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Introduction and Objectives: Metabolic Dysfunction-associated Fatty Liver Disease (MAFLD) has been recognized as the hepatic component of metabolic syndrome and has become a growing public health concern. Early and accurate detection of MAFLD is crucial for implementing appropriate intervention strategies and preventing progression to serious complications such as liver cirrhosis. We aimed to describe the diagnostic performance of the Hepatic Steatosis Index (HSI) in subjects with MAFLD and compare it with the Homeostatic Model Assessment of Insulin Resistance (HOMA), Waist-to-Hip Ratio (WHR), and Visceral Fat (SECA). Materials and Methods: Retrospective design study. Bioanthropometric, clinical, and biochemical variables were collected. The HSI was calculated using the formula HSI = 8 * ALT/AST + BMI + 2 (if diabetic) + 2 (if female). ROC curves and their areas were generated. Statistical significance was determined at p < 0.05. Results: A total of 585 subjects were evaluated, of whom 279 were classified with MAFLD (65.5% females) and 306 without MAFLD (76.8% females). Subjects with MAFLD exhibited higher values of age, BMI, WHR, HOMA, CAP, and HSI (Table 1). The HSI showed a diagnostic performance with an area under the curve (AUC) of 0.80. A cutoff point of 39.9 was established for the HSI, with a sensitivity of 63%, specificity of 74%, positive predictive value (PPV) of 73%, and negative predictive value (NPV) of 64%. The HSI demonstrated superior diagnostic performance compared to visceral fat (0.70), HOMA (0.70), and WHR (0.66) (Fig 1). Conclusions: The results of this study demonstrate that HOMA, visceral fat, and ICC can be useful as screening strategies in MAFLD. However, the Hepatic Steatosis Index (HSI) showed superior diagnostic performance compared to the other evaluated biomarkers. Therefore, it is suggested that HSI be considered a useful diagnostic tool in MAFLD.

Introduction and Objectives: Leflunomide is a drug used to treat autoimmune diseases. However, despite its therapeutic benefits, adverse effects have been reported after six months of treatment, including liver damage. Materials and Patients: A 19-year-old female from Acayucan, Veracruz, without significant hereditary or family history, drug addiction denied, with a pathological history of hypothyroidism for 2 years and rheumatoid arthritis since the age of 15, treated with leflunomide 20 mg, chloroquine 150 mg, levothyroxine 100 mcg. She presented in October 2022 with nausea, vomiting, postprandial abdominal pain, jaundice. Abdominal ultrasound revealed chronic calculous cholecystitis. Laparoscopic cholecystectomy was performed in December 2022 without complications. After surgical treatment, he persisted with jaundice, alteration of liver function tests of mixed pattern that evolves to cholestatic pattern (R factor 0.2, see Table 1). Non-reactive to viral hepatitis A, B and C, HIV, negative antibodies ANA, AML, AMA, anti-DNAds, anti-Smith, anti-Rho, complement C3 145 and C4 33. Cholangiography, with hepatomegaly, diffuse hepatic steatosis without evidence of biliary lesions. Liver biopsy showed features of portal and lobular hepatitis, intracytoplasmic and intracanalicular cholestasis, macrovesicular steatosis, and F2 fibrosis according to METAVIR (Fig. 1), which were not consistent with autoimmune or viral disease. RUCAM score with possible relation to hepatoxicity (4 points), so it is considered drug-induced liver injury (leflunomide). Results: Leflunomide was discontinued and treatment was adjusted to chloroquine 150 mg and prednisone 50 mg. Clinical and biochemical improvement was observed. Conclusions: This case highlights the importance of suspecting DILI in patients treated with potentially hepatotoxic drugs and with alterations in liver biochemistry. It is a rare disease for which there are no specific markers. Therefore, liver biopsy is a useful tool for early diagnosis.

Introduction and Objectives: Metabolic-associated fatty liver disease (MAFLD) poses a significant risk for progression to advanced liver diseases, underscoring the need for early detection. This study aims to assess and compare the diagnostic efficacy of non-invasive markers (APRI, FIB-4, Hepamet, and NAFLD Score (NFS) in detecting hepatic fibrosis among MAFLD patients. Materials and Patients: A retrospective examination was performed on adults with MAFLD who had undergone transient liver elastography. Hepatic fibrosis was identified at a cut-off point of ≥8 kPa. APRI, FIB-4, Hepamet, and NFS scores were evaluated with cut-off points determined via the Youden index. Receiver Operating Characteristic (ROC) curves and their areas were computed. All participants provided informed consent. Results: Our cohort consisted of 150 MAFLD patients, the median age of 55 years (48-65), comprising 66.2% (129) females and 33.88% (66) males. The median BMI was 32.1 (28.8-35.6), kPa was 5.6 (4.6-7.8), and CAP was 310 (280-341). Hepatic fibrosis was evident in 24.7% (37) of the participants. Among the evaluated scores, APRI exhibited superior diagnostic performance, achieving an area under the curve of 0.72, followed by FIB-4 (0.66), Hepamet (0.64), and NFS (0.62). The cut-off points of 0.50 for APRI, 1.65 for FIB-4, 0.05 for Hepamet, and -0.75 for NFS yielded sensitivities of 86%, 82%, 86%, and 81%, respectively (Fig 1). Conclusions: Non-invasive scoring systems, notably APRI, demonstrate valuable potential in evaluating hepatic fibrosis among Mexican MAFLD patients. Utilization of adjusted cut-off points enhances test efficiency, thereby facilitating early detection of individuals at greater risk of disease progression.

