Clinical review and literature analysis of hepatic epithelioid angiomyolipoma in alcoholic cirrhosis: A case report

BACKGROUND Hepatic epithelioid angiomyolipoma(HEA)has a low incidence and both clinical manifestations and imaging lack specificity.Thus,it is easy to misdiagnose HEA as other tumors of the liver,especially in the presence of liver diseases such as hepatitis cirrhosis.This article reviewed the diagnosis and treatment of a patient with HEA and alcoholic cirrhosis,and analyzed the literature,in order to improve the understanding of this disease.CASE SUMMARY A 67-year-old male patient with a history of alcoholic cirrhosis was admitted due to the discovery of a space-occupying lesion in the liver.Based on the patient’s history,laboratory examinations,and imaging examinations,a malignant liver tumor was considered and laparoscopic partial hepatectomy was performed.Postoperative pathology showed HEA.During outpatient follow-up,the patient showed no sign of recurrence.CONCLUSION HEA is difficult to make a definite diagnosis before surgery.HEA has the poten-tial for malignant degeneration.If conditions permit,surgical treatment is recom-mended.

Distinctive aspects of peptic ulcer disease,Dieulafoy'slesion,and Mallory-Weiss syndrome in patients withadvanced alcoholic liver disease or cirrhosis

AIM:To systematically review the data on distinctive aspects of peptic ulcer disease(PUD),Dieulafoy’s lesion(DL),and Mallory-Weiss syndrome(MWS)in patients with advanced alcoholic liver disease(a ALD),including alcoholic hepatitis or alcoholic cirrhosis.METHODS:Computerized literature search performed via Pub Med using the following medical subject heading terms and keywords:"alcoholic liver disease","alcoholic hepatitis","alcoholic cirrhosis","cirrhosis","liver disease","upper gastrointestinal bleeding","nonvariceal upper gastrointestinal bleeding","PUD",‘‘DL’’,‘‘Mallory-Weiss tear",and"MWS’’.RESULTS:While the majority of acute gastrointestinal(GI)bleeding with a ALD is related to portal hypertension,about 30%-40%of acute GI bleeding in patients with a ALD is unrelated to portal hypertension.Such bleeding constitutes an important complication of a ALD because of its frequency,severity,and associated mortality.Patients with cirrhosis have a markedly increased risk of PUD,which further increases with the progression of cirrhosis.Patients with cirrhosis or a ALD and peptic ulcer bleeding(PUB)have worse clinical outcomes than other patients with PUB,including uncontrolled bleeding,rebleeding,and mortality.Alcohol consumption,nonsteroidal anti-inflammatory drug use,and portal hypertension may have a pathogenic role in the development of PUD in patients with a ALD.Limited data suggest that Helicobacter pylori does not play a significant role in the pathogenesis of PUD in most cirrhotic patients.The frequency of bleeding from DL appears to be increased in patients with a ALD.DL may be associated with an especially high mortality in these patients.MWS is strongly associated with heavy alcohol consumption from binge drinking or chronic alcoholism,and is associated with a ALD.Patients with a ALD have more severe MWS bleeding and are more likely to rebleed when compared to non-cirrhotics.Preendoscopic management of acute GI bleeding in patients with a ALD unrelated to portal hypertension is similar to the management of a ALD patients with GI bleeding from portal hypertension,because clinical distinction before endoscopy is difficult.Most patients require intensive care unit admission and attention to avoid over-transfusion,to correct electrolyte abnormalities and coagulopathies,and to administer antibiotic prophylaxis.Alcoholics should receive thiamine and be closely monitored for symptoms of alcohol withdrawal.Prompt endoscopy,after initial resuscitation,is essential to diagnose and appropriately treat these patients.Generally,the same endoscopic hemostatic techniques are used in patients bleeding from PUD,DL,or MWS in patients with a ALD as in the general population.CONCLUSION:Nonvariceal upper GI bleeding in patients with a ALD has clinically important differences from that in the general population without a ALD,including:more frequent and more severe bleeding from PUD,DL,or MWS.

