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- Josefsson, Axel, 1984, et al.
(författare)
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Impact of peri-transplant heart failure & left-ventricular diastolic dysfunction on outcomes following liver transplantation
- 2012
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Ingår i: Liver International. - : Wiley. - 1478-3231 .- 1478-3223. ; 32:8, s. 1262-1269
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Tidskriftsartikel (refereegranskat)abstract
- Background & Aims: Assess the prevalence of peri-transplant heart failure and its potential relation to post-transplant morbidity and mortality. Methods: A retrospective study was performed on 234 consecutive cirrhotic patients undergoing liver transplantation in a single European center from 1999 to 2007 (mean age 52, 30% women, 36% with alcoholic liver disease, 24% with viral hepatitis, 18% cholestatic liver disease). Left ventricular diastolic dysfunction was defined as E/A ratio <= 1. We used the Boston classification for heart failure to assess the prevalence of peri-transplant heart failure. Patients were followed up for a mean of 4 years post-transplant (0.5-9 years). Results: Eighteen per cent of patients demonstrated diastolic dysfunction pretransplant. During the peri-transplantation period highly possible heart failure occurred in 27%. In logistic regression analysis, heart failure was independently related to lower mean arterial blood pressure (OR 0.94, 95% CR 0.91-0.98) and prolonged corrected QT time on ECG (OR 9.10, 95% CI 3.77-21.93) pretransplant. Peri-transplant mortality amounted to 5%, and was independently related to heart failure (OR 15.11, 95% CI 1.76-129.62) and the peri-transplant need of dialysis (OR 14.18, 95% CI 1.65-121.89). Heart failure was also associated with longer stay in the intensive care unit and peri-transplant cardiac events (P < 0.05). Long-term transplant-free mortality was independently related to diastolic dysfunction at baseline (Hazard ratio 4.82, 95% CI 1.78-13.06). Conclusion: Heart failure occurs in approximately a quarter of patients with cirrhosis following liver transplantation and it is an independent predictor of mortality and morbidity.
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| 2. |
- Benito de Valle, Maria, et al.
(författare)
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Mortality and cancer risk related to primary sclerosing cholangitis in a Swedish population-based cohort.
- 2012
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Ingår i: Liver international : official journal of the International Association for the Study of the Liver. - : Wiley. - 1478-3231. ; 32:3, s. 441-448
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Tidskriftsartikel (refereegranskat)abstract
- Background: Population-based studies on the epidemiology of primary sclerosing cholangitis (PSC) are sparse. Aims: To investigate mortality and risk of cancer, and to identify risk factors for hepatobiliary cancer and the combined end-point liver related death or liver transplantation (OLT) in a population-based PSC cohort in Västra Götaland, Sweden. Methods: Primary sclerosing cholangitis cases were identified in diagnostic registries. Case validation and follow up was provided through individual review of case files and linkage to the Swedish Cancer and Cause of Death registries. Standardized mortality ratio (SMR) and standardized incidence ratio (SIR) for cancer were calculated in relation to the background population. Cox's proportional hazards analysis was used to calculate crude and adjusted relative risks (RRs). Results: A total of 199 PSC patients were identified between 1992 and 2005. SMR in the PSC cohort was 4.20 (95% confidence interval (CI), 3.01–5.69). SIR for hepatobiliary cancer, cholangiocarcinoma and colorectal cancer were 177 (110–271), 868 (505–1390) and 2.87 (0.33–10.4) respectively. Age (RR=1.25 (1.01–1.53) per decade), female gender (RR=2.01 (1.09–3.72)), cholangitis (RR=2.56 (1.20–5.64)) and bilirubin (RR=3.95 (1.96–10.75) highest vs lowest quartile) were associated with the risk of liver related death or OLT. Age was associated with the risk of hepatobiliary cancer (RR 1.40 (1.01–1.95) per decade). Conclusions: Primary sclerosing cholangitis was associated with a four-fold increase in mortality in this population-based study. In accordance with previous studies, the risk of hepatobiliary cancer was dramatically increased. However, the increased risk of colorectal cancer reported in previous studies could not be confirmed.
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| 5. |
- Burza, Maria Antonella, 1980, et al.