Background and aims. Autoimmune hepatitis (AIH) is a chronic inflammatory condition of the liver in which the immunological mechanisms involved in tissue destruction and/or repair are still unclear. Different pro-inflammatory cytokines have been shown to play a determinant role in AIH pathogenesis. Here, we aim to compare the circulating levels of pro-and anti-inflammatory cytokines such as IL-6, TNF-α, IL-17A/F, IL-21, IL-22, IL-23, and IL-10 in patients with type 2 AIH compared to patients with type 1 AIH and healthy controls (HC). Fourty-six Mexican patients with AIH were recruited in our study. Patients were classified as type 1 or 2 AIH based on immune serological markers. Fourty-four serum samples from healthy individuals were included as controls. Serum cytokine levels were determined by ELISA technique.Results. Compared to healthy controls, serum levels of IL-17F, IL-21, IL-23, IL-10, IL-6, and TNF-α, but not IL-17A and IL-22, were significantly increased in AIH patients. When patients were grouped by aminotransferase activity, a biomarker of active disease, a positive correlation between serum IL-17F and alanine transaminase (rs: 0.4739; P = 0.0009) and aspartate transaminase (rs: 0.4984; P = 0.0004) levels was found. A cytokine signature profile associated with type 2 AIH was characterized by high serum IL-21 (type 1 AIH: 0.66 pg/mL; type 2 AIH: 331.1 pg/mL; P = 0.0042) and IL-22 (type 1 AIH: 0.1 pg/mL; type 2 AIH: 55.26 pg/mL; P = 0.0028) levels.Conclusions. We show for the first time, differential regulation of certain pro-inflammatory cytokines associated with disease progression and AIH type in Mexican patients.

Hepatoblastoma (HB) rarely occurs in adults. We report herein the unusual case of a 19-year-old, otherwise healthy woman with no history of liver disease who presented with upper abdominal pain and hepatomegaly. Tests for hepatitis B virus (HBV), hepatitis C virus (HCV) were negative, and AFP was normal. There was no evidence of liver cirrhosis. A well-demarcated solid mass of 14 cm in diameter, which was lobulated and partly necrotic, was detected in the liver by computed tomography (CT). At surgical exploration a large liver mass was detected occupying the entire right lobe. A right trisegmentectomy was performed with tumor grossly resected with microscopic residual disease (i.e positive margins). On microscopic examination the tumor was composed mainly of two components which were intermingled: epithelial and mesenchymal elements. The epithelial component was formed of small embryonal cells, grouped into nodules, scattered in cellular mesenchymal tissue. The diagnosis was mixed hepatoblastoma. The patient received 4 cycles of systemic chemotherapy with cisplatinum and adriamycin. Post-chemotherapy evaluation revealed recurrence of the hepatoblastoma in the remaining liver. She died 6 months later.

Introduction and Objectives: Autoimmune hepatitis (AIH) is a chronic immune-mediated disease with an estimated frequency of 11 to 25 subjects per 100 000 population. It has been reported that viral hepatitis can be a trigger for chronic active hepatitis with AIH criteria. Hepatitis E virus is infrequent in our environment, but it is recognized as the cause of about 20 million new infections per year, being described in case reports as a triggering factor of AIH. Materials and Patients: We present the case of a 39-year-old woman who debuts with jaundice and general condition attack, this, 20 days after her return from Qatar, referring to have consumed raw meat during her stay, denying chronic degenerative history, alcohol and drug consumption. Liver function tests showed changes with R factor >5 compatible with hepatocellular pattern, liver ultrasound showed no liver or biliary changes. AgsVHB (-), HCV (-), VHA IgG (+), IgM (-), AC VHE IgG (-), IgM (+), immunoglobulins IgA 342, IgG 1777 U, IgM 97 U, negative ANA, AML, AMA, anti-LKM-1 antibodies were reported, which was considered probable acute hepatitis E. Cholangioresonance was performed due to the increase in bilirubin at the expense of direct bilirubin, confirming the absence of biliary tract changes. Results: The patient was stable for 4 weeks with clinical improvement and a gradual decrease in bilirubin and transaminases, without evidence of liver damage or encephalopathy. After this period, the patient presented again with an abrupt rise in transaminases of more than 20 times the LSN. In view of these findings, an ultrasound-guided liver biopsy was performed. The histopathological report was consistent with autoimmune hepatitis, and treatment with prednisone and azathioprine was initiated, to which the patient responded favourably. The patient is currently asymptomatic and stable. Conclusions: It is important to consider that acute hepatitis due to HEV is increasingly recognised, although sometimes misdiagnosed and confused with other liver diseases. It is also important to highlight that autoimmune diseases may be preceded by a viral infection due to an inadequate immune response, which forces us to highlight liver biopsy as a useful tool when serological markers are insufficient.