Minimally invasive techniques for resection of centrally located tumors near the region of hepatic duct bifurcation poses technical concerns to many hepatobiliary surgeons. Excessive bleeding, inadvertent injury to the hilar plate with subsequent bile leak and abdominal sepsis, and involvement of the middle hepatic vein (MHV) often deter surgeons from using a minimally invasive technique in this circumstance. An emerging robotic method with advantages over conventional laparoscopy offers greater technical feasibility for peri-/juxtahilar dissections and MHV ligation/reconstruction. Although robotic portal vein resection and reconstruction has been established and widely reported in the literature, especially in pancreaticoduodenectomy or Klatskin tumor resection,1-5 technical descriptions of hepatic vein reconstruction remain limited. Herein, we describe our technique for robotic partial central hepatectomy for juxtahilar tumor, highlighting steps of MHV tangential reconstruction to avoid congestion of the associated hepatic parenchyma drained by the MHV trunk. A 57-year-old woman presented with a single 5 cm segment V hypermetabolic mass, concerning for metastatic breast cancer without evidence of extrahepatic disease. She had a multifocal invasive adenocarcinoma requiring partial mastectomy and antiestrogen treatment 11 years before her current presentation. Magnetic resonance imaging showed a 5 cm liver mass almost in contact with the hepatic duct bifurcation dorsally and laterally displacing the middle portion of the MHV. Robotic partial central hepatectomy under intermittent Pringle maneuver was undertaken using a meticulous crush-clamp technique to avoid injury to the hilar plate, and tangential reconstruction of the MHV using a curved vascular bulldog clamp was completed without intraoperative complications. The robotic operation was completely uneventful, with minimal blood loss, and the patient had an uneventful recovery followed by hospital discharge on postoperative day 3. A final pathology report was consistent with metastatic breast cancer with negative resection margins. At 16 months after the robotic liver resection, the patient remains without evidence of disease recurrence. Although robotic approaches to resection and reconstructive techniques for the portal vein and inferior vena cava have been discussed, very little is known about resection and reconstructive techniques for the major hepatic vein during robotic hepatic resection. Preservation of the major hepatic vein, such as MHV, is important to avoid parenchymal venous congestion of the corresponding liver sector, which in theory can compromise overall liver function in patients with marginal future liver remnant volume or hepatic functional reserve secondary to underlying liver disease. In the case presented here, the right anterior sector (segment 5/8) is dominant, with 37% portion volume, so adequate parenchymal venous drainage via MHV was clinically important and necessary. Adequate inflow, outflow, and biliary drainage are three widely known key factors that determine postoperative hepatic recovery and parenchymal regeneration. Another observation on the preoperative imaging was that a segment IV bile duct was focally dilated because of mechanical local tumor compression/involvement onto the segmental bile duct, which was directly located dorsal to this mass. Beyond this localized radiological finding, no clinical symptoms were observed. The tumor did not invade the roof of the hilar plate, so R-0 resection margins were easily obtained. A hepatic vein reconstruction technique such as shown in this video can be similarly applied for other major hepatic veins such as the right and left hepatic veins. We anticipate that this robotic technique for reconstructing major hepatic veins will become significantly more relevant in cases of upper segmental tumor resection, as reported by Procopio et al.6 As such, tumor resection using a robotic approach can be maximally optimized. Application of a robotic technique is safe and feasible for juxtahilar tumors requiring precise dissection and reconstruction of the major hepatic vein trunk. We believe that the robotic surgical system allows for challenging hepatic tumor resections in difficult locations and hepatic vascular preservation using reconstructive techniques.

