Little is known of national utilization practices and outcomes with ≥80y donors. Methods: Using UNOS registry data, all U.S. adult recipients of primary deceased donor LT from 2/05-1/12 were evaluated (n=36,318). Centers (n=132) were categorized based on the # of ≥80y livers transplanted: non- (n=95), low- (n=31, range: 1-7 grafts/center), and high-utilizers (n=6, range: 22-36 grafts/center). Regions (n=11) were categorized as low-, mid-, and high-MELD based on tertiles of median recipient LT-MELD. Cox models evaluated the effects of donor

age ≥80y on graft loss (death or re-LT). Cilomilast purchase Results: 244 ≥80y donor livers were transplanted. Donors ≥80y vs <80y differed by %female (63 vs 40%), %with diabetes (15 vs 11%) and/ or hypertension (73 vs 35%), %died of stroke (75 vs 42%), %donation

ACP-196 manufacturer after cardiac death (0 vs 5%), and %distributed nationally (33 vs 6%) [p<0.01 for all], but not by cold ischemia time (6.7 vs 6.6 hours; p=0.41). Recipients of ≥80y vs <80y livers were older (median 60 vs 55y), more likely to be female (42 vs 32%), less likely to have HCV (11 vs 27%), and had lower median laboratory LT-MELD (17 vs 20) [p<0.01 for all], but were similar for %hepatocellular carcinoma (18 vs 23%; p=0.07). Only 37/132 (28%) centers transplanted ≥80y livers, but 174/244 (71%) of the ≥80y livers were transplanted by 6 centers (high-utilizers), accounting for 2-8% of each center's total transplant volume; 3, 2, and 1 centers were in high-, mid-, and low-MELD regions, respectively. The adjusted hazard ratio (aHR) for graft loss

of ≥80y livers was 1.15 (95% CI 0.93-1.43; p=0.20). Low- and high-utilizers did not differ in graft survival of ≥80y livers (aHR 1.88, 95% CI 0.85-4.13, p=0.12). Overall graft survival of ≥80y vs <80y livers was 88% vs 91% at 3 months selleck inhibitor (p=0.07), 75% vs 79% at 1y (p=0.14), and 48% vs 47% at 3y after LT (p=0.67). Re-LT occurred in 7% and 5% recipients of ≥80y vs <80y livers (p=0.01); %re-LT for ≥80y graft recipients did not differ between low- and high-utilizers (7 vs 7%; p=0.97). Among ≥80y grafts that failed within 1y of LT, only recipient LT-MELD score predicted failure (OR 1.05 per MELD point, 95% CI 1.01-1.09; p=0.03). Conclusion: The vast majority of ≥80y donor livers are accepted and transplanted by only 6 U.S. LT centers. Graft survival with ≥80y livers was acceptable and did not vary by center experience with ≥80y donors. Codification of objective selection criteria may increase utilization of older donors while maintaining the currently observed post-LT outcomes. Disclosures: The following people have nothing to disclose: Suzanne R. Sharpton, Sandy Feng, Jennifer C.

As illustrated in Fig. 1, a range of CCrs12979860 genotype frequencies may evolve in patients with chronic HCV infection; this depends on the frequencies in uninfected subjects and

the rates of spontaneous resolution of infection. However, from this figure, it is obvious that a 67% CC genotype rate at rs12979860 should not develop in an uninfected population Panobinostat with a 45% CC genotype rate, as reported for HCV genotype 2/3 by Montes-Cano et al.,4 unless the clearance rate in patients carrying a non-CC genotype is higher than that in the CC genotype group. An alternative explanation might be that, for epidemiological reasons, HCV genotype 2/3 preferentially spreads in populations with higher frequencies of the CC genotype. We propose that these putative mechanisms should be explored, although, as suggested by Montes-Cano et al., a positive selection on the basis of unknown

virological or biological phenomena might also explain the high frequency of the CC genotype in patients with genotype 2/3. Magnus Lindh M.D.*, Martin Lagging M.D.*, Gunnar Norkrans M.D.*, Kristoffer Hellstrand M.D.*, * Department of Infectious Diseases, University of Gothenburg, Gothenburg, Sweden. “
“A young woman, aged 19, presented to the Emergency Department with abdominal pain and gastrointestinal bleeding. Pain had been present for 4 days and, on the day of admission, she had episodes of nausea and vomiting. Subsequently, check details she Sirolimus supplier began to vomit blood and also developed melena. She had been previously diagnosed with a hypercoagulable state resulting from a JAK-2 mutation and was known to have portal vein thrombosis with extension of the thrombosis into the splenic and superior mesenteric veins. She had also been previously diagnosed with esophageal varices but had not had episodes of gastrointestinal bleeding. She ceased treatment with warfarin 1 month prior to admission but restarted the drug after the onset of abdominal pain. Blood tests revealed a hemoglobin

