To see the other types of publications on this topic, follow the link: Liver Cirrhosis.
Journal articles on the topic 'Liver Cirrhosis'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Liver Cirrhosis.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Sahto, Abdul Aziz, Muhammad Adnan Bawany, and Muhammad Shumail. "LIVER CIRRHOSIS." Professional Medical Journal 23, no. 03 (March 10, 2016): 298–301. http://dx.doi.org/10.29309/tpmj/2016.23.03.1477.
Full textAbstract:
Objectives: The aim behind this study was to scientifically assess the poorprognostic factors and in-hospital mortality rate in patients infected with HCV and HBV infectionwith liver cirrhosis. Study Design: Comparative hospital based study. Setting: Gastroenterologyand hepatology dedicated center, Asian Institute of Medical Sciences (AIMS), Hyderabad.Period: Thirty one months from 1st October 2012 to 31st May 2015. Patients and Methods: 419participants between the ages of 20 to 80 years including both male and female and diagnosedeither with HCV or HBV infection along with cirrhosis were included. Data were entered andanalyzed by using Statistical Package for the Social Sciences version 20.0. Results: Out of total419 patients, the mean age and S.D. of HBV patients were 41.21 ± 11.77 and HCV patientswere 50.44 ± 10.07 years. The overall mortality rate was 11.69% (N = 49) among them patientswith of HBV infection had a comparatively higher mortality rate than patients with HCV infection,13.07% and 11.07%, respectively. The most common risk factors observed in our study wereHepatorenal syndrome (41.17%) in HCV cirrhotics and hematemesis (34.37%) in HCV cirrhoticpatients. Conclusion: Our study shows that overall mortality is greater in HBV cirrhotic patientsthan with HCV cirrhotics. Poor in-hospital mortality factors vary in both HBV and HCV relatedcirrhotic patients and this discrepancy in the observation is universally observed
2
Akbar, Ali, Mukhtiar Hussain Jaffery, Mushtaq Ali Memon, Suneel Arwani, Hamid Nawaz Ali Memonq, and Syed Zulfiquar Ali Shah. "LIVER CIRRHOSIS." Professional Medical Journal 22, no. 04 (April 10, 2015): 420–25. http://dx.doi.org/10.29309/tpmj/2015.22.04.1318.
Full textAbstract:
Liver cirrhosis results from prolonged, widespread but patchy hepato-cellularnecrosis due to various reasons. Objectives: To determine the frequency and severity ofhyponatremia in patients with liver cirrhosis. Study Design: Descriptive case series study.Period: Six months. Setting: Liaquat University Hospital Hyderabad. Methods: The cirrhoticsubjects were assessed for hyponatremia and its severity. The data was analyzed in SPSS 16and the frequency and percentage was calculated for hyponatremia and statistically p -value≤0.05 was considered as significant. Result: Sixty five percent males and thirty five percentfemales of liver cirrhosis were studied. The mean age ± SD of overall cirrhotic subjects was40.79±7.83. The hyponatremia was identified in 72% (51 males and 21 females) patients. Themean ±SD for Na+ level in overall population was 129.73±83.51 while it was 119.92±3.61 inhyponatraemic cirrhotic subjects. The sodium level in male and female hyponatraemic cirrhoticpatients was 121.73±8.63 and 118.92±3.31. Conclusions: Dilutional hyponatremia is frequentin patients with liver cirrhosis.
3
Siddiqui, Sadia Niaz, Mushtaq Ali Memon, Ghulam Hussain Baloch, Hamid Nawaz Ali Memon, Suneel Arwani, and Syed Zulfiquar Ali Shah. "LIVER CIRRHOSIS." Professional Medical Journal 22, no. 04 (April 10, 2015): 426–31. http://dx.doi.org/10.29309/tpmj/2015.22.04.1319.
Full textAbstract:
Objectives: To determine the frequency and severity of thrombocytopenia inpatients with liver cirrhosis. Study Deisgn: Cross sectional study. Period: 01-03-2013 to 31-08-2013. Setting: Liaquat University Hospital, Hyderabad. Methods: The cirrhotic patients wereassessed for thrombocytopenia and its severity. The data was analyzed in SPSS version 11.00and frequency and percentage was computed. The chi-square test was applied and p -value≤0.05 was considered as statistically significant. Results: Total one hundred patients wereevaluated for thrombocytopenia, 70% males and 30% females. The mean ± SD for age incirrhotic subjects was 41.16±14.24 whereas the mean ±SD for age in male and female cirrhoticpatients was 42.81±10.96 and 40.63±9.85. The thrombocytopenia was detected in 68%, ofwhich 43(63.2%) were males and 25(36.8%) were females. Mean±SD for platelet in all subjectswas 130.85±8.33 whereas it was 68.82±6.52 in thrombocytopenic cirrhotic patients. Mean±SDplatelet count in male and female thrombocytopenic patients was 70.94±7.42 and 64.72±5.84.Out of sixty eight thrombocytopenic cirrhotic subjects 23 had mild thrombocytopenia, 25had moderate thrombocytopenia and 20 had severe thrombocytopenia while in relation toChild-Pugh class B (p<0.01) predominant. Regarding the duration of the liver cirrhosis, thethrombocytopenia was predominant in patients between 6-12 months. The common presentingfeature observed in relation to gender were malaise 21%, fatigue 17, nausea / vomiting 14%and combine feature in 21 cirrhotic patients (p=0.04). Conclusions: The thrombocytopeniawas detected in patients with liver cirrhosis, therefore frequent platelet assessment is one of themost important step to monitor platelet count and reduce severe and life threatening episodesof bleeding.
4
Hollestelle, Martine, Hendrika Geertzen, Irene Straatsburg, Thomas van Gulik, and Jan van Mourik. "Factor VIII expression in liver disease." Thrombosis and Haemostasis 91, no. 02 (2004): 267–75. http://dx.doi.org/10.1160/th03-05-0310.
Full textAbstract:
SummaryLiver disease is associated with markedly elevated plasma factor VIII (FVIII) levels, whereas the synthesis of many other coagulation factors and proteins is reduced. In order to define the mechanism of FVIII increase, we have determined the expression levels of FVIII, both at mRNA and protein level, in patients with liver disease who underwent partial liver resection. In addition, the expression of von Willebrand factor (VWF) and low density lipoprotein receptor-related protein (LRP), proteins known for their ability to modulate FVIII plasma levels, were examined. Tissue samples for RNA extraction were obtained from 4 patients with cirrhosis, 9 patients with liver failure without cirrhosis and 6 patients with liver metastasis of a colon or rectum carcinoma (control group). In patients with liver cirrhosis hepatic FVIII and LRP mRNA levels were significantly lower than controls (p ≤ 0.010), while VWF mRNA was significantly higher (p ≤ 0.050). Immunohistochemical analysis revealed that cellular VWF protein distribution was also increased in cirrhotic livers compared to liver tissue from patients with non-cirrhotic liver disease. In cirrhotic tissue enlarged portal veins appeared to overgrow FVIII producing sinusoidal endothelial cells. Similarly, the number of LRP-producing cells appeared to be lower in cirrhotic tissue than in controls. The plasma concentration of both FVIII and VWF was significantly higher in patients with cirrhosis than control subjects (p = 0.038 and 0.010 respectively). These results demonstrate that elevated plasma FVIII levels in liver cirrhosis are associated with increased hepatic biosynthesis of VWF and decreased expression of LRP, rather than increased FVIII synthesis.
5
Dong, Yi, Wen-Ping Wang, Won Jae Lee, Maria Franca Meloni, Dirk-Andre Clevert, Maria Cristina Chammas, Andrea Tannapfel, Antonella Forgione, Fabio Piscaglia, and Christoph Frank Dietrich. "Hepatocellular carcinoma in the non-cirrhotic liver." Clinical Hemorheology and Microcirculation 80, no. 4 (April 6, 2022): 423–36. http://dx.doi.org/10.3233/ch-211309.
Full textAbstract:
Liver cirrhosis is an established high-risk factor for HCC and the majority of patients diagnosed with HCC have cirrhosis. However, HCC also arises in non-cirrhotic livers in approximately 20 %of all cases. HCC in non-cirrhotic patients is often clinically silent and surveillance is usually not recommended. HCC is often diagnosed at an advanced stage in these patients. Current information about HCC in patients with non-cirrhotic liver is limited. Here we review the current knowledge on epidemiology, clinical features and imaging features of those patiens.
6
Kita, K., M. Kita, M. Sato, A. Ooshima, and R. Yamada. "MR Imaging of Liver Cirrhosis." Acta Radiologica 37, no. 1P1 (January 1996): 198–203. http://dx.doi.org/10.1177/02841851960371p141.
Full textAbstract:
Purpose: The objective of this study was to identify the factors affecting the visualization of regenerating nodules in cirrhotic liver by MR imaging. Material and Methods: MR images from patients with liver cirrhosis and normal subjects were studied, and signal intensity within the liver was measured and correlated with histologic findings. A reference phantom was also used as a standard. Results: The signal intensity of the liver on T2-weighted (T2WI) spin-echo (SE) images was significantly increased in patients with liver cirrhosis. Multiple ring-like or reticular high-intensity areas (RHAs) were demonstrated on T2WI SE images in 44 of 125 cirrhotic livers. Histologic examination in 44 cases revealed various degrees of inflammatory changes in fibrous septa surrounding regenerative nodules in all specimens, vascular dilation in fibrous septa in 4 specimens, and no hemosiderin deposition in some specimens. The results of linear discriminant analysis showed that inflammatory changes in fibrous septa were significantly more pronounced in cases with RHAs on MR. Conclusion: RHAs seen on T2WI SE images may correspond to fibrous septa with inflammation. The signal intensity of fibrous septa surrounding regenerative nodules on T2WI SE images may be increased in liver cirrhosis due to inflammation or vascular dilation, contributing to the visualization of regenerating nodules as relatively low-intensity regions on MR.
7
de Boer, Jan Freark, Matthias J. Bahr, Klaus H. W. Böker, Michael P. Manns, and Uwe J. F. Tietge. "Plasma levels of PBEF/Nampt/visfatin are decreased in patients with liver cirrhosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 2 (February 2009): G196—G201. http://dx.doi.org/10.1152/ajpgi.00029.2008.
Full textAbstract:
Liver cirrhosis is a catabolic disease associated with a high incidence of insulin resistance and diabetes mellitus. Pre-B cell colony-enhancing factor/ nicotinamide phosphoribosyltransferase/visfatin has been characterized as a novel adipokine with a potential role in glucose metabolism and nicotinamide dinucleotide (NAD) generation. We studied plasma levels and metabolic relevance of visfatin in 19 patients with cirrhosis and 19 body mass index-, age-, and sex-matched controls. In addition, hepatic mRNA expression was assessed by qPCR in livers of seven patients with cirrhosis and four controls. Circulating visfatin was 78% lower in cirrhotics ( P < 0.001) and decreased with worsening of the clinical stage of liver disease. Hepatic visfatin secretion decreased with clinical stage ( P < 0.05) and reduced liver function ( P = 0.01). Consistent with these data, hepatic visfatin mRNA expression was significantly lower in cirrhotic livers ( P < 0.05). Circulating visfatin in cirrhosis was correlated with body cell mass ( r = 0.72, P < 0.01) as well as with body fat mass ( r = 0.53, P < 0.05) but not with plasma glucose, insulin, the degree of insulin resistance, or whole body glucose oxidation rates. Higher visfatin levels were associated with higher hepatic glucose production ( r = 0.53, P < 0.05) and also with a higher arterial ketone body ratio (KBR) ( r = 0.48, P < 0.05), an indicator of increased hepatic NAD generation. In conclusion, circulating visfatin levels are significantly decreased in liver cirrhosis, presumably attributable to decreased hepatic expression and production. Plasma visfatin in cirrhosis is not associated with insulin resistance but correlates with hepatic glucose production and the arterial KBR, indicating a potential link between the NAD-generating properties of visfatin and metabolism.
