Search

Serum phosphatidylethanol (PEth) testing has emerged as a promising biomarker for assessing recent alcohol consumption, surpassing the limitations of self-reported data. Limited clinical data exists comparing PEth levels and patients' reported alcohol intake. Compare PEth testing results with self-reported alcohol intake and assesses variables associated with underreporting. Single-center retrospective cohort of patients with a diagnosis of chronic liver disease and serum PEth. A patient's first positive PEth (>/=10 ng/mL) and self-reported alcohol consumption was used. PEth results were categorized as mild (10–20), moderate (20–200), or heavy (>200). Severity measures between self-report and PEth were assessed using Bhapkar's test and Bonferroni-adjusted McNemar's tests. Demographic data was analyzed using Chi-Square tests. 279 patients were included. 94 (33.7%) patients had consistency with self-report, and 185 patients had inconsistencies in their report (66.3%, p < 0.001). Of 279 patients, 161 (57.7%) underreported their alcohol consumption, and 55 (19.7%) heavy PEth patients underreported alcohol consumption as light. 58% of alcohol-related and 56.4% of non-alcohol-related cirrhotic patients underreported their alcohol use. In our cohort, only one third of self-reported alcohol consumption was consistent with the PEth level. Notably, 57.7% underreported alcohol intake. Our study reinforces the clinical importance of PEth testing as an objective clinical measure. [ABSTRACT FROM AUTHOR]

Purpose: Despite progressive implementation of image-guided point-shear wave elastography (pSWE) in guidelines as an alternative to transient elastography for the staging of fibrotic liver disease, pSWE is not widely adopted in clinical workflow. More information on reliability and validity of pSWE systems is needed. Therefore, we performed a phantom study to evaluate the validity and reliability of pSWE with ultrasound systems. Methods: Validity and reliability of pSWE measurements from three ultrasound systems were evaluated. Measurements were performed on an elasticity phantom with reference elasticities of 7 ± 1 (low) (median ± interquartile range (IQR)), 14 ± 2 (medium) and 26 ± 3 (high) kPa. Measurements were repeated in tenfold for each reference at 2, 3 and 4 cm depth. Results were considered valid when median elasticity ± IQR was between the uncertainty limits (IQR) for each reference elasticity value and reliable when IQR/median < 0.30. Results: pSWE with the systems provided valid results for all reference elasticities and focal depths, except for overestimation of high reference elasticity at 2 and 4 cm depth for one system (41.5 ± 4.3 and 39.0 ± 1.2 kPa, respectively). Measurements were reliable with a maximum IQR/median of 0.13, well below the guideline of IQR/median < 0.30. Discussion: The results support the use of pSWE as an alternative to invasive or non-image guided noninvasive techniques for liver fibrotic staging. Conclusions: pSWE with ultrasound systems from different vendors is valid and reliable and can therefore be implemented to optimize clinical workflow by performing imaging and elastography simultaneously. [ABSTRACT FROM AUTHOR]

Background: Doppler ultrasonography is essential to provide insights into hemodynamic alterations and liver function changes in pre-cirrhotic and cirrhotic patients. Utilizing Doppler examinations, this study aims to explore the correlation between hepatic arterial hemodynamics and Model for end-stage liver disease (MELD) scores in chronic liver disease patients. Methods: A study of 50 chronic liver disease patients included sonographic assessments, measuring liver, portal vein size, and flow. Hepatic artery velocity, resistive index (RI), pulsatility index (PI), and acceleration time (AT) were evaluated. Biochemical parameters (serum bilirubin, creatinine, INR) were used to calculate MELD scores, compared with different Doppler sonographic parameters. Results: The study found a mean peak systolic velocity (PSV) of 107.42 ± 48.10, with end-diastolic velocity (EDV) of 26.40 ± 14.68, RI of 0.74 ± 0.06, and PI of 1.47 ± 0.24. The mean MELD score was 19.28 ± 6.09. Correlations between MELD scores and PSV, EDV, RI, PI, and AT did not yield statistically significant correlations. 80% of subjects displayed high RI (> 0.7) values in the hepatic artery, and a significant correlation was found between portal vein thrombosis and hepatic artery PSV and RI (p < 0.05). Conclusions: Hepatic artery RI and PSV show a significant correlation with portal vein thrombosis. Doppler ultrasonography, while not directly tied to MELD scores, is valuable for non-invasive liver disease monitoring when invasive methods are impractical. Further research is needed to unravel the relationships between hemodynamic changes, MELD scores, and clinical outcomes in a broader patient population. [ABSTRACT FROM AUTHOR]