Correlation between hepatic blood flow and liver function in alcoholic liver cirrhosis

AIM: To elucidate the correlation between hepatic blood flow and liver function in alcoholic liver cirrhosis (AL-LC).

Vitamin D receptor gene polymorphisms and hepatocellular carcinoma in alcoholic cirrhosis

AIM: To assess the relationship between vitamin D re-ceptor (VDR) gene polymorphisms and the presence of hepatocellular carcinoma (HCC). METHODS: Two-hundred forty patients who underwent liver transplantation were studied. The etiologies of liver disease were hepatitis C (100 patients), hepatitis B (37) and alcoholic liver disease (103). A group of 236 healthy subjects served as controls. HCC in the explanted liver was detected in 80 patients. The following single nucle-otide gene polymorphisms of the VDR were investigatedby polymerase chain reaction and restriction fragment length polymorphism: FokI C>T (F/f), BsmI A>G (B/b), ApaI T>G (A/a) and TaqI T>C (T/t) (BAT). RESULTS: The frequencies of genotypes in patients without and with HCC were for FokI F/F = 69, F/f = 73, f/f = 18 and F/F = 36, F/f = 36, f/f = 8; BsmI b/b = 45, B/b = 87, B/B = 28 and b/b = 33, B/b = 35, B/B = 12; for ApaI A/A = 53, A/a = 85, a/a = 22 and A/A = 27, A/a = 38, a/a = 15; for TaqI T/T = 44, T/t = 88, t/t = 28 and T/T = 32, T/t = 38, t/t = 10. Carriage of the b/b genotype of BsmI and the T/T genotype of TaqI was signif icantly associated with HCC (45/160 vs 33/80, P < 0.05 and 44/160 vs 32/80, P < 0.05, respectively). The absence of the A-T-C protective allele of BAT was signif i-cantly associated with the presence of HCC (46/80 vs 68/160, P < 0.05). A strong association was observed between carriage of the BAT A-T-C and G-T-T haplotypes and HCC only in alcoholic liver disease (7/46 vs 12/36 vs 11/21, P < 0.002, respectively).CONCLUSION: VDR genetic polymorphisms are sig-nificantly associated with the occurrence of HCC in patients with liver cirrhosis. This relationship is more specific for patients with an alcoholic etiology.

Does an association exist between chronic pancreatitis and liver cirrhosis in alcoholic subjects?

AIM: To study the possible association between chronic pancreatitis (CP) and liver cirrhosis (LC) of alcoholic etiology,after excluding any other causes.METHODS: One hundred and forty consecutive alcoholic patients were subdivided into three groups: CP (n = 53),LC (n = 57),and asymptomatic alcoholic (n = 30).Clinical,biochemical and morphological characteristics,Child-Pugh index,indocyanine green test,and fecal pancreatic elastase-1 test were assessed.RESULTS: In patients with cirrhosis,major clinical manifestations of CP such as pancreatic pain and steatorrhea,as well as imaging alterations of CP such as calcifications,duct dilation and pseudocysts were absent; insulin-dependent diabetes was present in 5.3% of cases,and elastase-1 test was altered in only 7%,and severely altered in none.In patients with CP,clinical characteristics of cirrhosis such as ascites,encephalopathy and gastrointestinal hemorrhage were present in one case,Child-Pugh grade > A in 5.7%,and altered indocyanine green test in 1.9% cases.In asymptomatic alcoholism,there was only a non-coincident alteration of elastase-1 test and indocyanine test in 14.8% and 10%,respectively,but other characteristics of cirrhosis or CP were absent.An inverse correlation (r = -0.746) between elastase-1 test and indocyanine test was found in alcoholic patients.CONCLUSION: There is a scarce coincidence in clinical and morphological alterations among patients with CP or LC of alcoholic etiology,but an inverse correlation between pancreatic and liver function tests.These findings support that these alcoholic diseases evolve in a different manner and have different etiopathogenesis.

