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Aims Systemic amyloidosis is a multisystem disorder caused by the misfolding, aggregation, and deposition of certain proteins in various organs and tissues. Cardiac involvement is common and worsens the prognosis. Atrial fibrillation is the most frequent arrhythmia in cardiac amiloidosis (CA), but many cases of ventricular arrhythmias (VA) and sudden cardiac death (SCD) have been described. Methods and results We present a case of a 64-year-old man admitted following exertional syncope occurred after climbing a flight of stairs. In the previous 2 weeks he had experienced fatigue and poor tolerance to exertion; moreover, 2 days before he had another episode of transient loss of consciousness after exertion. His medical history included left gonarthrosis and surgery for right carpal tunnel syndrome one year before. Physical examination did not revealed signs of heart failure. A 12-lead electrocardiogram (ECG) showed a pseudoinfarction pattern with QS waves in V2 and V3 leads and low voltage in all limb leads (Figure 1). Routine blood tests revealed N-terminal pro-bran natriuretic peptide (NT-ProBNP) of 3436 pg/ml (n.v. 0–125) and high-sensitive troponin T of 67 pg/ml (n.v. < 58). A trans-thoracic echocardiogram showed left ventricle (LV) concentric thickening wall with granular and sparkling pattern, mild reduced ejection fraction, reduced global longitudinal strain with apical sparing, grade 3 diastolic disfunction, biatrial enlargement, mild mitral regurgitation, right ventricle free wall thickening (8 mm), mild reduced TAPSE, and mild pericardial effusion. Cardiac magnetic resonance (CMR) confirmed ventricular wall thickening with evidence at T1 mapping of interstitial infiltration more evident in the septum and inferior-lateral wall with apical savings (Figure 2). A total body 99mTc-HDP scintigraphy showed cardiac uptake with intensity similar to bone signal (Perugini Score 2) suggesting ATTR cardiac amyloidosis (Figure 3). Both kappa and lambda concentrations were normal. The genetic testing did not reveled mutations in the TTR gene. We concluded for a diagnosis of ATTR wild-type CA. The Holter ECG monitoring registered numerous ventricular ectopic beats and an episode of non-sustained ventricular tachycardia. A coronary angiography ruled out coronary artery disease. In consideration of the clinical-instrumental picture an ICD was implanted. Conclusions In conclusion, CA is still underdiagnosed. VA and SCD may further complicate the prognosis. Early diagnosis and adequate stratification of the arrhythmic risk are essential to ensure patients the best therapeutic strategies.

The caseous calcification of the mitral annulus (CCMA) is a rare variant of the mitral annulus calcification (MAC), with prevalence of 0.067% in general population. It is usually an asymptomatic condition but rarely it can cause severe mitral valve dysfunction, embolization, and conduction abnormalities. Transthoracic echocardiography (TTE) is a useful diagnostic tool. However, it can be necessary a multi-modality imaging approach for a differential diagnosis among other intra-cardiac masses. We are presenting a case of CCMA in an 88-year-old woman admitted to our department for acute decompensation of chronic heart failure. TTE has shown pathognomonic findings of CCMA. Tridimensional trans-esophageal echocardiography (3D TEE) gave a better characterization of the CCMA, avoiding further diagnostic procedures.

Myocarditis is an inflammatory disease of cardiac muscle with a variable clinical presentation, ranging from asymptomatic cases to different degrees of left ventricular systolic dysfunction up to heart failure and dilated heart disease. Ventricular arrhythmias (VA) can occur in patients with myocarditis and implantable cardioverter defibrillator (ICD) may be indicated in patients with life-threatening VA who are not in the acute phase of myocarditis and who are receiving optimal medical therapy. Reduced left ventricular ejection fraction (LVEF) below 35%, which is used as the main criterion for stratifying the risk of sudden cardiac death (SCD), has low sensitivity and low specificity for arrhythmic risk stratification in patients with myocarditis. Myocardial scar is the main determinant for VA in these patients. Cardiac magnetic resonance imaging (CMR), using late gadolinium enhancement(LGE), has an excellent ability to determinate the extension and characterization of myocardial scar, indeed CMR can potentially improve SCD risk stratification and indication for ICD implantation in patients with myocarditis. We present a case of a 36 years-old male presenting to the Emergency Department with a monomorphic sustained ventricular tachycardia in whom MRI revealed myocardial-pericardial recurrent inflammatory involvement and worsening disease progression. ICD was implanted in consideration of the high risk of life-threatening arrhythmias.