Background and Aims Inflammatory bowel disease [IBD] comprises an immune-mediated group of chronic gastrointestinal disorders. Patients with IBD may experience extraintestinal manifestations, such as hepatobiliary complications. This meta-analysis aims to assess the prevalence of different hepatic manifestations in IBD patients. Methods For this systematic review and meta-analysis, PubMed, Scopus, Web of Science, and Embase were searched until July 20, 2022, by specifying keywords for IBD, hepatic manifestations, and study type. Full texts of cohort studies in English that examined the prevalence of different hepatic manifestations were included in this study. The primary outcome was the overall prevalence of hepatic manifestations in IBD patients. For the statistical analysis, a proportion by random effect model meta-analysis was performed. The registration number for the protocol of this study in PROSPERO is CRD42022369595. Results From the 4421 articles retrieved from the primary search, 118 met the inclusion criteria and were included in the final analysis. After a pooled analysis of 1 729 128 patients, the overall prevalence of hepatic manifestations was 3.49% (95% confidence interval [CI]: 3.31–3.68%; I 2: 99.55%). The pooled prevalence of non-alcoholic fatty liver disease in 228 216 patients was 26.1% [95% CI: 22.1–30.2%; I 2: 99.018%]. After pooled analysis of 9642 patients, the prevalence of primary sclerosing cholangitis was 1.67% [95% CI: 1.47–1.88%; I 2: 99.10%]. The pooled prevalence of biliary stones was 4.1% [95% CI: 3.6–4.7%; I 2: 97.43%]. Autoimmune hepatitis (0.51% [95% CI: 0.26–0.75%]; I 2: 85.36%) and portal vein thrombosis (0.21% [95% CI: 0.08–0.33%]; I 2: 97.95%) are considered as rare manifestations. Conclusion This study summarizes the prevalence and importance of different hepatic manifestations in IBD patients. These findings are crucial for the management of extraintestinal manifestations, especially hepatic manifestations, in IBD patients. [ABSTRACT FROM AUTHOR]

To define sarcopenic obesity (SaO) among chronic liver disease (CLD) patients via CT and MRI, and assess its impact on liver disease severity. CLD patients referred from the Gastroenterology and Hepatology Department diagnosed as chronic hepatitis B (N :101), cirrhosis (N :110), and hepatocellular carcinoma (N :169) with available information on body height, weight, Child-Pugh and MELD scores within 2 weeks of CT or MRI scanning were included in the study. Cross-sectional examinations were retrospectively evaluated for skeletal muscle index (SMI) and visceral adipose tissue area (VATA). The disease severity was assessed by Child-Pugh and MELD scoring. The rate of sarcopenia and SaO in the cirrhotic patients was higher than that in the chronic hepatitis B patients (p <0.033 and p < 0.004, respectively). The rate of sarcopenia and SaO in HCC patients was higher than that in the chronic hepatitis B patients (p <0.001 and p <0.001, respectively). Sarcopenic patients in Chronic hepatitis B, cirrhotic, and HCC groups had higher MELD scores than nonsarcopenic patients (p <0.035, p <0.023, and p <0.024, respectively). Despite finding a similar increase in Child-Pugh scores in cirrhotic and HCC sarcopenic patients, results were statistically insignificant (p <0.597 and p <0.688). HCC patients with SaO had higher MELD scores than patients with other body composition catagories (p <0.006). Cirrhotic patients with SaO had higher MELD scores than nonsarcopenic obese patients (p <0.049). Chronic hepatitis B patients with obesity had low MELD scores (p <0.035). Cirrhotic and HCC patients with obesity had higher MELD scores (p <0.01 and p <0.024, respectively). Cirrhotic and HCC patients with obesity had higher Child-Pugh scores than nonobese patients but only HCC patients showed statistically significance (p <0.480 and p <0.001). Radiologic evaluation of SaO and harmonizing body composition with MELD scoring is critical in CLD management. [ABSTRACT FROM AUTHOR]