Towards an evaluation of alcoholic liver cirrhosis and nonalcoholic fatty liver disease patients with hematological scales

BACKGROUND Seeking potentially novel blood markers of liver fibrosis and steatosis is constantly of crucial importance.Despite a growing number of studies in this field of hepatology,a certain role of hematological indices in the course of liver disorders has not been fully elucidated,yet.AIM To evaluate a diagnostic accuracy of neutrophil-to-lymphocyte ratio(NLR),platelet-to-lymphocyte ratio(PLR)and mean platelet volume-to-platelet-ratio(MPR)in the course of alcoholic liver cirrhosis(ALC)and nonalcoholic fatty liver disease(NAFLD).METHODS One hundred forty-two patients with ALC,92 with NAFLD and 68 persons in control group were enrolled in the study.Hematological indices(NLR,PLR and MPR),indirect and direct markers of liver fibrosis(aspartate transaminase to alkaline transaminase ratio,aspartate transaminase to platelet ratio index,fibrosis-4,gamma-glutamyl transpeptidase to platelet ratio,procollagen Ⅰ carboxyterminal propeptide,procollagen Ⅲ aminoterminal propeptide,transforming growth factor-α,platelet-derived growth factor AB,laminin)were measured in each person.Model for end-stage liver disease(MELD)score in ALC group and NAFLD fibrosis score together with BARD score were calculated in NAFLD patients.Receiver operating characteristic(ROC)curves and area under the curve(AUC)values were applied to assess the sensitivity and specificity of examined markers and to evaluate proposed cut-offs of measured indices in the course of ALC and NAFLD.RESULTS MPR and NLR values in ALC patients were significantly higher in comparison to control group;PLR level was significantly lower.MPR and PLR correlated with assessed indirect and direct markers of liver fibrosis.MPR,NLR and PLR correlated with MELD score.NLR level in NAFLD patients was significantly higher in comparison to controls.MPR correlated with indirect markers of liver fibrosis and NAFLD fibrosis score.AUC values and proposed cut-offs for NLR,PLR and MPR in ALC patients were:0.821(>2.227),0.675(<70.445)and 0.929(>0.048),respectively.AUC values and proposed cut-offs for NLR,PLR and MPR in NAFLD group were:0.725(>2.034),0.528(>97.101)and 0.547(>0.038),respectively.CONCLUSION Hematological markers are inseparably connected with serological indices of liver fibrosis in ALC and NAFLD patients.MPR and NLR turned out to be the most powerful parameters in ALC patients.

Incidence, risk factors and outcome of de novo tumors in liver transplant recipients focusing on alcoholic cirrhosis

Orthotopic liver transplantation(OLT) is an established life-saving procedure for alcoholic cirrhotic(AC) patients, but the incidence of de novo tumors ranges between 2.6% and 15.7% and is significantly increased in comparison with patients who undergo OLT for other etiologies. Tobacco, a known carcinogen, has been reported to be between 52% and 83.3% in AC patients before OLT. Other risk factors that contribute to the development of malignancies are dose-dependent immunosuppression, advanced age, viral infections, sun exposure, and premalignant lesions(inflammatory bowel disease, Barrett's esophagus). A significantly more frequent incidence of upper aerodigestive(UAD) tract, lung, skin, and kidney-bladder tumors has been found in OLT recipients for AC in comparison with other etiologies. Liver transplant recipients who develop de novo non-skin tumors have a decreased long-term survival rate compared with controls. This significantly lower survival rate is more evident in AC recipients who develop UAD tract or lung tumors after OLT mainly because the diagnosis is usually performed at an advanced stage. All transplant candidates, especially AC patients, should be encouraged to cease smoking and alcohol consumption in the pre- and postOLT periods, use skin protection, avoid sun exposure and over-immunosuppression, and have a yearly otopharyngolaryngeal exploration and chest computed tomography scan in order to prevent or reduce the incidence of de novo malignancies. Although still under investigation, substitution of calcineurin inhibitors for sirolimus or everolimus may reduce the incidence of de novo tumors after OLT.

