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Background & Aims Subtle inter-patient genetic variation and environmental factors combine to determine disease progression in non-alcoholic fatty liver disease (NAFLD). Carriage of the PNPLA3 rs738409 c.444C >G minor allele (encoding the I148M variant) has been robustly associated with advanced NAFLD. Although most hepatocellular carcinoma (HCC) is related to chronic viral hepatitis or alcoholic liver disease, the incidence of NAFLD-related HCC is increasing. We examined whether rs738409 C >G was associated with HCC-risk in patients with NAFLD. Methods PNPLA3 rs738409 genotype was determined by allelic discrimination in 100 European Caucasians with NAFLD-related HCC and 275 controls with histologically characterised NAFLD. Results Genotype frequencies were significantly different between NAFLD-HCC cases (CC=28, CG=43, GG=29) and NAFLD-controls (CC=125, CG=117, GG=33) ( p =0.0001). In multivariate analysis adjusted for age, gender, diabetes, BMI, and presence of cirrhosis, carriage of each copy of the rs738409 minor (G) allele conferred an additive risk for HCC (adjusted OR 2.26 [95% CI 1.23–4.14], p =0.0082), with GG homozygotes exhibiting a 5-fold [1.47–17.29], p =0.01 increased risk over CC. When compared to the UK general population (1958 British Birth Cohort, n=1476), the risk-effect was more pronounced (GC vs. CC: unadjusted OR 2.52 [1.55–4.10], p =0.0002; GG vs. CC: OR 12.19 [6.89–21.58], p Conclusions Carriage of the PNPLA3 rs738409 C >G polymorphism is not only associated with greater risk of progressive steatohepatitis and fibrosis but also of HCC. If validated, these findings suggest that PNPLA3 genotyping has the potential to contribute to multi-factorial patient-risk stratification, identifying those to whom HCC surveillance may be targeted.

Background and aim: Non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) are both associated with insulin resistance. We assessed whether NAFLD is associated with impaired insulin sensitivity in PCOS women independently of age and total adiposity. Subjects and methods: We enrolled 14 young PCOS women with NAFLD, 14 women with PCOS alone and 14 healthy controls, who were matched for age, body mass index, and total body fat (by bio-impedance analyzer). NAFLD was diagnosed by the surrogate measure of abnormal serum alanine aminotransferase (ALT) concentrations (defined as ALT>19 U/l) after excluding other secondary causes of liver disease (alcohol, virus, and medications). Insulin sensitivity was measured by euglycemic hyperinsulinemic clamp. Results: Insulin sensitivity was markedly decreased (p

AIM To analyse the variations in branching patterns of the popliteal artery and infrapopliteal vessels using angiography. MATERIALS And METHODS Femoral angiograms of 1037 lower limbs in 568 patients were examined to assess the popliteal artery branching pattern. Variations of the infrapopliteal vessels supplying the foot were assessed in 662 limbs from the same cohort of patients. RESULTS Nine hundred and forty-one (90.7%) limbs had the usual branching pattern with anterior tibial artery (AT) arising first followed by the tibial–peroneal trunk (TPT), which then gives rise to the posterior tibial (PT) and peroneal (PR) arteries. Variations in popliteal branching pattern were seen in 96 (9.3%) limbs. The commonest variation is high origin of the AT in 47 (4.5%) limbs or trifurcation of the popliteal artery in 33 (3.2%) limbs with AT, PT and PR arising together with no true TPT. The course of AT with high origin either anterior or posterior to popliteus was almost equal [25 (2.4%) or 22 (2.1%) limbs, respectively]. Eleven limbs (1.1%) had high origin of PT and two (0.2%) had a high origin of the PR. Six hundred and fifty-five (99%) limbs had normal infrapopliteal vessels. Seven (1%) had hypoplasia–aplasia of the infrapopliteal vessels. Five (0.8%) limbs had a hypoplastic PT with the remaining 2 (0.2%) having either a hypoplastic–aplastic AT or hypoplasia–aplasia of both AT and PT. CONCLUSION Variations in the branching of the popliteal artery occur in about 10% of patients. Knowledge of these variations is important because of the potential consequences for the management of peripheral vascular disease.