Progressive lipoprotein impairment occurs in liver cirrhosis and is associated with increased morbidity and mortality. The present review aims to summarize the current evidence regarding the prognostic value of lipoprotein abnormalities in liver cirrhosis and to address the need of a better prognostic stratification of patients, including lipoprotein profile assessment. Low levels of lipoproteins are usual in cirrhosis. Much evidence supports the prognostic role of hypolipidemia in cirrhotic patients. In particular, hypocholesterolemia represents an independent predictor of survival in cirrhosis. In cirrhotic patients, lipoprotein impairment is associated with several complications: infections, malnutrition, adrenal function, and spur cell anemia. Alterations of liver function are associated with modifications of circulating lipids. Decreased levels of lipoproteins significantly impact the survival of cirrhotic patients and play an important role in the pathogenesis of some cirrhosis-related complications.

10.33590/emjhepatol/10310451

In patients with cirrhosis, adrenal insufficiency (AI) is reported during sepsis and septic shock and is associated with increased mortality. Consequently, the term "hepato-adrenal syndrome" was proposed. Some studies have shown that AI is frequent in stable cirrhosis as well as in cirrhosis associated with decompensation other than sepsis, such as bleeding and ascites. Moreover, other studies showed a high prevalence in liver transplant recipients immediately after, or some time after, liver transplantation. The effect of corticosteroid therapy in critically ill patients with liver disease has been evaluated in some studies, but the results remain controversial. The 250-μg adreno-cortico-tropic-hormone stimulation test to diagnose AI in critically ill adult patients is recommended by an international task force. However, in liver disease, there is no consensus on the appropriate tests and normal values to assess adrenal function; thus, standardization of normal ranges and methodology is needed. Serum total cortisol assays overestimate AI in patients with cirrhosis, so that direct free cortisol measurement or its surrogates may be useful measurements to define AI, but further studies are needed to clarify this. In addition, the mechanisms by which liver disease leads to adrenal dysfunction are not sufficiently documented. This review evaluates published data regarding adrenal function in patients with liver disease, with a particular focus on the potential limitations of these studies as well as suggestions for future studies.

Adrenal insufficiency is often present in cirrhosis. We hypothesize that a prolonged adrenocorticotropic hormone (ACTH) stimulus can restore cellular capacity of adrenal glands to secrete cortisol. Aim of our study was to assess adrenal responsiveness to prolonged ACTH stimulation in cirrhotics.Prospective observational study in 121 consecutively admitted cirrhotic patients undergoing a low dose short synacthen test and plasma ACTH measurement using a chemiluminescence immunoassay. Long synacthen test was performed if the low dose was abnormal.46 patients had abnormal low dose short test (38%), and 29 underwent the long test: 41% showed normal response (Group 1), 55% showed delayed response (Group 2) and 1 had abnormal response (4%). Baseline ACTH levels did not significantly differ between the two groups. Median basal cortisol was higher in Group 1 (296 vs. 198 nmol/L; p=0.02). Using ROC curve basal cortisol254 nmol/L was associated with a delayed long synacthen test response (AUC 0.78, p=0.001) with good accuracy (sensitivity 67%, specificity 81%).A delayed cortisol response after a prolonged ACTH stimulation is found in over fifty percent of cirrhotics with abnormal low dose short synacthen test, confirming that the mechanism of hypoadrenalism in these patients could be related both to adrenal cellular dysfunction and hypothalamus-pituitary adrenal axis impairment.

Renal failure is a common complication of cirrhosis and is associated with poor prognosis. Several reports have demonstrated the clinical utility of renal resistive indices in the assessment of renal function in cirrhosis patients. It is unknown whether the occurrence of diabetes affects renal haemodynamic indices in patients with cirrhosis. Therefore, the aim of our study was to compare renal Doppler indices in cirrhotic patients with and without type 2 diabetes mellitus (T2DM) and in diabetics without cirrhosis, and to relate the Doppler parameters to albuminuria. We evaluated 89 consecutive patients with normal renal functioning, including 37 with cirrhosis and T2DM (CD-Group), 41 with cirrhosis without diabetes (C-Group) and 11 with diabetes without cirrhosis (D-Group). The kidney pulsatility index (PI) and resistance index (RI) were measured by Doppler ultrasound. Renal function was expressed as the estimated glomerular filtration rate (eGFR) using the modification of diet in renal disease (MDRD) formula. Microalbuminuria (µAlb) was also evaluated. No significant differences were observed with respect to age, the Child-Pugh class or the serum creatinine level. The eGFR was mildly reduced in the CD-Group compared with the C-Group and D-Group, and µAlb was present in 24.4 % of the patients in the CD-Group and in 9 % of those in the D-Group. The PI and RI were significantly increased in the CD-Group and D-Group compared with the C-Group. Both the PI and RI were significantly associated with µAlb independent of age and Child-Pugh class. The novel finding of this study was that T2DM potentially impairs renal haemodynamics in patients with cirrhosis.

