Incidence Of Liver Transplantation Research Articles

Impact of decompensated cirrhosis in children: A population-based study.

We describe the proportion of children with compensated cirrhosis who develop decompensation in Ontario, Canada over the past two decades. This is a retrospective population-based cohort study using routinely collected health care data from Ontario, Canada held at ICES during 1997-2017. Diagnosis of cirrhosis was made using validated ICES definition, and decompensation events were defined according to validated coding. Rates of decompensation, type of decompensation, and incidence of liver transplantation after decompensation were analyzed. Databases were linked at the individual level and analyzed at ICES-Queen's. A total of 2,755 children with compensated cirrhosis were included and 9% (253) developed decompensation over a median follow-up of 7 years. Children most likely to suffer decompensation were younger (median age 10 versus 4 years, p < 0.001) and female (45% versus 52%, p = 0.03). Ascites (137/253, 54%) was the most frequent complication. 199/2755 (7%) of children with cirrhosis received liver transplantation, of which 64% (128/199) occurred after a decompensation event. Overall, a total of 132 (4.7%) deaths occurred during the study period, with 55 deaths following a decompensating event. We present the first study to describe rates of decompensation, type, and rate of liver transplantation after decompensation in pediatric cirrhosis at the population level. To improve the care of children with liver disease, early detection of liver disease, early initiation of specific treatments as well as identification of children who are at risk of becoming decompensated are crucial.

Acute heart failure after liver transplantation: A narrative review.

Acute heart failure (AHF) is an under recognized yet potentially lethal complication after liver transplantation (LT) surgery. The increase in incidence of liver transplantation amongst high-risk patients and the leniency in the criteria for transplantation, predisposes these patients to postoperative AHF and the antecedent morbidity and mortality. The inability of conventional preoperative cardiovascular testing to accurately identify patients at risk for post-LT AHF poses a considerable challenge to clinicians caring for these patients. Even if high-risk patients are identified, there is considerable ambiguity in the candidacy for transplantation as well as optimization strategies that could potentially prevent the development of AHF in the postoperative period. The intraoperative and postoperative management of patients who develop AHF is also challenging and requires a well-coordinated multidisciplinary approach. The use of mechanical circulatory support in patients with refractory heart failure has the potential to improve outcomes but its use in this complex patient population can be associated with significant complications and requires a stringent risk-benefit analysis on a case-by-case basis.

S1175 Clinical Response to Treatment for Acute Kidney Injury (AKI) in Patients With Cirrhosis

INTRODUCTION: The development of acute kidney injury (AKI) is associated with increase in morbidity/mortality in patients with cirrhosis. Revised ICA criteria now classify AKI into three stages (1: Cr increase by 0.3 mg/dl or 50–100% increase from baseline; 2: Cr increase by 100-200%;3: Cr increase by > 200% or Cr > 4 mg/dl) with management based on stage and response to therapy. AIM: To characterize cirrhotic patients admitted with AKI and response to therapy based on ICA AKI stages. METHODS: Retrospective study of inpatients with cirrhosis at single center from 1/2015–05/2019 who received treatment for AKI. Treatment was administered at the discretion of the treating hepatologist and included volume expansion (VE; albumin, lactated ringer, normal saline), vasoconstrictors (VC; midodrine or norepinephrine), and octreotide. Progression and regression of AKI and incidence of liver transplant were analyzed. RESULTS: One hundred seventy-nine patients (97M, 82F, mean age 59) were reviewed (40% Caucasians, 35% Hispanics, 9% Asians, 3% Black). Main cirrhosis etiologies included alcohol (36%), HCV (19%), NASH (11%), cryptogenic (8%) and others. At presentation mean MAP was 69 mmHg and mean Na MELD 31. Mean serum values included Na 130 mEq/l, TB 9 mg/dl, creatinine 2.0 mg/dL, INR 2.0. 135/179 patients had AKI present at admission. 104 (58%) patients developed Stage 1, 43 (24%) developed Stage 2, 32 (18%) developed Stage 3 AKI. 69 patients received VE only, 110 patients received VC and VE (Table 1). In VC group, 37% remained in same stage AKI as at admission, 45% progressed to higher stage AKI, 18% regressed to lower AKI stage (Table 2). Peak stages of AKI were Stage 1 (18%), Stage 2 (16%), and Stage 3 (66%). In VE group, 39% developed regression of AKI, 39% had no change, 22% had progression. Peak stages of AKI were Stage 1 (38%), Stage 2 (23%), Stage 3 (39%). 34% received liver transplant, 49% died, 4% were LTFU, 13% alive. Patients who received VE for AKI had higher response to treatment (P < 0.05) compared to VC group. Patients with AKI stage 2 and stage 3 at admission had higher odds of remaining in same stage of AKI regardless of receiving vasoconstrictors (table 3). Patients with lower MAP at presentation had higher mortality rate (P = 0.002). CONCLUSION: Development of AKI is associated with high rate of mortality and need for LT. Regression to lower stage of AKI noted in 20/179 (11%) of patients receiving vasoconstrictors. The lowest response rates to VC were seen in those with Stage 3 AKI.Table 1Table 2Table 3