To investigate the safety and complication rate of 2 vessel-sealing devices (VSDs) used for hepatic surgery in dogs. This was a retrospective study from 6 institutions from January 2012 through June 2024 including dogs that underwent a complete or partial liver lobectomy or a liver biopsy using a VSD as the sole method. Surgical complications based on the type of liver lobectomy, severity of complication, type of VSD used, mass size, and liver lobe location were reported as the percentage of dogs experiencing the event of interest. Group differences were compared using a 2-tailed Fisher exact or χ2 test. Maximal tumor diameter in relation to complication type was assessed using a Kruskal-Wallis test. Statistical significance was set at P = .05. 58 dogs were included in the study. For liver lobectomy cases, complications occurred in 42 of 48 dogs and were mostly minor. No differences in complications were noted based on liver mass size, liver lobe location, type of liver lobectomy performed, severity of complication, or type of VSD used. Intra- or postoperatively, biliary leakage occurred in 4 of 48 dogs. The complication rate for dogs undergoing a liver biopsy was 5 of 10 and consisted of minor bleeding in 90% of the cases. Despite the high incidence of minor complications, VSD can be safely used for hepatic surgery in dogs. The ability of the 2 VSDs used to seal bile ducts when a liver lobectomy is performed requires further investigation. VSDs can be considered an alternative method for performing liver lobectomies in dogs.

Nelumbinis folium [Nelumbonaceae; Nelumbo nucifera Gaertn.] is a traditional Chinese medicine. Although studies have reported the efficacy of lotus leaf in weight management, the underlying molecular pathways necessitate further studies. This study aimed to elucidate the effects of lotus leaf on gut microbiota and their metabolites, especially long-chain fatty acids (LCFA), and measure how the effects of lotus leaf on gut microbiota help control obesity. The 12-week Lotus Leaf Extract (LLE) treatment mitigated weight gain, reduced liver and white adipose tissue mass, and activated brown adipose tissue in high-fat diet-induced obese mice, indicating enhanced energy metabolism. LLE reversed gut microbiota dysbiosis by enriching Eubacterium sp. in the gut. Microbiota transplantation indicated that Eubacterium sp. contributes to fat browning and thermogenesis, thereby alleviating host obesity, glucose homeostasis, dyslipidemia, and hepatic steatosis. In addition, Eubacterium sp. significantly increased the levels of margaroleic acid in mouse serum. In summary, the study found that lotus leaf extract can prevent obesity by modulating the gut microbiota, which in turn activates BAT activity and promotes the browning of WAT.

Percutaneous image-guided interventions are minimally invasive alternatives to surgery for diagnosis and management of various abdominal disease processes. However, persistent misconceptions about these procedures continue to hinder their appropriate use. This review addresses common myths that can lead to unnecessary treatment delays or use of more invasive interventions, including concerns about the safety of splenic biopsy, rigid contraindications for antiplatelet medication use, bleeding risks with direct liver mass puncture, tumor seeding from renal biopsies, complications from multiple liver biopsy passes, and increased risk of liver biopsy in the setting of ascites. By clarifying these issues, this article aims to promote evidence-based use of percutaneous procedures.

Fidanacogene elaparvovec is a single-dose gene therapy designed to express the high-activity factor IX (FIX) variant FIX-R338L. Participants (N=15) with FIX activity ≤2% were dosed with 5×1011 vector genomes/kg infusion of fidanacogene elaparvovec and completed the 1-year dosing trial. After the initial 52 weeks, participants could enroll in long-term follow-up (LTFU) for 5 additional years. This reports includes final safety and efficacy data of the LTFU trial through 6 years post gene therapy, with additional patient-reported outcomes (PROs). Of 14 participants enrolled in the LTFU, 11 completed 6-years' follow-up. During Years 2 to 6, 9 serious adverse events (AEs) were reported in 4 participants (28.6%); none were considered treatment-related or resulted in study discontinuation or death. Eight participants had increased alanine aminotransferase levels, and 3 of 8 also had increased aspartate aminotransferase levels; none received corticosteroids. No liver masses, malignancies, thrombotic events, or FIX inhibitors were reported. FIX activity was maintained, with a mean FIX activity of 24.7% at Year 2 (n=14) and 26.1% at Year 6 (n=11). Mean treated annualized bleeding rates remained lower than 1.0 (median=0.0) during each year of follow-up. Ten participants (71%) had no treated bleeding events. None of the 14 enrolled participants resumed FIX prophylaxis. Improvements relative to pre-gene therapy in PROs and target joints were observed over the duration of follow-up. Overall, fidanacogene elaparvovec exhibited a favorable safety profile, sustained efficacy, and improved PROs for up to 6 years. This trial is registered at www.clinicaltrials.gov as #NCT03307980.

