A 23-month-old, 8-kg boy with known glucose-6-phosphate dehydrogenase (G6PD) deficiency presented with a coin lodged in the upper esophagus and required urgent rigid esophagoscopy under general anesthesia. Anesthetic management was planned to avoid drugs with oxidative potential and to minimize physiologic stressors that could contribute to hemolysis or methemoglobinemia. General anesthesia was performed using agents considered safe in patients with G6PD deficiency, with intraoperative management focused on maintaining normoxia using the lowest possible inspired oxygen concentration needed to maintain oxygen saturation above 95%, normothermia, and hemodynamic stability. The foreign body was removed without complications, and there were no clinical signs of hemolysis or methemoglobinemia during hospitalization. Postoperative monitoring included serial hemoglobin assessment and clinical surveillance for jaundice and dark urine for more than 24 hours, with no evidence of delayed hemolysis. A follow-up phone call at 72 hours confirmed that there were no symptoms. This case highlights a practical perioperative approach to emergent pediatric anesthesia in a patient with G6PD deficiency, emphasizing careful drug selection and proactive prevention and monitoring of oxidative triggers.

Hepatitis A virus (HAV) and hepatitis E virus (HEV) are common causes of acute viral hepatitis in developing countries where inadequate sanitation and contaminated water supplies facilitate fecal-oral transmission. Although both infections are usually self-limiting, co-infection may result in atypical presentations and pose diagnostic challenges. We report the case of a previously healthy 14-year-old girl who presented with a 5-day history of nausea, vomiting, and anorexia, followed by sudden-onset jaundice and dark urine. She denied fever, abdominal pain, pruritus, bleeding manifestations, or altered mental status. Physical examination revealed marked icterus without hepatosplenomegaly or stigmata of chronic liver disease. Laboratory investigations demonstrated significant hyperbilirubinemia and elevated liver transaminases. Serological testing confirmed acute HAV and HEV co-infection with positive anti-HAV IgM and anti-HEV IgM antibodies. Abdominal ultrasonography showed a normal-sized liver with altered echogenicity and a characteristic "starry sky" appearance, along with gallbladder wall thickening without calculi or sludge. The patient received supportive treatment, including intravenous fluids, antiemetics, and symptomatic care. Her clinical condition improved steadily, with resolution of symptoms and progressive normalization of liver function tests during hospitalization. She was discharged in stable condition and remained asymptomatic at 14-day follow-up, with complete biochemical and radiological recovery. This case highlights that HAV-HEV co-infection can present with isolated jaundice and minimal systemic symptoms despite significant hepatic involvement. Recognition of characteristic imaging findings and timely serological evaluation can facilitate early diagnosis. Favorable outcomes can be achieved with supportive management, while prevention through vaccination, safe drinking water, and improved hygiene remains essential in endemic regions.

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.

The illicit synthetic cannabinoid receptor agonist (SCRA) market has experienced multiple changes since its appearance in the 2010s and, most recently, in response to a class-wide SCRA ban imposed by China in 2021. The reemergence of "older" SCRAs, such as the highly potent indole- and indazole-3-carboxamide-containing drugs, has occurred due to the sale of unregulated precursors on grey-market and dark websites. This shift poses a significant threat to public health, and recent intoxication outbreaks associated with these types of SCRAs demonstrate the need for further toxicological research to aid in better understanding their metabolism and appropriate targets for toxicological testing. Testing for metabolites can extend the detection window of SCRAs as parent drugs are rapidly metabolized and present at low or potentially undetectable concentrations in biological samples, including urine. In these instances, metabolites may be more sensitive biomarkers of SCRA use. This study characterized the metabolites for the synthetic cannabinoids MDMB-BINACA (also known as MDMB-BUTINACA), MDMB-PICA, and AB-CHMINACA via in vitro human liver microsome (HLM) incubation and analysis by liquid chromatography-quadrupole time-of-flight mass spectrometry (LC-QTOF-MS). Biotransformations observed in this study included ester and amide hydrolysis, oxidation, carboxylation, and dealkylation. Nine metabolites were identified for MDMB-BINACA, five of which were verified through retrospective analysis of authentic samples. Nine metabolites were also identified for both MDMB-PICA and AB-CHMINACA, with two metabolites of AB-CHMINACA verified in authentic samples. Characterization of the metabolism of these potent drugs allows for the use of the identified biomarker to improve forensic toxicology analyses and interpretation, especially when the use of synthetic cannabinoids is suspected.

