Early diagnosis of biliary atresia (BA) remains challenging, although timely recognition is critical for achieving favorable surgical outcomes. We present two infants in whom gadoxetic acid-enhanced MRI demonstrated imaging findings that supported early suspicion of BA. Two neonates with persistent cholestasis underwent routine laboratory evaluation, targeted ultrasonography, and hepatocyte-specific magnetic resonance imaging using gadoxetic acid. This contrast agent is actively taken up by functioning hepatocytes and is normally excreted into the biliary system during the delayed hepatobiliary phase, allowing functional assessment of bile formation and excretion. MRI findings, particularly biliary excretion on delayed images, were evaluated and correlated with intraoperative cholangiography. In both infants, hepatic parenchymal enhancement after contrast administration was preserved, indicating intact hepatocellular uptake. However, no biliary excretion was observed on delayed hepatobiliary-phase images. Intraoperative cholangiography confirmed biliary atresia in both cases. Although the diagnosis of biliary atresia is traditionally based on clinical findings, laboratory parameters, and ultrasonography, these approaches may remain inconclusive in some patients. Our findings suggest that gadoxetic acid-enhanced MRI, by demonstrating preserved hepatocellular uptake with absent biliary excretion, may serve as a useful adjunctive diagnostic tool and contribute to earlier and more confident identification of biliary atresia.

BACKGROUND Thyrotoxicosis is associated with well-recognized and clinically significant complications, including congestive heart failure and cardiac arrhythmias. The relationship between hyperthyroidism and hepatic dysfunction is complex, with several proposed pathophysiological mechanisms; however, direct cholestatic injury is frequently overlooked. Although mild liver enzyme elevation is common in hyperthyroidism, clinically overt jaundice is rare. Nevertheless, increasing evidence from case reports and case series suggests that thyrotoxicosis, especially Graves disease, can result in cholestatic-pattern jaundice. This temporal association is supported by substantial improvements in jaundice and liver biochemistry after antithyroid therapy. CASE REPORT A 62-year-old woman presented with a 1-month history of right upper quadrant abdominal pain, unintentional weight loss, and jaundice. Laboratory evaluation demonstrated cholestatic-pattern liver injury, and abdominal ultrasound revealed a solitary gallstone without evidence of acute or chronic cholecystitis. Abdominal computed tomography demonstrated right-sided heart failure with pericardial and bilateral pleural effusions and congestive hepatopathy. Endoscopic retrograde cholangiopancreatography showed no filling defects, excluding biliary obstruction. Because the patient had persistent sinus tachycardia, thyroid function tests were performed. The findings were consistent with primary hyperthyroidism and elevated thyroid-stimulating hormone receptor antibodies); thyroid ultrasound and scintigraphy results supported toxic multinodular goiter. Treatment with methimazole led to dramatic improvement of the jaundice. Given the possibility of competing etiologies, thyrotoxicosis was considered the most likely contributing factor to cholestatic jaundice onset. CONCLUSIONS This case highlights the importance of considering hyperthyroidism in the differential diagnosis of jaundice, particularly in diagnostically challenging cases.

Autoimmune hepatitis (AIH) is classically a chronic immune-mediated inflammatory liver disease; however, it may present abruptly as acute severe hepatitis and, in a minority of cases, progress to liver failure. Early recognition and prognostic stratification are essential in severe presentations, as some patients may require urgent referral for liver transplantation. We report a 66-year-old female presenting with jaundice and marked hepatocellular injury who rapidly progressed to acute-on-chronic liver failure (ACLF) with multiorgan dysfunction. Despite supportive care and an extensive etiological workup, her condition deteriorated with hepatic encephalopathy, acute kidney injury consistent with hepatorenal syndrome, and infectious complications. A transjugular liver biopsy demonstrated intense inflammatory activity with prominent lymphoplasmacytic infiltrates and interface hepatitis, supporting AIH on a background of previously unrecognized chronic liver disease. Given poor prognostic indicators (Model for End-Stage Liver Disease-Sodium (MELD-Na) score >30 and ACLF grade 3), she was urgently referred to a transplant center and successfully underwent emergency liver transplantation. This case highlights the importance of maintaining a high index of suspicion for AIH in cases of acute liver injury of unclear etiology, performing early and serial prognostic reassessment, and expediting transplant evaluation when advanced organ failure develops.

The American Academy of Pediatrics identified significant hemolysis as a significant neurotoxic risk factor for newborns with jaundice in its 2022 guideline for managing hyperbilirubinemia. The guideline recommends starting phototherapy at a lower level than otherwise if significant hemolysis is present. Currently, the optimal way to measure hemolysis is by determining an infant's level of end-tidal carbon monoxide corrected for ambient carbon monoxide (ETCOc). However, it is unclear what the optimal ETCOc level is for determining significant hemolysis. Given the differences in ETCOc levels among infants of different backgrounds, the most reasonable conclusion would be for each unit to determine the mean ± standard deviation ETCOc level of an inclusive group of 200-500 infants in their unit. Each unit could then decide whether to use the 95th, 75th, or some other percentile value as their unit's indicator of significant hemolysis.

A 91-year-old Chinese man with a 30-year history of diabetes and 5-year history of hypertension presented in January 2026 with acute epigastric pain and obstructive jaundice. Unenhanced CT showed dilated bile ducts with multiple linear hyperattenuating structures mimicking biliary stones. ERCP after sphincterotomy yielded abundant blood clots but no calculi, with persistent active bleeding; cholangioscopy revealed an irregular friable bleeding lesion at the left hepatic duct/hilar confluence. Fully covered metal and plastic stents were placed, with marked reduction of bleeding. Follow-up CT two weeks later showed a 5.5×3.6 cm segment-VI mass with wash-in/wash-out enhancement, consistent with hepatocellular carcinoma. Intraductal blood clots can mimic biliary stones; cholangioscopy localized the bleeding source during ERCP and redirected management.

