], compared to the non-lethal outcome in control Blvra [WT] mice. Quantification of circulating unconjugated bilirubin in Pcc-infected mice revealed dose response effect whereby the mutant strains failed to reach a protective ∼20-30 μM (∼1-2 mg/dL) threshold. These findings establish the antimalarial effect of BVRA oxidoreductase activity and define a threshold of circulating bilirubin required for malaria protection, informing on therapeutic development and biomarker-guided strategies.