Lipin-1 deficiency is a rare inherited metabolic disorder and a major genetic cause of severe, recurrent rhabdomyolysis in early childhood, carrying a significant risk of acute kidney injury and mortality if unrecognized. We report the case of a male toddler who first presented at 19 months of age with dark urine and intercurrent viral illness. Initial investigations demonstrated hematuria/myoglobinuria, proteinuria, and markedly elevated transaminases, leading to a presumptive diagnosis of glomerulonephritis. Creatine kinase (CK) was not measured at that time, and the episode was retrospectively felt to represent missed rhabdomyolysis. The patient subsequently presented similarly with abdominal pain and dark urine when profound rhabdomyolysis was identified by checking CK (CK >120,000 U/L). Aggressive hyperhydration led to biochemical improvement, and genetic testing confirmed a homozygous pathogenic LPIN1 exon 18 deletion. Since diagnosis, he has experienced multiple recurrent episodes of rhabdomyolysis, predominantly triggered by viral infections, requiring repeated admissions and intensive metabolic management. Notably, this patient also has a background of global developmental delay (GDD). To our knowledge, this represents the first reported case describing an association between LPIN1 deficiency and developmental delay. Emerging experimental and clinical evidence suggests a potential biological link between LPIN1 dysfunction, impaired myelination, and abnormal neurodevelopment, raising the possibility that developmental delay may be an under-recognized phenotypic feature of this condition. This case highlights the importance of considering rhabdomyolysis in children presenting with dark urine and intercurrent illness and the critical role of early CK measurement in preventing missed diagnoses. Prompt recognition of LPIN1 deficiency is essential, as delayed treatment may result in life-threatening complications and avoidable morbidity.

Urinary tract infections (UTIs) are among the most common diseases in companion animals, but empirical antibiotic treatments without culture often lead to recurrence and resistance. Vagococcus species are rarely reported as pathogens in animals, and Vagococcus lutrae has not previously been described in dogs. We report the first case of V. lutrae-associated cystitis in a dog in Türkiye. An 8-year-old female English Setter developed persistent dysuria and hematuria after surgery for pelvic trauma. Despite multiple antibiotic treatments (enrofloxacin, ceftriaxone, ciprofloxacin, amoxicillin-clavulanic acid), no clinical improvement was observed. On presentation, hematology indicated leukocytosis with regenerative anemia, and ultrasonography revealed bladder wall thickening and intraluminal hyperechoic material consistent with cystitis. Urine obtained by cystocentesis appeared dark red, alkaline (pH 9), and contained struvite crystals and urothelial cells. Urine culture obtained by cystocentesis yielded a pure growth of Gram-positive cocci identified as V. lutrae using MALDI-TOF mass spectrometry. Antibiotic susceptibility testing showed resistance to commonly used antimicrobials, including amoxicillin, ceftriaxone, ciprofloxacin, doxycycline, and gentamicin, but susceptibility to daptomycin, vancomycin, and teicoplanin. Supportive therapy was initiated; however, the patient died on the third day of treatment. This case suggests the potential pathogenic relevance of V. lutrae in dogs and emphasizes the importance of culture and sensitivity testing in recurrent or treatment-resistant UTIs to guide appropriate antimicrobial therapy.

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.

Acute kidney injury (AKI) is a severe and frequent complication following bee stings, with a reported incidence of 30-50%. Early identification is clinically challenging due to the delayed rise in serum creatinine. This retrospective study aimed to develop and validate an interpretable machine learning model for the early prediction of AKI in bee-sting patients. We included 305 patients admitted between January 2018 and September 2025, of whom 99 (32.5%) developed AKI according to Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Least Absolute Shrinkage and Selection Operator (LASSO) regression was employed for feature selection from 33 baseline variables, identifying eight key predictors, including lactate, creatinine, and dark urine. Six machine learning algorithms - logistic regression, random forest, support vector machine, neural network, extreme gradient boosting (XGBoost), and light gradient boosting machine - were developed and evaluated. The XGBoost model demonstrated superior performance, achieving an area under the receiver operating characteristic curve of 0.964 and an accuracy of 92.6% on the test set. SHapley Additive exPlanations analysis was applied to interpret the optimal model, highlighting creatinine, lactate dehydrogenase, lactate, and dark urine as the most influential predictors. A clinically applicable nomogram was constructed and showed good calibration and utility. In conclusion, this study successfully developed a high-performance and interpretable XGBoost model for early prediction of bee-sting-induced AKI. The validated nomogram provides an accessible bedside decision-support tool to facilitate timely risk stratification and intervention, potentially improving patient outcomes.