of 7.6 g/dL (76 g/l) with an international normalized ratio (INR) of 2.1. After fluid resuscitation and the correction of coagulopathy, upper gastrointestinal endoscopy was performed. Esophageal varices of moderate size were present but did not appear to be responsible for bleeding. However, there was a bleeding lesion in the duodenal cap that seemed likely to be related to a duodenal varix (Figure 1). A contrast-enhanced computed tomography scan showed extensive thromboses in the portal venous system with the formation of a portal cavernoma. An endoscopic ultrasound study confirmed the presence of periduodenal varices (Figure 2) and a subsequent angiogram confirmed the presence of extensive portal thromboses with large intra-abdominal collaterals that precluded treatment with a transjugular intrahepatic portosystemic shunt.

As illustrated in Fig. 1, a range of CCrs12979860 genotype frequencies may evolve in patients with chronic HCV infection; this depends on the frequencies in uninfected subjects and

the rates of spontaneous resolution of infection. However, from this figure, it is obvious that a 67% CC genotype rate at rs12979860 should not develop in an uninfected population Small molecule library with a 45% CC genotype rate, as reported for HCV genotype 2/3 by Montes-Cano et al.,4 unless the clearance rate in patients carrying a non-CC genotype is higher than that in the CC genotype group. An alternative explanation might be that, for epidemiological reasons, HCV genotype 2/3 preferentially spreads in populations with higher frequencies of the CC genotype. We propose that these putative mechanisms should be explored, although, as suggested by Montes-Cano et al., a positive selection on the basis of unknown

virological or biological phenomena might also explain the high frequency of the CC genotype in patients with genotype 2/3. Magnus Lindh M.D.*, Martin Lagging M.D.*, Gunnar Norkrans M.D.*, Kristoffer Hellstrand M.D.*, * Department of Infectious Diseases, University of Gothenburg, Gothenburg, Sweden. “
“A young woman, aged 19, presented to the Emergency Department with abdominal pain and gastrointestinal bleeding. Pain had been present for 4 days and, on the day of admission, she had episodes of nausea and vomiting. Subsequently, selleck kinase inhibitor she Hydroxychloroquine chemical structure began to vomit blood and also developed melena. She had been previously diagnosed with a hypercoagulable state resulting from a JAK-2 mutation and was known to have portal vein thrombosis with extension of the thrombosis into the splenic and superior mesenteric veins. She had also been previously diagnosed with esophageal varices but had not had episodes of gastrointestinal bleeding. She ceased treatment with warfarin 1 month prior to admission but restarted the drug after the onset of abdominal pain. Blood tests revealed a hemoglobin

of 7.6 g/dL (76 g/l) with an international normalized ratio (INR) of 2.1. After fluid resuscitation and the correction of coagulopathy, upper gastrointestinal endoscopy was performed. Esophageal varices of moderate size were present but did not appear to be responsible for bleeding. However, there was a bleeding lesion in the duodenal cap that seemed likely to be related to a duodenal varix (Figure 1). A contrast-enhanced computed tomography scan showed extensive thromboses in the portal venous system with the formation of a portal cavernoma. An endoscopic ultrasound study confirmed the presence of periduodenal varices (Figure 2) and a subsequent angiogram confirmed the presence of extensive portal thromboses with large intra-abdominal collaterals that precluded treatment with a transjugular intrahepatic portosystemic shunt.