Budd-Chiari like syndrome in decompensated alcoholic steatohepatitis and liver cirrhosis

A rare case of pseudo-Budd-Chiari Syndrome in a patientwith decompensated alcoholic liver disease is reported.Although clinical and radiological findings suggestedBudd-Chiari Syndrome, the liver biopsy revealedmicronodular cirrhosis and absence of histological signsof hepatic outflow obstruction.

Muscle hematoma:A critically important complication of alcoholic liver cirrhosis

An iliopsoas hematoma can occur either spontaneously or secondary to trauma or bleeding tendency due to hemophilia and anticoagulant therapy.Although liver cirrhosis is commonly associated with coagulopathy, iliopsoas hematoma is very rare.We herein,present a case of bilateral iliopsoas hematoma in a patient with alcoholic cirrhosis,and review the literature on muscle hematoma associated with cirrhosis.A 56-year-old man with alcoholic cirrhosis was admitted in a state of shock with anemia.The cause of anemia could not be detected,and the patient was treated conservatively. The site of bleeding was not detected with either gastroduodenal endoscopy or upper abdominal computed tomography,the latter of which did not include the iliopsoas muscle.He died on the 10th day of admission and bilateral iliopsoas hematomas were found on autopsy.An iron stain was positive in the iliopsoas muscle.Eight cases of muscle hematoma associated with cirrhosis,including the present case, were found in a review of the literature.Four of these cases involved the rectus abdominis muscle,3 involved the iliopsoas muscle and 1 involved combined muscles.Alcoholic cirrhosis accounted for 75%of the cases.One case(12.5%)was associated with virus- related cirrhosis,and another with combined virus- and alcohol-related cirrhosis.The mortality rate was 75%despite early diagnosis and low risk scores for cirrhosis.Muscle hematoma in patients with cirrhosis isclosely related to alcoholism,and the mortality rate of the condition is extremely high.In conclusion,muscle hematoma should be recognized as an important complication of cirrhosis.

Hemodynamics in the immediate post-transplantation period in alcoholic and viral cirrhosis

AIM:To study the hemodynamics in the immediate post transplant period and compare patients with alcoholic vs viral cirrhosis. METHODS:Between 2000-2003,38 patients were transplanted for alcoholic cirrhosis and 28 for postviral cirrhosis.Heart rate(HR),central venous pressure(CVP), mean arterial pressure(MAP),pulmonary capillary wedge pressure(PCWP),cardiac index(CI),systemic vascular resistance index(SVRI),pulmonary artery pressure(PAP),and pulmonary vascular resistance index(PVRI)were measured immediately and 24 h post transplantation. RESULTS:Hyperdynamic circulation persisted at 24 hfollowing transplantation with an elevated CI of 5.4± 1.3 L/(min×m 2 )and 4.9±1.0 L/(min×m 2 )in the viral and alcoholic groups,respectively,and was associated with a decreased SVRI.Within the first 24 h, there was a significant decrease in HR and increase in MAP;the extent of the change was similar in both groups.The CVP,PCWP,and SVRI increased,and CI decreased in the viral patients,but not the alcoholic patients.Alcoholics showed a lower PVRI(119±52 dynes/(cm 5 ×m 2 )vs 166±110 dynes/(cm5×m2),P< 0.05)and PAP(20±7 mmHg vs 24±7 mmHg,P< 0.05)compared to the viral group at 24 h. CONCLUSION:Hyperdynamic circulation persists in the immediate post-transplant period with a faster improvement in the viral group.Alcoholic patients have a more pronounced pulmonary vasodilatation.