Cholecystocolonic fistula (CCF) is a rare type of cholecystoenteric fistula, which are sometimes diagnosed incidentally in patients undergoing cholecystectomy. They are usually a complication of chronic cholecystitis, often secondary to gallstones, and they are difficult to diagnose due to their rarity and vague clinical presentation. If untreated, they can lead to complications such as acute cholangitis, biliary peritonitis, and biliary cirrhosis. This highlights the importance of early recognition of CCF and timely treatment. While the generally accepted management is surgical, there are no consensus guidelines available. We present a case of a 79-year-old with a CCF, diagnosed preoperatively in the setting of workup for acute cholangitis and choledocholithiasis. She presented with four days of right-sided abdominal pain and one day of vomiting and new jaundice. She was initially hypotensive with elevated inflammatory markers, hyperbilirubinaemia, and deranged liver function tests. Contrast-enhanced CT revealed an 11 mm distal common bile duct calculus with hepatic biliary dilatation, gas in the gallbladder lumen, and a large gallstone in the hepatic flexure, which were suggestive of an underlying CCF. She underwent a laparoscopic converted to open cholecystectomy with transcystic bile duct exploration and choledochotomy, as well as right hemicolectomy due to extensive oedema and inflammation surrounding the CCF. This was later followed by endoscopic retrograde cholangiopancreatography (ERCP) and biliary sphincterotomy. Her CCF and acute cholangitis were thus successfully treated with surgical intervention, and she recovered well. The rare occurrence of CCF highlights the importance of having a high index of clinical suspicion preoperatively as well as maintaining surgical flexibility if it is encountered during an operation. Early recognition and surgical intervention of CCF are important to prevent life-threatening complications.

Saw palmetto (SP) is a widely used herbal supplement for benign prostatic hyperplasia (BPH) and is generally considered safe. However, rare cases of SP-associated drug-induced liver injury (DILI) have been reported. We describe a case of cholestatic hepatitis attributed to SP, highlighting the diagnostic challenges associated with herbal supplement use and polypharmacy. A 70-year-old male with a history of BPH, hypertension, chronic obstructive pulmonary disease, atrial fibrillation, and cholecystectomy presented with one month of jaundice, pruritus, and pale stools. Physical examination demonstrated scleral icterus without abdominal tenderness. Laboratory evaluation revealed an alkaline phosphatase level of 215 U/L, total bilirubin of 7.3 mg/dL (direct bilirubin = 5.0 mg/dL), alanine aminotransferase of 305 U/L, aspartate aminotransferase of 133 U/L, and an international normalized ratio of 3.8 while receiving warfarin therapy for atrial fibrillation. Viral hepatitis serologies were negative. Right upper quadrant ultrasonography demonstrated mild biliary ductal prominence, and magnetic resonance cholangiopancreatography excluded biliary obstruction. Liver injury was initially attributed to congestive hepatopathy because of newly reduced left ventricular ejection fraction (34%-40%). However, the patient remained clinically euvolemic, liver biochemistries failed to improve, and progressive hyperbilirubinemia prompted further evaluation. A detailed medication history revealed over-the-counter SP use for approximately four months, discontinued two months before presentation, and a recent one-week course of trimethoprim-sulfamethoxazole for a urinary tract infection. Transjugular liver biopsy with measurement of the hepatic venous pressure gradient (6 mmHg) demonstrated cholestatic hepatitis with portal and lobular inflammation, eosinophilic infiltration, and bile duct proliferation, consistent with DILI. Right and left heart catheterization demonstrated normal filling pressures and the absence of obstructive coronary artery disease, making congestive hepatopathy unlikely. Warfarin was reversed with vitamin K and transitioned to apixaban because of concern for potential hepatotoxicity. The patient was treated with ursodiol and cholestyramine, resulting in gradual improvement in liver enzymes and bilirubin, and was discharged with close hepatology and cardiology follow-up. This case highlights SP as a rare but important suspected cause of cholestatic DILI. Although causality cannot be definitively established because of concomitant exposure to other drugs, SP was considered the most likely implicated agent based on the temporal relationship with exposure, exclusion of alternative etiologies, compatible histopathologic findings, and clinical improvement after its discontinuation. Clinicians should routinely inquire about over-the-counter and herbal supplement use when evaluating unexplained liver injury. Increased awareness, comprehensive medication reconciliation, and improved regulation of dietary supplements may facilitate earlier recognition and reduce preventable hepatotoxicity.

Commercial jaundice meters rely on reflectance data from specific wavelengths for Transcutaneous bilirubin (TcB) measurements. However, skin color bias is introduced due to melanin contribution. In this study, we evaluated melanin concentration as an objective indicator of neonatal skin pigmentation and assessed the performance of melanin corrected TcB measurements (TcBcorr). A total of 333 neonates were categorized into four groups using the Neomar skin color scale. Melanin concentration estimated from neonatal reflectance spectra strongly correlated with Neomar classification (Spearman's r = 0.90), with group differences confirmed by Kruskal-Wallis and Dunn's tests. TcBcorr values showed good agreement with total serum bilirubin (TSB) across all color groups with minimal bias (-0.06 to 0.11 mg/dL). Compared with commercial TcBmeter readings, skin color bias is reduced, particularly in the darker groups (colors 3 and 4). Chromophore-decoupled diffuse reflectance spectroscopy offers a skin color unbiased, clinically reliable approach for TcB measurements across diverse populations.