Backgrounds and aims: Adrenal insufficiency (AI) has been reported in patients with stable cirrhosis. A lack of substrates has been suggested as a possible contributing pathogenic mechanism leading to glucocorticoid deficiency in these subjects. To better explore this hypothesis, we studied lipoproteins in cirrhotics with and without AI. Methods. A total of 81 cirrhotic patients and 30 normal volunteers were enrolled. The severity of liver disease was graded by Child-Pugh score. Total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglyceride (TG), and apolipoprotein AI (Apo-AI) levels were evaluated. HDL subfractions were measured by gradient gel electrophoresis. Adrenal function was assessed by the Low-Dose Short Synacthen Test. Results. Cirrhotic patients showed a significant reduction of TC, HDL, LDL, TG, and Apo-AI levels compared with controls. HDL3 was significantly lower, while HDL2 was higher, in cirrhotics compared with the controls. AI was observed in 26 patients. TC, TG, HDL, and Apo-AI were significantly reduced in cirrhotics with AI compared with those with normal adrenal function. HDL2 and HDL3 did not differ between these two groups. Delta cortisol was related to TC (r = 0.30, p < 0.01), TG (r = 0.22, p = 0.05), and Apo-AI (r = 0.37, p < 0.001). Multivariate analysis revealed that Apo-AI and HDL were independently associated with AI. Conclusion. Our study shows that TC, TG, HDL, and Apo-AI are reduced in cirrhotics with AI. In particular, because both HDL and Apo-AI play a primary role in providing substrates for steroidogenesis to adrenal cells, this deficiency may contribute to the pathogenesis of AI in these patients.

Adrenal Insufficiency (AI), defined as deficient production or action of glucocorticoids resulting from either a structural damage of adrenal glands (primary adrenal insufficiency) or an impairment of the hypothalamic-pituitary axis (secondary adrenal disease), is being reported with increasing frequency in patients with liver disease, and some authors proposed the term “hepato-adrenal syndrome”. The prevalence of AI in patients with liver disease varies widely according to the study population: critically ill patients (33-92%), stable cirrhosis (31-60%), or decompensated cirrhosis, such as variceal bleeding (30-48%) and ascites (26-64%). However there is no current consensus about diagnostic criteria to define AI in patients with liver disease, and its prognostic relevance in stable cirrhosis is still unclear.

Measurements of serum levels of total cortisol can overestimate the prevalence of adrenal dysfunction in patients with cirrhosis because they have low concentrations of corticosteroid-binding globulin and albumin. We used measurements of serum total cortisol and serum free cortisol after the low-dose short Synacthen test (LDSST) to assess adrenal dysfunction.We studied 79 patients with stable cirrhosis; adrenal dysfunction was defined by peak concentrations of total cortisol ≤494 mmol/L and/or peak concentrations of free cortisol ≤33 nmol/L after the LDSST. We determined free cortisol index (FCI) scores and calculated free cortisol levels by using Coolens' equation. The Cox regression model was used to assess the relationship between adrenal dysfunction and outcomes (death or liver transplant).On the basis of measurement of total cortisol, 34% of patients had adrenal dysfunction, and on the basis of measurement of free cortisol, 29% had adrenal dysfunction. There was agreement between total cortisol and free cortisol levels in 22% of patients; in 13%, adrenal dysfunction was diagnosed only on the basis of total cortisol and in 6% only on the basis of free cortisol (κ coefficient, 0.56; P.01). Low concentrations of corticosteroid-binding globulin (21 vs 54 μg/mL, P.01) led to an overestimation of adrenal dysfunction that was based on measurement of total cortisol. Measurements of calculated free cortisol constantly overestimated free cortisol concentrations, with variations as large as 87% for baseline values and up to 84% after stimulation. Adrenal insufficiency, defined by FCI scores12, was detected in 30% of patients; among them, 23% also had subnormal peak levels of free cortisol (κ coefficient, 0.70; P.001). Adrenal dysfunction was not significantly associated with patient outcomes, on the basis of Cox model analysis.Adrenal insufficiency, defined by LDSST, is frequent in patients with stable cirrhosis, on the basis of measurements of total and free cortisol. FCI scores are better than measurement of total cortisol in assessing adrenal function in patients with cirrhosis. We did not associate adrenal dysfunction with outcome, but further studies are needed.