To define sarcopenic obesity (SaO) among chronic liver disease (CLD) patients via CT and MRI, and assess its impact on liver disease severity. CLD patients referred from the Gastroenterology and Hepatology Department diagnosed as chronic hepatitis B (N :101), cirrhosis (N :110), and hepatocellular carcinoma (N :169) with available information on body height, weight, Child-Pugh and MELD scores within 2 weeks of CT or MRI scanning were included in the study. Cross-sectional examinations were retrospectively evaluated for skeletal muscle index (SMI) and visceral adipose tissue area (VATA). The disease severity was assessed by Child-Pugh and MELD scoring. The rate of sarcopenia and SaO in the cirrhotic patients was higher than that in the chronic hepatitis B patients (p <0.033 and p < 0.004, respectively). The rate of sarcopenia and SaO in HCC patients was higher than that in the chronic hepatitis B patients (p <0.001 and p <0.001, respectively). Sarcopenic patients in Chronic hepatitis B, cirrhotic, and HCC groups had higher MELD scores than nonsarcopenic patients (p <0.035, p <0.023, and p <0.024, respectively). Despite finding a similar increase in Child-Pugh scores in cirrhotic and HCC sarcopenic patients, results were statistically insignificant (p <0.597 and p <0.688). HCC patients with SaO had higher MELD scores than patients with other body composition catagories (p <0.006). Cirrhotic patients with SaO had higher MELD scores than nonsarcopenic obese patients (p <0.049). Chronic hepatitis B patients with obesity had low MELD scores (p <0.035). Cirrhotic and HCC patients with obesity had higher MELD scores (p <0.01 and p <0.024, respectively). Cirrhotic and HCC patients with obesity had higher Child-Pugh scores than nonobese patients but only HCC patients showed statistically significance (p <0.480 and p <0.001). Radiologic evaluation of SaO and harmonizing body composition with MELD scoring is critical in CLD management. [ABSTRACT FROM AUTHOR]

There are well-described racial and ethnic disparities in the burden of chronic liver diseases. Hispanic persons are at highest risk for developing nonalcoholic fatty liver disease, the fastest growing cause of liver disease. Hepatitis B disproportionately affects persons of Asian or African descent. The highest rates of hepatitis C occur in American Indian and Alaskan Native populations. In addition to disparities in disease burden, there are also marked racial and ethnic disparities in access to treatments, including liver transplantation. Disparities also exist by gender and geography, especially in alcohol-related liver disease. To achieve health equity, we must address the root causes that drive these inequities. Understanding the role that social determinants of health play in the disparate health outcomes that are currently observed is critically important. We must forge and/or strengthen collaborations between patients, community members, other key stakeholders, health care providers, health care institutions, professional societies, and legislative bodies. Herein, we provide a high-level review of current disparities in chronic liver disease and describe actionable strategies that have potential to bridge gaps, improve quality, and promote equity in liver care. [ABSTRACT FROM AUTHOR]

There are well-described racial and ethnic disparities in the burden of chronic liver diseases. Hispanic persons are at highest risk for developing nonalcoholic fatty liver disease, the fastest growing cause of liver disease. Hepatitis B disproportionately affects persons of Asian or African descent. The highest rates of hepatitis C occur in American Indian and Alaskan Native populations. In addition to disparities in disease burden, there are also marked racial and ethnic disparities in access to treatments, including liver transplantation. Disparities also exist by gender and geography, especially in alcohol-related liver disease. To achieve health equity, we must address the root causes that drive these inequities. Understanding the role that social determinants of health play in the disparate health outcomes that are currently observed is critically important. We must forge and/or strengthen collaborations between patients, community members, other key stakeholders, health care providers, health care institutions, professional societies, and legislative bodies. Herein, we provide a high-level review of current disparities in chronic liver disease and describe actionable strategies that have potential to bridge gaps, improve quality, and promote equity in liver care. [ABSTRACT FROM AUTHOR]

SARS-CoV-2 vaccinations were found to be highly effective in phase 3 clinical trials. However, these trials have not reported data regarding the subgroup of liver disease or excluded patients with liver disease. The effectiveness of COVID-19 vaccines among liver cirrhosis (LC) patients is unclear. We conducted this meta-analysis to assess the effectiveness of SARS-CoV-2 vaccination in LC patients. A comprehensive literature search was conducted to include all the relevant studies that compared the outcomes of LC patients who received SARS-CoV-2 vaccines vs. unvaccinated patients. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) were calculated by the Mantel-Haenszel method within a random-effect model. Four studies with 51,834 LC patients (20,689 patients received at least one dose vs 31,145 were unvaccinated) were included. COVID-19–related complications, including hospitalization (RR 0.73, 95% CI 0.59–0.91, P = 0.004), mortality (RR 0.29, 95% CI 0.16–0.55, P = 0.0001), and need for invasive mechanical ventilation (RR 0.29, 95% CI 0.11–0.77, P = 0.01), were significantly lower in the vaccinated group compared to the unvaccinated group. SARS-CoV-2 vaccination in LC patients reduced COVID-19–related mortality, intubation, and hospitalization. SARS-CoV-2 vaccination is highly effective in LC. Further prospective studies, preferably randomized controlled trials, are necessary to validate our findings and determine which vaccine is superior in patients with LC. [ABSTRACT FROM AUTHOR]