Perivascular epithelioid cell tumor (PEComa) is a rare liver tumor, with few cases reported in the literature. Clinical decisions regarding patients diagnosed with PEComa are based on studies with small sample sizes. Differential diagnosis between PEComa and other types of liver lesions is challenging due to non-specific radiological findings associated with this type of liver mass. We report the case of a 51-year-old female patient followed at the outpatient hepatology clinic of Patras, General University Hospital, Greece, for chronic hepatitis B. The patient was asymptomatic, with positive hepatitis B surface antigen and normal liver function tests. An area with abnormal echogenicity and a diameter of 28mm was observed in an abdominal ultrasound during routine follow up. Magnetic resonance imaging (MRI) was performed, and a mass with a diameter of 30.6mm was found on surgical liver segment IV. A follow-up MRI 8months later showed the lesion had increased to 36mm and exhibited suspicious radiological characteristics. Surgical excision of liver segment IV was performed. Post-surgical pathological analysis of the tumor confirmed a diagnosis of PEComa, with no evidence of vascular or lymphatic invasion. The low mitotic index, the size of the tumor and the lack of nuclear atypia or diffuse pleomorphic morphology supported a favorable tumor behavior. In conclusion, PEComas are rare liver tumors without pathognomonic radiological features. Surgical excision of these masses is the safest treatment option, and post-surgical pathological analysis is essential for the diagnosis and prognosis of these patients.

Pancreatic Ductal Adenocarcinoma (PDAC) has a dismal five-year survival rate of 13% and is closely associated with cachexia. Cancer cachexia is a multifactorial syndrome characterized by irreversible wasting of skeletal muscles, fat loss and systemic inflammation. While cachexia is known to confer resistance to immune checkpoint inhibition in several cancers, the bidirectional relationship between cachexia and the immune system in PDAC remains unclear, necessitating the development of novel preclinical models. Our laboratory has characterized a novel pancreatic cancer cachexia model in C57BL/6J mice by utilizing the pancreatic cancer cell line called KPCL-4 derived from KPC-LSIY mice (KrasLSL-G12D/+Tp53LSL-R172H/+Pdx1-Cre/R26LSL-LSIY). KPCL-4 cells were orthotopically injected into the pancreas of male and female C57BL/6J mice and hallmarks of cachexia were assessed at endpoint by measurement of tumor weight, terminal tumor-adjusted body weight, skeletal muscle, adipose tissue, liver and spleen masses, proteolytic markers and grip strength. Plasma cytokine and chemokine concentrations were quantified by Luminex assay and high-dimensional flow cytometry was used to investigate changes in tumor-infiltrating immune populations. We observed a sex bias in cachexia presentation despite similar tumor weights in male and female mice, whereby males exhibited a >5% decrease in terminal tumor-adjusted body weight (p < 0.001), >50% fat loss (p < 0.001), upregulation of proteolytic markers in skeletal muscles (p < 0.01) and reduction in skeletal muscle mass (p < 0.05), function (p < 0.01) and cross-sectional area (p < 0.0001) whereas females demonstrated conserved skeletal muscle mass with 33% fat loss (p < 0.05), reduction in muscle cross-sectional area (p < 0.0001) and splenomegaly (p < 0.01). While intra-tumoral immune populations did not exhibit sex-specific differences, plasma cytokine concentrations were differentially upregulated in males and females, suggesting functional differences in immune cells as potent drivers of sex bias in KPCL-4-driven cachexia. The KPCL-4 orthotopic PDAC model exhibits prominent hallmarks of cachexia and serves as a novel platform for investigating the complex interplay between cancer cachexia and immunomodulation.