To investigate whether interindividual variation in CYP2E1 levels can be explained by genetic polymorphism, we analysed DNA samples from 40 healthy individuals by single-strand conformational polymorphism analysis for polymorphisms in the CYP2E1 coding sequence and promoter region. DNA sequencing of samples showing mobility shifts on single-strand conformational polymorphism detected polymorphisms at positions -316 (A to G), -297 (T to A), -35 (G to T), 1107 (G to C; intron 1), 4804 (G to A Val179Ile; exon 4) and 10157 (C to T; exon 8). All individuals positive for either A(-316)G, G(-35)T, G(4804)A or the previously described RsaI polymorphism at -1019 were also positive for T(-297)A, which had the highest allele frequency of the observed polymorphisms (0.20). A(-316)G, G(-35)T and G(4804)A were detected at allele frequencies of 0.022, 0.052 and 0.013, respectively. The functional significance of the upstream polymorphisms was examined by preparing constructs of positions -549 to +3 of CYP2E1 containing the observed combinations of the polymorphisms fused to luciferase reporter genes and transfecting HepG2 cells. For the G(-35)T/T(-297)A construct, a 1.8-fold increase in luciferase activity compared with the wild-type sequence (P = 0.06) and 2.5-fold compared with T(-297)A only (P = 0.025) was observed. No significant difference in activity was observed between the other constructs. The significance of the predicted Val179Ile base change from G(4804)A was determined by expression of the wild-type and mutated full length cDNAs in lymphoblastoid cells. No significant difference in kinetic constants for chlorzoxazone hydroxylation between mutant and wild-type was observed. In summary, this study demonstrated six novel CYP2E1 polymorphisms, including three upstream of the promoter, but with the possible exception of G(-35)T, none appeared to be of functional significance.

Available evidence supports the concept that alcoholic liver disease (ALD) is a multifactorial disease with a heritable component. A number of polymorphic genes with small and additive effects will thus encode susceptibility to this ‘polygenic’ disease. Molecular genetic studies of ALD are in their infancy, and methods available for the genetic dissection of complex traits are discussed. Some candidate genes have been identified, and studies have been undertaken to test for association between specific alleles and ALD susceptibility. There is evidence to support a role for alleles of two genes encoding enzymes involved in the oxidative metabolism of alcohol (acetaldehyde dehydrogenase2∗2 and cytochrome P4502E1 c2 allele) in susceptibility to ALD. More recently, attention has focused on cytokines, and there are now data showing association of specific alleles of both tumour necrosis factor alpha and interleukin-10 with predisposition to ALD. These candidate genes need to be subjected to rigorous evaluation in different populations. Such research should help to define more precisely the molecular mechanisms underlying the development of ALD in a sub-population (

Chronic HCV (hepatitis C virus)-associated cirrhosis represents a major indication for liver transplantation. Bile acids contribute to hepatic stellate cell activation as a key event in fibrogenesis. The aim of the present study was to investigate the role of bile acids and polymorphisms in bile acid level-regulating genes on fibrosis progression. A total of 206 subjects with chronic HCV infection were included for ABCB11 (ATP-binding cassette, subfamily B, member II) 1331T>C and NR1H4 (nuclear receptor) −1G>T genotyping, 178 of which were analysed for fibrosis stage. Exclusion criteria were HBV (hepatitis B virus) or HIV coinfection, alcohol >40 g/day and morbid obesity. A total of 358 patients with NAFLD (non-alcoholic fatty liver disease) were genotyped for comparison with a non-viral liver disease. Caucasian individuals (n = 110), undergoing liver resection for focal hepatic metastasis, served as controls. The ABCB11 1331C allele was significantly overrepresented in HCV patients compared with controls {allelic frequency 62.9%; OR (odds ratio), 1.41 [95% CI (confidence interval), 1.012–1.965]}. Median plasma bile acid levels were not significantly increased in the CC compared with TT genotype [7.2 (1–110) μmol/l compared with 3.5 (1–61) μmol/l; values are medians (range). A significant association between the presence of cirrhosis and ABCB11 genotype (CC compared with CT or TT, P=0.047) was observed in the χ2 test and independent of other risk factors of age, gender, body mass index and disease duration in multivariate analysis (P = 0.010). No such association could be observed in fatty liver patients with regard to advanced fibrosis (F≥2). The common ABCB11 1331CC genotype, which is present in 40% of HCV patients and renders the carrier susceptible to increased bile acid levels, is associated with cirrhosis.