Results: Complete data were available in 301 patients with cirrhosis (cryptogenic n = 94, non-cryptogenic n = 207). Patients with cryptogenic cirrhosis were older (mean selleck chemical age 66.4 vs. 60.7, p < 0.0001), had more females (43.6% vs. 26.6%, p = 0.003), less severe disease severity (Child Pugh C 8.5% vs 15.9%, p = 0.042) and a higher prevalence of the metabolic syndrome (83% vs. 51.2%, p < 0.0001)

compared with non-cryptogenic cirrhosis. During the 5-year study period, adults with cryptogenic cirrhosis had a longer total hospital admission stay compared to non-cryptogenic cirrhosis (median 10.5 vs 8 days, p = 0.08). Further analysis demonstrated a longer hospital admission duration for cryptogenic cirrhosis due to non-liver related morbidity (median 19.0 days vs. 13.0 days, p = 0.04), rather than liver related morbidity (median 14.0 days vs 11.0 days, p = 0.06). A higher proportion of stroke (6% vs 2%, p = 0.02) and cardiovascular disease (6% vs 3%, p = 0.05) were responsible for the increased hospitalization for non-liver related morbidity in

cryptogenic compared to non-cryptogenic cirrhotic patients. Kaplan-Meier survival analysis showed no significant difference in survival between both types of cirrhosis during the period of study (Log rank statistic 0.56). Conclusion: Cryptogenic Sotrastaurin cirrhosis is associated with an increased morbidity, but not mortality, compared to non-cryptogenic cirrhosis. This difference is due to a greater burden of non-liver related complications in the selleck chemicals former. Key Word(s): Na Presenting Author: KALAIYARASI KALIYAPERUMAL Additional Authors: Na Corresponding Author: KALAIYARASI KALIYAPERUMAL Affiliations: Tan Tock Seng Hospital Objective: We present a 57 year old gentleman, who has liver cirrhosis from likely chronic systemic iron overload, haemolysis and iron deposition due to a rare form of non transfusion dependant thalassaemia. His medical problems include hypergonadotrophic hypogonadism, osteoporosis and subclinical hypothyroidism. He had never undergone any blood or blood product transfusions in the past. He is a teetotaller. On physical examination he had

short stature, bronze skin, scleral icterus and multiple stigmata of chronic liver disease with hepatosplenomegaly. He had biochemical evidence of hemolysis and iron overload in addition to raised aspartate aminotransferase and unconjugated hyperbilirubinemia. Investigations done to rule out other causes of liver cirrhosis was negative in particular HFE gene mutation analysis (C282Y and H63D mutations were not detected). An ultrasound of the liver showed coarsened liver echo texture and nodular surface outline. Fibroscan stiffness reading was 27.4 kPa. Oesophagogastroduodenoscopy (OGD) showed the presence of portal hypertensive gastropathy. DNA sequence analysis revealed a rare IVSInt1 mutation in his Beta globin gene, forming an extremely rare and unusual compound heterozygote for a Beta globin and an unknown HPFH thalassaemia mutation.

The presence of a membrane in the inferior vena cava also influences therapy as many of these patients are treated by dilatation of the inferior vena cava rather than surgical shunts or transjugular intrahepatic portosystemic shunts (TIPS). In the patient illustrated below, membranous obstruction of the inferior vena cava was associated with vascular collaterals that resulted in an unusual appearance on a chest radiograph. A 42-year-old woman was investigated because of fatigue, mild dyspnea

and a 3-month history of peripheral edema. Physical examination revealed two varicose vessels on her left back. A chest radiograph showed an abnormality in the left lower lobe of her lung that raised the possibility of lung cancer (Figure 1). However, a Doppler ultrasound study and an abdominal computed tomography scan showed a narrow segment between the inferior RAD001 in vitro vena cava and the right atrium consistent with a Budd-Chiari syndrome. The diagnosis was confirmed by angiography that demonstrated complete

obstruction of the inferior vena cava (arrowhead) and CHIR-99021 price the formation of numerous collateral vessels (1 represents the inferior vena cava; 2, left renal vein; 3, ascending lumbar vein; 4, left subphrenic vein; 5, right subphrenic vein) as shown in Figure 2. A dilated cardiac septal vein (arrow) created the abnormality on the chest radiograph. This vein was linked to the left subphrenic vein in the cardiac septum and entered into the superior vena cava through the left brachiocephalic vein. After balloon dilatation of the inferior vena cava, blood was shown to enter the right atrium and pressure in the inferior vena cava fell from 16 mmHg to 9 mmHg. Various investigations did not reveal a hypercoagulable state. Treatment resulted in improvement in symptoms and a reduction in the size of the abnormality on the chest radiograph. Contributed by “
“To the Editor: We read with great interest the practice guidelines for the diagnosis and selleck inhibitor management of autoimmune hepatitis recently issued by the American Association for the Study of Liver Diseases

(AASLD).1 In particular, we appreciate the new definition of biochemical remission, which now requires not only normal bilirubin and gamma-globulin levels but also normal serum aminotransferases; this is at variance with the 2002 definition,2 which considers aminotransferase levels lower than twice the upper limits of normal to be sufficient. According to the 2002 criteria, nearly 80% of patients with autoimmune hepatitis enter remission within 3 years. The recently coined new definition will result in a tremendous change in the rate of response to immunosuppressive treatment for autoimmune hepatitis. Here we present our own experience, which has already been published in part,3 and compare the different response rates according to the 2002 and 2010 definitions of remission.