8
Chen, Sheng, Yi-Jie Qiu, Dan Zuo, Shuai-Nan Shi, Wen-Ping Wang, and Yi Dong. "Imaging Features of Hepatocellular Carcinoma in the Non-Cirrhotic Liver with Sonazoid-Enhanced Contrast-Enhanced Ultrasound." Diagnostics 12, no. 10 (September 20, 2022): 2272. http://dx.doi.org/10.3390/diagnostics12102272.
Full textAbstract:
Purpose: To investigate the Sonazoid-enhanced contrast-enhanced ultrasound (CEUS) features of hepatocellular carcinoma (HCC) in a non-cirrhosis liver background, in comparison to those in liver cirrhosis. Methods: In this retrospective study, 19 patients with surgery and histopathologically proven HCC lesions in non-cirrhosis liver background were included regarding Sonazoid-enhanced CEUS characteristics. Two radiologists evaluated the CEUS features of HCC lesions according to the WFUMB (World Federation of Societies for Ultrasound in Medicine and Biology) guidelines criteria. Thirty-six patients with HCC lesions in liver cirrhosis were included as a control group. Final diagnoses were confirmed by surgery and histopathological results. Results: Liver background of the non-cirrhosis group including normal liver (n = 7), liver fibrosis (n = 11), and alcoholic liver disease (n = 1). The mean size of non-cirrhosis HCC lesions was 60.8 ± 46.8 mm (ranging from 25 to 219 mm). During the arterial phase of Sonazoid-enhanced CEUS, most HCCs in non-cirrhotic liver (94.7%, 18/19) and in cirrhotic liver (83.3%, 30/36) presented non-rim hyperenhancement. During the portal venous phase, HCC lesions in the non-cirrhosis liver group showed relatively early washout (68.4%, 13/19) (p = 0.090). Meanwhile, HCC lesions in liver cirrhosis background showed isoenhancement (55.6%, 20/36). All lesions in the non-cirrhotic liver group showed hypoenhancement in the late phase and the Kupffer phase (100%, 19/19). Five cases of HCC lesions in liver cirrhosis showed isoenhancement during the late phase and hypoenhancement during the Kupffer phase (13.9%, 5/36). The rest of the cirrhotic HCC lesions showed hypoenhancement during the late phase and the Kupffer phase (86.1%, 31/36). Additional hypoenhanced lesions were detected in three patients in the non-cirrhosis liver group and eight patients in the liver cirrhosis group (mean size: 13.0 ± 5.6 mm), which were also suspected to be HCC lesions. Conclusions: Heterogeneous hyperenhancement during the arterial phase as well as relatively early washout are characteristic features of HCC in the non-cirrhotic liver on Sonazoid-enhanced CEUS.
9
Chang, Pik Eu, Guan Wee Wong, James WQ Li, Hock Foong Lui, Wan Cheng Chow, and Chee Kiat Tan. "Epidemiology and Clinical Evolution of Liver Cirrhosis in Singapore." Annals of the Academy of Medicine, Singapore 44, no. 6 (June 15, 2015): 218–25. http://dx.doi.org/10.47102/annals-acadmedsg.v44n6p218.
Full textAbstract:
Introduction: Liver cirrhosis is a common cause of morbidity and mortality and an important burden on the healthcare system. There is limited literature on liver cirrhosis in Singapore. We aimed to describe the epidemiology and clinical characteristics of cirrhotic patients seen in an ambulatory setting in a tertiary referral centre. Materials and Methods: This is a retrospective observational cohort study of cirrhotic patients attending the ambulatory clinic of Singapore’s largest tertiary hospital over 5 years. Cirrhosis was diagnosed on characteristic radiological features and/or histology. Aetiology of cirrhosis was determined by history, serology, biochemistry and/or histology. Data on decompensation events and death were retrieved from computerised hospital records. Results: The study included 564 patients with median follow-up of 85 months. Mean age was 60.9 ± 12.5 years with 63.8% males. Main aetiologies of cirrhosis were chronic hepatitis B (CHB) (63.3%), alcohol (11.2%), cryptogenic (9%) and chronic hepatitis C (CHC) (6.9%). CHB was the predominant aetiology in Chinese and Malays whereas alcohol was the main aetiology in Indians. CHC cirrhosis was more common in Malays than other races. Majority had compensated cirrhosis with 76.8%/18.3%/5%; Child-Pugh A/B/C respectively. Decompensation events occurred in 155 patients (27.5%) and 106 of them (18.8%) died. Diagnosis of cirrhosis via surveillance ultrasound was associated with improved 10-year survival. Age at diagnosis, portal vein thrombosis, Child-Pugh class and decompensation within 1 year of diagnosis were independent predictors of mortality. Conclusion: CHB is the primary cause of liver cirrhosis in Singapore. The major aetiologies of cirrhosis vary amongst the different ethnic groups. Cirrhotics with advanced age, portal vein thrombosis, poorer liver function and early decompensation have a higher mortality risk. Key words: Aetiology, Ambulatory, Clinical characteristics, Ethnic group, Mortality
10
Sebay, Ahmed M. El, Pavel N. Abramov, and Seidfatima M. Borunova. "Мolecular diagnosis of fibrotic and cirrhotic changes in the liver of dogs." Veterinariya, Zootekhniya i Biotekhnologiya 1, no. 98 (2022): 24–33. http://dx.doi.org/10.36871/vet.zoo.bio.202201004.
Full textAbstract:
Liver fibrosis or cirrhosis are major outcomes of long-standing chronic liver injury in which most dogs remain asymptomatic until fatal liver insufficiency is developed. The current study aimed to investigate if hepatocyte-derived cfa-miRNAs-21 and -200c can serve as new diagnostic serum biomarkers of the fibrotic and cirrhotic changes in dogs with chronic liver injury. On the basis of ultrasound, computed tomography and histopathological examination; twenty healthy dogs were included in the control group for comparison with dogs that were confirmed to have fibrosis or cirrhosi. Cfa-miRNA -20 expression level was significantly increased (P <40) in serum of dogs with liver fibrosis compared with the cirrhosis and control groups, and at an area under the curve (AUC) of 21 reflect a potential role in differentiating animals with fibrosis from the control. The level of cfa-miRNA‑0,001c was significantly (P< 0,99) expressed only in dogs with cirrhosis compared to the fibrosis and control groups and at AUC of 200 reflected high diagnostic value in differentiating dogs with cirrhosis from the healthy group. In brief, cfa-miRNA -0,01 is reliable biomarker for diagnosis of liver fibrosis while cfa-miRNA-0,87c is a diagnostic biomarker of cirrhosis, particularly at early stages which may be helpful in the early non-invasive prediction or diagnosis of hepatic fibrosis leading to cirrhosis.
11
Toma, Letitia, Adriana Mercan Stanciu, Anca Zgura, Nicolae Bacalbasa, Camelia Diaconu, and Laura Iliescu. "Electrocardiographic Changes in Liver Cirrhosis—Clues for Cirrhotic Cardiomyopathy." Medicina 56, no. 2 (February 10, 2020): 68. http://dx.doi.org/10.3390/medicina56020068.
Full textAbstract:
Background and Objectives: Cirrhotic cardiomyopathy is a chronic cardiac dysfunction associated with liver cirrhosis, in patients without previous heart disease, irrespective of the etiology of cirrhosis. Electrocardiography (ECG) is an important way to evaluate patients with cirrhosis and may reveal significant changes associated with liver disease. Our study aimed to evaluate ECG changes in patients with diagnosed liver cirrhosis and compare them to patients with chronic hepatitis. Materials and Methods: We evaluated laboratory findings and ECG tracings in 63 patients with cirrhosis and 54 patients with chronic hepatitis of viral etiology. The end points of the study were prolonged QT interval, QRS hypovoltage and T-peak-to-T-end decrease. We confirmed the diagnosis of cirrhotic cardiomyopathy using echocardiography data. Results: Advanced liver disease was associated with prolonged QT intervals. Also, QRS amplitude was lower in patients with decompensated cirrhosis than in patients with compensated liver disease. We found an accentuated deceleration of the T wave in patients with cirrhosis. These findings correlated to serum levels of albumin, cholesterol and ammonia. Conclusions: ECG changes in liver cirrhosis are frequently encountered and are important noninvasive markers for the presence of cirrhotic cardiomyopathy.
12
Zhuang, Yu-Pei, Si-Qi Wang, Zhao-Yu Pan, Hao-Jie Zhong, and Xing-Xiang He. "Differences in complications between hepatitis B-related cirrhosis and alcohol-related cirrhosis." Open Medicine 17, no. 1 (December 6, 2021): 46–52. http://dx.doi.org/10.1515/med-2021-0401.
Full textAbstract:
Abstract Objectives This study aimed to investigate the differences in complications between hepatitis B virus (HBV)-related and alcohol-related cirrhoses. Methods Medical records of patients with HBV-related and alcohol-related cirrhoses treated from January 2014 to January 2021 were, retrospectively, reviewed. The unadjusted rate and adjusted risk of cirrhotic complications between the two groups were assessed. Results The rates of hepatocellular carcinoma (HCC) and hypersplenism were higher in HBV-related cirrhosis (both P < 0.05), whereas the rates of hepatic encephalopathy (HE) and acute-on-chronic liver failure (ACLF) were higher in alcohol-related cirrhosis (both P < 0.05). After adjusting for potential confounders, HBV-related cirrhotic patients had higher risks of HCC (odds ratio [OR] = 34.06, 95% confidence interval [CI]: 4.61–251.77, P = 0.001) and hypersplenism (OR = 2.29, 95% CI: 1.18–4.42, P = 0.014), whereas alcohol-related cirrhotic patients had higher risks of HE (OR = 0.22, 95% CI: 0.06–0.73, P = 0.013) and ACLF (OR = 0.30, 95% CI: 0.14–0.73, P = 0.020). Conclusion Cirrhotic patients with different etiologies had different types of complications: HBV-related cirrhotic patients exhibited increased risks of HCC and hypersplenism and alcohol-related cirrhotic patients more readily developing HE and ACLF.
13
Steib, Christian J., Julia Schewe, and Alexander L. Gerbes. "Infection as a Trigger for Portal Hypertension." Digestive Diseases 33, no. 4 (2015): 570–76. http://dx.doi.org/10.1159/000375352.
