In a dairy herd in the state of Goiás, Central-West Brazil, a cow died following an acute illness characterized by jaundice and hemoglobinuria. Necropsy revealed jaundice, dark-red urine and dark-red discoloration of the kidneys, and a diffusely copper-colored liver with two extensive, firm lesions surrounded by hyperemic halos in the right and left lobes. Histopathological analysis showed multifocal coagulative necrosis in the liver, accompanied by abundant intralesional bacillary structures and multifocal thrombosis. Renal lesions included tubular cell degeneration and necrosis, intracellular hyaline droplet accumulation, and occasional proteinaceous casts within the tubular lumen. PCR and sequencing confirmed the presence of Clostridium haemolyticum DNA in the liver lesions. Based on the characteristic clinical presentation and pathological findings, the diagnosis of bacillary hemoglobinuria was established, with further molecular evidence of the clostridial agent. To our knowledge, this is the first reported case of bacillary hemoglobinuria in the Central-West region of Brazil, and an unusual report in the Tropical Zone in the country, especially in dairy cattle.

Babesiosis is a tick-borne infection caused by intraerythrocytic Babesia parasites and may result in severe hemolytic anemia and systemic complications. Coinfection with other Ixodes-borne pathogens may further complicate diagnosis and management. We report a 45-year-old immunocompetent man working as a landscaper in Connecticut who presented with syncope following two weeks of fever, fatigue, diaphoresis, arthralgias, jaundice, and dark urine. Laboratory evaluation revealed profound hemolytic anemia with a hemoglobin of 6.8 g/dL, elevated lactate dehydrogenase (LDH), undetectable haptoglobin, reticulocytosis, and stage 1 acute kidney injury. Peripheral blood smear demonstrated characteristic Maltese cross formations, with approximately 0.6% parasitemia, and polymerase chain reaction (PCR) testing confirmed Babesia microti and Borrelia burgdorferi coinfection. Direct antiglobulin testing for immunoglobulin G (IgG) was negative. The patient required intensive care monitoring and transfusion and improved following treatment with atovaquone, azithromycin, and doxycycline. Subsequent outpatient evaluation identified asymptomatic Strongyloides stercoralis infection, which was treated with ivermectin. This finding was clinically significant because warm autoimmune hemolytic anemia is a recognized complication of babesiosis and may require corticosteroid therapy, which can precipitate potentially life-threatening Strongyloides hyperinfection in patients with occult infection. This case highlights that severe babesiosis may occur despite low-level parasitemia and emphasizes the importance of recognizing coinfections and obtaining a detailed occupational and environmental exposure history, particularly when future immunosuppressive therapy may be considered.

Background and Objectives: The association between SARS-CoV-2 infection, COVID-19 vaccination, and the development of rhabdomyolysis remains unclear. This systematic review aimed to comprehensively synthesize and analyze the available evidence on the occurrence of rhabdomyolysis in the context of SARS-CoV-2 infection and COVID-19 vaccination. Materials and Methods: A literature search was conducted in PubMed, Scopus, EMBASE, and Web of Science. The review followed PRISMA 2020 guidelines, assessing methodological quality. Statistical analyses were performed using STATA v18. Results: A total of 133 patients with rhabdomyolysis associated with SARS-CoV-2 infection were identified from 93 case reports and 7 case series; the median age was 45.5 years (IQR: 24-62), with a predominance of males (72.9%). Additionally, 13 observational studies comprising 818 patients with rhabdomyolysis associated with SARS-CoV-2 infection were included. Among cases associated with SARS-CoV-2 vaccination, 20 patients were identified from 20 case reports; the median age was 52.5 years (IQR: 22.5-76.5), with a predominance of males (75%). These cases were primarily associated with mRNA-based vaccines, particularly Pfizer-BioNTech BNT162b2 (50%) and Moderna (20%), and occurred predominantly after the first and second doses. The most frequent clinical manifestations in both groups were fever, myalgia, and dark urine. Clinical outcomes were favorable in most patients, both among infection-associated cases (72.2%) and vaccination-associated cases (80%). Conclusions: Rhabdomyolysis has been documented during SARS-CoV-2 infection, although its true frequency remains uncertain, whereas cases following COVID-19 vaccination do not establish causality or platform-specific risks.