Targeting an Early and Substantial Increase in Mean Arterial Pressure Is Critical in the Management of Type 1 Hepatorenal Syndrome: A Combined Retrospective and Pilot Study

Appreciation of the central role for arterial vasodilatation in the pathogenesis of hepatorenal syndrome (HRS) has led to routine use of vasoconstrictors in combination with albumin as a medical therapy for HRS. Various vasoconstrictors have been explored but the optimal approach for such therapies has not yet been established. The purpose of this study was to examine the role of targeting an early and substantial increase in mean arterial pressure (MAP) in the management of type 1 HRS, a condition associated with very poor prognosis. A total of 59 patients with type 1 HRS who received a combination therapy of vasoconstrictors and albumin were enrolled into a retrospective cohort study. Subjects having a substantial increase of more than 10mmHg in MAP by day 3 after initiation of therapy were categorized as MAP responders and the rest as MAP non-responders. In addition, five patients were enrolled into a prospective pilot study in which a titration protocol of vasoconstrictors was followed to achieve early goal-directed therapy (EGDT). MAP responders achieved significantly higher incidence of treatment success or total response, less requirement of dialysis and more incidence of liver transplantation. More importantly, this response is associated with better short-term and long-term overall survival as well as transplant-free survival. The effectiveness of such an approach was further confirmed in the pilot study which followed an EGDT protocol. Using an early and substantial increase in MAP as a therapeutic target is associated with favorable clinical outcomes in the management of type 1 HRS.

Cytomegalovirus Infection After Liver Transplantation Incidence, Risks, and Benefits of Prophylaxis

Background Cytomegalovirus (CMV) infection and related disease is a feared complication after liver transplantation. Antiviral prophylaxis is recommended in clinical practice guidelines depending on the CMV status of both donor and recipient as well as the individual risk profile. Methods We retrospectively analyzed 211 liver transplant recipients with respect to the incidence of CMV infection after transplantation, the influence of donor and recipient CMV status, and the effect of antiviral prophylaxis. In addition, the underlying liver disease and immunosuppressive regimen were compared with the incidence of CMV infection. Patients were divided into 4 groups according to CMV donor/recipient (D/R) profile: group A (D−/R−) 28 patients (13.3%), group B (D−/R+) 64 patients (30.3%), group C (D+/R+) 79 patients (37.4%), and group D (D+/R−) 40 patients (19.0%). Results CMV infection was observed in 17.9%, 29.7%, 24.1%, and 22.5% of the patients, respectively, with no significant difference in infection rates between the groups. CMV infection occurred in 5 patients (17.9%) in the presumed low-risk profile (group A), despite an antiviral prophylaxis in 4 out of these 5 patients. In contrast, CMV infection occurred in only 9/40 patients (22.5%) in the presumed high-risk profile (group D). The most frequent infection rates were found in groups B and C (R+ groups). After successful treatment of CMV infection, no recurrence was detected. Underlying liver disease or immunosuppressive protocol had no influence on CMV infection. Conclusion Approximately one fourth of patients will acquire CMV infection after liver transplantation independent of donor/recipient status. Surprisingly, antiviral prophylaxis does not seem to be sufficient to reduce this proportion of patients, either in presumed high-risk or in presumed low-risk situations.

Steroids in the management of PBC: Why do we need them?

Steroids in the management of PBC: Why do we need them?