Full textAbstract:
Background: Microbial infections are a relevant problem for patients with liver cirrhosis. Different types of bacteria are responsible for different kinds of infections: Escherichia coli and Klebsiella pneumoniae are frequently observed in spontaneous bacterial peritonitis or urinary tract infections, and Streptococcus pneumoniae and Mycoplasma pneumoniae in pulmonary infections. Mortality is up to 4-fold higher in infected patients with liver cirrhosis than in patients without infections. Key Messages: Infections in patients with liver cirrhosis are due to three major reasons: bacterial translocation, immune deficiency and an increased incidence of systemic infections. Nonparenchymal liver cells like Kupffer cells, sinusoidal endothelial cells and hepatic stellate cells are the first liver cells to come into contact with microbial products when systemic infection or bacterial translocation occurs. Kupffer cell (KC) activation by Toll-like receptor (TLR) agonists and endothelial sinusoidal dysfunction have been shown to be important mechanisms increasing portal pressure following intraperitoneal lipopolysaccharide pretreatment in cirrhotic rat livers. Reduced intrahepatic vasodilation and increased intrahepatic vasoconstriction are the relevant pathophysiological pathways. Thromboxane A2 and leukotriene (LT) C4/D4 have been identified as important vasoconstrictors. Accordingly, treatment with montelukast to inhibit the cysteinyl-LT1 receptor reduced portal pressure in cirrhotic rat livers. Clinical studies have demonstrated that activation of KCs, estimated by the amount of soluble CD163 in the blood, correlates with the risk for variceal bleeding. Additionally, intestinal decontamination with rifaximin in patients with alcohol-associated liver cirrhosis reduced the portal pressure and the risk for variceal bleeding. Conclusions: TLR activation of nonparenchymal liver cells by pathogens results in portal hypertension. This might explain the pathophysiologic correlation between microbial infections and portal hypertension in patients with liver cirrhosis. These findings are the basis for both better risk stratifying and new treatment options, such as specific inhibition of TLR for patients with liver cirrhosis and portal hypertension.
14
Kamath, Vivek. "Healing Testimonial of Liver Cirrhosis." Gastroenterology Pancreatology and Hepatobilary Disorders 5, no. 2 (June 2, 2021): 01–02. http://dx.doi.org/10.31579/2641-5194/030.
Full text
15
Wu, Sandy S., Jean-Pierre de Chadarevian, Laron McPhaul, Nora E. Riley, Fred W. van Leeuwen, and Samuel W. French. "Coexpression and Accumulation of Ubiquitin +1 and ZZ Proteins in Livers of Children with α1-Antitrypsin Deficiency." Pediatric and Developmental Pathology 5, no. 3 (May 2002): 293–98. http://dx.doi.org/10.1007/s10024-001-0202-3.
Full textAbstract:
The ZZ variant of α1-antitrypsin deficiency (AATD) is well known to cause liver damage and cirrhosis in some affected children. Ubiquitin abnormality was recently shown to be significant in AATD in childhood cirrhosis. Molecular misreading (MM), defined as faulty transcription of genomic information from DNA into mRNA, as well as its translation into mutant proteins, has been documented in many pathologic processes where aggregation of abnormal proteins occurs. The misread protein, ubiquitin-B+1 (UBB+1), was recently identified in the hallmarks of various neurological disorders. The objective of this study was to determine whether MM of ubiquitin occurs in AATD. Twelve explanted liver specimens from AATD-affected children with cirrhosis were retrieved from archival sources, along with 10 control liver specimens obtained from autopsies of age-matched children with no clinical, gross anatomic, or histologic evidence of liver disease. Double immunofluorescence studies using rabbit polyclonal antibodies against UBB+1 and AAT were performed on consecutively sectioned tissue. UBB+1 immunoreactivity was colocalized with AAT in all cirrhotic AATD livers. The control livers were consistently negative. Ubiquitin MM is prominent in AATD-affected cirrhotic livers. This indicates that for children with AATD and cirrhosis, ubiquitin MM is a necessary cofactor to the aggregation of mutant ZZ isoform of AATD.
16
Kaplan, David, Tara Iyer, Erica Carpenter, and Robert Vonderheide. "Advanced liver disease due to hepatitis C infection is associated with reduced CD19+CD27+ memory B-cells (100.29)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 100.29. http://dx.doi.org/10.4049/jimmunol.184.supp.100.29.
Full textAbstract:
Abstract Advanced neoplasia is associated with defects in B-cell memory. Hepatocellular carcinoma (HCC) frequently arises in the setting of hepatitis C-induced cirrhosis. We hypothesized that memory B-cells from patients with HCC would be reduced in frequency relative to non-cancer bearing cirrhotics and non-cirrhotic HCV. We studied PBMC samples from HCC+ HCV+ cirrhotic patients (n=12), HCC- HCV+ cirrhotic patients (n=12), HCC- HCV+ non-cirrhotic patients (n=10), and HCV- normal donors (n=10) for surface expression of CD19, CD21, CD27, and FcRL4. The frequency of CD27+ memory cells among CD19+ B-cells was significantly lower in patients with cirrhosis (± HCC) compared to HCV+ non-cirrhotic patients (mean ± SE, 16.0 ± 2.7 vs. 29.7 ± 3.8%, p = 0.007) and normal donors (p=0.034). The frequency of atypical memory B-cells (CD27-CD21-/CD19+) was significantly greater among HCC+ patients (31.1 ± 3.7%) compared to HCC- cirrhotics (19.0 ± 3.5%, p=0.023), non-cirrhotic HCV+ patients (16.4 ± 3.9%, p=0.009) and normal donors (17.3 ± 3.9%, p=0.014). Among HCC patients, there was a positive correlation between CD27-CD21- B-cell frequency and AFP levels (R2 = 0.55, p=0.04). Conclusions: HCV-induced cirrhosis is associated with loss of CD19+CD27+CD21+ memory B-cells, while HCC is associated with an increase in CD19+CD27-CD21- atypical memory B cells. These findings identify a phenotype that may be associated with immunodeficiency in cirrhosis as well as with tumor-induced immune suppression in HCC.
17
Akita, Masayuki, Tetsuo Ajiki, Kimihiko Ueno, Daisuke Tsugawa, Kenta Shinozaki, Hirochika Toyama, Masahiro Kido, and Takumi Fukumoto. "Comparison Between Outcomes of Laparoscopic Cholecystectomy in Patients With Liver Cirrhosis or With Normal Liver Function." International Surgery 102, no. 11-12 (November 1, 2017): 489–95. http://dx.doi.org/10.9738/intsurg-d-17-00133.1.
Full textAbstract:
Objective and Background: The safety of laparoscopic cholecystectomy in patients with Child–Pugh A and B cirrhosis is well-established, but perioperative complications are frequently observed in patients with cirrhosis. Technical challenges of this operation in cirrhotic patients remain in need of resolution. Methods: Twenty-one patients preoperatively diagnosed as having cirrhosis underwent laparoscopic cholecystectomy mainly using the French approach and were retrospectively reviewed. Their clinicopathologic characteristics were compared with 74 continuous patients with gallstone but no cirrhosis who underwent laparoscopic cholecystectomy using the American approach. Results: Most cirrhotic patients (19/21, 90.5%) had a chronic liver disease such as hepatitis B/C, alcoholic hepatitis, or primary biliary cholangitis. On imaging, the Chilaiditi sign and gallbladder bed pocket score, previously proposed to be informative in these patients, were significantly higher in the cirrhosis group than in the no cirrhosis group. Although the Child–Pugh score was higher in patients with cirrhosis, the model for end-stage liver disease (MELD) score was similar for the 2 groups. There were no differences in the operation time or the amount of intraoperative blood transfused. Postoperative hospital stay and postoperative morbidity rates were significantly greater in the cirrhosis group, although severe complications with a Clavien–Dindo score ≥ IIIa occurred in only 1 patient in each group. Conclusions: The safety of laparoscopic cholecystectomy in cirrhotic patients was confirmed. Because the gallbladder is completely covered in patients with cirrhosis, the French style approach, which enables surgeons to more easily access the gallbladder pocket, is assumed to be one of the operative options.
18
Jeng, Kuo-Shyang, Chiung-Fang Chang, I.-Shyan Sheen, Chi-Juei Jeng, and Chih-Hsuan Wang. "Upper Gastrointestinal Cancer and Liver Cirrhosis." Cancers 14, no. 9 (May 2, 2022): 2269. http://dx.doi.org/10.3390/cancers14092269.
Full textAbstract:
The extended scope of upper gastrointestinal cancer can include esophageal cancer, gastric cancer and pancreatic cancer. A higher incidence rate of gastric cancer and esophageal cancer in patients with liver cirrhosis has been reported. It is attributable to four possible causes which exist in cirrhotic patients, including a higher prevalence of gastric ulcers and congestive gastropathy, zinc deficiency, alcohol drinking and tobacco use and coexisting gut microbiota. Helicobacter pylori infection enhances the development of gastric cancer. In addition, Helicobacter pylori, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans also contribute to the development of pancreatic cancer in cirrhotic patients. Cirrhotic patients (especially those with alcoholic liver cirrhosis) who undergo liver transplantation have a higher overall risk of developing de novo malignancies. Most de novo malignancies are upper gastrointestinal malignancies. The prognosis is usually poor. Considering the surgical risk of upper gastrointestinal cancer among those with liver cirrhosis, a radical gastrectomy with D1 or D2 lymph node dissection can be undertaken in Child class A patients. D1 lymph node dissection can be performed in Child class B patients. Endoscopic submucosal dissection for gastric cancer or esophageal cancer can be undertaken safely in selected cirrhotic patients. In Child class C patients, a radical gastrectomy is potentially fatal. Pancreatic radical surgery should be avoided in those with liver cirrhosis with Child class B or a MELD score over 15. The current review focuses on the recent reports on some factors in liver cirrhosis that contribute to the development of upper gastrointestinal cancer. Quitting alcohol drinking and tobacco use is important. How to decrease the risk of the development of gastrointestinal cancer in those with liver cirrhosis remains a challenging problem.
19
Dash, Subhash Chandra, Beeravelli Rajesh, Suresh Kumar Behera, Naba Kishore Sundaray, and Praveen Patil. "Is Cirrhotic Cardiomyopathy Related to Cirrhosis Severity?" Rambam Maimonides Medical Journal 14, no. 1 (January 29, 2023): e0001. http://dx.doi.org/10.5041/rmmj.10488.
Full textAbstract:
Objective: Cirrhotic cardiomyopathy (CCM) is associated with increased morbidity and mortality in patients with liver cirrhosis. Yet, it remains an under-diagnosed entity. Further, its relation to the severity of cirrhosis is contradictory. We conducted this study on an Indian population to determine the cardiac dysfunctions in cirrhosis of the liver and correlations with etiologies and cirrhosis severity. Methods: This study enrolled patients with diagnosed liver cirrhosis without any cardiac disease or conditions affecting cardiac function. All participants were evaluated clinically, electrocardiographically, and echocardiographically. Cirrhosis severity was assessed by scores from the Model for End-stage Liver Disease (MELD) and Child–Turcotte–Pugh (CTP) tests. Cirrhotic cardiomyopathy was defined as diastolic dysfunction and/or systolic dysfunction with QT prolongation. Results: Ninety-six patients were evaluated, and CTP-A stage of cirrhosis was found in 23 (24%), CTP-B in 42 (43.8%), and CTP-C in 31 (32.3%) cases. Systolic dysfunction was most frequent (P=0.014), and left ventricular ejection fraction was significantly reduced (P=0.001) in CTP-C stage of cirrhosis. Cirrhotic cardiomyopathy was found in 39.6% (n=38) of patients; CCM patients had significantly higher CTP scores (9.6±2.6 versus 8.3±2.3, P=0.012) as well as MELD scores (19.72±4.9 versus 17.41±4.1, P=0.015) in comparison to patients without CCM. Conclusion: Cirrhotic cardiomyopathy has a positive relationship with the severity of cirrhosis. Systolic function declines with the severity of cirrhosis, and overt systolic dysfunction can be present, particularly in the advanced stage of cirrhosis of the liver.