Background/aimsThe aim of this study was to assess the effect of functional ENPP1(ectoenzyme nucleotide pyrophosphate phosphodiesterase 1)/PC-1 (plasma cell antigen-1) and IRS-1 (insulin receptor substrate-1) polymorphisms influencing insulin receptor activity on liver damage in non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, whose progression is associated with the severity of insulin resistance.Patients and methods702 patients with biopsy-proven NAFLD from Italy and the UK, and 310 healthy controls. The Lys121Gln ENPP1/PC-1 and the Gly972Arg IRS-1 polymorphisms were evaluated by restriction analysis. Fibrosis was evaluated according to Kleiner. Insulin signalling activity was evaluated by measuring phosphoAKT levels by western blotting in a subset of obese non-diabetic patients.ResultsThe ENPP1 121Gln and IRS-1 972Arg polymorphisms were detected in 28.7% and 18.1% of patients and associated with increased body weight/dyslipidaemia and diabetes risk, respectively. The ENPP1 121Gln allele was significantly associated with increased prevalence of fibrosis stage >1 and >2, which was higher in subjects also positive for the 972Arg IRS-1 polymorphism. At multivariate analysis, the presence of the ENPP1 121Gln and IRS-1 972Arg polymorphisms was independently associated with fibrosis >1 (OR 1.55, 95% CI 1.24 to 1.97; and OR 1.57, 95% CI 1.12 to 2.23, respectively). Both polymorphisms were associated with a marked reduction of ∼70% of AKT activation status, reflecting insulin resistance and disease severity, in obese patients with NAFLD.ConclusionsThe ENPP1 121Gln and IRS-1 972Arg polymorphisms affecting insulin receptor activity predispose to liver damage and decrease hepatic insulin signalling in patients with NAFLD. Defective insulin signalling may play a causal role in the progression of liver damage in NAFLD.

Objectives Report the New Zealand national experience of endovascular repair of acute traumatic thoracic aortic injuries (TTAIs). Design Retrospective analysis of the New Zealand thoracic aortic stent database between December 2001 and December 2007. Materials and methods Of the 134 patients on the database, 27 patients (20%) underwent endovascular repair of TTAI. Data collected included age, sex, cause of injury, details of the procedure, complications and mortality. Results Most patients were young, median age 20 (15–78), male (n = 19, 70%), and involved in motor vehicle accidents (n = 23, 85%). Median length of aorta stented was 117 mm (77–200 mm). Great vessel origins were covered intentionally in 23 (85%) patients, four (17%) requiring a hybrid procedure. Average procedure time was 98.3 min (35–180). Primary technical success was 96%, secondary technical success 100%. Endoleaks were observed in four (15%) patients, one requiring a second endovascular procedure. There were no conversions to open surgery. Procedure-related complications occurred in four (15%) patients. No patient developed cord injury. All cause mortality at 30 days is one (4%) and at discharge is two (7%) due to associated poly-trauma. Conclusion Our results add further evidence of the safety of endovascular repair of thoracic aortic injury and compare favourably with those of other centres.

