Hepatitis A virus (HAV) infections occur predominantly in children, and are usually self-limiting. However, 75-95% of the infections in adults are symptomatic (mostly with jaundice), with the illness symptoms usually persisting for a few weeks. Atypical manifestations include relapsing hepatitis, prolonged cholestasis, and complications involving renal injury. Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is a severe, drug-induced hypersensitivity reaction characterized by skin rash, fever, lymph-node enlargement, and internal organ involvement. We describe a 22-year-old male who presented with acute kidney injury and was diagnosed with prolonged cholestatic hepatitis A. The patient also developed DRESS syndrome due to antibiotic and/or antiviral treatment. To our knowledge, this is the first report of histopathologically confirmed DRESS syndrome due to antibiotic and/or antiviral treatment following HAV infection with cholestatic features and renal injury.
Background/Aims The nonspecific clinical presentation of acute hepatitis A (AHA) mandates the detection of anti-hepatitis A virus IgM antibodies (IgM anti-HAV) in the serum for obtaining a definitive diagnosis. However, IgM anti-HAV might not be present during the early phase of the disease. The aim of this study was to determine the optimal time for repeating the IgM anti-HAV test (HAV test) in AHA patients with a negative initial test. Methods In total, 261 patients hospitalized with AHA were enrolled for this retrospective study. AHA was diagnosed when the test for IgM anti-HAV was positive and the serum alanine aminotransferase (ALT) level was ≥400 IU/L. Repeat HAV test was conducted after 1-2 weeks if the initial HAV test was negative but AHA was still clinically suspected. Results The results of the initial HAV test were negative in 28 (10.7%) patients. The intervals from symptom onset to the initial-HAV-test day and from the peak-ALT day to the initial-HAV-test day were significantly shorter in the negative-initial-HAV-test group, but on multivariate analysis only the latter was significantly associated with negative results for the initial HAV test (β=-0.978; odds ratio [95% confidence interval]=0.376 [0.189-0.747]; P=0.005). The HAV test was positive in all patients when it was performed at least 2 days after the peak-ALT day. Conclusions The results of HAV tests were significantly associated with the interval from the peak-ALT day to the HAV-test day. The optimal time for repeating the HAV test in clinically suspicious AHA patients with a negative initial HAV test appears to be at least 2 days after the peak-ALT day.
Liver cirrhosis (LC) is a disease with a high rate of prevalence and one of the most common causes of mortality in the Republic of Korea (hereafter "Korea"). In Korea, the main etiologies of LC have been found to be chronic hepatitis B (CHB), alcohol, and chronic hepatitis C (CHC). In patients with complications such as ascites, variceal bleeding, and encephalopathy, the 5-year survival rates were 32%, 21%, and 40%, respectively, reflecting the poor prognosis of patients with LC. Consequently, a clinical practice guideline appropriate for the medical milieu of Korea is important for both patients and clinicians. In 2005, the Korean Association for the Study of the Liver established a guideline for the treatment of LC that is now widely used. However, it is currently necessary to revise and update the clinical practice guideline based on new evidence over the past 6 years regarding the diagnosis, treatment, and prevention of LC. Therefore, the Korean Association for the Study of the Liver undertook a revision and update of the clinical practice guideline co-organized by the Liver Cirrhosis Clinical Research Center. This guideline was based on an interdisciplinary (hepatology, radiology, pathology, and preventive medicine) approach. A panel of experts selected by the Korean Association for the Study of the Liver and Liver Cirrhosis Clinical Research Center met several times to discuss and write this guideline during 2005-2011. This guideline was written in light of published studies retrieved from MEDLINE, EMBASE, and Cochrane Library. The panel aimed to address 5 subjects: diagnosis of LC, anti-fibrotic therapy for LC, variceal bleeding, ascites, and hepatic encephalopathy. The evidence and recommendations made in this guideline have been graded according to the GRADE (Grading of Recommendations Assessment Development and Evaluation) system. The strength of evidence has been classified into 3 levels: A (high-quality evidence), B (moderate-quality evidence), and C (low-quality evidence). The strength of recommendation has been classified into 2 categories: strong and weak (Table 1). Where there was no