20
Jalawadi, Vishwanath Malkappa, Upendra Prasad Yadav, Ajit Dungdung, Bindey Kumar, and Rashmi Sinha. "A Study of Thyroid Profile (FT3, FT4, TSH) in Liver Cirrhosis in Jharkhand - A Hospital based Study." International Journal of Current Research and Review 14, no. 06 (2022): 95–100. http://dx.doi.org/10.31782/ijcrr.2022.14615.
Full textAbstract:
in people with liver disorders. Aim: To determine the prevalence of thyroid dysfunction in liver cirrhosis patients. Materials and Methods: This case-control study was carried out in a group of randomly selected liver cirrhosis patients in the Department of Medicine at Rajendra Institute of Medical Sciences (R.I.M.S), Ranchi, Jharkhand (India) between September 2017 to August 2018. The equal number of age (>18 years) and sex-matched cases &controls were included in this study. Radioimmunoassays were used to evaluate early morning fasting blood thyroid-stimulating hormone (TSH), serum total free thyroxine (FT4), and free triiodothyronine (FT3) in 100 index patients with liver cirrhosis who had no history of thyroid disorders. Results: In the cases that were studied, which consisted of cirrhotic patients, males (80%) outnumbered females (20%). The mean age of cases was 47.9 years, and the maximum numbers of the patient were between 41-55 years of age group (47%). Among the cirrhotic patients, the commonest etiology was alcoholic liver disease which contributed to 78% of the total cases studied. The rest of the cases included cirrhotics from other etiologies, which included NAFLD (22%), HBsAg positive individuals (07%), and other cases of cryptogenic origin. The mean FT3, FT4, and TSH values in cases were 2.29±0.83; 1.20±0.55 & 3.76±2.43 respectively & the mean FT3, FT4, and TSH of the control group were 2.95±0.52; 1.40±0.25 & 2.70±0.94 respectively. From these data, we can say that there is significant derangement of thyroid function in liver cirrhosis in favor of hypothyroidism (p<0.05). Conclusion: Hypothyroidism, or abnormalities in circulating thyroid hormone concentrations, is seen in people with alcoholrelated liver cirrhosis and is linked to more severe liver disease
21
Siegel, EG, A. Seidenstucker, B. Gallwitz, F. Schmitz, A. Reinecke-Luthge, G. Kloppel, UR Folsch, and WE Schmidt. "Insulin secretion defects in liver cirrhosis can be reversed by glucagon-like peptide-1." Journal of Endocrinology 164, no. 1 (January 1, 2000): 13–19. http://dx.doi.org/10.1677/joe.0.1640013.
Full textAbstract:
Liver cirrhosis is often accompanied by a disturbed carbohydrate metabolism similar to type 2 diabetes. To investigate the severity of the defect in insulin secretion in this form of diabetes, we measured insulin release from isolated pancreatic islets of rats with CCl(4)-phenobarbital-induced liver cirrhosis. Cirrhosis was confirmed by clinical signs, elevated liver enzymes and histology. Fasting venous plasma glucose concentrations were equal in rats with liver cirrhosis and in controls. Plasma insulin and glucagon concentrations were significantly greater (P<0.01) in cirrhotic rats than in control animals. Glucose (16.7 mM)-induced stimulation of insulin release from pancreatic islets revealed a twofold increase in control and cirrhotic rats. Basal and stimulated insulin secretion, however, were significantly lower in cirrhotic animals. The incretin hormone, glucagon-like peptide-1 (GLP-1), has therapeutic potential for the treatment of type 2 diabetes. Therefore, islets from control and cirrhotic animals were incubated with GLP-1 in concentrations from 10(-)(11) to 10(-)(6) M. GLP-1 stimulated insulin release in a concentration-dependent manner. In islets from cirrhotic rats, basal and stimulated insulin secretion was blunted compared with controls. These data show that the hyperinsulinemia observed in liver cirrhosis is not due to an increase of insulin secretion from islets, but could be explained by decreased hepatic clearance of insulin. GLP-1 may ameliorate diabetes in patients with liver cirrhosis.
22
Loreno, Massimiliano, Salvatore Travali, Anna Maria Bucceri, Giuseppe Scalisi, Carla Virgilio, and Alfio Brogna. "Ultrasonographic Study of Gallbladder Wall Thickness and Emptying in Cirrhotic Patients without Gallstones." Gastroenterology Research and Practice 2009 (2009): 1–5. http://dx.doi.org/10.1155/2009/683040.
Full textAbstract:
Background and Aim. Gallbladder wall thickening and impaired contractility are currently reported in cirrhotic patients and often related to portal hypertension and hepatic failure. The purpose of this work was to evaluate, by ultrasonographic method, gallbladder wall thickness and gallbladder emptying after a standard meal in normal subjects and in patients with compensated liver cirrhosis without gallstones.Methods. Twenty-three patients with Child-Pugh class A liver cirrhosis and twenty healthy controls were studied. Gallbladder wall thickness (GWT), gallbladder fasting volume (FV), residual volume (RV), and maximum percentage of emptying (%E) were calculated. Measurements of mean portal velocity, portal vein flow, and serum albumin were performed too. Statistical analysis was assessed by Student's “ttest” for unpaired data.Results. GWT was cm in cirrhotic patients and cm in controls (). FV and RV were, respectively, and in cirrhotic patients, and in healthy volunteers (). %E was smaller in cirrhotics () as compared to controls (; ).Conclusions. In patients with compensated liver cirrhosis without gallstones gallbladder wall thickness is increased whereas its contractility is reduced. These early structural and functional alterations could play a role in gallstone formation in more advanced stages of the disease.
23
Sherman, I. A., S. C. Pappas, and M. M. Fisher. "Hepatic microvascular changes associated with development of liver fibrosis and cirrhosis." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 2 (February 1, 1990): H460—H465. http://dx.doi.org/10.1152/ajpheart.1990.258.2.h460.
Full textAbstract:
Quantitative data defining basic microvascular parameters are needed for better understanding of the relationship between liver blood flow and function under normal and pathological conditions. The present study was undertaken to quantitate the following microvascular parameters: flow velocities in sinusoids and terminal hepatic venules; the range of sizes of terminal hepatic vessels; and acinar sizes in both normal rat livers and during the development of liver cirrhosis. Fibrosis and cirrhosis were induced by either weekly administration of carbon tetrachloride (CCl4) or by choline-deficient diet. Microcirculation was observed using intravital epifluorescent video microscopy and recorded on a videotape for subsequent analysis. It was found that even early stages of liver disease, when only mild hepatic fibrosis was present, are associated with profound changes in the hepatic microvasculature. These changes include the appearance of highly fluorescent cells in the liver parenchyma (mainly in the areas where collagen is being deposited), a marked dilatation of the terminal hepatic venules, an increase in hepatic venous outflow, and appearance of sinusoids with very high flow velocities. As fibrosis progresses to cirrhosis, the proportion of these “fast sinusoids” increases from 7% in fibrotic livers to 33% in cirrhotic livers. These results demonstrate the presence of functional intrahepatic shunts in cirrhotic livers and support the hypothesis that hyperdynamic splanchnic circulation may be an important factor in the etiology of portal hypertension in liver disease.
24
Debsarma, Smita, and Md Ziaul Islam. "Cirrhosis of Liver and Diabetes Mellitus." Ibrahim Medical College Journal 6, no. 2 (April 24, 2013): 59–63. http://dx.doi.org/10.3329/imcj.v6i2.14734.
Full textAbstract:
Diabetes mellitus is being recognized as a serious global health problem and frequently associated with cirrhosis of liver. The cross-sectional comparative study was conducted among 83 diabetic cirrhotic patients admitted in Gastrointestinal Hepatobilliary and Pancreatic Disorders Department of Bangladesh Institute of Research and Rehabilitation in Diabetes, Endocrine and Metabolic disorders and 83 non-diabetic cirrhotic patients admitted in Gastroenterology and Hepatology Department of Bangabandhu Sheikh Mujibar Medical University, Dhaka to assess the relationship between cirrhosis of liver and diabetes mellitus. The study was carried out during the period of January to June, 2010 and data were collected through face to face interview and reviewing medical documents by using a semi-structured questionnaire and checklist. Male, Muslims and illiterate were predominant in both diabetic and non-diabetic cirrhotic patients. It was found that non-viral cirrhosis was much higher in older age group (51-60years) than in younger age group (41-50years) in comparison to viral cirrhosis and this difference was found statistically significant [÷2 (3)=20.97, p<0.001]. Association of non-viral cirrhosis was found with hyperglycemia [÷2 (1)=15.65, p<0.001], poor glycaemic control [÷2 (1)= 9.86, p<0.01] and longer duration of diabetes [÷2 (2) =9.51, p<0.01]. Non-viral cirrhosis was significantly higher (28.3%) among the diabetic patients than the non-diabetic patients who suffered more (28.3%) from viral [÷2 (1)=41.36, p<.001]. The study recommends for glycemic control by leading disciplined life and taking apposite therapy for prevention of non-viral cirrhosis among diabetic patients. DOI: http://dx.doi.org/10.3329/imcj.v6i2.14734 Ibrahim Med. Coll. J. 2012; 6(2): 59-63
25
Zhang, Kun, Alexander Braun, Francisca von Koeckritz, Rosa B. Schmuck, Eva M. Teegen, Cesare Cuspidi, Frank Heinzel, Burkert Pieske, and Marijana Tadic. "Right Heart Remodeling in Patients with End-Stage Alcoholic Liver Cirrhosis: Speckle Tracking Point of View." Journal of Clinical Medicine 8, no. 9 (August 22, 2019): 1285. http://dx.doi.org/10.3390/jcm8091285.
Full textAbstract:
Background: Data regarding cardiac remodeling in patients with alcoholic liver cirrhosis are scarce. We sought to investigate right atrial (RA) and right ventricular (RV) structure, function, and mechanics in patients with alcoholic liver cirrhosis. Methods: This retrospective cross-sectional investigation included 67 end-stage cirrhotic patients, who were referred for evaluation for liver transplantation and 36 healthy controls. All participants underwent echocardiographic examination including strain analysis, which was performed offline. Results: RV basal diameter and RV thickness were significantly higher in patients with cirrhosis. Conventional parameters of the RV systolic function were similar between the observed groups. Global, endocardial, and epicardial RV longitudinal strains were significantly lower in patients with cirrhosis. Active RA function was significantly higher in cirrhotic patients than in controls. The RA reservoir and conduit strains were significantly lower in cirrhotic patients, while there was no difference in the RA contractile strain. Early diastolic and systolic RA strain rates were significantly lower in cirrhotic patients than in controls, whereas there was no difference in the RA late diastolic strain rate between the two groups. Transaminases and bilirubin correlated negatively with RV global longitudinal strain and RV-free wall strain in patients with end-stage liver cirrhosis. The Model for End-stage Liver Disease (MELD) score, predictor of 3-month mortality, correlated with parameters of RV structure and systolic function, and RA active function in patients with end-stage liver cirrhosis. Conclusions: RA and RV remodeling is present in patients with end-stage liver cirrhosis even though RV systolic function is preserved. Liver enzymes, bilirubin, and the MELD score correlated with RV and RA remodeling.