In liver cirrhosis, hepatoadrenal syndrome has been described recently as a progressive impairment in the adrenocortical reserve, with deficient production or action of glucocorticoids resulting in adrenal insufficiency. Data on the treatment of this syndrome are scarce. We report a case of a 60-year-old male patient referred to our hospital because of rectal bleeding and bilateral leg swelling. He complained of marked weakness, bilateral leg swelling, and shortness of breath with exertion for the last 2 months. Biochemistry and imaging indicated liver cirrhosis. Because of the weakness and persistent hypotension, we performed a low-dose synacthen test, which indicated adrenal insufficiency (baseline cortisol level 1.8 μg/dl, increasing to 3.5 and 3.7 μg/dl at 20 and 30 min, respectively). The patient's general condition improved promptly after corticosteroid supplementation.

Background & Aims To evaluate renal failure (RF) in cirrhosis to determine and quantify its prognostic significance. Methods Studies were identified by MEDLINE, EMBASE, Cochrane, ISI Web of Science (1977–2010); search terms included renal failure, mortality, and cirrhosis. Included studies (n=74) reported >10 patients and mortality data (8088 patients). Mortality at 1, 3, and 12months was evaluated with respect to Child-Pugh score, serum creatinine, ascites, ICU status or sepsis, prospective study design, and publication year. Pooled odds ratio (POR) for death was compared for RF vs . non-RF (5668 patients). Results Overall median mortality for RF patients was 67%: 58% at 1month and 63% (IQR 54–79) at 12months. POR for death RF vs. non-RF patients was 7.6 (95%CI 5.4–10.8). Overall mortality before 2005 (1264 patients) was 74% and after 2005 (2833 patients) was 63% with a marked reduction only at 30days (71% vs. 52%). Conclusions This study provides a measure of the increased risk of death in cirrhosis with renal failure. RF increases mortality 7-fold, with 50% of patients dying within one month. Preventative strategies for RF are needed.

Relative adrenal insufficiency (AI) occurs in patients with cirrhosis with sepsis, but not with variceal bleeding. We evaluated adrenal function in cirrhotic patients with and without bleeding.Twenty cirrhotic patients with variceal bleeding were evaluated using the short synacthen test (SST) and 10 using the low-dose synacthen test (LDSST) followed by SST. The control group included 60 stable cirrhotic patients, assessed by LDSST (n = 50) or SST (n = 10), and 14 healthy volunteers. AI was diagnosed using SST, based on peak cortisol levels ≤ 18 μg/dL in nonstressed patients or Δmax9 μg/dL or a total cortisol level10 μg/dL in stressed patients with variceal bleeding-the current criteria for critical illness-related corticosteroid insufficiency. Using LDSST, diagnosis was based on peak concentrations of cortisol ≤ 18 μg/dL in nonstressed patients and25 μg/dL (or Δmax9 μg/dL) in patients with variceal bleeding. We evaluated patients with levels of serum albumin2.5 g/dL, to indirectly assess cortisol binding.All healthy volunteers had normal results from LDSSTs and SSTs. Patients with variceal bleeding had higher median baseline concentrations of cortisol (15.4 μg/dL) than stable cirrhotic patients (8.7 μg/dL, P = .001) or healthy volunteers (10.1 μg/dL, P = .01). Patients with variceal bleeding had higher median peak concentrations of cortisol than stable cirrhotic patients (SST results of 32.7 vs 21 μg/dL, P = .001; LDSST results of 9.3 vs 8.1 μg/dL; nonsignificant), with no differences in Δmax in either test. These differences were greater with variceal bleeding than in stable cirrhotic patients with AI. Subanalysis of patients with albumin levels2.5 g/dL did not change these differences.Cirrhotic patients with variceal bleeding have AI. Despite higher baseline concentrations of serum cortisol and subnormal Δmax values, they did not have adequate responses to stress, and therefore had critical illness-related corticosteroid insufficiency.