Objectives: The aim of the study was to assess the sleep characteristics among patients with chronic liver diseases (CLDs) and find the relationship between variables of their demographic and sleep disorder. Methods: This descriptive cross-sectional study was designed to achieve the stated goals of patients with CLD in the Al-Najaf Center for Gastroenterology and Hepatology in Al-Sadr Medical City from November 1, 2020, to June 1, 2021. The sample was selected from 120 adult patients =18 years using non-probability sampling (purposeful) with CLD (disease duration of six months or more). The questionnaire consisted of two socio-demographic parts with clinical data (18 items) and a general health questionnaire (28 items) with 4 implicit subscales, including insomnia and anxiety level. Results: There was a strong significant relationship between sleep disorder and age (P=0.001), occupational status (P=0.001), daily activity (P=0.001), BMI (P=0.001), and duration of disease (P=0.001), gender (P=0.021), educational level (P=0.04), marital status (P=0.049), and type of disease (P=0.01). However, there was no significant relationship between sleep disorder and the remaining demographic and clinical data. Discussion: In conclusion, there is a relationship between the sleep disorder of CLD patients and their socio-demographic data. There is a strong significant relationship between patients' physical status and their sleep disorder (P=0.001). This result means that the disease has a significant effect on sleep. [ABSTRACT FROM AUTHOR]

Objectives: Hepatic osteodystrophy (HOD) is a well-recognized complication of chronic liver diseases (CLD), but the influential factors associated with this complication were studied scarcely in a rural Indian population. The study aims to evaluate the prevalence of HOD and variables that might influence it among cases diagnosed with CLD. Materials and Methods: It is a cross-sectional observational design survey that was performed in a hospital among the two-hundred cases and controls with a 1:1 ratio who were age (>18 years) and gender matched in a period between April and October 2021. They were subjected to etiological workup, hematological and biochemical investigations, and Vitamin D levels. Then, dual-energy X-ray absorptiometry was used to measure the bone mineral densitometry (BMD) for whole-body, lumbar spine (LS), and hip. HOD was diagnosed according to the WHO criteria. Then, the Chi-square test and conditional logistic regression analysis were used to investigate the influential factors of HOD in CLD patients. Results: The whole-body, LS-spine, and hip BMDs in CLD cases were found to be significantly lower as compared to controls. When the participants among both groups were stratified by age and gender, a significant difference in LS-spine and hip BMD was observed in elderly patients (>60 years), and in both the male and female patients. HOD was found in 70% of CLD patients. After multivariate analysis in CLD patients, we identified that being a male patient (odds ratio [OR] = 3.03), older age (OR = 3.54), duration of illness for more than 5 years (OR = 3.89), decompensated liver dysfunction with Child–Turcotte–Pugh-B and C grading (OR = 8.28), and low level of Vitamin D (OR = 18.45) were the risk factors for HOD. Conclusion: This study concludes that severity of illness and lower level of Vitamin D were the main influential factors for HOD. Supplementation of Vitamin D and calcium in the patients can abate the risk of fractures in our rural communities. [ABSTRACT FROM AUTHOR]