BACKGROUND Legionella pneumophila is a common and often severe cause of community-acquired pneumonia. Infection with this organism is also known to be associated with a wide range of extrapulmonary manifestations, such as neurologic deficits, hyponatremia, acute kidney injury, and elevated liver enzymes. Other complications, such as rhabdomyolysis and hypertriglyceridemia, are rare. CASE REPORT A rare presentation of Legionella infection was observed in a 34-year-old man, characterized by severe rhabdomyolysis, acute kidney injury (AKI), and hypertriglyceridemia. The patient presented with severe muscle cramps, weakness, dark urine, diarrhea, fever, and chills. Initial laboratory evaluations revealed significantly elevated creatine kinase (163 600 U/L), creatinine (7.79 mg/dL), and transaminases (AST 1179 U/L, ALT 184 U/L), in conjunction with hyponatremia. A chest X-ray and computed tomography (CT) showed left basilar pneumonia, and a positive Legionella urine antigen test confirmed the diagnosis. A fasting lipid panel also revealed profound hypertriglyceridemia (1173 mg/dL). The patient's only identified risk factor for Legionella infection was vaping. Despite aggressive therapeutic interventions, including intravenous fluids and azithromycin, AKI progressed, necessitating hemodialysis. The patient also received treatment for alcohol withdrawal and severe hypertension. While creatine kinase, AST, and ALT levels gradually decreased, BUN and creatinine remained elevated at discharge, with ongoing plans for outpatient hemodialysis. CONCLUSIONS Legionella pneumonia can present with a diverse array of extrapulmonary manifestations. This case illustrates the diverse and potentially life-threatening systemic complications associated with Legionella infection.

Hepatitis A virus (HAV) infection is usually self-limited, but a minority of cases progress to acute liver failure (ALF), particularly, in resource-limited settings. We report a previously healthy 19-year-old woman who presented with 20 days of jaundice, dark urine, and hepatic encephalopathy. Baseline tests showed total bilirubin 18.3 mg/dL, aspartate aminotransferase 281 U/l, alanine aminotransferase 341 U/l, international normalized ratio (INR) 1.23, and positive anti-HAV immunoglobulin M/immunoglobulin G. Although she did not meet formal ALF criteria at presentation, within 72 hours, she progressed to ALF, with bilirubin rising to 28 mg/dL, INR to 1.8, and ammonia to 140 µg/dL; ultrasonography revealed hepatomegaly. In the absence of liver transplantation or continuous renal replacement therapy, a resource-adapted supportive bundle was implemented, including intravenous N-acetylcysteine, vitamin K, neuroprotection, glucose control, early enteral nutrition, conservative transfusion, and infection surveillance. Clinical and biochemical parameters improved, and she was discharged after approximately 4 weeks, with recovery on follow-up. This case highlights early warning signs and the feasibility of a structured non-transplant management pathway for HAV-associated ALF in constrained settings.

A 46-year-old man with non-Hodgkin lymphoma (NHL) in remission since 2014 presented with progressive dizziness, fatigue, and dark-colored urine. Laboratory workup revealed hemoglobin levels of 5.9 g/dL, elevated lactate dehydrogenase (LDH), hyperbilirubinemia, low haptoglobin, and a positive direct Coombs test for IgG, C3, and poly-specific antibodies, confirming warm autoimmune hemolytic anemia (wAIHA). Immunoglobulin profiling showed low IgM and IgA with high-normal IgG, suggesting chronic immune dysregulation, whereas abdominal imaging revealed mesenteric calcifications, raising concern for residual lymphomatous tissue potentially driving ongoing autoimmune activation. Despite corticosteroids and intravenous immunoglobulin (IVIG), persistent hemolysis necessitated four units of packed red blood cell (PRBC) transfusions and escalation to rituximab, after which gradual clinical stabilization was achieved, highlighting the refractory nature of wAIHA in the setting of previous lymphoproliferative malignancy. Serial monitoring of hemoglobin, reticulocyte count, and LDH throughout the clinical course demonstrated dynamic trends consistent with partial but meaningful immunosuppression, underscoring the value of longitudinal laboratory surveillance in guiding therapeutic escalation decisions. The presence of mesenteric calcifications, combined with a skewed immunoglobulin profile, provided important structural and immunologic clues to the underlying pathophysiology, illustrating how multimodal diagnostic evaluation can reveal occult contributors to delayed autoimmune phenomena even in the absence of overt malignancy recurrence. This case underscores the importance of recognizing delayed AHA in NHL survivors and the necessity of long-term hematologic surveillance, periodic cross-sectional imaging, and a low threshold for multidisciplinary consultation even after prolonged remission.