Spontaneous remission of hepatic myelopathy in a patient with alcoholic cirrhosis:A case report

BACKGROUND Hepatic myelopathy(HM)is a rare neurological complication of advanced cirrhosis.Prognosis of patients with HM is generally poor without timely liver transplantation or interventional therapy.Self-resolving HM in patients with alcoholic cirrhosis has never been reported.CASE SUMMARY A 53-year-old man with alcoholic cirrhosis and recurrent overt hepatic encephalopathy for 1 year was admitted for lower extremity weakness,slow movement,and stumbling gait.The patient was diagnosed with HM after excluding other causes of spastic paraparesis.The patient refused liver transplantation.However,the patient kept total abstinence and received a multidisciplinary treatment for complications of decompensated cirrhosis.The symptoms of HM resolved gradually after 2 years of treatment.All complications of alcoholic cirrhosis resolved after 4 years of follow-up.CONCLUSION The case demonstrates that HM can resolve in patients without liver transplantation after total abstinence and systemic management of complications.

Peculiar characteristics of portal-hepatic hemodynamics of alcoholic cirrhosis

Alcohol-related cirrhosis is a consequence of heavy and prolonged drinking. Similarly to patients with cirrhosis of other etiologies, patients with alcoholic cirrhosis develop portal hypertension and the hepatic, splanchnic and systemic hemodynamic alterations that follow. However, in alcoholic cirrhosis, some specific features can be observed. Compared to viral cirrhosis, in alcohol-related cirrhosis sinusoidal pressure is generally higher, hepatic venous pressure gradient reflects portal pressure better, the portal flow perfusing the liver is reduced despite an increase in liver weight, the prevalence of reversal portal blood flow is higher, a patent paraumbilical vein is a more common finding and signs of hyperdynamic circulations, such as an increased cardiac output and decreased systemic vascular resistance, are more pronounced. Moreover, alcohol consumption can acutely increase portal pressure and portal-collateral blood flow. Alcoholic cardiomyopathy, another pathological consequence of prolonged alcohol misuse, may contribute to the hemodynamic changes occurring in alcohol-related cirrhosis. The aim of this review was to assess the portal-hepatic changes thatoccur in alcohol-related cirrhosis, focusing on the differences observed in comparison with patients with viral cirrhosis. The knowledge of the specific characteristics of this pathological condition can be helpful in the management of portal hypertension and its complications in patients with alcohol-related cirrhosis.

Elevated nitric oxide and 3',5' cyclic guanosine monophosphate levels in patients with alcoholic cirrhosis

AIM: To evaluate whether serum levels of nitric oxide (NO ·) and plasma levels of cyclic guanosine monophosphate (cGMP) and total glutathione (GSH) are altered in patients with alcoholic cirrhosis and to examine their correlation with the severity of liver disease.METHODS: Twenty-six patients with alcoholic liver cirrhosis were studied. Serum levels of NO · and plasma levels of cGMP and GSH were measured in 7 patients with compensated alcoholic cirrhosis (Child-Pugh A) and 19 patients with advanced cirrhosis (Child-Pugh B and C). The model for end-stage liver disease (MELD) score was evaluated. Sixteen healthy volunteers served as controls. Liver enzymes and creatinine levels were also tested.RESULTS: NO · and cGMP levels were higher in patients with Child-Pugh B and C cirrhosis than in Child-Pugh A cirrhosis or controls (NO ·: 21.70 ± 8.07 vs 11.70 ± 2.74; 21.70 ± 8.07 vs 7.26 ± 2.47 μmol/L, respectively; P < 0.001) and (cGMP: 20.12 ± 6.62 vs 10.14 ± 2.78; 20.12 ± 6.62 vs 4.95 ± 1.21 pmol/L, respectively; P < 0.001). Total glutathione levels were lower in patients with Child-Pugh B and C cirrhosis than in patients with Child-Pugh A cirrhosis or controls (16.04 ± 6.06 vs 23.01 ± 4.38 or 16.04 ± 6.06 vs 66.57 ± 26.23 μmol/L, respectively; P < 0.001). There was a significant correlation between NO · and cGMP levels in all patients with alcoholic cirrhosis. A significant negative correlation between reduced glutathione/glutathione disulfide and the MELD score was found in all cirrhotic patients.CONCLUSION: Our results suggest a role for oxidative stress in alcoholic liver cirrhosis, which is more significant in decompensated patients with higher levels of NO ·and cGMP and lower GSH levels than in compensated and control patients. Altered mediator levels in decompensated patients may influence the hemodynamic changes in and progression of liver disease.