Drug-Induced Liver Injury: An Analysis of 461 Incidences Submitted to the Spanish Registry Over a 10-Year Period

Drug-Induced Liver Injury: An Analysis of 461 Incidences Submitted to the Spanish Registry Over a 10-Year Period

Drug-Induced Liver Injury: An Analysis of 461 Incidences Submitted to the Spanish Registry Over a 10-Year Period

Progress in the understanding of susceptibility factors to drug-induced liver injury (DILI) and outcome predictability are hampered by the lack of systematic programs to detect bona fide cases. A cooperative network was created in 1994 in Spain to identify all suspicions of DILI following a prospective structured report form. The liver damage was characterized according to hepatocellular, cholestatic, and mixed laboratory criteria and to histologic criteria when available. Further evaluation of causality assessment was centrally performed. Since April 1994 to August 2004, 461 out of 570 submitted cases, involving 505 drugs, were deemed to be related to DILI. The antiinfective group of drugs was the more frequently incriminated, amoxicillin-clavulanate accounting for the 12.8% of the whole series. The hepatocellular pattern of damage was the most common (58%), was inversely correlated with age (P < .0001), and had the worst outcome (Cox regression, P < .034). Indeed, the incidence of liver transplantation and death in this group was 11.7% if patients had jaundice at presentation, whereas the corresponding figure was 3.8% in nonjaundiced patients (P < .04). Factors associated with the development of fulminant hepatic failure were female sex (OR = 25; 95% CI: 4.1-151; P < .0001), hepatocellular damage (OR = 7.9; 95% CI: 1.6-37; P < .009), and higher baseline plasma bilirubin value (OR = 1.15; 95% CI: 1.09-1.22; P < .0001). Patients with drug-induced hepatocellular jaundice have 11.7% chance of progressing to death or transplantation. Amoxicillin-clavulanate stands out as the most common drug related to DILI.

Ursodeoxycholic acid for primary biliary cirrhosis.

Primary biliary cirrhosis is a rare autoimmune liver disease and an effective treatment has been difficult to establish. Some randomised clinical trials have found an effect of ursodeoxycholic acid for primary biliary cirrhosis. Evaluate the beneficial effects and adverse effects of peroral ursodeoxycholic acid for primary biliary cirrhosis versus placebo or no intervention. The Controlled Trials Register of The Cochrane Hepato-Biliary Group, The Cochrane Library, MEDLINE, EMBASE and the full text of the identified studies were searched until April 2001. The electronic searches were done by entering the search terms 'ursodeoxycholic acid', 'UDCA', 'primary biliary cirrhosis', and 'PBC'. Randomised clinical trials evaluating ursodeoxycholic acid administered perorally at any dose versus placebo or no intervention in patients with primary biliary cirrhosis diagnosed by any method. Only trials using an adequate method for randomisation were included, regardless of blinding and language. The methodologic quality of the randomised clinical trials was evaluated by components and the Jadad-score. The following outcomes were extracted: mortality, liver transplantation, pruritus, other clinical symptoms (jaundice, portal pressure, (bleeding) oesophageal varices, ascites, hepatic encephalopathy, hepato-renal syndrome, autoimmune conditions), liver biochemistry, liver function, liver biopsy findings, quality of life, and adverse events. All analyses were performed according to the intention-to-treat method. A total of 16 randomised clinical trials evaluating ursodeoxycholic acid against placebo (n = 15) or no intervention (n = 1) in 1422 patients were identified. The median Jadad-score was 3 (range 1-5). A number of trials described as double blind had problems with the blinding. Neither mortality (odds ratio = 0.94; 95% confidence interval (CI) 0.60 to 1.48), liver transplantation (odds ratio = 0.83; 95% CI 0.52 to 1.32), mortality or liver transplantation (odds ratio = 0.90; 95% CI 0.65 to 1.26), pruritus, fatigue, autoimmune conditions, quality of life, liver histology, or portal pressure were significantly affected by ursodeoxycholic acid (given in doses of 8-15 mg/kg/day for three months to five years). However, ursodeoxycholic acid significantly (P < 0.05) reduced ascites, jaundice, and biochemical variables such as serum bilirubin and liver enzymes. Ursodeoxycholic acid was not significantly associated with adverse events. Including data after patients had been switched onto open label ursodeoxycholic acid confirmed the findings regarding the lack of a significant effect of ursodeoxycholic acid on mortality and mortality or liver transplantation. A significant (P = 0.04) effect was, however, observed on the incidence of liver transplantation (odds ratio = 0.68; 95% CI 0.48 to 0.98). Ursodeoxycholic acid has a marginal therapeutic effect for primary biliary cirrhosis. On the positive side, ursodeoxycholic acid has few side effects. The general usage of ursodeoxycholic acid for primary biliary cirrhosis needs reevaluation.