Objectives: The influence of chronic liver disease (CLD) on emergent neurosurgical outcomes in patients with spontaneous intracerebral hemorrhage (ICH) remains unclear. CLD is usually associated with coagulopathy and thrombocytopenia, which contribute to a high rebleeding rate and poor prognosis after surgery. This study aimed to confirm the outcomes of spontaneous intracranial hemorrhage in patients with CLD after emergent neurosurgery. Materials and Methods: We reviewed the medical records of all patients with spontaneous ICH from February 2017 to February 2018 at the Buddhist Tzu Chi Hospital, Hualien, Taiwan. This study was approved by the Review Ethical Committee/Institutional Board Review of Hualien Buddhist Tzu Chi Hospital (IRB111-051-B). Patients with aneurysmal subarachnoid hemorrhage, tumors, arteriovenous malformations, and those younger than 18 years were excluded. Duplicate electrode medical records were also removed. Results: Among the 117 enrolled patients, 29 had CLD and 88 did not. There were no significant differences in essential characteristics, comorbidities, biochemical profile, Glasgow coma scale (GCS) score at admission, or ICH sites. The length of hospital stay (LOS) and length of intensive care unit stay (LOICUS) are significantly longer in the CLD group (LOS: 20.8 vs. 13.5 days, P = 0.012; LOICUS: 11 vs. 5 days, P = 0.007). There was no significant difference in the mortality rate between the groups (31.8% vs. 28.4%, P = 0.655). The Wilcoxon rank-sum test for liver and coagulation profiles between survivors and the deceased revealed significant differences in the international normalized ratio (P = 0.02), including low platelet counts (P = 0.03) between survivors and the deceased. A multivariate analysis of mortality found that every 1 mL increase in ICH at admission increased the mortality rate by 3.9%, and every reduction in GCS at admission increased the mortality rate by 30.7%. In our subgroup analysis, we found that the length of ICU stay and LOS are significantly longer in patients with CLD who underwent emergent neurosurgery: 17.7 ± 9.9 days versus 7.59 ± 6.68 days, P = 0.002, and 27.1 ± 7.3 days versus 16.36 ± 9.08 days, P = 0.003, respectively. Conclusions: From our study's perspective, emergent neurosurgery is encouraged. However, there were more prolonged ICU and hospital stays. The mortality rate of patients with CLD who underwent emergent neurosurgery was not higher than that of patients without CLD. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study was designed to evaluate whether fat and iron affect the apparent diffusion coefficient (ADC) values of the liver parenchyma in the settings of fibrosis and inflammation. PATIENTS AND METHODS: We evaluated the diffusion-weighted images (DWIs) of 58 patients with chronic liver disease and 48 control subjects. Liver specimens of patients were assessed for fibrosis, necroinflammation, iron, and steatosis. Liver ADCs, spleen ADCs, and normalized liver ADCs (defined as the ratio of the liver ADC to spleen ADC) values were analyzed after stratifying patients with either fibrosis stages or histology activity index (HAI) scores. The relationship between ADC values and histopathological findings was studied using multiple linear regression analysis. RESULTS: The median liver and normalized liver ADC values were significantly lower in higher stages of fibrosis and HAI scores. Compared to the control group, patients with the highest stages of fibrosis and inflammation had significantly higher spleen ADCs. The effect of the fibrosis stage on liver ADC and normalized liver ADC values was significant in the setting of inflammation, whereas the degree of steatosis and iron grade did not affect these ADC values. CONCLUSIONS: ADC values can distinguish both later stages of liver fibrosis and inflammation. There is no significant effect of fat and iron on ADC values. Therefore, DWI may be reliable in evaluating liver fibrosis and inflammation. [ABSTRACT FROM AUTHOR]

Hepatic encephalopathy (HE) is a potentially reversible neurocognitive complication of cirrhosis. It has been reported in at least 30% of patients with cirrhosis and imposes a significant economic burden on caregivers and the healthcare system. Ammonia has been recognized as the culprit in HE development, and all the currently approved treatments mostly act on this toxin to help with HE resolution. After a brief overview of HE characteristics and pathophysiology, this review explores the current accepted treatments for this debilitating complication of cirrhosis. This is followed by an overview of the novel available therapies and a brief focus on future treatment modalities for HE. [ABSTRACT FROM AUTHOR]