clear evidence, the recommendations were based on the consensus expert opinion(s) in literature and that of the writing committee. Table 1 Grading evidence and recommendations 1. Diagnosis of LC LC is a pathologically defined disease, and is clinically classified as compensated and decompensated LC. Decompensated LC includes cases with ascites, variceal bleeding, hepatic encephalopathy, or jaundice. Image studies for diagnosing LC are CT, abdominal ultrasound, and MRI. Typical findings of these images are nodular liver surface, splenomegaly, and the presence of intra-abdominal collateral vessels, which mean increasing portal venous pressure. Although there are not established criteria for the diagnosis of compensated LC, imaging studies may be helpful for the diagnosis of LC b y integrating laboratory findings such as albumin, bilirubin, or prothrombin time and platelet values. 1-1. Diagnostic approach-patient history, physical examination, and laboratory tests When dealing with patients with LC, evaluation of the cause, severity, and stage is the first step. In patients with chronic liver disease, history taking (drug use, blood transfusion, or alcohol use), physical examination (jaundice, ascites, spider angioma, hepatomegaly, or splenomegaly), and symptom such as fatigue from hepatitis should be assessed. In patients with LC, a whole blood test including platelet count, liver function test (albumin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gamma glutamyl transpeptidase), prothrombin time, abdominal ultrasound, abdominal CT, and endoscopy should be carried out to confirm the presence or absence of cirrhosis. In addition, laboratory tests for hepatitis B or C virus infection are needed for the evaluation of its cause. Generally, the Child-Pugh score is used to assess the severity of LC. In clinical practice for the diagnosis of LC, findings of portal hypertension such as ascites, hepatic encephalopathy, or varices, imaging findings, and laboratory findings are common diagnostic tools. Recently, it was found that nodularity of the liver surface, a platelet count of less than 100,000/mm3, albumin less than 3.5 g/dL, and an international normalized ratio of 1.3 or more are related to the presence of LC. Presence of one condition of these findings showed a specificity of 90.42% and a sensitivity of 61.11%.1
Pegylated interferon and ribavirin combination therapy is accepted as the standard antiviral treatment for chronic hepatitis C regardless of HCV genotype. This combination therapy achieves higher response rates than previous therapy, but, nevertheless, a large proportion of patients suffer from treatment failure or adverse events. Recent clinical studies of viral kinetics during antiviral treatment have led to the introduction of response-guided therapy, the concept of 'customized therapy depending on viral response', which focuses on modulation of the treatment period depending on the viral response to create a sustained viral response without unnecessary medication and costs. New upcoming direct-acting antivirals (DAAs) maximize response rate, and triple therapy including DAAs along with pegylated interferon and ribavirin combination therapy could soon be the standard therapy. In this article, we reviewed the factors affecting treatment, response guided treatment, retreatment after failure of standard treatment, management of adverse events during treatment, and new treatment options.
BACKGROUND/AIMS:We aimed to determine the association between the co-expression patterns of Notch1, Snail, and p53 proteins (NSP) and the postoperative prognosis of hepatocellular carcinoma (HCC).METHODS:The immunoblot data for molecular expression (147 HCC/corresponding non-HCC tissues and 15 dysplastic nodules) and the sequencing data for p53 mutations (110 HCCs) were obtained from our previous study. Data analyses were restricted to cases with HCC differentiation grade III (n=47), due to its high p53 mutation rate.RESULTS:Nineteen of the 47 patients (40.4%) -comprising 12 in the liver and 7 in distant organs-had relapsed at 1-2 years after surgery. There was no relationship between p53 mutation and postoperative recurrence in the grade III HCCs. Seven (87.5%) of the eight relapsed cases with Notch1, Snail, and p53 (wild) co-expression experienced recurrence only within the liver, and all tumors were smaller than 5 cm in diameter. Extrahepatic relapse occurred mostly in HCC patients with tumors larger than 5 cm in diameter, without any deviation in the NSP pattern.CONCLUSIONS:The results of this preliminary study suggest that the co-expression of Notch1, Snail, and p53 (wild) is not inferior to the patterns with p53 mutation as an indicator of postoperative recurrence of grade III HCC.