Neuroendocrine and circadian dysfunctions are thought to underlie bipolar disorder (BD) and could be implemented as markers of complex symptom conditions, including the presence of Post-Traumatic Stress Disorder (PTSD) comorbidity. The primary objective of this study was to investigate neuroendocrine profiles in different BD phenotypes through the measure of nocturnal urinary levels of Cortisol (stress-response factor) and 6-sulfatoxymelatonin (aMT6s; light/dark signal) in euthymic BD patients diagnosed with PTSD (PTSD group) or with major depressive episodes without trauma symptoms (DEP group). Both groups were compared against healthy controls (CTL). Nighttime urinary levels of aMT6s and Cortisol were analyzed by competitive ELISA, with ensuing values normalized for specific gravity. The Cortisol-to-aMT6s ratio (Cort/aMT6s) was calculated as an exploratory proxy for the homeostatic balance between HPA-mediated catabolic/coping activities and Melatonin-related reparative functions. Clinical severity and psychosocial activities were assessed by using mood HAM-D, YMRS, trauma IES-R and functioning WSAS scales. Results revealed distinct biological patterns: PTSD subjects showed increased nocturnal Cortisol compared to DEP and CTL groups, whereas DEP patients exhibited lower aMT6s levels and an elevated Cort/aMT6s ratio. Cortisol and aMT6s correlated positively in PTSD, while the ratio correlated positively with Cortisol solely in controls. Clinically, Cortisol correlated positively with IES-R and functional impairment (WSAS), whereas aMT6s correlated negatively with HAM-D and YMRS scores. Present findings suggest a possible neuroendocrine divergence in BD patients with depression versus PTSD: nocturnal Melatonin deficiency may be associated with depression, while HPA-axis hyperactivity and altered crosstalk between the two systems may characterize PTSD comorbidity, with the Cort/aMT6s ratio as a potential index of impaired daily functioning. These results could be promising for the use of biomarkers linked to allostatic and circadian responses within the BD spectrum.

Congenital portosystemic shunts (CPS) are rare vascular malformations associated with hepatic and extrahepatic complications, including hepatopulmonary syndrome (HPS). We present a 16-year-old adolescent with no relevant medical history who presented with episodes of abdominal pain, jaundice, and dark urine. Ultrasound revealed a heterogeneous liver with multiple hyperechoic nodules and no visualization of the intrahepatic portal vein. Angiography demonstrated an extrahepatic portocaval shunt at the level of the portal trunk, with no opacification of the intrahepatic portal tree and low portal pressures; liver biopsy revealed regenerative nodular hyperplasia. Subsequently, he developed hypoxemia with orthodeoxygenation and required home oxygen therapy. He was placed on the waiting list and received an orthotopic liver transplant from a deceased donor. This case highlights the need for timely diagnosis, proper anatomical characterization, and individualized treatment planning in CPS associated with HPS.

We report a 35-year-old man with chronic hepatitis B infection and decompensated liver cirrhosis who presented with an 8-month history of progressive fatigue, exertional limb weakness, anorexia, and dark urine, which partially improved following hepatoprotective and anti-cholestatic therapy. One day before admission, his condition deteriorated abruptly, with fever, chills, diarrhea, profound fatigue, and rapidly progressive bilateral lower-extremity oedema. Laboratory evaluation revealed severe systemic inflammation and coagulopathy, including a white blood cell count of 8.4 × 10[9]/L with neutrophil predominance (absolute neutrophil count, 7.6 × 10[9]/L; neutrophil percentage, 90.7%), severe thrombocytopenia (23 × 10[9]/L), markedly elevated inflammatory markers (C-reactive protein, 68.7 mg/L; procalcitonin, 5.81 ng/mL; interleukin-6, >5000 pg/mL), hypoalbuminemia, and prolonged prothrombin time. Empirical antimicrobial therapy was initiated immediately. Blood cultures obtained on admission became positive within 24 hours and were subsequently identified as Vibrio vulnificus. Antimicrobial therapy was adjusted according to susceptibility testing, and surgical incision, drainage, and debridement were performed for progressive lower-extremity soft tissue infection. The patient gradually improved after pathogen-directed antimicrobial therapy and surgical source control and was discharged after clinical stabilization. This case highlights the importance of early recognition, appropriate antimicrobial therapy, and timely surgical intervention in severe V. vulnificus infection, particularly among patients with underlying liver disease.