Adrenal insufficiency (AI) is reported in critically ill patients with cirrhosis and is associated with increased mortality. It is unclear if AI is an underlying condition or triggered by critical events (e.g. sepsis). We investigated AI in cirrhosis without infection or hemodynamic instability.A total of 101 consecutive patients with cirrhosis were studied. AI was defined by a total serum cortisol (TC)18 μg/dl at 20 or 30 min after injection of 1 μg of tetracosactrin. Transcortin, calculated free cortisol (cFC), and free cortisol index (FCI) were assessed in a subgroup of 41 patients, with FCI12 representing normal adrenal function.AI was present in 38 patients (38%). Child score (median, 10 vs 7, p0.0001), MELD score (median, 17 vs 12, p0.0001), ascites (68% vs 37%, p0.01), basal TC (median,7.6 vs 14.9 μg/dl, p0.001), albumin (28 ± 0.8 vs 33 ± 0.7 g/L, p0.0001), INR (median, 1.6 vs 1.2, p0.0001), total bilirubin (median, 51 vs 31 μmol/L, p0.05), total cholesterol (median, 120 vs 142, p0.05), and LDL (median, 76 vs 81, p0.05) were significantly different between those with and without AI. ROC curves showed a basal TC ≤ 12.8 μg/dl to be a cut-off value closely associated with AI. The cFC was significantly related to TC for baseline values (R=0.94, p0.0001), peak values (R=0.90, p0.0001), and delta values (R=0.95, p0.0001), in patients with and without AI. However, no patient had a FCI12.AI defined by an abnormal response to 1 μg tetracosactrin is frequent in stable patients with cirrhosis, in the absence of infections or hemodynamic instability and is related to the severity of liver disease. However, evaluation of the true incidence of AI should comprise direct assays of free cortisol. Clinical consequences of AI need to be explored.

Received February 14, 2011; accepted May 9, 2011.Liver transplantation for hepatocellular carcinoma(HCC) and cirrhosis is complicated by the prognosis ofboth diseases. Although there is reasonable prognos-tic evidence for the likelihood of surviving cirrhosiswith and without liver transplantation, the issue withHCC is the likelihood of its recurrence as well as itsconsequences. For patients with HCC, there iscurrently only 1 drug (sorafenib) that has been shownto increase survival (in the pretransplant setting), andthe median increase is only 3 months.

We read with interest the article by Parkes et al in Gut 1 and fully agree with the authors' aims in evaluating the performance of a non-invasive marker of fibrosis, the enhanced liver fibrosis (ELF) test, with respect to clinically meaningful end points of liver-related complications and mortality. However, we believe that the methodology used is inappropriate and has led to potentially misleading conclusions. The authors have previously shown that ‘severe fibrosis’, i.e. stage 3 (‘bridging fibrosis’) and 4 (cirrhosis) in patients with non-alcoholic steatohepatitis is better predicted by an ELF panel score of 9.9–10.35.2 They also showed that ELF scores are not significantly different between different liver disease aetiologies. In this paper,1 they …

Introduction Adrenal Insufficiency (AI) defined by low dose short synacthen test (LDSST) in stable cirrhosis is frequent using serum total cortisol (TC). However no published data exist on directly measured plasma free cortisol (FC) after LDSST. Aim We prospectively assessed adrenal insufficiency defined by LDSST in stable cirrhosis using TC and FC. Method Patients with stable cirrhosis without shock and/or sepsis were prospectively studied using the LDSST. AI was defined by a peak-TC Results 78 consecutive patients with cirrhosis were studied (Viral: 16, Alcoholic: 41; other: 21). Basal TC (365±192 mmol/l) and peak TC (571±216 mmol/l) were significantly related to basal FC (26±24 nmol/l) and peak FC (53±34 nmol/l) respectively: for baseline values R=0.78, p Conclusion AI defined by LDSST is frequent in stable patients with cirrhosis, using both total cortisol and free cortisol criteria. However in patients with more advanced liver disease and/or low total cortisol level, discrepancy exists between the rates of diagnosis of AI using the total and free cortisol criteria. Thus in these patients AI should be confirmed by free cortisol measurement.