Non-alcoholic fatty liver disease (NAFLD) is associated with an increased risk of cardiovascular disease in type 2 diabetes. Currently, there is a lack of information on associations between NAFLD and microvascular complications of diabetes. We assessed the associations between NAFLD and both chronic kidney disease (CKD) and retinopathy in a large cohort of type 2 diabetic individuals using a cross-sectional design.Prevalence rates of retinopathy (by ophthalmoscopy) and CKD (defined as overt proteinuria and/or estimated GFRor= 60 ml min(-1) 1.73 m(-2)) were assessed in 2,103 type 2 diabetic individuals who were free of diagnosed cardiovascular disease and viral hepatitis. NAFLD was ascertained by patient history, blood sampling and liver ultrasound.NAFLD patients had higher (p0.001) age- and sex-adjusted prevalence rates of both non-proliferative (39 vs 34%) and proliferative/laser-treated retinopathy (11 vs 5%), and CKD (15 vs 9%) than counterparts without NAFLD. In logistic regression analysis, NAFLD was associated with increased rates of CKD (odds ratio 1.87; 95% CI 1.3-4.1, p=0.020) and proliferative/laser-treated retinopathy (odds ratio 1.75; 1.1-3.7, p=0.031) independently of age, sex, BMI, waist circumference, hypertension, diabetes duration, HbA(1c), lipids, smoking status and medications use.Our findings suggest that NAFLD is associated with an increased prevalence of CKD and proliferative/laser-treated retinopathy in type 2 diabetic individuals independently of numerous baseline confounding factors. Further studies are required to confirm the reproducibility of these results and to evaluate whether NAFLD contributes to the development or progression of CKD and retinopathy.

Publisher Summary This chapter discusses the alcoholic liver disease. Alcohol was recognized to be a cause of liver damage by the ancient Greeks, and it is currently the most common cause of liver disease in the Western World. The magnitude and range of the health and socio-economic problems attributable to alcohol abuse are enormous. An appreciation of the absorption, distribution, metabolism and elimination of alcohol is critical to understanding the variety of biochemical disturbances that are commonly observed in alcoholic patients such as hyperuricemia, hyperlipidemia and hypoglycemia. Alcohol metabolism underlies several of the mechanisms considered to play a role in the pathogenesis of alcohol-related liver damage and some of the more recent explanations for interindividual susceptibility to alcoholic liver disease. Alcohol metabolism is discussed in terms of the fate of a unit of alcohol following ingestion. Chronic alcohol abuse produces a wide range of morphological changes in the liver, the most frequent being fatty liver, alcoholic hepatitis and cirrhosis. Biochemical and hematological tests can confirm the presence of alcohol abuse and indicate the presence of liver damage, however are not useful in determining the severity of the histological lesion.

Fuzzy logic controls are actively explored in an increasing number of manufacturing and process industries. The main goal is to improve manufacturing productivity. This paper is intended to fill the need of applying logical industrial control using fuzzy rules. With improved knowledge of fuzzy logic, users' interests and success rate of potential applications will grow. In this paper, we present idiosyncrasies of industrial control needs and understanding fuzzy logic for industrial controls. We then discuss the process of evolving applications and examples of industrial controls. Several justifications using fuzzy logic and practical ways to apply are presented. The overall goal is to increase successful applications of fuzzy logic controls in the manufacturing and process environment. >

Introduction The detection of non-alcoholic steatohepatitis (NASH) within non-alcoholic fatty liver disease (NAFLD) is important both for ascertaining prognosis and the stratification of patients for existing interventions and emerging therapies. Liver biopsy is considered the reference standard for assessing NASH. The aim of this study was to develop a biomarker of NASH which would be able to detect NASH prior to the development of significant hepatic fibrosis. Candidate biomarkers of hepatic inflammation, apoptosis and liver fibrosis were selected on the basis of biological plausibility and previous association with NAFLD. Method 172 patients with NAFLD and no evidence of other liver disease were consecutively recruited from two centres. 84 patients from the first centre were included as a training cohort and 88 patients from the second centre as a validation cohort. Liver biopsies were performed on all patients and scored using the NAFLD activity score (NAS). 36 patients with advanced fibrosis were excluded from the analysis. Serum samples were taken on all patients and tested for five matrix proteins (HA, P3NP, TIMP-1, Procollagen 4 and YKL-40) and 19 haematological and biochemical parameters including HOMA-IR. Stepwise multiple linear regression was used to determine the relationship of the multiple variables to the NAS score. Results A model combining terminal peptide of pro-collagen III (P3NP) and tissue inhibitor of matrix metalloproteinase 1 (TIMP-1) was found to significantly correlate with the NAS score in the training cohort (R=0.643, R2=0.413, p Conclusion This model appears to have good diagnostic performance for the detection of NASH in both the training and validation cohorts. Our results appear promising and if confirmed in further studies this model will be of clinical utility in detecting the minority of patients with NAFLD who have NASH and are at risk of developing progressive liver disease.