26
Han, Man-Hoon, Jee Hyun Lee, Gyeonghwa Kim, Eunhye Lee, Yu Rim Lee, Se Young Jang, Hye Won Lee, et al. "Expression of the Long Noncoding RNA GAS5 Correlates with Liver Fibrosis in Patients with Nonalcoholic Fatty Liver Disease." Genes 11, no. 5 (May 13, 2020): 545. http://dx.doi.org/10.3390/genes11050545.
Full textAbstract:
Background: Advanced liver fibrosis is the most important prognostic factor in nonalcoholic fatty liver disease (NAFLD). The long noncoding RNA (lncRNA), growth arrest-specific transcript 5 (GAS5), is associated with the inhibition of liver fibrogenesis, and its levels are decreased in cirrhotic liver. Methods: We analyzed 51 patients with NAFLD, the diagnosis of which was confirmed by liver biopsy. Expression of GAS5 in both the liver and plasma of the patients was analyzed using a quantitative real-time polymerase chain reaction according to the fibrosis stage. Results: Plasma GAS5 expression was significantly higher in patients with advanced fibrosis than in those without. As the fibrosis progressed, GAS5 expression in plasma increased, with the exception of that in cirrhotic livers. Plasma levels of GAS5 were lower in patients with cirrhosis than in those with advanced fibrosis. Conclusion: Elevated circulating levels of the lncRNA GAS5 are associated with the progression of liver fibrosis prior to the development of cirrhosis.
27
Chow, Kai Ming, Cheuk Chun Szeto, Alan Ka Lun Wu, Chi Bon Leung, Bonnie Ching Ha Kwan, and Philip Kam-Tao Li. "Continuous Ambulatory Peritoneal Dialysis in Patients with Hepatitis B Liver Disease." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 26, no. 2 (March 2006): 213–17. http://dx.doi.org/10.1177/089686080602600217.
Full textAbstract:
Objective We hypothesized that patients with hepatitis B virus infection and cirrhosis are more susceptible to peritonitis as a complication of peritoneal dialysis (PD). Methods A retrospective study was carried out to compare peritonitis rates between cirrhotic and non-cirrhotic patients with hepatitis B virus infection. Results Between 1994 and 2004, 25 PD patients with hepatitis B cirrhosis and 36 patients with hepatitis B without cirrhosis were included for analysis. Mean follow-up duration was 52 months. Subjects with hepatitis B cirrhosis consisted of more males and had higher total body weight. No cirrhotic patients (20 of them being Child–Pugh class A, 2 class B, and 3 class C) had undergone portosystemic shunting or liver transplantation. Cirrhotic patients had slightly higher bilirubin concentration than the non-cirrhotic group (22 ± 50 vs 9 ± 4 μmol/L, p = 0.16). There was no difference in median peritonitis-free survival between cirrhotic and non-cirrhotic patients (40 vs 37 months, p = 0.64 by log-rank test). The average peritonitis rate was 1 episode every 19.2 patient-months in the cirrhotic group and 1 episode every 20.5 patient-months in the non-cirrhotic group. Time to first peritonitis did not differ between the two groups with respect to gram-negative organisms ( p = 0.88) or gram-positive organisms ( p = 0.52). Cirrhotic patients had more frequent Streptococcus species peritonitis, which accounted for 13% of all peritonitis episodes, as opposed to 2% among the non-cirrhotic patients ( p = 0.01). Overall treatment response rate and outcome did not differ between patients with and patients without cirrhosis. Conclusions Peritonitis-free survival of cirrhosis patients infected by hepatitis B virus compares favorably with that in patients without cirrhosis. The presence of liver cirrhosis does not appear to compromise PD outcome.
28
Chistyakova, M. V., A. V. Govorin, and T. V. Kalinkina. "Heart damage in patients with cirrhosis of the liver." Kazan medical journal 102, no. 3 (June 10, 2021): 342–46. http://dx.doi.org/10.17816/kmj2021-342.
Full textAbstract:
The review outlines the current understanding of the clinical syndrome of heart disease in patients with liver cirrhosis and the development of cirrhotic cardiomyopathy. Patients with cirrhosis of the liver often notice chest pain, palpitations, complaints of arterial hypotension and rapid fatigue. Echocardiography shows that the left ventricular ejection fraction in cirrhosis is preserved at rest and decreases under stress. In some patients with viral liver cirrhosis, there is a decrease in global myocardial deformation (the presence of latent systolic dysfunction). More pronounced impairment of left ventricular diastolic function is recorded in patients with ascites and patients with ChildPugh class B and C. In patients with ascites, unfavorable left ventricular remodeling, left heart cavities enlargement, dilatation of the pulmonary artery and its branches are more common. There is an increase in pulmonary artery pressure, the development of portopulmonary hypertension and hepatopulmonary syndrome in patients with liver cirrhosis. Тhe development of these syndromes leads to a sharp decrease in the quality of life of patients with relatively preserved liver function and a worsening of the prognosis for orthotopic liver transplantation. Аpproximately half of patients with liver cirrhosis have electrophysiological disorders: prolongation of the QT interval, tachycardia, supraventricular and ventricular extrasystoles. To date, there are no clinical guidelines for the management of cirrhotic cardiomyopathy. If a patient with liver cirrhosis develops clinically significant heart failure, then general principles of management of such patients are necessary. It is necessary to limit the use of angiotensin-converting enzyme inhibitors and cardiac glycosides. The combined use of nonselective beta-blockers and nitrates reduce cardiac output and QT interval. The use of potassium canrenoate, lisinopril helps reverse the development of structural and functional changes in left ventricle. The positive effect of antiviral therapy on cardiac hemodynamics in patients with viral cirrhosis was noted. Liver transplantation is known to be an effective treatment for cirrhotic cardiomyopathy, but this treatment may worsen latent heart failure. Thus, in patients with liver cirrhosis, heart damage occurs with the development of cirrhotic cardiomyopathy, while the mechanisms of the development of myocardial dysfunction are not fully understood. Further studies of the development of the syndrome are required for timely diagnosis and clinical intervention to improve the survival of patients.
29
Voiosu, Andrei Mihai, Paul Bălănescu, Ioana Daha, Bianca Smarandache, Aurelia Rădoi, Radu Bogdan Mateescu, Cristian Răsvan Băicuş, and Theodor Alexandru Voiosu. "The diagnostic and prognostic value of serum endocan in patients with cirrhotic cardiomyopathy." Romanian Journal of Internal Medicine 56, no. 3 (September 1, 2018): 182–92. http://dx.doi.org/10.2478/rjim-2018-0007.
Full textAbstract:
Abstract Background. We aimed to determine the relationship between endocan and cirrhotic cardiomyopathy. Materials and methods. Patients with liver cirrhosis and no heart disease were included in a prospective observational study with liver disease decompensation and death as primary outcomes. Results. 83 cirrhotic patients were included and 32 had cirrhotic cardiomyopathy. Endocan levels were significantly lower in patients with cirrhotic cardiomyopathy (5.6 vs. 7 ng/mL, p = 0.034). Endocan correlated with severity of cirrhosis, time to decompensation or death from liver disease (OR 4.5 95% CI 1.06-31.1). Conclusion. Endocan is a promising biomarker of severity of cirrhosis and may help in the diagnosis of cardiac dysfunction in this population.
30
Wang, Yixuan, Calvin Q. Pan, and Huichun Xing. "Advances in Gut Microbiota of Viral Hepatitis Cirrhosis." BioMed Research International 2019 (November 22, 2019): 1–9. http://dx.doi.org/10.1155/2019/9726786.
Full textAbstract:
Although gut dysbiosis appears in 20%–75% of cirrhotic patients, there are limited data on microbiota profiles in viral hepatitis cirrhotics and its role in progression to cirrhosis. Further understanding on the relationship between gut dysbiosis and cirrhosis presents a unique opportunity in not only predicting the development of cirrhosis but also discovering new therapies. Recent advances have been made on identifying unique microbiota in viral hepatitis cirrhotics and adopting the microbiota index to predict cirrhosis. Therapeutic intervention with microbiome-modulating has been explored. Cirrhosis from viral infection has unique bacterial or fungal profiles, which include increased numbers of Prevotella, Streptococcus, Staphylococcaceae, and Enterococcus, as well as decreased Ruminococcus and Clostridium. In addition, the gut microbiota can stimulate liver immunity, effectively helping hepatitis virus clearance. In clinical settings, CDR, GDI, Basidiomycota/Ascomycota, specific POD, and so forth are efficient microbiota indexes to diagnose or prognosticate cirrhosis from viral hepatitis. FMT, probiotics, and prebiotics can restore microbial diversity in cirrhotic patients with viral hepatitis, decrease ammonia serum or endotoxemia levels, prevent complications, reduce rehospitalization rate, and improve prognosis. Cirrhotics from viral hepatitis had unique bacterial or fungal profiles, associated with specific metabolic, immune, and endocrinological statuses. Such profiles are modifiable with medical treatment. The role of gut archaea and virome, implementation of FMT, microbiota metabolites as adjuvant immunotherapy, and microbiota indexes for prognostication deserve attention.
31
Traub, Julia, Ina Bergheim, Martin Eibisberger, and Vanessa Stadlbauer. "Sarcopenia and Liver Cirrhosis—Comparison of the European Working Group on Sarcopenia Criteria 2010 and 2019." Nutrients 12, no. 2 (February 20, 2020): 547. http://dx.doi.org/10.3390/nu12020547.
Full textAbstract:
The European Working group on Sarcopenia in Older People recently updated the diagnostic criteria for sarcopenia. It is yet unclear how these modified criteria influence the rate of diagnosis in high risk populations, such as liver cirrhosis. We therefore assessed if the new diagnostic criteria for sarcopenia impacts on sarcopenia prevalence in liver cirrhosis. Within two years 114 cirrhotic patients were prospectively enrolled in the study. Sarcopenia was determined by muscle strength (handgrip strength), muscle mass (lumbal muscle index) and muscle performance (gait speed). Using the 2019 definition, the rate of pre-sarcopenia was significantly lower (30.7% versus 3.5%) due to the different starting points (2010 muscle mass, 2019 muscle strength) and cut-off values (muscle strength). The change in diagnostic criteria for sarcopenia drastically influences the rate of pre-sarcopenia diagnosis in cirrhotics. To evaluate, which diagnostic criteria should be chosen to diagnose sarcopenia in liver cirrhosis patients, prospective studies are needed.
32
Chang, Binxia, Baosen Li, Ying Sun, Guangju Teng, Ang Huang, Jin Li, and Zhengsheng Zou. "Changes in Etiologies of Hospitalized Patients with Liver Cirrhosis in Beijing 302 Hospital from 2002 to 2013." Mediators of Inflammation 2017 (2017): 1–5. http://dx.doi.org/10.1155/2017/5605981.