Maternal nutrient restriction (MNR) heightens disease susceptibility in offspring through epigenetic modifications that alter the development of essential organs. This study investigates how restriction alters the fetal sheep hepatic methylome and its potential regulatory influence on gene expression. Using a monozygotic twin model generated through embryo splitting, we examined hepatic DNA methylation responses to maternal nutrient restriction (50% vs. 100% NRC nutritional requirements; n = 4 per group) from gestational day (GD) 35 to 135 in pregnant sheep. At GD 135, conceptus (fetal-placental unit) development was assessed; although fetal weight was unaffected (p > 0.10), restricted fetuses exhibited reduced liver mass (p < 0.05). Whole-genome bisulfite sequencing (WGBS) of fetal liver identified 1,636,305 differentially methylated CpG sites (dmCpGs) in the Group-Level Analyses and 42,231 dmCpGs in the Twin-Pair Analyses. At the Group-Level, 40,533 promoter, 126,667 exonic, and 785,381 intronic sites were identified, whereas the Twin-Pair subset contained 1314, 7116, and 22,239, respectively. Site-level shifts and functional enrichment across features highlighted GPCR-cAMP/calcium-PI3K/AKT signaling, phosphoinositide metabolism, ECM/integrin-focal adhesion networks, thyroid hormone signaling, and Rho-family GTPases. These findings indicate that maternal nutrient restriction modifies the fetal hepatic methylome through coordinated signaling, metabolic, and structural reconfigurations that create conditions conducive to metabolic disease.

Un uncommon diagnosis of liver masses.

Obesity promotes metabolic dysfunction-associated steatotic liver disease (MASLD). Gut microbiota can influence MASLD through local communication between the gut and liver. Bacterial components are often conceptualized only as contributors to chronic inflammation. However, certain postbiotics can protect against chronic inflammation and dysmetabolism by activating specific immune responses during obesity. Site-specific innate immune training can direct compartmentalized immune responses. We hypothesized that site-specific immunomodulation by gut-derived inactivated bacterial-based stimuli (i.e., postbiotics) would improve features of MASLD. We found that biweekly subcutaneous injections of an inactivated bacterial preparation of a gut bacterium (QBECO from Escherichia coli) improved markers of steatosis, inflammation, and fibrosis indicative of MASLD in obese mice. QBECO lowered liver mass, triglycerides, F4/80 macrophages, eosinophil peroxidase activity, and collagen content in the liver without altering food intake or body mass in obese mice. QBECO increased whole body lipid oxidation without altering total energy expenditure in obese mice. QBECO had an immunomodulatory effect that lowered liver eosinophil peroxidase activity, lowered liver nitrite/arginase ratio, and increased CD163 positive cells, a marker of M2 macrophages in the liver of obese mice. We confirmed that multiple gut bacteria-derived postbiotics improved MASLD as injections of an inactivated bacterial preparation of Proteus mirabilis (QBPMI) also lowered markers of steatosis, inflammation, and fibrosis in obese mice. A postbiotic from Klebsiella variicola (QBKPN), a bacterium typically pathogenic outside the gut, did not alter MASLD in obese mice. Therefore, site-specific immunomodulators derived from gut bacteria can improve the hallmarks of MASLD without causing weight loss.NEW & NOTEWORTHY This study demonstrates that site-specific immunomodulators (SSIs), prepared from inactivated bacteria, can attenuate liver steatosis, inflammation, and fibrosis in a mouse model of obesity and metabolic dysfunction-associated steatotic liver disease (MASLD). Gut bacteria-derived SSIs improved hallmarks of MASLD without altering body weight or food intake, but an SSI derived from a bacterium typically pathogenic outside the gut did not alter MASLD. Therefore, gut-derived SSI postbiotics can improve MASLD.