Introduction Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disease in many countries. There remains considerable uncertainty about natural history and prognosis. Few studies, totalling Methods Patients with 2 liver biopsies >1 year apart were identified from the Newcastle Hospitals NAFLD clinic. Clinical and laboratory data were collected from the time of liver biopsy. Results 108 patients (mean age 48 ± 12 years; 66% male; 48% diabetic) were identified with ≥2 liver biopsies (median interval 6.6 years, range 1.3–22.6). 81 (75%) patients had NASH and 27 patients with NAFL. Overall 45 (42%) patients had progression of fibrosis, 43 (40%) had no change in fibrosis, while 20 (18%) had fibrosis regression. The mean rate of fibrosis was 0.08 ± 0.25 stages/year overall, increasing to 0.29 ± 0.24 stages/year in progressors. Importantly, no significant difference in the proportion exhibiting fibrosis progression was found between those with NAFL or NASH at index biopsy (10/27 (37%) vs. 36/83 (43%) p = 0.65). 12/27 (44%) with NAFL at baseline progressed to NASH at follow-up biopsy, whereas 6/75 (8%) with NASH regressed to NAFL. Weight change was a significant factor associated with inter-biopsy change in disease activity measured by NAFLD activity score (r s, =0.23 p = 0.026). Of 10 patients with NAFL who had fibrosis progression, 3 progressed by 1 stage, 5 by 2 stages and 2 by 3 stages; all had NASH on the follow-up biopsy. Of concern, 6 of 27 (22%) patients with baseline NAFL had reached stage 3 fibrosis at the follow up biopsy, but none were cirrhotic. Among the patients with NAFL, 80% of those who had fibrosis progression were diabetic at the time of follow-up liver biopsy compared with 25% of non-progressors (p = 0.005). The FIB-4 score was the only significant baseline factor that predicted fibrosis progression (OR 2.1 [95% CI: 1.1–3.9], p = 0.02). However, the AUROC was only 0.63 (p = 0.04). Conclusion Contrary to current dogma, this study suggests that NAFL is not entirely benign and has the potential to progress to NASH and clinically significant fibrosis, particularly if patients develop diabetes. Disclosure of Interest None Declared.

We report the case of a 48-year-old man with neurofibromatosis presenting with sudden-onset abdominal pain, profound hypotension, and a drop in hemoglobin. CT scan demonstrated a massive hematoma within the right lobe of the liver with rupture into the peritoneal cavity. Angiography demonstrated diffuse abnormalities of the hepatic circulation with fusifom, ectatic, and stenotic segments. Acute extravasation from a peripheral branch of the right hepatic artery was identified and successfully embolized with subsequent hemodynamic stabilization of the patient. To the best of our knowledge this is the first case report of this kind in a patient with type I neurofibromatosis.