Previous studies show that mortality from chronic liver disease (CLD) and cirrhosis is increasing in the United States. However, there are limited data on sex-specific mortality trends by age, race, and geographical location. The aim of this study was to conduct a comprehensive time-trend analysis of liver disease–related mortality rates in the National Center of Health Statistics (NCHS) database. CLD and cirrhosis mortality rates between 20002020 (age-adjusted to the 2000 standard U.S. population) were collected from the NCHS database and categorized by sex and age into older adults (≥55 years) and younger adults (<55 years), race (Non-Hispanic-White, Non-Hispanic-Black, Hispanic, Non-Hispanic-American-Indian/Alaska-Native, and Non-Hispanic-Asian/Pacific-Islander), U.S. state, and cirrhosis etiology. Time trends, annual percentage change (APC), and average APC (AAPC) were estimated using Joinpoint Regression using Monte Carlo permutation analysis. We used tests for parallelism and identicalness for sex-specific pairwise comparisons of mortality trends (two-sided P value cutoff =.05). Between 20002020, there were 716,651 deaths attributed to CLD and cirrhosis in the U.S. (35.68% women). In the overall population and in older adults, CLD and cirrhosis-related mortality rates were increasing similarly in men and women. However, in younger adults (246,149 deaths, 32.72% women), the rate of increase was greater in women compared with men (AAPC = 3.04 vs 1.08, AAPC-difference = 1.96; P <.001), with non-identical non-parallel data (P values <.001). The disparity was driven by Non-Hispanic-White (AAPC = 4.51 vs 1.79, AAPC-difference = 2.71; P <.001) and Hispanic (AAPC = 1.89 vs –0.65, AAPC-difference = 2.54; P =.001) individuals. The disparity varied between U.S. states and was seen in 16 states, mostly in West Virginia (AAPC = 4.96 vs 0.88, AAPC-difference = 4.08; P <.001) and Pennsylvania (AAPC = 2.81 vs –1.02, AAPC-difference = 3.84; P <.001). Etiology-specific analysis did not show significant sex disparity in younger adults. Mortality rates due to CLD and cirrhosis in the U.S. are increasing disproportionately in younger women. This finding was driven by higher rates in Non-Hispanic White and Hispanic individuals, with variation between U.S. states. Future studies are warranted to identify the reasons for these trends with the ultimate goal of improving outcomes. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinomas (HCCs) usually arise from chronic liver disease (CLD). Precancerous cells in chronically inflamed environments may be 'epigenetically primed', sensitising them to oncogenic transformation. We investigated whether epigenetic priming in CLD may affect HCC outcomes by influencing the genomic and transcriptomic landscapes of HCC. Analysis of DNA methylation arrays from 10 paired CLD‐HCC identified 339 shared dysregulated CpG sites and 18 shared differentially methylated regions compared with healthy livers. These regions were associated with dysregulated expression of genes with relevance in HCC, including ubiquitin D (UBD), cytochrome P450 family 2 subfamily C member 19 (CYP2C19) and O‐6‐methylguanine‐DNA methyltransferase (MGMT). Methylation changes were recapitulated in an independent cohort of nine paired CLD‐HCC. High CLD methylation score, defined using the 124 dysregulated CpGs in CLD and HCC in both cohorts, was associated with poor survival, increased somatic genetic alterations and TP53 mutations in two independent HCC cohorts. Oncogenic transcriptional and methylation dysregulation is evident in CLD and compounded in HCC. Epigenetic priming in CLD sculpts the transcriptional landscape of HCC and creates an environment favouring the acquisition of genetic alterations, suggesting that the extent of epigenetic priming in CLD could influence disease outcome. [ABSTRACT FROM AUTHOR]

This review evaluates the ability of the fibrosis index based on four factors (FIB-4) identifying fibrosis stages, long-time prognosis in chronic liver disease, and short-time outcomes in acute liver injury. FIB-4 was accurate in predicting the absence or presence of advanced fibrosis with cut-offs of 1.0 and 2.65 for viral hepatitis B, 1.45 and 3.25 for viral hepatitis C, 1.30 (<65 years), 2.0 (≥65 years), and 2.67 for non-alcoholic fatty liver disease (NAFLD), respectively, but had a low-to-moderate accuracy in alcoholic liver disease (ALD) and autoimmune hepatitis. It performed better in excluding fibrosis, so we built an algorithm for identifying advanced fibrosis by combined methods and giving work-up and follow-up suggestions. High FIB-4 in viral hepatitis, NAFLD, and ALD was associated with significantly high hepatocellular carcinoma incidence and mortality. Additionally, FIB-4 showed the ability to predict high-risk varices with cut-offs of 2.87 and 3.91 in cirrhosis patients and predict long-term survival in hepatocellular carcinoma patients after hepatectomy. In acute liver injury caused by COVID-19, FIB-4 had a predictive value for mechanical ventilation and 30-day mortality. Finally, FIB-4 may act as a screening tool in the secondary prevention of NAFLD in the high-risk population. [ABSTRACT FROM AUTHOR]