We report a severe case of human hepatic fascioliasis in a 60-year-old woman from Azerbaijan who had been misdiagnosed with liver cancer and treated oncologically for approximately two years without clinical improvement. The patient presented with complaints of pain in the right hypochondrium, intermittent fever, general weakness, anorexia, weight loss, and insomnia. Laboratory evaluation revealed marked eosinophilia. Imaging studies demonstrated heterogeneous hepatic lesions compatible with inflammatory and necrotic changes. Coprological examination confirmed the presence of Fasciola eggs. To our knowledge, this represents one of the first clinically documented cases of human hepatic fascioliasis reported from Azerbaijan. The patient was treated with triclabendazole administered in two courses of three days each, separated by a 10-day interval, along with supportive hepatoprotective therapy and B complex vitamins. Following treatment, clinical symptoms resolved completely, eosinophil levels normalized, and follow up stool examinations were negative. Two months after therapy, laboratory parameters approached normal physiological values. This case emphasizes the importance of including hepatic fascioliasis in the differential diagnosis of liver masses, particularly in patients with eosinophilia and relevant epidemiological exposure. Early recognition prevents unnecessary invasive procedures and prolonged oncological treatment

BackgroundThis study investigates the differentiation of liver focal nodular hyperplasia (FNH) from liver malignant tumor (MT) by a combination of T2-weighted imaging (T2WI), diffusion-derived vessel density (DDVD), slow diffusion coefficient (SDC), and apparent diffusion coefficient (ADC). Based on the odds ratio (OR) for a sign to suggest the possibility of a lesion being FNH, we propose a liver mass sum score (LiverMss-FNH) scheme to facilitate the diagnosis.MethodsLiver diffusion-weighted magnetic resonance imaging included 13 cases of FNH and 82 cases of MT. DDVD was calculated from b=0 and b=10 s/mm2 images, SDC was calculated from b=500 and b=800 s/mm2 images, and ADC was calculated from b=0 and b=800 s/mm2 images. For liver semi-quantitative analysis, relative to the adjacent liver signal, a liver lesion’s signal was assigned to five categories: low signal, iso-signal, slightly high signal, high signal, and markedly high signal. The lesion on T2WI being not high signal was assigned a sub-score “1” (otherwise scored 0); the lesion being iso-signal on DDVD was assigned a sub-score “1.5” (otherwise scored 0); the lesion on SDC being not high signal was assigned a sub-score “1” (otherwise scored 0); the lesion on ADC being not low signal was assigned a sub-score “0.5” (otherwise scored 0); the existence of stellate scar was assigned a sub-score “0.5” (otherwise scored 0). The sum of these five sub-scores was termed LiverMss-FNH.ResultsA total of 26 MT cases had large (median 8.1 cm, standard deviation: 4.2 cm) and very heterogeneous masses which were very unlikely to be FNH. The remaining 13 FNH cases (median 3.8 cm, standard deviation: 1.7 cm) and 56 MT cases (median 4.9 cm, standard deviation: 4.3 cm; hepatocellular carcinoma, n=40; metastasis, n=12; intrahepatic cholangiocarcinoma, n=4) were evaluated with LiverMss. Liver lass lesion being not high signal on T2WI, being iso-signal on DDVD, being not high signal on SDC, being not low signal on ADC, and the existence of stellate scar had ORs of 49.1, 45.8, 30, 8.5, and 13.3, respectively, favoring the diagnosis of FNH. A total of 69.2% (9/13) of the FNH had LiverMss-FNH ≥4.0, while the remaining 4 cases (30.8%) all had a LiverMss-FNH of 3.0. A total of 89.3% (50/56) of the MT had LiverMss-FNH ≤1.5.ConclusionsLiver FNH tend to have lower DDVD signal and lower SDC signal than liver MT. A LiverMss ≥4 can strongly suggest the diagnosis for a liver mass being FNH, and while a LiverMss-FNH ≤1.5 can strongly suggest the diagnosis for a liver mass being MT.