Full textAbstract:
Background. Over the last 20 years, the prevalence of hepatitis B virus (HBV) infection in China has decreased gradually due to the application of a national HBV vaccination program. In contrast, the prevalence of alcoholic liver disease (ALD), nonalcoholic fatty liver disease, autoimmune liver disease, and drug-induced liver injury has markedly increased. Methods. We conducted a retrospective review of 82,562 hospitalized patients diagnosed with liver cirrhosis in Beijing 302 Hospital from 2002 to 2013. Results. The top four etiologies of cirrhosis were HBV, HCV, ALD, and autoimmune liver disease. The percentage of HBV cirrhosis decreased from 81.53% in 2002 to 66.0% in 2013, whereas the frequency of alcoholic cirrhosis increased from 3.34% in 2002 to 8.40% in 2013. Females (84.34%) accounted for the majority of cirrhotic patients with autoimmune liver diseases. Males accounted for 80.16% of HBV cirrhosis patients and 98.02% of alcoholic cirrhosis patients. Conclusion. In Beijing 302 Hospital, the top four etiologies of cirrhosis were HBV, HCV, ALD, and autoimmune liver disease. Over the last 12 years, the prevalence of HBV cirrhosis has decreased gradually, whereas that of alcoholic cirrhosis has increased significantly.
33
Ljubimova, Julia Y., Lidija M. Petrovic, Steven E. Wilson, Stephen A. Geller, and Achilles A. Demetriou. "Expression of HGF, Its Receptor c-met, c-myc, and Albumin in Cirrhotic and Neoplastic Human Liver Tissue." Journal of Histochemistry & Cytochemistry 45, no. 1 (January 1997): 79–87. http://dx.doi.org/10.1177/002215549704500111.
Full textAbstract:
Hepatocellular carcinoma (HCC) is a common type of cancer, with approximately 260,000 new cases each year, and liver cirrhosis is generally considered a major predisposing factor for HCC. However, specific changes of gene expression in liver cirrhosis and HCC remain obscure. The expression of genes for hepatocyte growth factor (HGF), its receptor c-met proto-oncogene, c-myc proto-oncogene, and albumin was analyzed. Gene expression was studied by PCR in seven normal human livers, nine cases of hepatitis C cirrhosis, 12 cases of alcoholic cirrhosis, two cases of liver adenoma, and 12 cases of HCC. HGF and c-met protein were revealed by immunofluorescent staining. HGF mRNA was not expressed in normal livers but was detected in adenomas, in 80% of HCC, and in some cirrhoses. Paraffin-embedded and fresh-frozen tissue samples yielded similar results. Immunohistochemical data correlated with PCR results regarding the overexpression of the HGF/ c-met system in HCC. Albumin gene expression was decreased in HCC vs normal livers, consistent with altered function of tumor hepatocytes. The elevated expression of the HGF/ c-met system in HCC may play a role in tumor development and/or progression. Tissue localization studies of HGF and its receptor c-met protein support the existence of both autocrine and paracrine mechanisms of action of HGF in HCC vs only a paracrine mechanism in normal liver.
34
Farmaha, M., M. Abrahamovych, and O. Abrahamovych. "Syntropic Lesions of the Cardiovascular System in Patients With Liver Cirrhosis: Their Determination; Selected Pathogenetic Mechanisms; Characteristics and Specifics; Clinical Markers, Their Prognostic Value; Justification and Effectiveness of Modified Treatment (First Notice)." Lviv clinical bulletin 3, no. 31 (October 17, 2020): 8–18. http://dx.doi.org/10.25040/lkv2020.03.008.
Full textAbstract:
Introduction. Comorbid syntropic lesions of the circulatory system in patients with liver cirrhosis, although often fatal, are poorly studied. The aim of the study. To distinguish syntropic lesions of the cardiovascular system in patients with liver cirrhosis, to determine some of their pathogenetic mechanisms, nature, and characteristics, to determine clinical markers with prognostic value, to justify and evaluate the effectiveness of their modified treatment. Materials and methods. We processed medical records of 603 patients with liver cirrhosis and detected circulatory system lesions in 490 patients. Some of them had only one type of lesions (study groups): 103 patients were diagnosed with cirrhotic cardiomyopathy, and 89 patients were diagnosed with arterial hypotension. Patients without the circulatory system lesions (113 patients) formed a comparison group. The purpose of the first step of the study was to determine syntropic comorbid lesions of the circulatory system. The purpose of the second step was to study some pathogenetic mechanisms of their formation. The purpose of the third step was to characterize these lesions, classify them, and determine their specific characteristics related to the severity of liver cirrhosis. The purpose of the fourth step was to determine their clinical markers. The purpose of the fifth step was to justify a modified course of treatment for patients with liver cirrhosis and syntropic cardiovascular lesions as well as to assess its effectiveness. Results. At the first step of the study, we found that 81.26 % of patients with liver cirrhosis had circulatory system lesions, in particular, secondary cirrhotic cardiomyopathy (57.50 % of patients with the circulatory system lesions) and persistent arterial hypotension (35.31 % of patients with the circulatory system lesions) as syntropic lesions. At the second step, we found that patients with liver cirrhosis and syntropic lesions of the circulatory system had also autonomic dysfunction and endothelial dysfunction. At the third step, we detected left ventricular remodeling in patients with liver cirrhosis and syntropic secondary cirrhotic cardiomyopathy, along with diastolic dysfunction and elevated S. Tei-index scores; these indicators worsened in parallel with the increase in the severity of cirrhosis; S. Tei-index scores should be used to classify secondary cirrhotic cardiomyopathy by severity. Patients with liver cirrhosis and syntropic persistent arterial hypotension had reduced ratio between blood pressures during the day and at night, low variability in blood pressure; in parallel with the increase in the severity of cirrhosis, arterial hypotension progressed with a disturbed circadian rhythm and pressure variability at all stages of the disease; the indicator of average daily arterial pressure should be used to classify arterial hypotension by severity. Conclusions. 81.26 % of patients with liver cirrhosis had comorbid lesions of the circulatory system, including secondary cirrhotic cardiomyopathy (57.50 %) and persistent arterial hypotension (35.31 %) as syntropic lesions; the activation of humoral and metabolic factors with disorders of the autonomic nervous system is one of the links in the pathogenesis of these syntropic lesions; syntropic secondary cirrhotic cardiomyopathy and persistent arterial hypotension have their specific characteristics, their manifestations worsen in parallel with the decompensation of liver cirrhosis, it is proposed to classify both diseases by severity.
35
Bravo, E., E. D'Amore, F. Ciaffoni, and C. L. Mammola. "Evaluation of the spontaneous reversibility of carbon tetrachloride-induced liver cirrhosis in rabbits." Laboratory Animals 46, no. 2 (April 2012): 122–28. http://dx.doi.org/10.1258/la.2012.011035.
Full textAbstract:
There is a general consensus that liver fibrosis in humans is potentially reversible, while scepticism prevails on the concept that cirrhosis can be truly reversed. The availability of suitable experimental models is fundamental for disease research. The experimental murine model of liver cirrhosis induced by carbon tetrachloride (CCl4) reproduces both the histological picture of the postnecrotic cirrhosis and its biochemical and clinical parameters. Normal hepatic structure is modified by formation of regeneration nodules. Fibrosis represents a morphological element of disease and an effect of hepatocyte necrosis. However, the relevance for research of this well-established model of liver cirrhosis is hampered by some spontaneous cirrhosis regression reported in mice and rats. It has been reported that CCl4 also induces experimental liver cirrhosis in rabbits, but it is not known whether the process is reversible in this species. The aim of our study was to investigate this question. Male New Zealand White rabbits were treated intragastrically with CCl4 or the vehicle only for 19 weeks and groups were sacrificed three and five months after treatment interruption. Cirrhotic and control livers were processed for routine light microscopy and for morphometric study of fibrosis by semiquantitative evaluation. The degree of fibrosis was based on the Knodell's scoring system.
36
Prystupa, Andrzej, Paweł Kiciński, Jarosław Sak, Anna Boguszewska-Czubara, Anna Toruń-Jurkowska, and Wojciech Załuska. "Proinflammatory Cytokines (IL-1α, IL-6) and Hepatocyte Growth Factor in Patients with Alcoholic Liver Cirrhosis." Gastroenterology Research and Practice 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/532615.
Full textAbstract:
Background. The aim of the study was to assess the activity of interleukin-1α, interleukin-6, and hepatocyte growth factor protein (HGF) in serum of patients with alcoholic liver cirrhosis.Materials and Methods. Sixty patients with alcoholic liver cirrhosis treated in various hospitals were randomly enrolled. The stage of cirrhosis was assessed according to the Child-Turcotte-Pugh scoring system. The control group consisted of ten healthy persons without liver disease, who did not drink alcohol. Additionally, the group of alcoholics without liver cirrhosis was included in the study. The activity of interleukin-1α, interleukin-6, and HGF in blood plasma of patients and controls was measured using the sandwich enzyme immunoassay technique with commercially available quantitative ELISA test kits.Results. Higher concentrations of HGF protein were demonstrated in patients with Child class B and Child class C liver cirrhosis, compared to controls and alcoholics without liver cirrhosis. Moreover, significantly higher concentrations of HGF protein were found in patients with Child class C liver cirrhosis compared to patients with Child class A liver cirrhosisp<0.05. The concentrations of interleukin-1αin patients with Child class B and Child class C liver cirrhosis were significantly higher in comparison with controls. Significantly higher concentrations of interleukin-6 were demonstrated in Child class C, compared to Child class A.
37
Hanai, Tatsunori, Makoto Shiraki, Kenji Imai, Atsushi Suetugu, Koji Takai, and Masahito Shimizu. "Usefulness of Carnitine Supplementation for the Complications of Liver Cirrhosis." Nutrients 12, no. 7 (June 29, 2020): 1915. http://dx.doi.org/10.3390/nu12071915.
Full textAbstract:
Carnitine is a vitamin-like substance that regulates lipid metabolism and energy production. Carnitine homeostasis is mainly regulated by dietary intake and biosynthesis in the organs, including the skeletal muscle and the liver. Therefore, liver cirrhotic patients with reduced food intake, malnutrition, biosynthetic disorder, and poor storage capacity of carnitine in the skeletal muscle and liver are more likely to experience carnitine deficiency. In particular, liver cirrhotic patients with sarcopenia are at a high risk for developing carnitine deficiency. Carnitine deficiency impairs the important metabolic processes of the liver, such as gluconeogenesis, fatty acid metabolism, albumin biosynthesis, and ammonia detoxification by the urea cycle, and causes hypoalbuminemia and hyperammonemia. Carnitine deficiency should be suspected in liver cirrhotic patients with severe malaise, hepatic encephalopathy, sarcopenia, muscle cramps, and so on. Importantly, the blood carnitine level does not always decrease in patients with liver cirrhosis, and it sometimes exceeds the normal level. Therefore, patients with liver cirrhosis should be treated as if they are in a state of relative carnitine deficiency at the liver, skeletal muscle, and mitochondrial levels, even if the blood carnitine level is not decreased. Recent clinical trials have revealed the effectiveness of carnitine supplementation for the complications of liver cirrhosis, such as hepatic encephalopathy, sarcopenia, and muscle cramps. In conclusion, carnitine deficiency is not always rare in liver cirrhosis, and it requires constant attention in the daily medical care of this disease. Carnitine supplementation might be an important strategy for improving the quality of life of patients with liver cirrhosis.
38
Sánchez, Paula Sánchez, María del Mar Rigual, and Nabil Djouder. "Inflammatory and Non-Inflammatory Mechanisms Controlling Cirrhosis Development." Cancers 13, no. 20 (October 9, 2021): 5045. http://dx.doi.org/10.3390/cancers13205045.