Hepatic lymphangiomas are extremely rare; moreover cystic lymphangiomas usually arise in areas such as the neck and axilla, where loose connective tissue allows the expansion oflymphatic channels.The case of a 65-year old male is described, who presented with a solitary lymphangioma in the liver.The lesion was discovered incidentally and due to diagnostic uncertainty was removed surgically.A short review of histology, clinical presentation and preoperative diagnos- tic difficulties of hepatic lymphangiomas is given.
Serum ferritin is an independent predictor of histologic severity and advanced fibrosis in patients with nonalcoholic fatty liver disease. Kris V. Kowdley, Patricia Belt, Laura A Wilson, Matthew M. Yeh, Brent A. Neuschwander-Tetri, Naga Chalasani, Arun J. Sanyal, and James E. Nelson; for the NASH Clinical Research Network. Hepatology 2012;55:77-85. Nonalcoholic fatty liver disease (NAFLD) is now recognized as a major cause of chronic liver diseases, including liver cirrhosis and hepatocellular carcinoma (HCC) in Western countries.1,2 Like alcoholic liver disease, NAFLD covers a wide spectrum of disorders from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. Approximately 30% of the US population and 20% of the Korean population have NAFLD.1,3 Just as all heavy drinkers do not progress to cirrhosis and HCC, nor do all patients with nonalcoholic steatosis progress. In addition to its high prevalence, one of the challenges facing hepatologists is the diagnosis and risk stratification of NAFLD. There is no proven serologic marker to confirm the disease, which is diagnosed by excluding a history of alcohol consumption and other causes of liver disease using various serologic tests; sometimes a liver biopsy is needed. Moreover, after the diagnosis, it is not clear who will progress to cirrhosis or HCC. Central obesity is a well-known risk factor and hyperglycemia, diabetes, and age are associated with advanced fibrosis.1,4 However, to evaluate the risk of disease progression, a liver biopsy is essential. Recently non-invasive methods to distinguish between simple steatosis and significant fibrosis have been introduced. Serological tests have been investigated, including α2-macroglobulin, apolipoprotein A-I, hyaluronic acid, the platelet count, bilirubin, and gamma-glutamyl transpeptidase.2 Direct and indirect inflammation mediators such as interleukin-6 (IL-6), CC-chemokine ligand 2, and N-glycans gave positive results, but further studies are needed to determine whether these have diagnostic roles.2 An apoptosis product, cytokeratin- 18 (CK-18) fragments, was also associated with NASH or fibrosis.5 Recently, hepatic iron overload and its correlation with chronic liver disease have been considered.6,7 With recent progress in understanding iron metabolism in patients with hereditary hemochromatosis at the molecular level, accumulating evidence suggests a link between altered iron metabolism and NAFLD. In the last decade, many studies have found a relationship between hepatic iron and NASH or its progress.8-11 Iron (ferrum in Latin), atomic number 26, is the most common element on Earth. It is essential in most living organisms. Iron binds to cofactors in hemes, myoglobin, cytochrome P450, and catalases. When body iron accumulates, it promotes oxidative free-radical reactions, which have harmful effects. In hereditary hemochromatosis, accumulated iron in the liver, heart, and pancreas leads to cirrhosis, heart failure, and diabetes. Even mild iron overload might aggravate insulin resistance, diabetes, atherosclerosis, colonic neoplasia, and NAFLD.6,12-15 Moreover, iron depletion therapy, such as with a phlebotomy, improves the metabolic complications and elevated liver enzymes in patients with NAFLD.16 Iron is strictly regulated by a mechanism similar to that for glucose control.17 Like glucose and insulin, the serum iron level is regulated by a hepatic peptide hormone, hepcidin. An elevated iron level stimulates hepcidin synthesis, which decreases the iron-exporter ferroportin in macrophages and intestinal cells and reduces serum iron, just as insulin controls excess glucose.17,18 Currently, people in developed countries consume an overabundance of food. Since most food contains glucose and iron, excessive eating can increase the risks of hyperglycemia and iron overloading. Since accumulated iron is difficult to remove, males and the elderly are at higher risk for iron accumulation than females and younger people. Females lose body iron via regular menstruation. This iron-theory may explain the gender difference in cardiovascular diseases, although it has not been confirmed whether iron has the same effects on chronic liver diseases.19 Kowdley et al20 investigated the serum ferritin level and histological findings, including iron deposition, in 628 patients with NAFLD. This large cross-sectional study revealed that an elevated serum ferritin (>1.5×UNL) was associated with