Methods: Male hepatocyte-specific Pten-deficient mice (AlbCrePten), which develop spontaneously steatohepatitis and HCC, fed Control Diet (CD) or High Fat Diet (HFD) were randomly divided between exercise and sedentary groups. The exercise groups run on a motorized treadmill for 60 min/day, 5 days/week during 32 weeks. At sacrifice, the body and liver weights were measured. The number and the size of nodules were registered. Livers and tumors were analysed by histology; steatosis and NAFLD activity score (NAS) were graded. Results: After 32 weeks of regular exercise, body weight, but not liver weight, was significantly reduced by exercise in CD-fed mice. No difference was observed in HFD-fed mice. Under CD, 71% of exercised mice developed nodules larger than 10mm vs. 100% in the sedentary group. The mean number of HCCs per liver was reduced by exercise (1.8±0.8 vs 2.8±2.3), as well as the total tumor volume per liver (444±551 vs 945±1007mm3). Under HFD, 50% of exercised and sedentary mice developed nodules. The mean number and the total number of HCCs per liver were similar in both groups (2.8±0.8 vs 2.8±0.8 and 484±474 vs 480±317mm3 respectively). Exercise did not affect steatosis in CD-fed mice (1.4±0.7 vs 1.6±0.8), but exercise reduced steatosis in HFD-fed mice (1.3±0.7 vs 2.3±0.7, p < 0.01). Exercise decreased the NAS in HFD-fed mice (2.1±1.2 vs 4.7±1.9, p < 0.03), but this effect was absent in CD-fed mice (2.2±0.1 vs 2.8±1.4). Conclusion: These data show a benefit of regular exercise on the development of HCC in an experimental model of NASH characterized by overactivation of the mTOR pathway. This beneficial effect was lost under high fat diet and independent of the improvement of NASH histology. The mechanisms underlying these effects remain to be determined. This research received funding from the European Community’s Seventh Framework Programme (FPZ/2007–2013).

Blood ethanol concentrations after separate oral dosing and intravenous infusion of ethanol (0.15 g/kg) were measured in 16 control subjects and 13 subjects treated with ranitidine. All subjects underwent routine upper gastrointestinal endoscopy. Peak blood ethanol concentrations, and area under the blood ethanol/time curve, were significantly higher in the ranitidine group after oral, but not intravenous, ethanol administration. The first pass metabolism, as calculated by the difference between the area under the curves, was significantly lower in the ranitidine group. In addition, all subjects withdrawn from ranitidine (n = 6) had a significant reduction in peak blood ethanol concentration and area under the curve after repeat dosing with oral ethanol. Both groups were well matched for age, sex, indications for endoscopy, findings at endoscopy, and gastric histology. These findings show that ranitidine increases the bioavailability of low dose ethanol and has possible short term forensic, and longterm physical implications for moderate drinkers who are taking the drug.

Introduction Alcoholic liver disease (ALD) is a significant and increasing threat to the health of the British population. It remains one of the commonest indications for liver transplantation and a leading cause of death. Despite this, the long term clinical course and predictive factors of survival in advanced ALD have not been well described. We aimed to identify factors that predict 15-year survival in out-patients with biopsy-proven advanced ALD. Methods Patients attending clinic in our institution during early 1996 (n=134) with biopsy proven advanced (stage III or IV) ALD were followed-up for 15 years or until death or transplantation. At baseline, clinical data including alcohol and smoking history, BMI and features of portal hypertension were recorded. Laboratory data (bilirubin, creatinine, sodium, PT, INR and platelet count) were collected. On biopsy, the presence of cirrhosis and histological features (fat severity, lymphocyte and neutrophil infiltration) were scored semi-quantitatively. Results Median age was 51 (29–67) and the majority (72%) were male. All patients had a history of alcohol excess (>80 g/day for men, 50 g/d for women). Patients were followed until death (n=97; median 62 m), OLT (n=5; median 96 m) or are still alive (n=32; median 187 m). Overall, the 5, 10 and 15-year survival was 64, 40 and 26%, respectively. Patient baseline characteristics are shown according to outcome (Abstract PWE-285 table 1). In multivariate analysis age (p=0.01), smoking (p=0.01), persistent drinking (p Conclusion In out-patients with biopsy-proven advanced ALD, clinical but not histological factors determine prognosis. Age, persistent alcohol intake, smoking habit and serum albumin are independent poor prognostic factors. Abstinence from alcohol and smoking cessation should be the priorities in the long-term management of ALD. Competing interests None declared.