Hepatic venous pressure gradient: Inaccurately estimates portal venous pressure gradient in alcoholic cirrhosis and portal hypertension

BACKGROUND Portal hypertension(PHT)in patients with alcoholic cirrhosis causes a range of clinical symptoms,including gastroesophageal varices and ascites.The hepatic venous pressure gradient(HVPG),which is easier to measure,has replaced the portal venous pressure gradient(PPG)as the gold standard for diagnosing PHT in clinical practice.Therefore,attention should be paid to the correlation between HVPG and PPG.METHODS Between January 2017 and June 2020,134 patients with alcoholic cirrhosis and PHT who met the inclusion criteria underwent various pressure measurements during transjugular intrahepatic portosystemic shunt procedures.Correlations were assessed using Pearson’s correlation coefficient to estimate the correlation coefficient(r)and determination coefficient(R^(2)).Bland-Altman plots were constructed to further analyze the agreement between the measurements.Disagreements were analyzed using paired t tests,and P values<0.05 were considered statistically significant.RESULTS In this study,the correlation coefficient(r)and determination coefficient(R2)between HVPG and PPG were 0.201 and 0.040,respectively(P=0.020).In the 108 patients with no collateral branch,the average wedged hepatic venous pressure was lower than the average portal venous pressure(30.65±8.17 vs.33.25±6.60 mmHg,P=0.002).Hepatic collaterals were identified in 26 cases with balloon occlusion hepatic venography(19.4%),while the average PPG was significantly higher than the average HVPG(25.94±7.42 mmHg vs 9.86±7.44 mmHg;P<0.001).The differences between HVPG and PPG<5 mmHg in the collateral vs no collateral branch groups were three cases(11.54%)and 44 cases(40.74%),respectively.CONCLUSION In most patients,HVPG cannot accurately represent PPG.The formation of hepatic collaterals is a vital reason for the strong underestimation of HVPG.

Development of risky varices in alcoholic cirrhosis with a well-maintained nutritional status

AIM: To compare the nutritional status between alcoholic compensated cirrhotic patients and hepatitis C virus(HCV)-related cirrhotic patients with portal hypertension.METHODS: A total of 21 patients with compensated cirrhosis(14 with HCV-related cirrhosis and seven with alcoholic cirrhosis) who had risky esophageal varices were investigated. In addition to physical variables, including the body mass index, triceps skinfold thickness, and arm-muscle circumference, the nutritional status was also assessed using the levels of pre-albumin(pre-ALB), retinol-binding protein(RBP) and non-protein respiratory quotient(NPRQ) measured with an indirect calorimeter.RESULTS: A general assessment for the nutritional status with physical examinations did not show a significant difference between HCV-related cirrhosis and alcoholic cirrhosis. However, the levels of pre-ALB and RBP in alcoholic compensated cirrhotic patients were significantly higher than those in HCV-related compensated cirrhotic patients. In addition, the frequency of having a normal nutritional status(NPRQ ≥ 0.85 and ALB value > 3.5 g/d L) in alcoholic compensated cirrhotic patients was significantly higher than that in HCV-related compensated cirrhotic patients.CONCLUSION: According to our small scale study, alcoholic compensated cirrhotic patients can develop severe portal hypertension even with a relatively well-maintained liver function and nutritional status compared with HCV-related cirrhosis.

Trends of alcoholic liver cirrhosis readmissions from 2010 to 2018:Rates and healthcare burden associated with readmissions