The impact of cryptogenic cirrhosis on skeleton has not been studied in Indian context. So this study investigated bone health in male patients with early cryptogenic cirrhosis as defined by Child-Turcot-Pugh A (CTP-A) categorization and compared it with patients diagnosed to have hepatitis B related chronic liver disease (CLD) on treatment and age, sex-matched healthy controls. It was a cross-sectional study, in which thirty male subjects were recruited in each group. Bone mineral density (BMD), trabecular bone score (TBS), hip structural analysis (HSA) and bone mineral parameters were assessed. The mean ±SD age of the study subjects was 39.3 ± 9.2 years. The mean 25-hydroxy vitamin D was significantly lower in subjects with cryptogenic cirrhosis as compared to controls (p = 0.001). Subjects with cryptogenic cirrhosis had significantly lower (1.297 ± 0.099) TBS as compared to hepatitis-B related CLD (1.350 ± 0.094) control subjects (1.351 ± 0.088) (p = 0.04). BMD at the hip and lumbar spine was also significantly lower in subjects with cryptogenic cirrhosis as compared to hepatitis-B related CLD and healthy age matched controls (p < 0.05). Most components of HSA were significantly affected in subjects with cryptogenic cirrhosis as compared to control subjects (p < 0.05). Patients with cryptogenic cirrhosis had significantly low TBS and BMD lumbar spine and hip as well as poor proximal hip geometry which may be good predictor of future fragility fractures. [ABSTRACT FROM AUTHOR]

Microvesicles (MVs) play a role in inflammation, coagulation, and vascular homeostasis in liver disease. To characterize circulating plasma MVs profile in patients with decompensated cirrhosis and acute kidney injury (AKI). We measured the levels of total, endothelial, platelet, tissue factor (TF)+, leukocyte and hepatocyte MVs by new generation flow-cytometry in a prospective cohort of patients with decompensated cirrhosis with and without AKI. Eighty patients with decompensated cirrhosis were recruited (40 each with and without AKI). Patients with cirrhosis with AKI had significantly higher calcein+ (total), endothelial, and platelet-MVs. Conversely, TF+, leukocyte, and hepatocyte-MVs were comparable between groups. Resolution of AKI was associated with significantly decreased total and endothelial-MVs that became comparable with those in patients without AKI. Platelet MVs significantly decreased but remained higher compared to patients without AKI. TF+MVs significantly decreased and became lower than patients without AKI. Leukocyte and hepatocyte-MVs remained unchanged. Creatinine (OR 4.3 [95%CI 1.8–10.7]), MELD (OR 1.13 [95%CI 1.02–1.27]), any bleeding (OR 9.07 [95%CI 2.02–40.6]), and hepatocyte-MVs (OR 1.04 [95%CI 1.02–1.07]) were independently associated with 30-day mortality. AKI worsened vascular and cellular homeostasis in patients with cirrhosis, particularly by inducing endothelial dysfunction and platelet activation. AKI did not worsen systemic inflammation and hepatocytes activation. [ABSTRACT FROM AUTHOR]

Lusutrombopag is an oral platelet production promoter for thrombocytopenia in patients with chronic liver disease (CLD) that is usually administered before an invasive procedure. However, not all patients showed adequate platelet elevation. To the best of our knowledge, there is only one case report published so far on patients treated with lusutrombopag before tooth extraction. Here, we reported three cases of CLD complicated by thrombocytopenia treated with lusutrombopag before tooth extraction, whose platelet count (PLC) increased appropriately in two cases but did not rise in the third case, necessitating platelet transfusion. Case 1 was that of a 72-year-old male with cirrhosis, hepatocellular carcinoma, hypertension, chronic renal failure, and low PLC (4.7 × 104/μL). Case 2 was that of a 67-year-old female with cirrhosis, diabetes, and chronic renal failure, low PLC (3.6 × 104/μL). Both the PLCs of cases 1 and 2 increased appropriately after the administration of lusutrombopag, and we were able to perform extraction without platelet transfusion. Case 3 was that of a 56-year-old female with idiopathic portal hypertension, giant spleen, portal vein embolism, and systemic lupus erythematosus, whose PLC was reduced at 2.9 × 104/μL. Abdominal ultrasonography revealed an abnormal enlargement of the spleen. The PLC did not increase after lusutrombopag administration, and platelet transfusion was required during surgery in this case. Furthermore, PLC did not increase on the day after platelet transfusion. Therefore, this suggested that PLC did not increase by lusutrombopag or platelet transfusion because of splenomegaly caused by idiopathic portal hypertension. [ABSTRACT FROM AUTHOR]