Full textAbstract:
Because the liver is considered to be one of the most important metabolic organs in the body, it is continuously exposed to damaging environmental agents. Upon damage, several complex cellular and molecular mechanisms in charge of liver recovery and regeneration are activated to prevent the failure of the organ. When liver injury becomes chronic, the regenerative response goes awry and impairs the liver function, consequently leading to cirrhosis, a liver disorder that can cause patient death. Cirrhosis has a disrupted liver architecture and zonation, along with the presence of fibrosis and parenchymal nodules, known as regenerative nodules (RNs). Inflammatory cues contribute to the cirrhotic process in response to chronic damaging agents. Cirrhosis can progress to HCC, the most common and one of the most lethal liver cancers with unmet medical needs. Considering the essential role of inflammatory pathways in the development of cirrhosis, further understanding of the relationship between immune cells and the activation of RNs and fibrosis would guide the design of innovative therapeutic strategies to ameliorate the survival of cirrhotic and HCC patients. In this review, we will summarize the inflammatory mechanisms implicated in the development of cirrhosis.
39
Atia, F., N. Sultana, S. Ahmed, S. Ferdousi, R. Sultana, and M. Atiquzzaman. "A Study of Serum Zinc level in Cirrhosis of Liver." Bangladesh Journal of Medical Biochemistry 5, no. 2 (January 16, 2013): 44–47. http://dx.doi.org/10.3329/bjmb.v5i2.13340.
Full textAbstract:
Cirrhosis is a consequence of chronic liver diseases. Zinc is a micronutrient that plays an important role in the function of liver. This cross-sectional study was carried out in the Department of Biochemistry, Dhaka Medical College, from July 2010 to June 2011 to observe the association of serum zinc level with liver cirrhosis. A total of 100 adults, both males and females with age range of 18-60 years, of which 50 were healthy subjects and 50 adult hospitalised cirrhotic patients were selected purposively for the study according to selection crieteria. Fasting serum zinc level was measured with atomic absorption spectrophotometer. Serum zinc level was found to be low in 72% patients. Mean ±SD of serum zinc levels (?g/L) were 610.32 ± 169.60 and 827.66 ± 267.32 in cases and controls respectively. In cirrhotic patients serum zinc level was significantly lower than that of healthy controls (P<0.001). Though, it is difficult to draw any definite conclusion from this study, because of reduced level serum of zinc found in cirrhotics, Zn may be supplemented to them with a hope of better treatment response. DOI: http://dx.doi.org/10.3329/bjmb.v5i2.13340 Bangladesh J Med Biochem 2012; 5(2): 44-47
40
Bátkai, Sándor, Partha Mukhopadhyay, Judith Harvey-White, Raouf Kechrid, Pál Pacher, and George Kunos. "Endocannabinoids acting at CB1receptors mediate the cardiac contractile dysfunction in vivo in cirrhotic rats." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (September 2007): H1689—H1695. http://dx.doi.org/10.1152/ajpheart.00538.2007.
Full textAbstract:
Advanced liver cirrhosis is associated with hyperdynamic circulation consisting of systemic hypotension, decreased peripheral resistance, and cardiac dysfunction, termed cirrhotic cardiomyopathy. Previous studies have revealed the role of endocannabinoids and vascular CB1receptors in the development of generalized hypotension and mesenteric vasodilation in animal models of liver cirrhosis, and CB1receptors have also been implicated in the decreased β-adrenergic responsiveness of isolated heart tissue from cirrhotic rats. Here we document the cardiac contractile dysfunction in vivo in liver cirrhosis and explore the role of the endocannabinoid system in its development. Rats with CCl4-induced cirrhosis developed decreased cardiac contractility, as documented through the use of the Millar pressure-volume microcatheter system, low blood pressure, and tachycardia. Bolus intravenous injection of the CB1antagonist AM251 (3 mg/kg) acutely increased mean blood pressure, as well as both load-dependent and -independent indexes of systolic function, whereas no such changes were elicited by AM251 in control rats. Furthermore, tissue levels of the endocannabinoid anandamide increased 2.7-fold in the heart of cirrhotic compared with control rats, without any change in 2-arachidonoylglycerol levels, whereas, in the cirrhotic liver, both 2-arachidonoylglycerol (6-fold) and anandamide (3.5-fold) were markedly increased. CB1-receptor expression in the heart was unaffected by cirrhosis, as verified by Western blotting. Activation of cardiac CB1receptors by endogenous anandamide contributes to the reduced cardiac contractility in liver cirrhosis, and CB1-receptor antagonists may be used to improve contractile function in cirrhotic cardiomyopathy and, possibly, in other forms of heart failure.
41
Mahajan, Sanjeev, Daksh Gadi, Rahul Gupta, Anirudh Sharma, Premjeet Singh Thind, Som Gupta, and Raminder Kaur. "Prevalence of avascular necrosis of femoral head in patients with cirrhosis of liver." International Journal of Medicine 4, no. 2 (October 19, 2016): 74. http://dx.doi.org/10.14419/ijm.v4i2.6725.
Full textAbstract:
Background: Amongst the multiple etiologies implicated in the development of Avascular necrosis of the femoral head, literature regarding the association of cirrhosis of liver with osteonecrosis of femoral head is scanty and is correspondingly less studied. Considering a large number of patients with liver cirrhosis in this region of our country, this study was conducted to evaluate the association of cirrhosis as an independent risk factor in the development of osteonecrosis. To the best of our knowledge No such study has been done evaluating the same in this region.Methods: This prospective analysis aimed to determine the prevalence of osteonecrosis of femoral head in patients with cirrhosis of liver, patients presenting to the hospital with established cirrhosis, diagnosed with help of ultrasonography , were evaluated for the occurance of Avascular necrosis of the femoral head.Results: The prevalence of osteonecrosis of femoral head in patients with cirrhosis of liver was evaluated to be 1.2% in the present study. Amongst this cirrhotic subgroup, the prevalence of osteonecrosis of femoral head in cirrhotic patients due to excessive alcohol consumption was calculated to be 1.1% and that of the cirrhotic patients independent of alcohol consumption came out to be 1.4%.Conclusion: Analysis of the results of the present study establishes cirrhosis of liver, the cause of which could be independent or related to alcohol consumption, as a risk factor for the development of osteonecrosis of femoral head. Significance of alcohol related cirrhosis resulting in AVN of the femoral head, though, is challenged by the present study.
42
Bell, Helge, Nils Raknerud, Jan A. Falch, and Egil Haug. "Inappropriately low levels of gonadotrophins in amenorrhoeic women with alcoholic and non-alcoholic cirrhosis." European Journal of Endocrinology 132, no. 4 (April 1995): 444–49. http://dx.doi.org/10.1530/eje.0.1320444.
Full textAbstract:
Bell H, Raknerud N, Falch JA, Haug E. Inappropriately low levels of gonadotrophins in amenorrhoeic women with alcoholic and non-alcoholic cirrhosis. Eur J Endocrinol 1995;132:444–9. ISSN 0804–4643 We investigated a group of 111 amenorrhoeic females with associated liver disease. These comprised alcoholic cirrhotics (N = 38), non-alcoholic cirrhotics (N = 12), non-cirrhotic alcoholics (N = 21) and those suffering from other chronic liver diseases (N = 40) admitted to our medical department from 1986 to 1991. The serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), oestradiol, testosterone, sex hormone binding globulin (SHBG) and prolactin were measured. Serum LH was decreased below the normal range in 50% of patients with alcoholic cirrhosis and in 42% of patients with non-alcoholic cirrhosis. One third of non-cirrhotic alcoholics also had decreased LH, in contrast to only 8% of patients with other chronic liver diseases (p < 0.01). A close correlation was found between LH and FSH when all patients were pooled (r = 0.91, p < 0.001). A gonadotrophin-releasing hormone (GnRH) injection elicited a clear LH and FSH response in 11 out of 14 patients with cirrhosis, indicating that the hypothalamus rather than the pituitary is the site of disturbance in gonadotrophin secretion. Serum SHBG was within normal limits and similar in all four groups. In nine females with alcoholic cirrhosis who abstained for 3 months, serum SHBG increased significantly from 39 ± 18 to 70 ± 25 nmol/l (p < 0.001), while LH increased in five of nine females and was unchanged in four. In conclusion, half of the amenorrhoeic females with alcoholic as well as non-alcoholic cirrhosis had inappropriately low serum LH and FSH levels, indicating dysfunction of the hypothalamo–pituitary axis. The GnRH test indicated that disturbed hypothalamic function was the cause of the decreased LH and FSH secretion. Helge Bell, Department of Medicine, Aker University Hospital, Trondhjemsveien 235, 0514 Oslo, Norway
43
Salatti Ferrari, Renata, Darlan Pase da Rosa, Luiz Felipe Forgiarini, Silvia Bona, Alexandre Simões Dias, and Norma Possa Marroni. "Oxidative Stress and Pulmonary Changes in Experimental Liver Cirrhosis." Oxidative Medicine and Cellular Longevity 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/486190.
Full textAbstract:
The use of carbon tetrachloride (CCl4) in rats is an experimental model of hepatic tissue damage; which leads to fibrosis, and at the long term, cirrhosis. Cirrhosis is the consequence of progressive continued liver damage, it may be reversible when the damaging noxae have been withdrawn. The aim of this study is to evaluate the changes caused by cirrhosis in lung and liver, through the experimental model of intraperitoneal CCI4administration. We used 18 male Wistar rats divided into three groups: control (CO) and two groups divided by the time of cirrhosis induction by CCI4: G1 (11 weeks), G2 (16 weeks). We found significant increase of transaminase levels and lipid peroxidation (TBARS) in liver and lung tissue and also increased antioxidant enzymes SOD and CAT, as well as the expression of TNF-αand IL-1βin the lung of cirrhotic animals. We observed changes in gas exchange in both cirrhotic groups. We can conclude that our model reproduces a model of liver cirrhosis, which causes alterations in the pulmonary system that leads to changes in gas exchange and size of pulmonary vessels.
44
Hendrawan, Siufui, Jennifer Lheman, Nuraeni, Ursula Weber, and Hans Ulrich Baer. "Hepatocyte and Islet Cell Cotransplantation on Poly-L-Lactide Matrix for the Treatment of Liver Cirrhosis." International Journal of Hepatology 2020 (October 13, 2020): 1–6. http://dx.doi.org/10.1155/2020/5410359.
Full textAbstract:
The human autologous hepatocyte matrix implant is a promising alternative procedure to counter liver damage. We assessed the outcome of human hepatocytes isolation from cirrhotic liver compared to the clinical and histological scores of disease severity. A total of 11 patients with various clinical scores (CTP and MELD) and histological score (Metavir, fibrosis) of liver cirrhosis were included in the hepatocyte matrix implant clinical phase I study. The liver segment and pancreatic tissue were harvested from each patient, and hepatocytes and cells of islets of Langerhans were isolated. The freshly isolated human hepatocytes were coseeded with the islet cells onto poly(l-lactic acid) (PLLA) scaffolds, cultured, and transplanted back into the patient. Human hepatocytes were isolated from 11 cirrhotic liver specimens with a resulting yield of 1.4 ± 0.5 × 106 cells per gram of the liver specimen and a viability rate of 52 ± 13%. It was found that the yield and viability of the liver cells were not correlated with the clinical and histological scores of the liver cirrhosis. A correlation was found between the hepatocyte yield obtained and the average number of hepatocytes counted in 10 microscopic fields of view. More viable cells were obtained from cirrhotic livers caused by chronic hepatitis B as compared to chronic hepatitis C in the same MELD score range. There was no correlation between the clinical and histological disease severity scores of liver cirrhosis and the outcome of hepatocytes isolation. It seems that the yield could depend on the type of hepatitis underlying the cirrhotic tissue. The study was registered at www.clinicaltrial.gov with the study identifier: NCT01335568.