Metabolic dysfunction-associated steatotic liver disease (MASLD) spans from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH) and can progress to cirrhosis or hepatocellular carcinoma. Despite its prevalence, effective therapies are lacking. Recent genome-wide association studies identified a common missense variant (rs2642438) in the Mitochondrial Amidoxime Reducing Component 1 (MTARC1) gene that protects against liver cirrhosis without increasing cardiovascular disease risk. Biochemical and disease risk signatures associated with carriers of this missense variant also aligned with those of a known loss-of-function MTARC1 variant, suggesting mARC1 inhibition as a potential MASLD treatment. To validate mARC1 loss-of-function as protective against MASLD, we generated Mtarc1 knockout (KO) mice and placed them on a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD). Effects of Mtarc1 KO on obesity and type 2 diabetes were explored using a high-fat diet. Hepatocytes from Mtarc1 KO mice were isolated to explore the molecular mechanisms by which Mtarc1 KO impacts lipid metabolism. Mtarc1 KO mice exhibited no vital growth or development defects. With a high-fat diet-induced obesity model, obese Mtarc1 KO mice exhibited reduced liver mass and lower cholesterol levels, with no effect on glucose homeostasis. In a CDAHFD-induced MASLD model, mARC1 deficiency significantly reduced liver steatosis, profibrosis, and inflammation. Untargeted metabolomics profiling further showed hepatic enrichment of phospholipids in Mtarc1 KO mice. Primary hepatocytes isolated from Mtarc1 KO mice exhibited reduced lipid droplet accumulation, decreased fatty acid uptake, and increased lipid secretion. These findings support mARC1 inhibition as a promising therapeutic strategy for MASLD/MASH.

To investigate the effects of aerobic exercise, caloric restriction, and their combined intervention on NLRP3 inflammasome activation and macrophage M1/M2 polarization in the liver of db/db mice, and to elucidate their potential mechanisms in alleviating hepatic inflammation. Thirty-two mice were randomly divided into four groups (n=8/group): control (CON), aerobic exercise (AE), caloric restriction (CR), and combined intervention (ECR). The AE group underwent treadmill running at 50%-55% VO2max for 1 h/day, 5 days/week. The CR group received 70% of the CON group’s daily food intake. The ECR group combined both interventions for 12 weeks. Body weight and food intake were monitored weekly. Post-intervention, liver mass, lipid profiles (TC, TG, LDL-C, HDL-C), hepatic morphology (HE staining), lipid deposition (Oil Red O staining), and protein levels of iNOS, Arg-1, IL-1β, IL-10, NLRP3, Cleaved-Caspase-1, and ASC (Western blot) were analyzed. Macrophage polarization was assessed via immunofluorescence (F4/80, CD86, CD206). Data were analyzed using one-way ANOVA (significance levels: *p &lt; 0.05, **p &lt; 0.01) (1). CR, AE, and ECR groups exhibited significantly lower body weight than CON, with ECR showing the most pronounced reduction (p &lt; 0.05). (2) ECR significantly reduced TC and LDL-C levels compared to CON (p &lt; 0.05). (3) All interventions improved hepatic histology and lowered NAFLD activity scores (NAS), with ECR outperforming AE and CR (p &lt; 0.01). (4) CR and ECR reduced lipid droplet area, with ECR showing superior efficacy (p &lt; 0.01). (5) AE, CR, and ECR suppressed IL-1β and iNOS while elevating IL-10 and Arg-1, with ECR achieving the most significant effects (p &lt; 0.01). NLRP3, Cleaved-Caspase-1, and ASC expression were markedly reduced in ECR versus CON and AE (p &lt; 0.05). (6) ECR decreased F4/80+/CD86+ (M1) co-localization and increased F4/80+/CD206+ (M2) co-localization compared to all groups (p &lt; 0.01). Conclusion: (1) Aerobic exercise primarily induces M2 polarization and anti-inflammatory cytokine upregulation, while caloric restriction suppresses M1 polarization and pro-inflammatory factors. The combined intervention demonstrated superior effects by integrating both mechanisms. (2) NLRP3 inflammasome inhibition correlates with improved macrophage polarization, with the combined intervention exerting stronger suppression on NLRP3 pathway proteins than individual interventions.

Activated hepatic stellate cells are required for Hippo-YAP activation and functional liver regeneration following portal vein ligation in mice.