BACKGROUND Alcoholic liver cirrhosis(ALC)is a chronic liver disease with varying disease severity.Readmissions of ALC are associated with poor outcomes.AIM To identify and assess trends of readmissions for ALC over an eight-year period.METHODS This retrospective interrupted trend study analysed 30-d readmissions of ALC in the United States from 2010 to 2018 using the National Readmissions Database.Hospitalization for ALC was the reason for index admission obtained using the International Classification of Diseases codes(571.2 and K70.3X).Biodemographic characteristics and hospitalization trends were highlighted over time.A multivariate regression analysis model was used to calculate the trend for riskadjusted odds of 30-d all-cause ALC readmissions,ALC specific readmission rate,ALC readmission proportion,inpatient mortality,mean length of stay(LOS)and mean total hospital cost(THC)following adjustments for age,gender,grouped Charlson Comorbidity Index,insurance,mean household income,and hospital characteristics.RESULTS There was a trend towards increasing total 30-d readmissions of ALC from 7660 in 2010 to 15085 in 2018(P<0.001).Patients readmitted for ALC were noted to have an increasing comorbidity burden over time.We noted a rise in the risk-adjusted 30-d all-cause readmission of ALC from 24.9%in 2010 to 29.9%in 2018(P<0.001).ALC-specific readmission rate increased from 6.3%in 2010 to 8.4%in 2018(P<0.001)while ALC readmission proportion increased from 31.4%in 2010 to 36.3%in 2018(P<0.001).Inpatient mortality for 30-d readmissions of ALC declined from 10.5%in 2010 to 8.2%in 2018(P=0.0079).However,there was a trend towards increasing LOS from 5.6 d in 2010 to 6.3 d in 2018(P<0.001)and increasing THC from 13790 dollars in 2010 to 17150 dollars in 2018(P<0.001).The total days of hospital stay attributable to 30-d readmissions of ALC increased by 119.2%while the total attributable hospital costs increased by 149%by the end of 2018.CONCLUSION There was an increase in the 30-d readmission rate and comorbidity burden for ALC;however,inpatient mortality declined.Additionally,there was a trend towards increasing LOS and THC for these readmissions.

Randomized controlled trial of Qing Gan Huo Xue Prescription in the treatment of alcoholic liver cirrhosis

Objective:To evaluate the efficacy of Qing Gan Huo Xue Prescription(QGHXP)in the treatment of patients with alcoholic liver cirrhosis(ALC)of damp and heat stasis syndrome.Methods:A total of 69 patients with ALC were randomly divided into TCM group(n=35)and control group(n=34).The TCM group was given QGHXP 1 pack TID orally.Control group received polyene phosphatidylcholine capsule 456 mg TID for 24 weeks.The observation measurements are symptom efficacy rate,serum level of liver enzyme,and non-invasive liver cirrhosis evaluation,including liver stiffness measurement(LSM)examininged by FibroTouch,APRI score,FIB-4 index and Maddrey discriminant function.Results:The symptom efficacy rate of the experimental group and the control group was 85.70%and 61.80%(P=0.024).Liver enzyme levels(serum ALP,γ-GT,AST and ALT)of TCM group were lower than those of control group(P<0.05).LSM of TCM group was reduced after treatment,and was significant lower than control group(14.19±1.49)vs.(15.06±1.24)(P<0.05).The APRI scores,FIB-4 index and Maddrey discriminant functions of TCM group were lower than those of control group(P<0.05).Conclusion:QGHXP is an effective alternative for the treatment of damp and heat stasis syndrome of ALC in improving liver function and clinical symptoms.

Pleomorphic hepatocellular carcinoma following consumption of hypericum perforatum in alcoholic cirrhosis

Hepatocellular carcinoma (HCC) often develops in patients with underlying liver disease, yet HCC with syncytial giant cells (SGCs) is extremely rare. Herein, we report a 55-year-old man with a 6-year history of alcoholic cirrhosis who during his regular checkup presented with marked elevation of alpha-fetoprotein. Clinical examination and imaging analyses revealed a tumor-like lesion in segment 4 of the liver, which was removed by limited wedge resection. Histological analysis by hematoxylin and eosin staining indicated pleomorphic and atypical nodules, with some SGCs, embedded within the boundaries of the neoplastic lesion. The adjacent liver parenchyma showed microvesicular steatosis, pericellular fibrosis, and moderate hemosiderin accumulation (grade 2, as determined by Prussian blue iron stain) in hepatocytes and Kupffer cells but no copper accumulation (as determined by orcein stain). Immunohistochemical analysis showed hepatocyte antigen-positive staining for the neoplastic cells and SGCs. The diagnosis was made for cirrhosis-related HCC with SGCs. The previous reports of pleomorphic HCC have featured osteoclast-like (i.e., mesenchymal type) giant cells, making this case of epithelial type giant cells very rare. The patient&#x02019;s 6-month history of hypericum perforatum/St John&#x02019;s wort self-medication may have prompted the cirrhosis or HCC progression or the unusual SGC manifestation.