advanced hepatic fibrosis (odds ratio [OR], 1.66; 95% confidence interval [CI], 1.05-2.62; P=0.028) and a higher NAFLD Activity Score (NAS) (OR, 1.99; 95% CI, 1.06-3.75; P=0.033). An elevated serum ferritin (seen in approximately 20% of the subjects) was associated with greater iron accumulation in the body (i.e., a high serum iron and transferrin-iron saturation) and greater hepatic iron deposition in both the reticuloendothelial system and hepatocytes. The patients with an increased serum ferritin also had higher serum transaminases and gamma-glutamyl transferase, and a lower platelet count. Interestingly, even in patients without a hepatic iron overload on histology, a higher serum ferritin was correlated with an advanced stage. This suggests the presence of systemic inflammation unrelated to iron overload. There are a few contradictory reports on the role of the iron burden in patients with NAFLD.21,22 It is not clear whether the elevated serum ferritin is a consequence of systemic inflammation or a marker of iron overload in patients with NAFLD. The study by Kowdley et al20 seems to keep to the middle path. I would like to know more about the proportion of patients who had an elevated serum ferritin, but no iron deposition, in their study. Further studies to confirm the role of iron in NAFLD are needed. Should we use this simple, sensitive, and inexpensive test in all patients with NAFLD? Before approving its clinical use, one should consider the fact that most of the subjects in this study were severely obese (average BMI 34 kg/m2) and had metabolic syndrome (69%). The study population might differ from the real general population. In less-obese populations, the serum ferritin might differ and the iron burden might not be complicated. The cut-off level for the serum ferritin (1.5×UNL) in this study was subjective and needs further supporting data. In summary, not all patients with NAFLD progress to cirrhosis or HCC. It is not clear what factor(s) contribute to advanced liver disease. Dysregulated iron overload might be a contributing factor. Serum ferritin, a marker of iron accumulation, is related to advanced fibrosis in patients with NAFLD. However, it can also be elevated with systemic inflammation. Nevertheless, serum ferritin may be a simple, useful marker for obese patients with NAFLD. Further studies should confirm the role of iron overload and the meaning of hyperferritinemia in patients with chronic liver diseases, including NAFLD.
See the Original "Rapid normalization of alanine aminotransferase predicts viral response during combined peginterferon and ribavirin treatment in chronic hepatitis C patients" on page 41.
BACKGROUND/AIMS:The treatment for chronic hepatitis C (CHC) is removal of the virus in order to prevent progression to liver cirrhosis and hepatocellular carcinoma (HCC). Few data have been presented regarding the clinical significance of changes in the alanine aminotransferase (ALT) level in this context. We analyzed the patterns of changes in ALT level and investigated the relationship between the rapid normalization of ALT and sustained virologic response (SVR) after combined treatment with peginterferon and ribavirin.METHODS:CHC patients (n=370) were classified into four groups according to the initial ALT level and subsequent changes: (1) initially abnormal ALT level and sustained abnormal ALT level during treatment, (2) initially abnormal ALT level but achievement of ALT normalization, (3) initially normal ALT level and variable ALT abnormality during treatment, and (4) initially normal ALT level and sustained normalization of ALT level during treatment. We subdivided groups 1 and 2 into those with patterns of decreased and normalization of ALT, with or without rapid normalization. We checked the end-treatment response (ETR) and SVR rates in each group and the factors associated with SVR, including patterns of changes in ALT level.RESULTS:A total of 168 patients completed the therapy (age=54.34±10.64 years [mean±SD], 95 males [56.5%], genotype 1:82 [48.8%]). SVR was achieved in 115 (68.45%) of the completely treated patients. The SVR rate was significantly lower in group 1 than in group 2 (37.8 vs. 81.6%, P<0.001), and significantly higher in the rapid normalization group than in the group without rapid normalization (78.5% vs. 41.2%, P<0.001). Multiple logistic regression analysis revealed that age (odds ratio [OR]=0.94, 95% confidence interval [CI]=0.91-0.98, P=0.005), viral genotype (OR=2.76, 95% CI=1.20-6.38, P=0.017), and initial hepatitis C virus RNA titer (OR=0.28, 95% CI=0.10-0.75, P=0.012) were identified as independent significant predictive factors for SVR.CONCLUSIONS:The SVR rate is significantly associated with normalization, and especially rapid normalization of ALT. Rapid normalization of ALT by 4 weeks after treatment might be a useful response factor that is readily available in clinical practice, and especially for genotype 1 patients.