(författare)
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PNPLA3 I148M (rs738409) genetic variant and age at onset of at-risk alcohol consumption are independent risk factors for alcoholic cirrhosis
- 2014
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Ingår i: Liver International. - : Wiley. - 1478-3223 .- 1478-3231. ; 34:4, s. 514-520
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Tidskriftsartikel (refereegranskat)abstract
- Background & Aims Environmental and genetic factors contribute to alcoholic cirrhosis onset. In particular, age at exposure to liver stressors has been shown to be important in progression to fibrosis in hepatitis C individuals. However, no definite data on the role of age at onset of at-risk alcohol consumption are available. Moreover, patatin-like phospholipase domain-containing protein 3 (PNPLA3) I148M (rs738409) variant has been associated with alcoholic cirrhosis, but only in cross-sectional studies. The aim of this study was to investigate the role of age at onset of at-risk alcohol consumption and PNPLA3 I148M variant on alcoholic cirrhosis incidence. A total of 384 at-risk alcohol drinkers were retrospectively examined. The association among age at onset of at-risk alcohol consumption, PNPLA3 I148M variant and cirrhosis incidence was tested. A higher incidence of alcoholic cirrhosis was observed in individuals with an older (>= 24years) compared with a younger (<24) age at onset of at-risk alcohol consumption (P-value<0.001). Moreover, PNPLA3 148M allele carriers showed an increased incidence of cirrhosis (P-value<0.001). Both age at onset of at-risk alcohol consumption and PNPLA3148M allele were independent risk factors for developing cirrhosis (H.R. (95% C.I.): 2.76 (2.18-3.50), P-value<0.001; 1.53(1.07-2.19), P-value=0.021 respectively). The 148M allele was associated with a two-fold increased risk of cirrhosis in individuals with a younger compared with an older age at onset of at-risk alcohol consumption (H.R. (95% C.I.): 3.03(1.53-6.00) vs. 1.61(1.09-2.38). Age at onset of at-risk alcohol consumption and PNPLA3 I148M genetic variant are independently associated with alcoholic cirrhosis incidence.
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| 7. |
- Marschall, Hanns-Ulrich, 1954, et al.
(författare)
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Gallstone disease in Swedish twins is associated with the Gilbert variant of UGT1A1.
- 2013
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Ingår i: Liver international : official journal of the International Association for the Study of the Liver. - : Wiley. - 1478-3231. ; 33:6, s. 904-8
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND & AIMS: The Gilbert syndrome-associated functional TATA box variant UGT1A1*28 (A(TA)7 TAA) was found to increase susceptibility to pigment gallstone formation in patients with haemolytic anaemia. Further studies in extensive cohorts demonstrated an increased risk of this variant for cholesterol gallstone disease (GD). We now investigated this polymorphism as a determinant of symptomatic GD in Swedish twins. METHODS: The Swedish Twin Registry was merged with the Hospital Discharge and Causes of Death Registries and searched for GD-related diagnoses among monozygotic (MZ) twins living in the Stockholm area. In addition, we screened the TwinGene database for GD. In total, we found 44 MZ twin pairs with and eight MZ twins without GD to be evaluable. GD-free twins from TwinGene (109 concordantly MZ and 126 independent DZ) served as controls. UGT1A1*28 genotyping was performed using TaqMan assays. RESULTS: Overall, 58 and 8 of 106 twins with GD were hetero- and homozygous UGT1A1 risk allele carriers respectively. The case-control association tests showed a significantly (P<0.05) increased risk of developing GD (OR=1.62, 95% CI 1.00-2.63) in heterozygotes carriers and in addition, a trend (P=0.075) for an increased risk among carriers (OR=1.52, 95% CI 0.97-2.44) of the risk allele. CONCLUSION: These data from Swedish twins confirm the Gilbert variant as risk factor for GD. Our observation is in line with nucleation in bilirubin supersaturated bile representing an initial step in cholelithogenesis.
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| 10. |
- Thulin, Petra, et al.
(författare)
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Keratin-18 and microRNA-122 complement alanine aminotransferase as novel safety biomarkers for drug-induced liver injury in two human cohorts
- 2014
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Ingår i: Liver international (Print). - : Wiley. - 1478-3223 .- 1478-3231. ; 34:3, s. 367-378
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND & AIMS:There is a demand for more sensitive, specific and predictive biomarkers for drug-induced liver injury (DILI) than the gold standard used today, alanine aminotransferase (ALT). The aim of this study was to qualify novel DILI biomarkers (keratin-18 markers M65/M30, microRNA-122, glutamate dehydrogenase and alpha-foetoprotein) in human DILI.METHODS:Levels of the novel biomarkers were measured by enzyme-linked immunosorbent assay or real-time quantitative reverse-transcription PCR (qRT-PCR) in two human DILI cohorts: a human volunteer study with acetaminophen and a human immunodeficiency virus (HIV)/tuberculosis (TB) study.RESULTS:In the acetaminophen study, serum M65 and microRNA-122 levels were significantly increased at an earlier time point than ALT. Furthermore, the maximal elevation of M65 and microRNA-122 exceeded the increase in ALT. In the HIV/TB study, all the analysed novel biomarkers increased after 1 week of treatment. In contrast to ALT, the novel biomarkers remained stable in a human cohort with exercise-induced muscular injury.CONCLUSIONS:M65 and microRNA-122 are potential biomarkers of DILI superior to ALT with respect to sensitivity and specificity.
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