Alcoholic liver disease:Utility of animal models

Alcoholic liver disease(ALD) is a major cause of acute and chronic liver injury. Extensive evidence has been accumulated on the pathological process of ALD during the past decades. However, effective treatment options for ALD are very limited due to the lack of suitable in vivo models that recapitulate the full spectrum of ALD. Experimental animal models of ALD, particularly rodents, have been used extensively to mimic human ALD. An ideal animal model should recapitulate all aspects of the ALD process, including significant steatosis, hepatic neutrophil infiltration, and liver injury. A better strategy against ALD depends on clear diagnostic biomarkers, accurate predictor(s) of its progression and new therapeutic approaches to modulate stop or even reverse the disease. Numerous models employing rodent animals have been established in the last decades to investigate the effects of acute and chronic alcohol exposure on the initiation and progression of ALD. Although significant progress has been made in gaining better knowledge on the mechanisms and pathology of ALD, many features of ALD are unknown, and require further investigation, ideally with improved animal models that more effectively mimic human ALD. Although differences in the degree and stages of alcoholic liver injury inevitably exist between animal models and human ALD, the acquisition and translational relevance will be greatly enhanced with the development of new and improved animal models of ALD.

Liver transplantation and alcoholic liver disease:History,controversies,and considerations

Alcohol consumption accounts for 3.8% of annual global mortality worldwide, and the majority of these deaths are due to alcoholic liver disease(ALD), mainly alcoholic cirrhosis. ALD is one of the most common indications for liver transplantation(LT). However, it remains a complicated topic on both medical and ethical grounds, as it is seen by many as a "self-inflicted disease". One of the strongest ethical arguments against LT for ALD is the probability of relapse. However, ALD remains a common indication for LT worldwide. For a patient to be placed on an LT waiting list, 6 mo of abstinence must have been achieved for most LT centers. However, this "6-mo rule" is an arbitrary threshold and has never been shown to affect survival, sobriety, or other outcomes. Recent studies have shown similar survival rates among individuals who undergo LT for ALD and those who undergo LT for other chronic causes of end-stage liver disease. There are specific factors that should be addressed when evaluating LT patients with ALD because these patients commonly have a high prevalence of multisystem alcohol-related changes. Risk factors for relapse include the presence of anxiety or depressive disorders, short pre-LT duration of sobriety, and lack of social support. Identification of risk factors and strengthening of the social support system may decrease relapse among these patients. Family counseling for LT candidates is highly encouraged to prevent alcohol consumption relapse. Relapse has been associated with unique histopathological changes, graft damage, graft loss, and even decreased survival in some studies. Research has demonstrated the importance of a multidisciplinary evaluation of LT candidates. Complete abstinence should be attempted to overcome addiction issues and to allow spontaneous liver recovery. Abstinence is the cornerstone of ALD therapy. Psychotherapies, including 12-step facilitation therapy, cognitive-behavioral therapy, and motivational enhancement therapy, help support abstinence. Nutritional therapy helps to reverse muscle wasting, weight loss, vitamin deficiencies, and trace element deficiencies associated with ALD. For muscular recovery, supervised physical activity has been shown to lead to a gain in muscle mass and improvement of functional activity. Early LT for acute alcoholic hepatitis has been the subject of recent clinical studies, with encouraging results in highly selected patients. The survival rates after LT for ALD are comparable to those of patients who underwent LT for other indications. Patients that undergo LT for ALD and survive over 5 years have a higher risk of cardiorespiratory disease, cerebrovascular events, and de novo malignancy.