The presence of a membrane in the inferior vena cava also influences therapy as many of these patients are treated by dilatation of the inferior vena cava rather than surgical shunts or transjugular intrahepatic portosystemic shunts (TIPS). In the patient illustrated below, membranous obstruction of the inferior vena cava was associated with vascular collaterals that resulted in an unusual appearance on a chest radiograph. A 42-year-old woman was investigated because of fatigue, mild dyspnea

and a 3-month history of peripheral edema. Physical examination revealed two varicose vessels on her left back. A chest radiograph showed an abnormality in the left lower lobe of her lung that raised the possibility of lung cancer (Figure 1). However, a Doppler ultrasound study and an abdominal computed tomography scan showed a narrow segment between the inferior learn more vena cava and the right atrium consistent with a Budd-Chiari syndrome. The diagnosis was confirmed by angiography that demonstrated complete

obstruction of the inferior vena cava (arrowhead) and Everolimus the formation of numerous collateral vessels (1 represents the inferior vena cava; 2, left renal vein; 3, ascending lumbar vein; 4, left subphrenic vein; 5, right subphrenic vein) as shown in Figure 2. A dilated cardiac septal vein (arrow) created the abnormality on the chest radiograph. This vein was linked to the left subphrenic vein in the cardiac septum and entered into the superior vena cava through the left brachiocephalic vein. After balloon dilatation of the inferior vena cava, blood was shown to enter the right atrium and pressure in the inferior vena cava fell from 16 mmHg to 9 mmHg. Various investigations did not reveal a hypercoagulable state. Treatment resulted in improvement in symptoms and a reduction in the size of the abnormality on the chest radiograph. Contributed by “
“To the Editor: We read with great interest the practice guidelines for the diagnosis and selleckchem management of autoimmune hepatitis recently issued by the American Association for the Study of Liver Diseases

(AASLD).1 In particular, we appreciate the new definition of biochemical remission, which now requires not only normal bilirubin and gamma-globulin levels but also normal serum aminotransferases; this is at variance with the 2002 definition,2 which considers aminotransferase levels lower than twice the upper limits of normal to be sufficient. According to the 2002 criteria, nearly 80% of patients with autoimmune hepatitis enter remission within 3 years. The recently coined new definition will result in a tremendous change in the rate of response to immunosuppressive treatment for autoimmune hepatitis. Here we present our own experience, which has already been published in part,3 and compare the different response rates according to the 2002 and 2010 definitions of remission.

The pharmacokinetics of sumatriptan and naproxen did not differ according to whether sumatriptan/naproxen sodium was administered during a migraine attack or a migraine-free period. The pharmacokinetics of 2 sumatriptan/naproxen sodium tablets administered 2 hours apart were consistent with the pharmacokinetic predictions from a single dose of the combination tablet.

The adverse-event profile of the sumatriptan/naproxen sodium combination tablet did not appear to differ from that of the individual components of the same or similar Natural Product Library screening dosage strengths administered alone or in combination. In addition, the incidence of adverse events with 2 sumatriptan/naproxen sodium tablets administered 2 hours apart was lower than that with the single dose. Conclusion.— The combination tablet of sumatriptan/naproxen sodium has unique pharmacokinetic properties. The rapid absorption of sumatriptan with the delayed-release properties of naproxen sodium from sumatriptan/naproxen sodium might contribute to its therapeutic advantage over monotherapy with either component. No clinically meaningful effects of food, administration during a migraine attack, or administration of a second tablet (2 hours after initial dose) on the pharmacokinetics or safety

of sumatriptan/naproxen sodium were observed. “
“The trigeminal autonomic cephalalgias (TACs) are a group of primary headache disorders that feature short duration, repetitive attacks of severe unilateral head pain accompanied by prominent ipsilateral cranial autoniomic features. The TACs likely have a strong genetic determination, most evidently demonstrated by Trichostatin A several cluster headache studies. Key insights into their pathophysiology are derived from the cranial distribution of the pain, prominence of cranial autonomic features, attack patterns,