Objective: To compare the diagnostic accuracy of CT scan in identifying solitary liver lesions, in reference to histopathology as the gold standard. Study Design: Cross-sectional Study. Place and Duration of Study: Department of Gastroenterology, Pak Emirate Military Hospital, Rawalpindi, Pakistan, from Jan to Jun 2023. Methodology: A total of 180 patients of both genders, aged 30 to 70 years, who were clinically diagnosed of a solitary liver lesion were included. CT was studied for liver lesions, attenuation value was obtained, and diagnosis was then confirmed with aspiration, cytology, and histopathology by a consultant pathologist. Data was recorded on a proforma and analyzed through SPSS. Results: The Mean age of 51.82±5.98 years. Male patients were 135(75%), and 45(25%) were female patients. CT scan diagnosed 101(56.1%) patients, while histopathology diagnosed 96(53.3%) patients with malignant liver lesions. CT scan has shown sensitivity of 91.6%, specificity 84.5% and diagnostic accuracy of 88%, PPV 87.1% and NPV 89.8% in the diagnosis of malignant liver lesions. Conclusion: The results of our study showed that a CT scan is a useful tool in diagnosing malignant liver masses and helps to avoid unnecessary liver biopsy.

Sarcopenia, characterized as a reduction of skeletal muscle mass and functional capacity, remains a relevant but insufficiently studied issue in pediatric patients with inflammatory bowel disease. Loss of muscle mass may negatively affect the course of inflammatory bowel disease, increase the frequency of complications, and reduce treatment effectiveness. Recent studies have highlighted a possible association between sarcopenia and hepatobiliary manifestations in patients with inflammatory bowel disease. However, due to the limited number of studies and the absence of diagnostic guidelines, the prevalence of sarcopenia in children with inflammatory bowel disease and concomitant hepatobiliary manifestations remains unclear.Objective. To assess the prevalence of sarcopenia in children with inflammatory bowel disease and to determine associations between reduced muscle mass and laboratory markers of liver injury.Materials and Methods. Thirty-six children with inflammatory bowel disease were examined, including 18 with ulcerative colitis and 18 with Crohn’s disease. Laboratory markers were analyzed. Body composition was assessed using bioelectrical impedance analysis, and total psoas muscle area (tPMA) was measured via computed tomography or magnetic resonance imaging.Results: Sarcopenia based on tPMA (z-score &lt; –2) was found in 61% of patients. A decrease of skeletal muscle mass measured by bioimpedance analysis was observed in 19.4% of children, more frequently in those with hepatobiliary manifestations. A strong correlation between tPMA and body composition parameters was found.Conclusion: These findings emphasize the importance of comprehensive nutritional assessment in children with inflammatory bowel disease, especially in the presence of hepatobiliary manifestations. Further prospective studies on sarcopenia in these patients are needed.

Phosphorus is an essential component of bone and energy metabolism; however, the mechanism involved in the regulation of phosphorus under postmenopausal conditions remains insufficiently understood. Interestingly, the disruption of estrogen status can alter mineral homeostasis. Meanwhile, phytoestrogens and probiotics may offer a non-pharmacological strategy to support mineral homeostasis; nonetheless, evidence of their impact on phosphorus distribution remains limited. Thus, this study aimed to evaluate the effect of daidzein, tempeh, and Lactobacillus acidophilus on phosphorus distribution in ovariectomized (OVX) rats. A total of 64 female Wistar rats were allocated to sham-operated (n = 8) or OVX (n = 56) groups. Following a three-week calcium-deficient diet, the OVX rats were randomized to seven dietary interventions for six weeks: control (O), alendronate (OB), daidzein (10 mg/kg diet/day; OD), tempeh (250 g/kg diet/day; OT), probiotic L. acidophilus (1 × 1010 CFU/day; OL), daidzein + probiotic (ODL), or tempeh + probiotic (OTL). Food intake, body mass, and phosphorus concentrations in feces, the femur, kidney, pancreas, spleen, heart, and liver were analyzed. OVX groups (O, 366 ± 14 g; p = 0.01; OD, 361 ± 18 g; p = 0.02; OL, 358 ± 29 g; p = 0.04) gained significantly more body mass than sham controls (311 ± 30 g). Dietary interventions with daidzein, tempeh, and L. acidophilus enhanced phosphorus deposition in the femur, kidney, and pancreas compared with the OVX controls. The OT group showed the highest femoral phosphorus levels (178,111 ± 32,628 mg/kg d.w., p = 0.02), while the ODL group revealed elevated phosphorus levels in the kidney (12,966 ± 462 mg/kg d.w.; p = 0.01). The OD (914 ± 115 mg/kg d.w.; p < 0.001), ODL (913 ± 39 mg/kg d.w.; p < 0.001), and OTL (926 ± 70 mg/kg d.w.; p < 0.001) groups showed significantly increased levels of pancreatic phosphorus. A positive correlation was noted between the pancreatic and femoral phosphorus levels (r = 0.33; p = 0.02). Alendronate treatment had no significant effect. Dietary daidzein, tempeh, and probiotics modulate phosphorus distribution in postmenopausal rats. These results support the translational potential of dietary bioactives to improve phosphorus metabolism in postmenopausal women.