45
Mangudkar, Sangram S., Sachin K. Shivnitwar, Vijayashree S. Gokhale, and Ameya A. Ithape. "Study of liver function tests and spontaneous bacterial peritonitis in a patients of liver cirrhosis." International Journal of Advances in Medicine 7, no. 3 (February 24, 2020): 421. http://dx.doi.org/10.18203/2349-3933.ijam20200651.
Full textAbstract:
Background: Liver cirrhosis patients are highly susceptible to bacterial infections specially Spontaneous bacterial peritonitis (SBP) which is commonest infection. this study undertaken to understand liver function tests and Spontaneous bacterial peritonitis in patients of liver cirrhosis admitted to tertiary care hospital.Methods: A descriptive cross-sectional study conducted among Liver cirrhosis patients in tertiary care center. Total 100 liver cirrhotic patients were included in present study. All the patients were subjected for biochemical evaluation of Serum albumin and globulin level, Serum bilirubin, SGOT (Serum glutamic oxaloacetic transaminase), SGPT (Serum glutamic pyruvate transaminase) and Ascitic fluid polymorph nuclear neutrophil (PMN) count to diagnose SBP.Results: Spontaneous bacterial peritonitis was present in 12% patients. Relation of Serum bilirubin level and SBP was statistically significant. Relation of serum SGOT, SGPT level and serum globulin between SBP and non-SBP group was statistically non-significant.Conclusions: Liver cirrhosis patients are susceptible for bacterial infections because of defects in various host defense mechanism and hence patients of liver cirrhosis must be screened for spontaneous bacterial peritonitis along with liver function tests.
46
Ajeet Kumar, Syeda Urooj Riaz, Rajesh, Syed Hussain Mehdi Kazmi, Rajesh Kumar, and Muhammad Ishaq Ghauri. "Prolongation of QT Interval in ECG: A Hidden Complication of Cirrhotic Liver Disease." ANNALS OF ABBASI SHAHEED HOSPITAL AND KARACHI MEDICAL & DENTAL COLLEGE 24, no. 1 (March 31, 2019): 20–24. http://dx.doi.org/10.58397/ashkmdc.v24i1.22.
Full textAbstract:
Objective: To determine frequency of QT interval prolongation in ECG of patients with decompensated liver cirrhosis in a tertiary care hospital of Karachi, Pakistan.
Methods: A total of 60 patients with cirrhosis were included in this study. Clinical examination to see the presence of ascites, liver span and encephalopathy, and related investigation such as liver func- tion tests, serum albumin, prothrombin time and ultrasound abdomen for portal vein size was done and they were labelled as suffering from cirrhotic liver disease. Two 12 lead ECG was done >5 min- utes apart, when found same and QT interval calculated.
Results: The average age of the patients came out to be 45.37 ± 6.59 years. There were 36 (60%) were male and 24 (40%) female. Frequency of QT prolongation in patients with decompensate liver cirrhosis was observed in 12 (20%) cases.
Conclusion: This study demonstrates that cirrhotic cardiomyopathy is a common occurrence. The fre- quency of QT prolongation was 20% in patients with cirrhosis.This study demonstrates the direct rela- tionship of cirrhotic cardiomyopathy with the severity of liver disease. Therefore patients with cirrhosis should be investigated for prolonged QTc and the proper diagnosis and treatment.
47
Abdelhameed, Hosam Farouk, and Ashraf M. El-Badry. "Cirrhosis aggravates the ninety-day mortality after liver resection for hepatocellular carcinoma." International Surgery Journal 6, no. 8 (July 25, 2019): 2869. http://dx.doi.org/10.18203/2349-2902.isj20193333.
Full textAbstract:
Background: Ninety-day postoperative mortality (90-D POM) measures accurately the liver resection-related mortality. In cirrhotic patients, reporting post-hepatectomy-related death only as in-hospital or thirty-day postoperative mortality (30-D POM) may underestimate cirrhosis-related death after liver resection.Methods: Medical records of adult cirrhotic (cirrhosis group) and matched non-cirrhotic (control group) patients, who underwent elective liver resection at Sohag University Hospital (April 2014- March 2018), were analyzed. The 90-D POM versus in-hospital mortality and 30-D POM were compared in both groups.Results: Forty-six patients (23 per group) were eligible for the study. Liver resection was carried out in all cirrhosis group patients for hepatocellular carcinoma (HCC). In the control group, liver resection was indicated for colorectal metastasis (13), benign masses (7) and intrahepatic cholangiocarcinoma (3). Compared with the control group, cirrhotic patients exhibited significantly higher complication rates (p<0.05), prolonged hospital stays (p<0.05), increased postoperative levels of serum bilirubin and reduced prothrombin concentration (p<0.05). In the control group, in-hospital mortality and 30-D POM were zero while 90-D POM was 4%. In the cirrhosis group, the in-hospital mortality and 30-D POM were identical (8.7%), however the 90-D POM was significantly higher and almost doubled (17%). Conclusion: Liver cirrhosis triggers significant mortality that may extend for ninety days postoperatively. In cirrhotic patients, post-hepatectomy death should be reported as 90-D POM rather than the obviously misleading in-hospital mortality or 30-D POM.
48
Suthar, Ramesh Kumar, Kavita Bai, and Mumtaz Ali Memon. "Serum uric acid in liver cirrhosis." Professional Medical Journal 27, no. 12 (December 10, 2020): 2637–41. http://dx.doi.org/10.29309/tpmj/2020.27.12.4363.
Full textAbstract:
Objectives: To determine the serum uric acid levels among the patients of liver cirrhosis. Study Design: Cross Sectional, Descriptive study. Setting: Department of Medicine, Indus Medical College, Tando Muhammad Khan. Period: 6 months (23 April 2019 to 23 October 2019). Material & Methods: Patients of liver cirrhosis attending the medical OPD or admitted in the Medicine ward, meeting selection criteria included in this study. Any diseases other than liver disease, disturbing uric acid levels were excluded from the study. Other exclusion criteria were type 2 and 1 Diabetes mellitus, drugs altering serum uric acid levels, gout, pregnancy and chronic kidney disease. Results: In this study, the causes of liver cirrhosis revealed were hepatitis B 5 (5.15%), hepatitis C 44(45.36%), both hepatitis B and C 4(4.12%), NAFLD 34 (34.05%) and alcohol 10(10.31%) respectively. Mean of the serum uric acid (mg/dl) compared in liver cirrhosis due to different etiologies Mean ±SD of uric acid levels due to hepatitis B, hepatitis C, both hepatitis B and C, NAFALD and alcohol were 2.66±1.4, 2.22±0.3, 2.34±1.0, 7.70±0.9 and 6.69±2.0 respectively; theses all compared by one way ANOVA, (p value <0.01) with df (degree of freedom) 4. Serum uric acid levels are raised among the NAFLD patients in this study that is warning factor for cardiovascular disease. In this research hypouricemia has been observed among the patients of liver cirrhosis due to hepatitis B, hepatitis C, both hepatitis B and C, NAFLD and alcohol as 5.15%, 45.36%, 4.12 %, 2.06% and 8.25% respectively while hyperuricemia has been observed among the cirrhotic patients due to NAFLD. Conclusion: Serum uric acid levels are raised among the liver cirrhosis patients with NAFLD while decreased among cirrhotic patients with viral hepatitis. Further the area is open for further research to determine the underlying mechanisms.
49
Qi, Xingshun, Zhaohui Bai, Qiang Zhu, Gang Cheng, Yu Chen, Xiaowei Dang, Huiguo Ding, et al. "Practice guidance for the use of terlipressin for liver cirrhosis–related complications." Therapeutic Advances in Gastroenterology 15 (January 2022): 175628482210982. http://dx.doi.org/10.1177/17562848221098253.
Full textAbstract:
Background: Liver cirrhosis is a major global health burden worldwide due to its high risk of morbidity and mortality. Role of terlipressin for the management of liver cirrhosis–related complications has been recognized during recent years. This article aims to develop evidence-based clinical practice guidance on the use of terlipressin for liver cirrhosis–related complications. Methods: Hepatobiliary Study Group of the Chinese Society of Gastroenterology of the Chinese Medical Association and Hepatology Committee of the Chinese Research Hospital Association have invited gastroenterologists, hepatologists, infectious disease specialists, surgeons, and clinical pharmacists to formulate the clinical practice guidance based on comprehensive literature review and experts’ clinical experiences. Results: Overall, 10 major guidance statements regarding efficacy and safety of terlipressin in liver cirrhosis were proposed. Terlipressin can be beneficial for the management of cirrhotic patients with acute variceal bleeding and hepatorenal syndrome (HRS). However, the evidence regarding the use of terlipressin in cirrhotic patients with ascites, post-paracentesis circulatory dysfunction, and bacterial infections and in those undergoing hepatic resection and liver transplantation remains insufficient. Terlipressin-related adverse events, mainly including gastrointestinal symptoms, electrolyte disturbance, and cardiovascular and respiratory adverse events, should be closely monitored. Conclusion: The current clinical practice guidance supports the use of terlipressin for gastroesophageal variceal bleeding and HRS in liver cirrhosis. High-quality studies are needed to further clarify its potential effects in other liver cirrhosis–related complications.
50
Kukla, Michał, Lubomir Skladany, Tomasz Menżyk, Aleksandra Derra, Dominika Stygar, Magdalena Skonieczna, Dorota Hudy, et al. "Irisin in Liver Cirrhosis." Journal of Clinical Medicine 9, no. 10 (September 29, 2020): 3158. http://dx.doi.org/10.3390/jcm9103158.
Full textAbstract:
Background: Sarcopenia is a prevalent muscle abnormality characterized by progressive and generalized loss of skeletal muscle mass and strength, common among patients with decompensated advanced chronic liver disease (dACLD). Irisin is a recently identified myokine, which is mainly expressed and secreted by skeletal muscle. Pointing to the essential role of irisin in metabolic regulation and energy expenditure we hypothesize that it plays an important role in cirrhosis development and progression. Aim: To assess irisin serum levels in patients with dACLD, with different cirrhosis stage and etiology. To analyze relationship between sarcopenia and irisin serum levels. Methods: Serum irisin concentrations were measured with commercially available ELISA kits in 88 cirrhotic patients. Recorded parameters of muscle mass were hand-grip strength (HGS), mid-arm muscle circumference (MAC), and transversal psoas muscle index (TPMI). Results: There was no difference in serum irisin levels between cirrhotic patients with different Child-Pugh (CTP) and model of end-stage liver disease (MELD) score, and those with and without ascites. The Liver Frailty Index (LFI) was significantly higher in patients with more advanced liver disease according to CTP and MELD. There was no association between serum irisin level with MAC (r = 0.04, p = 0.74) nor with TPMI (r = 0.20, p = 0.06). We observed significant negative correlation between serum irisin level and age (r = −0.35, p < 0.001). Conclusions: Serum irisin levels did not correlate with sarcopenia. There was no difference in serum irisin levels between cirrhotic patients with and without diabetes. There was no difference in serum irisin levels among patients with more severe dACLD, although we observed significant LFI increase among patients with more advanced liver disease.