and distinctive therapeutic responses. These aspects are explored with regard to studies of the trigeminovascular system, selleck the trigeminal-autonomic reflex, the neuroendocrine system, functional neuroimaging, and various treatments used in clinical practice. “
“A small case series is presented of preadolescent patients with indomethacin-responsive headache. Preadolescent indomethacin-responsive headache is a rare and poorly understood entity, with few published cases in the literature. Two young children had similar presentations of indomethacin-responsive headaches. Both patients experienced frequent paroxysmal episodes of sudden-onset severe frontal or temporal head pain. The events lasted seconds to minutes in duration, and varied in frequency ranging from multiple episodes per week to multiple events per day. There were no associated autonomic or migrainous symptoms, and a comprehensive work-up revealed no secondary causes for the debilitating headaches. Both patients had dramatic clinical improvement with indomethacin.

To test the direct effects of α-GalCer on liver damage, mice were injected with α-GalCer only (group name: α-GC) or α-GalCer and then CFA/IFA without 2-OA-BSA (group name: α-GC/CFA) throughout the protocol. Sera were obtained on all mice at 4 and 12 weeks postimmunization and titers of immunoglobulin M (IgM) and IgG anti-PDC-E2 autoantibodies were measured by enzyme-linked immunosorbent assay (ELISA). All mice were sacrificed at either 4 or 12 weeks postimmunization and thence examined for liver histopathology, including mononuclear cell phenotypes. Furthermore, to confirm XAV-939 clinical trial the biologic effects of α-GalCer administration, a nested group of mice were assayed 24 hours after

the α-GalCer injection for cytokine production and liver DC phenotypes. Sera from the same mice were also collected at times 0, 2, 6,

10, 24, and 48 hours following the α-GalCer injection and analyzed for serum levels of interferon gamma (IFN-γ) and IL-4 by ELISA. All experiments were performed following approval of the Animal Welfare Committees of National Taiwan University and the University of California at Davis. The methodology for all of the surrogate readouts are described below. Serum titers of IgM and IgG anti-PDC-E2 autoantibodies were measured by ELISA using our well-standardized recombinant autoantigens, including the use of positive and negative controls. Briefly, purified recombinant PDC-E2 at 1 μg/mL in carbonate buffer (pH 9.6) was coated onto ELISA plates at 4°C overnight. After blocking with 1% casein (Sigma-Aldrich) for 1 hour, diluted sera were added for see more 2 hours at room temperature. The ELISA plates were washed with PBS-tween 20 followed by the addition of horseradish peroxidase (HRP)-conjugated goat antimouse IgG (1:10,000, Zymed Laboratories, Carlsbad, CA) and IgM (1:10,000, Invitrogen,

Camarillo, CA). The plates were incubated for another hour and immunoreactivity was detected by measuring the optical density (O.D.) at 450 nm after exposure for 20 minutes to tetramethylbenzidine (TMB) substrate (R&D systems, Minneapolis, MN). Livers were perfused with PBS containing 0.2% BSA (PBS/0.2% BSA) (Sigma-Aldrich), passed through a 100-μm nylon mesh, and resuspended in PBS/0.2% BSA. The parenchymal selleck chemicals cells were removed as pellets after centrifugation at 100g for 1 minute and the nonparenchymal cells were washed in PBS/0.2% BSA three times (440 g, 5 minutes) to remove hepatocytes. Mononuclear cells were then isolated using Histopaque-1077 (Sigma-Aldrich). After centrifugation, collected cells were washed with PBS/0.2% BSA and viability of cells was confirmed by trypan blue dye exclusion. Cell numbers were determined by a hemacytometer (Hausser Scientific, Horsham, PA). Cell population and cytokine secretion of iNKT cells were measured by flow cytometry.