Background and Clinical Significance: Tarui disease, or glycogen storage disease type VII, is a rare autosomal recessive metabolic myopathy caused by muscle phosphofructokinase deficiency. Its manifestations include exercise intolerance, exertional myalgia, muscle cramps, myoglobinuria, rhabdomyolysis, hyperuricemia, and compensated hemolysis. The hematologic phenotype may obscure the underlying metabolic disorder and raise concern for a clonal myeloid neoplasm. Case Presentation: A 23-year-old man was referred for persistent mild thrombocytopenia following evaluation for jaundice and hepatosplenomegaly. He had undergone cholecystectomy at 18 years of age and reported exercise-induced myalgia, muscle cramps, and episodes of dark urine. Laboratory investigations demonstrated mild monocytosis, reticulocytosis, thrombocytopenia, hyperuricemia, elevated lactate dehydrogenase, and predominantly unconjugated hyperbilirubinemia, with a negative direct antiglobulin test. Selected inherited hemolytic disorders, hemoglobinopathies, and paroxysmal nocturnal hemoglobinuria were excluded. Bone marrow examination showed marked erythroid hyperplasia and mild megakaryocytic dysplasia. Testing for JAK2, CALR, and MPL mutations and an extended myeloid next-generation sequencing panel identified no pathogenic variants, and monocytosis resolved during follow-up. Whole-exome sequencing identified a homozygous PFKM missense variant, NM_001354735.1:c.1087A>T, p.(Ile363Phe), classified as a variant of uncertain significance. The patient subsequently developed severe rhabdomyolysis, with a creatine kinase level of 225,000 U/L and recovered after intensive intravenous hydration without renal impairment. Conclusions: Tarui disease should be considered in young patients with compensated hemolysis, hyperuricemia, exertional muscle symptoms, dark urine, or rhabdomyolysis, even when hematologic abnormalities suggest a myeloid disorder. The highly concordant phenotype and homozygous PFKM variant support a clinically probable diagnosis, although pathogenicity remains unconfirmed. Functional and segregation evidence may strengthen causal interpretation and support future variant reclassification.

Energy drinks are multi-ingredient beverages whose clinically apparent hepatotoxicity is described mainly in case reports. A 25-year-old man with obesity and approximately three years of daily high-volume energy drink consumption (1-2.5 L/day) presented with epigastric pain, dark urine, jaundice, and systemic inflammation. His admission total bilirubin was 8.0 mg/dL, alanine aminotransferase 380 U/L, aspartate aminotransferase 187 U/L, gamma-glutamyl transferase 471 U/L, and alkaline phosphatase 232 U/L. The resulting R ratio was 4.5, indicating a mixed biochemical pattern. Computed tomography and magnetic resonance cholangiopancreatography excluded biliary obstruction and demonstrated hepatosplenomegaly, diffuse hepatic edema, and enlarged porta hepatis lymph nodes. Viral and autoimmune investigations were unrevealing. Core liver biopsy showed centrilobular and midzonal cholestasis with bilirubinostasis, minimal lobular inflammation, portal lymphogranulocytic infiltrates, preserved bile ducts, and no fibrosis. The energy drink exposure was stopped. Empiric antibiotics, ursodeoxycholic acid, and intravenous methylprednisolone were administered. By discharge on hospital day 18, bilirubin and C-reactive protein had substantially decreased; aminotransferases remained elevated but were declining from their peak. At four months, aspartate aminotransferase, alkaline phosphatase, and C-reactive protein were within the supplied institutional reference ranges, while alanine aminotransferase and gamma-glutamyl transferase had markedly improved. A retrospective updated Roussel Uclaf Causality Assessment Method score of 3 supported only a possible product-level association. This case illustrates that biochemical classification and histology may diverge and that causality should not be assigned to a single energy drink ingredient when the exact formulation, dose, and untreated dechallenge are unavailable.