BACKGROUND/AIMS:Newly developed and potent antiviral agents suffer from the problem of drug resistance. Multidrug resistance is a major impediment in the treatment of patients with chronic hepatitis B (CHB). In line with American Association for the Study of Liver Diseases guidelines, adefovir dipivoxil (ADV) add-on therapy is recommended in the case of lamivudine resistance, while tenofovir disoproxil fumarate (TDF) is recommended for ADV or entecavir (ETV) resistance. TDF is currently not available in Korea. ADV+ETV combination therapy may be a viable alternative to TDF in patients with either ADV or ETV resistance. However, the efficacy of ADV+ETV combination therapy in patients with CHB and multidrug resistance is unclear. This study investigated the efficacy of ADV+ETV combination therapy in patients with multidrug resistance.METHODS:Twenty-five patients were enrolled and were administered ADV+ETV combination therapy for at least 6 months. Blood was drawn at baseline and at 3, 6, 9, and 12 months after commencing treatment, and the following blood parameters were analyzed: alanine transaminase, hepatitis B e-antigen (HBeAg), anti-hepatitis B e-antigen, and hepatitis B virus (HBV) DNA levels. The initial virological response (IVR) was defined as an HBV DNA level of <4 log(10) copies/mL after 6 months of combination therapy.RESULTS:The IVR rate was 76%. The proportion of patients with a high viral load (≥5.0 log) dropped from 76% at baseline to only 5% after 6 months of treatment. The biochemical response rate during the first 6 months was 71%. HBeAg was lost in 2 patients (10%).CONCLUSIONS:ADV+ETV combination therapy induced a good IVR in CHB patients who were refractory to more than 2 antiviral agents. This regimen may be a good alternative to TDF in Korea, where that drug is not available.
BACKGROUND/AIMS:Low-dose metronomic chemotherapy involves the frequent administration of comparatively low doses of cytotoxic agents with no extended breaks, and it may be as efficient as and less toxic than the conventional maximum tolerated dose therapy. This study evaluated the feasibility and therapeutic efficacy of metronomic chemotherapy in patients with advanced hepatocellular carcinoma (HCC) with major portal vein thrombosis (PVT).METHODS:Thirty consecutive HCC patients with major PVT with or without extrahepatic metastasis were prospectively allocated to metronomic chemotherapy consisting of epirubicin being infused through the correct hepatic artery at a dose of 30 mg/body surface area (BSA) every 4 weeks, and cisplatin (15 mg/BSA) and 5-fluorouracil (50 mg/BSA) every week for 3 weeks, with intervening 1 week breaks. The treatment response was assessed using response evaluation criteria in solid tumors (RECIST).RESULTS:In total, 116 cycles of metronomic chemotherapy were administered to the 30 patients, with a median of 3 cycles given to individual patients (range, 1-15 cycles). Six patients (20.0%) achieved a partial response and six patients (20.0%) had stable disease. The median time to disease progression and overall survival were 63 days (range, 26-631 days) and 162 days (95% confidence interval; range, 62-262 days), respectively. Overall survival was significantly associated with baseline alpha-fetoprotein level (P=0.001) and tumor response (P=0.005). The baseline alpha-fetoprotein level was significantly associated with the disease control rate (P=0.007). Adverse events were tolerable and managed successfully with conservative treatment.CONCLUSIONS:Metronomic chemotherapy may be a safe and useful palliative treatment in HCC patients with major PVT.