Of these patients, 340 subsequently developed HCC. The risk of HCC in patients with chronic HCV increased in proportion to BMI with a hazard ratio of 1.86 for overweight http://www.selleckchem.com/products/ch5424802.html patients and 3.10 for obese patients as compared to underweight patients.90 Recently, Konishi et al. published a study of a cohort of chronic HCV patients without a previous diagnosis of diabetes mellitus.91 The study demonstrated that the presence of diabetes mellitus, as evidenced by a positive 75 g oral glucose tolerance test, independently increased the risk of HCC development in patients with chronic HCV.91 NAFLD and its

associated risk factors appear to act synergistically with other conditions to promote HCC.92 The data suggesting that hepatic steatosis, obesity, and diabetes mellitus increase the risk of HCC development in chronic HCV strengthens the notion that they are risk factors for

the development of HCC in NASH. Treatment of these conditions related to NASH may decrease the risk of carcinogenesis associated with chronic HCV, and should be further evaluated. Multiple case reports of HCC in the setting of NASH have been published and reviewed in the literature (Table 3).8, 52, 57, 93-109 Male patients make up the majority of cases with a mean age at diagnosis of 66.7 (range = 45-82). The patients are typically older at presentation than patients with HCC related to other RG7420 manufacturer chronic liver diseases. This older age at presentation correlates to reports of older ages at presentation in patients with CC and HCC compared to alcohol-related, HBV-related, and HCV-related HCC controls.50 The majority of the patients with HCC in the setting of NASH also have underlying diabetes (64%), obesity (58%), or this website other manifestations of the metabolic syndrome which is consistent with previous findings. Patients typically have large, well-differentiated tumors at the time of presentation

which may be secondary to a delayed diagnosis. Up to 50% of patients have HCC at the time of initial referral, and rarely patients present with HCC in the absence of cirrhosis.8, 93, 94, 96, 101, 105-109 The fact that HCC can arise in the setting of NASH without underlying cirrhosis raises the interesting possibility that carcinogenesis can occur in NAFLD in the absence of advanced liver disease.108 Three recent case studies of patients with HCC in the setting of NASH support the findings of previous case reports.57, 107, 109 Hashizume et al. reviewed nine patients with HCC in NASH. The majority of patients were male and the median age of diagnosis was 71.5 years. All of the patients had diagnoses of diabetes, hypertension, or hypertriglyceridemia, and the majority showed clinical evidence of insulin resistance and the metabolic syndrome. Three of nine patients developed HCC without evidence of underlying cirrhosis. The review supports the associations of age, cirrhosis, diabetes, and obesity with the risk for HCC.107 Chagas et al.

Conclusion: QLFTs independently predict risk for future clinical outcomes. By improving risk assessment, QLFTs could enhance the noninvasive monitoring, counseling, http://www.selleckchem.com/products/Y-27632.html and management of patients with chronic HCV. (HEPATOLOGY 2012) Chronic hepatitis C virus (HCV) is a major cause of liver disease, cirrhosis, and hepatocellular carcinoma (HCC) in the United States and worldwide.1-4 Early detection of patients with significant hepatic impairment, who are at risk for future decompensation, is a priority of clinical management. Progression of liver disease is defined histologically by accumulation of fibrosis and physiologically by impairment

of hepatic function and blood flow. Increased Ishak fibrosis score5, 6 or increased hepatic venous pressure gradient (HVPG)7-9 indicate greater severity of liver disease and identify patients

at risk for future clinical complications. Quantifying fibrosis requires the performance of liver biopsy, and measuring HVPG is technically complex and requires catheterization of the jugular vein. Both liver biopsy and HVPG measurement learn more are associated with potentially severe complications, prone to sampling error, and may not be embraced by patients. Accurate noninvasive methods for staging of disease are needed. One noninvasive approach is to develop models based on clinical findings and standard blood tests. Child-Turcotte-Pugh (CTP) classification10 and model for end-stage liver disease (MELD) score11, 12 are, perhaps, the best known and most commonly applied. Both were developed to predict surgical mortality or mortality after transjugular intrahepatic portal-systemic shunt (TIPS) in patients with advanced cirrhosis. Neither are applicable to the patient with earlier-stage or clinically compensated disease.13 Other models target patients with compensated selleck inhibitor disease. The Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) Trial investigators developed a model based upon bilirubin, albumin, aspartate aminotransferase/alanine aminotransferase (AST/ALT), and platelet count.14

This model identified high-risk patients, 59% of whom developed clinical outcomes in 3.5 years of follow-up. But, the high-risk cutoff was insensitive; only 46% of the patients who eventually developed outcomes were identified. Hepatic elastography and serum fibrosis markers correlate with stage of fibrosis, as well as risk for cirrhosis or varices.15-18 In one study, hyaluronic acid, YKL-40, and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), combined with standard laboratory tests, were significantly associated with disease progression.18 Further studies of elastography and serum fibrosis markers in predicting future risk for clinical outcomes are needed to validate their prognostic value.