Focal nodular hyperplasia (FNH) is a benign hepatic lesion that is typically asymptomatic and most often found incidentally. Biliary obstruction caused by FNH is rare and can create diagnostic uncertainty, particularly when imaging can mimic vascular lesions, hepatocellular adenoma, bile duct adenoma, or congenital hepatobiliary abnormalities. We present the case of a 38-year-old woman with hypertension who was noted to have persistently abnormal liver enzymes on routine outpatient blood tests. She denied symptoms such as jaundice, pruritus, pale stools, dark urine, weight loss, nausea, vomiting, or abdominal pain. Laboratory tests showed a chronic cholestatic-predominant pattern with elevated alkaline phosphatase, mildly elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT), fluctuating hyperbilirubinemia, and markedly elevated gamma-glutamyl transferase (GGT). Ultrasound revealed intrahepatic biliary ductal dilatation and indeterminate cystic areas within the liver. Computed tomography revealed chronic biliary ductal dilatation, hepatic parenchymal deformity, a mass-like hypertrophied hepatic segment, and a central arterial-enhancing structure initially concerning for aneurysm or pseudoaneurysm. Magnetic resonance imaging (MRI) and magnetic resonance cholangiopancreatography (MRCP) demonstrated marked intrahepatic biliary dilatation, an arterially enhancing lesion suspicious for atypical FNH, and a second exophytic lesion causing mass effect on the biliary tree. Differentials included atypical adenoma, intrahepatic bile duct adenoma, vascular lesion, or congenital anomaly. Because serial imaging remained indeterminate, percutaneous liver biopsy was performed. Histopathology showed preserved lobular architecture, intermittent thin fibrous septa, focal sinusoidal dilatation, ductular reaction, and map-like glutamine synthetase staining with membranous beta-catenin staining, supporting the diagnosis of FNH. This case highlights an atypical presentation of FNH causing chronic intrahepatic biliary obstruction and emphasizes the importance of integrating imaging, multidisciplinary review, and histopathology when benign hepatic lesions present atypically and influence management decisions.

Leptospirosis is a neglected tropical disease that is widespread in tropical and subtropical regions. The lack of rapid and sensitive diagnostic tools continues to limit the early identification of the disease. In this study, a graphene quantum dots-based aptasensor was developed for the detection of Leptospira interrogans. Graphene quantum dots were synthesized and used as fluorescence transducers, which are covalently conjugated with cell surface-specific DNA aptamer targeting the pathogen. The synthesized quantum dots exhibited quasi-spherical morphology with particle size ranging from ~ 2.5 nm. Upon target recognition, the GQD-aptamer conjugate exhibited concentrationdependent fluorescence quenching, showing a linear response over the range of 10[3]-10[8] CFU/mL (R[2] = 0.958) and a limit of detection of 10[3] CFU mL[-1]. The assay was completed within 15 min. The sensing platform was further evaluated under biologically relevant conditions, including protein-containing buffer, heat-treated cells, diluted serum, and artificial urine samples. In addition to spectroscopic analysis, dark-field microscopy revealed pronounced aggregation and clustering of Leptospira cells following treatment with the GQD-aptamer conjugate. The combined spectroscopic and microscopic findings support the proposed sensing mechanism and highlight the potential of the developed GQD-aptamer platform as a rapid fluorescence-based aptasensor for Leptospira, with future applicability towards point-of-care diagnostic development.

Carnitine palmitoyltransferase II (CPT II) deficiency is a rare inherited disorder of long-chain fatty acid oxidation that may present in adulthood with episodic myopathy and rhabdomyolysis. Severe episodes can be life-threatening and may result in acute kidney injury (AKI), particularly when triggered by infection or metabolic stress.

Acute appendicitis (AAP) and acute cholecystitis (AC) are two of the most common surgical emergencies, yet their synchronous occurrence is exceptionally rare and diagnostically challenging. We report the case of a 49-year-old male patient who presented with a 10-day history of diffuse abdominal pain, nausea, vomiting, anorexia, and dark urine. Examination revealed abdominal tenderness with positive Murphy's and rebound signs. Laboratory tests demonstrated leukocytosis, neutrophilia, and elevated liver enzymes. Imaging with combined ultrasound and computed tomography confirmed both an inflamed, stone-bearing gallbladder and an enlarged, fluid-filled appendix. Diagnostic laparoscopy revealed active pelvic purulence and a severely inflamed gallbladder with dense inflammation at the hepatocystic triangle. Prioritizing definitive source control while avoiding iatrogenic biliary manipulation in a contaminated field, cholecystectomy was deferred. The patient underwent an appendectomy, which was converted to an open gridiron approach due to severe adhesions and tissue friability obscuring the appendiceal base. Index histopathology confirmed perforated AAP with serositis. Postoperatively, the patient was readmitted on day 14 with a superficial incisional surgical-site infection; this was successfully managed with bedside drainage and antibiotics after imaging ruled out deep intra-abdominal collections. Three months later, the patient underwent an uncomplicated interval laparoscopic cholecystectomy, with final histopathology confirming chronic cholecystitis. The rarity of this presentation highlights the need for high clinical suspicion. Synchronous perforated AAP with AC remains a rare diagnostic challenge in atypical abdominal pain. Early multimodal imaging and individualized operative planning, including staged intervention when severe inflammation or unsafe anatomy precludes simultaneous resection, may be considered to optimize patient safety.