Introduction The identification of fibrosis in patients with NAFLD is important for ascertaining prognosis and stratifying patients for emerging therapeutic interventions. Use of both direct marker panels (liver matrix components) and indirect marker panels (simple biochemical tests) have been described for the detection of fibrosis in NAFLD. The aim of this study was to compare the performance of direct and indirect serum marker panels in the detection of fibrosis in NAFLD as compared with liver biopsy. Methods From two centres, 177 patients were recruited and underwent percutaneous liver biopsy. Fibrosis staging was assessed using Kleiner criteria by two senior liver-histopathologists. Serum at the time of biopsy was used to calculate six indirect marker panels of fibrosis (APRI, BAAT, BARD, Cirrhosis discriminate score, NAFLD fibrosis index and Fib4). These panels were compared with the ELF Test (HA, TIMP1, PIIINP) and HA alone. Diagnostic accuracy was assessed using receiver operating characteristic curves which were compared using the method of DeLong. Results The distribution of fibrosis stages in the cohort were as follows: F0 39.5% (n=70), F1 19.2% (n=34), F2 17.5% (n=31), F3 13.6% (n=24), F4 10.2% (n=18). While ELF and HA alone had the best performance overall, the ELF test was better than HA in its ability to discriminate minimal fibrosis (p=0.02) and cirrhosis (p=0.06). All indirect serum markers tested had significantly worse performance than ELF in the detection of cirrhosis (p Conclusion In patients with NAFLD, direct serum marker panels have superior performance compared to indirect marker panels allowing superior stratification and prognostication. The performance of HA alone is enhanced by the addition of PIIINP and TIMP1. Competing interests None declared.

Type 1 collagen is the predominant collagen in cirrhotic livers. Each type 1 collagen molecule contains three subunits, two are identical (the α 1 chains) and the sequence of the third ( α 2 ) is very similar. They are encoded at the non-synthenic loci, COL1A1 and COL1A2 and restriction site dimorphisms have been described at each locus. Genetic factors have been invoked as a basis for increased susceptibility to alcoholic cirrhosis. One hypothesis is that genetically determined differences in type 1 collagen may be involved in this predisposition. We have examined this by analysing restriction fragment length polymorphisms at each type 1 collagen locus in leucocyte DNA from 56 unrelated patients with alcoholic cirrhosis and 74 local unrelated healthy controls. Based on the presence or absence of these restriction site dimorphisms four possible haplotypes were generated at COL1A1 and COL1A2 . We found no significant difference in allele frequencies between alcoholic cirrhotics and controls and, unlike a previous small study, we found no particular haplotype of either gene was associated with alcoholic cirrhosis. Our study provides no evidence for involvement of type 1 collagen structural genes in a genetic predisposition to cirrhosis in alcoholics.

Objectives To evaluate data in the New Zealand Thoracic Aortic Stent database to try and identify a scoring system that could predict 30-day mortality in patients undergoing stenting of the descending thoracic aorta (TEVAR). Design Retrospective analysis of the New Zealand thoracic aortic stent database between December 2001 and August 2007. Materials and methods The 30-day mortality of the 122 patients is 7.38% ( n = 9). Risk factors were recorded based on the Society of Thoracic Surgeons (STS) risk score. Glasgow aneurysm score was calculated and the pathology being treated analysed. Univariate analyisis was carried out. Results The mortality of three pathology groups was compared. 30-day mortality was 2.04% ( n = 1) in the elective aneurysm group, 17.95% ( n = 7) in the complicated Stanford type B dissection group, and 0% ( n = 0) in the trauma group. Thirty-day mortality is significantly higher in the dissection group compared with the elective aneurysm ( p = 0.02) and trauma ( p = 0.03) groups. The most frequent risk factors in the dissection group of patients were peripheral vascular disease, smoking and hypertension. Although percentage mortality is higher with increasing GAS, the results are not statistically significant ( p = 0.34). No independent risk factors were identified from the STS risk score data. Conclusion No specific risk score system seems to be able to predict mortality in TEVAR patients.