631 OUTCOME OF LIVER TRANSPLANTATION (LT) FOR HEPATOCELLULAR CARCINOMA (HCC) ACCORDING TO DIFFERENT TRANSPLANT CRITERIA: A META-ANALYSIS G. Germani, M. Garcovich, K. Gurusamy, C. Toso, G. Fede, E. Tsochatzis, A.K. Burroughs. The Royal Free Sheila Sherlock Liver Centre and Division of Surgery, University College London, Hepato-Pancreatico-Biliary and Liver Transplant Unit, University Department of Surgery, Royal Free Campus, UCL Medical School, London, UK; Services de Chirurgie Viscerale et Transplantation Hopitaux Universites de Geneve, Geneva, Switzerland E-mail: germani.giacomo@gmail.com

Background: Little is known on changes of replication of HCV replication during chemotherapy and on correlated hepatic flares. Aims: To evaluate changes in HCV-RNA load in plasma and PBMC of patients with onco-hematological diseases (OHD) during and after chemotherapy (CT). Methods: Thirty-six consecutive patients with OHD (21 with B-cell nonHodgkin Lymphoma, 9 chronic lymphocytic leukemia, 5 multiple myeloma and 1 Hodgkin Lymphoma), naive for CT, were enrolled: 8 were antiHCV/HCV-RNA positive (HCV-POS group) and 28 anti-HCV negative (HCV-NEG group). Twenty-three patients, 7 in HCV-POS and 16 in HCVNEG group, received Rituximab-based CT for 4-6 months. HCV-RNA was searched by a ultra-sensitive real time RT-PCR in Light Cycler 1.5 on plasma and PBMC samples collected before, during and after CT. Results: In all the 7 patients treated with Rituximab-based CT in the HCVPOS group, an increase in HCV load of at least of 1.5 log in plasma and of 1.1 in PBMC was observed during CT. A hepatic flare (increase in ALT> 4 times the previous values) occurred after CT discontinuation in these 7 patients; in the patient with cirrhosis the hepatic flare was associated with decompensation. The remaining patient in the HCV-POS group receiving Rituximab-sparing CT for chronic lymphocytic leukemia had cirrhosis, but she did not show an increase in HCV load, both in plasma and in the PBMC, nor a hepatic flare nor decompensation of liver disease. HCV-RNA was never detected in plasma and PBMC samples of the 28 patients in HCV-NEG group neither before, during nor after CT. Conclusion: HCV-RNA positive OHD patients treated with Rituximab show a consistent increase in HCV load under CT and develop a hepatic flare, lifethreatening in cirrhotic patients. None of 28 anti-HCV/HCV-RNA negative OHD patients became HCV-RNA positive during or after CT, excluding in patients under a consistent immune-suppression a reactivation and probably the presence of the so called “occult HCV replication”. OC-35

Background Alcohol is the most common cause of liver disease in the Western world today. Randomised clinical trials have addressed the question whether propylthiouracil has any efficacy in patients with alcoholic liver disease. Objectives The objectives were to assess the efficacy of propylthiouracil on mortality, clinical symptoms and complications, liver biochemistry, and liver histology in patients with alcoholic liver disease. Adverse events were also analysed. Search strategy The Cochrane Hepato-Biliary Group Controlled Trials Register (searched July 2001), The Cochrane Controlled Trials Register (Cochrane Library Issue 3, 2001), MEDLINE (January 1966 to July 2001), EMBASE (January 1985 to July 2001) were searched. These electronic searches were combined with full text searches. Manufacturers and researchers in the field were also contacted. Selection criteria Randomised clinical trials studying patients with alcoholic steatosis, alcoholic fibrosis, alcoholic hepatitis, and/or alcoholic cirrhosis were included. Interventions encompassed propylthiouracil at any dose versus placebo or no intervention. The trials could be double-blind, single-blind, or unblinded. The trials could be unpublished or published as an article, an abstract, or a letter and no language limitations were applied. Data collection and analysis All analyses were performed according to the intention-to-treat method. The statistical package (RevMan and MetaView) provided by the Cochrane Collaboration was used. The methodological quality of the randomised clinical trials was evaluated by components of quality and the Jadad-scale. Main results Combining the results of six randomised clinical trials including 710 patients demonstrated no significant effects of propylthiouracil versus placebo on mortality (Peto odds ratio (OR) 0.91, 95% confidence interval (CI) 0.59 to 1.40), liver related mortality (OR 0.78, 95% CI 0.45 to 1.33), complications of the liver disease (OR 1.14, 95% CI 0.58 to 2.24), or liver histology. Propylthiouracil was associated with a non significant trend towards an increased risk of non-serious adverse events (OR 1.49, 95% CI 0.74 to 2.99) and with the seldom occurrence of serious adverse events (leukopenia). Reviewer's conclusions This systematic review could not demonstrate any significant efficacy of propylthiouracil on any clinically important outcomes (mortality, liver related mortality, liver complications, and liver histology) of patients with alcoholic liver disease and propylthiouracil was associated with adverse events. Accordingly, there is no evidence for using propylthiouracil for alcoholic liver disease outside randomised clinical trials.