The article presents the results of an experimental study of the cumulative properties of the new combined preparation “ImunoHepaVerm”, which contains fenbendazole, milk thistle (Silybum marianum), and purple coneflower (Echinacea purpurea). The aim of the study was to comprehensively evaluate the potential cumulative effects of the preparation under conditions of its repeated administration to laboratory animals. The research was conducted on white rats weighing 205–220 g in accordance with current requirements of biomedical experiments and international standards for the ethical use of laboratory animals. The preparation was administered intragastrically on an empty stomach in increasing doses over 14 days using the subchronic toxicity test method. Throughout the experiment, clinical observations of the animals were performed, and upon completion, morphological, hematological, and biochemical analyses were conducted. The calculated cumulation coefficient of the drug “ImmunoHepaVerm” was 3.25. The obtained results demonstrated that repeated administration of “ImunoHepaVerm” did not lead to mortality, significant behavioral disturbances, or changes in body weight. Most organ-to-body mass coefficients remained within physiological ranges; the only significant change was a moderate decrease in the liver mass coefficient, which may reflect adaptive reactions of hepatocytes to prolonged exposure to the preparation. Hematological parameters mostly corresponded to control values; however, a slight decrease in hemoglobin levels and an increase in eosinophil and monocyte counts were observed, indicating activation of the immune response. Biochemical analysis revealed a moderate increase in aminotransferase and alkaline phosphatase activity, as well as a reduction in total protein and albumin levels. Nevertheless, these changes were not toxic in nature and reflected functional load on the liver. Overall, the findings confirm that “ImunoHepaVerm” does not exhibit cumulative toxicity and may be recommended for further preclinical studies aimed at assessing its safety and therapeutic efficacy.

This study was to explore the effects of O-GlcNAc transferase (OGT) inhibition on the liver pathological changes in spontaneously obese mice. Ten 6-week-old male ob/ob mice were randomly divided into a control group and a drug-treated group (receiving intraperitoneal injection of the OGT inhibitor OSMI-1). After 60 days of treatment, mouse liver tissue and serum samples were collected, and the expression levels of liver OGT and lipolysis-related proteins were detected by Western blot. Serum biochemical indexes were detected by full-automatic biochemical analyzer, and serum high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were detected by corresponding kits. Liver pathological changes were detected by HE staining, oil red O staining, glycogen staining, and Masson staining. The results showed that compared with the control group, the body weight and liver mass of mice in the drug-treated group were significantly reduced. The levels of OGT protein expression and O-GlcNAc glycosylation modification in the liver were significantly down-regulated. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bile acid (TBA), lactate dehydrogenase (LDH), total cholesterol (TCHO), and triglycerides (TRIG) were significantly decreased. The levels of serum HDL-C and LDL-C were significantly reduced, and the expression levels of lipolysis-related proteins, including carnitine palmitoyltransferase 1A (CPT1A), CPT2, acyl-CoA oxidase 1 (ACOX1), and peroxisome proliferator-activated receptor α (PPARα) were significantly down-regulated. The number of hepatic lipid droplets was decreased significantly, the liver tissue had multiple nuclei and fewer vacuoles, the glycogen content was decreased significantly, and the collagen fiber content was increased significantly. These results suggest that OGT inhibition can improve abnormal serum indicators and accumulation of liver fat in spontaneously obese mice, thereby reducing liver pathological changes.