An 80-year-old woman with hilar cholangiocarcinoma was hospitalized due to sudden-onset abdominal pain. Computed tomography revealed hepatic necrosis accompanied with emphysematous change in the superior segment of the right liver (S7/S8), implying spontaneous rupture, based on the presence of perihepatic free air. Although urgent percutaneous drainage was performed, neither pus nor fluids were drained. These findings suggest emphysematous hepatitis with a hepatic mass. Despite the application of intensive care, the patient's condition deteriorated rapidly, and she died 3 days after admission to hospital. Liver gas has been reported in some clinical diseases (e.g., liver abscess) to be caused by gas-forming organisms; however, emphysematous hepatitis simulating emphysematous pyelonephritis is very rare. The case reported here was of fatal emphysematous hepatitis in a patient with hilar cholangiocarcinoma.
Reports of metastatic hepatocellular carcinoma (HCC) without a primary liver tumor are rare. Here we present a case of isolated HCC that had metastasized to the pelvic bone without a primary focus. A 73-year-old man presented with severe back and right-leg pain. Radiological examinations, including computed tomography (CT) and magnetic resonance imaging (MRI), revealed a huge mass on the pelvic bone (13×10 cm). He underwent an incisional biopsy, and the results of the subsequent histological examination were consistent with metastatic hepatocellular carcinoma. The tumor cells were positive for cytokeratin (AE1/AE3), hepatocyte paraffin 1, and glypican-3, and negative for CD56, chromogranin A, and synaptophysin on immunohistochemical staining. Examination of the liver by CT, MRI, positron-emission tomography scan, and angiography produced no evidence of a primary tumor. Radiotherapy and transarterial chemoembolization were performed on the pelvic bone, followed by systemic chemotherapy. These combination treatments resulted in tumor regression with necrotic changes. However, multiple lung metastases developed 1 year after the treatment, and the patient was treated with additional systemic chemotherapy.
Background/Aims Hepatocellular carcinoma (HCC), which is the third most common cancer in Korea, has a very poor prognosis. However, only a few studies have performed a comprehensive survival-related analysis in all patients who were consecutively diagnosed and treated over a given period of time. The aim of this study was to determine the 5-year survival rate and its prognostic factors among HCC patients. Methods In total, 257 patients who were consecutively diagnosed with HCC between January 2000 and December 2003 were followed until death or until December 2008. We analyzed their survival outcomes according to their clinical characteristics, tumor staging, and treatment modalities, and determined the independent prognostic factors affecting survival. Results The patients were aged 59±10 years (mean±SD). During the follow-up period, 223 patients (86.8%) died and the overall median survival was 10.8 months; the 1-, 3-, and 5-year survival rates were 44.4%, 21.0%, and 12.1%, respectively. The outcomes in patients with tumor node metastasis (TNM) stage I or II and Child-Pugh class A or B were significantly better with surgical resection than with other treatment modalities (P<0.01). Patients who underwent supplementary transcatheter arterial chemoembolization as a second-line treatment after surgical resection had better outcomes than those who underwent surgical resection alone (P=0.02). Initial symptoms, Child-Pugh class, serum alpha-fetoprotein, tumor size, portal vein thrombosis, and TNM stage were found to be independent prognostic factors for survival among HCC patients. Conclusions This retrospective cohort study elucidated survival outcomes and prognostic factors affecting survival in HCC patients at a single center.
Ciliated hepatic foregut cyst (CHFC) is a rare developmental disorder of the liver. Diagnoses of CHFC has become frequent during the past two decades due to technological progress and increased use of various imaging modalities.1 Clinically and radiologically, this lesion can be difficult to distinguish from the other cystic neoplasms of the liver. In this issue, we present a case of CHFC and discuss the typical histopathologic findings.
BACKGROUND/AIMS:It has been shown that the drug-eluting beads loaded with doxorubicin (DEBDOX) are effective for the treatment of hepatocellular carcinoma (HCC). However, the optimal safety and efficacy still remain to be established by using various bead sizes, doxorubicin doses, and the degree of stasis.The aim of this study was to determine the optimal safety and efficacy of DEBDOX in the treatment of HCC.METHODS:Analysis of a 503-patient prospective, multicenter, multinational Bead Registry Database from 2007 to 2010 identified 206 patients who had been treated for HCC with DEBDOX. Primary endpoints were to compare safety, tolerance, response rates, and overall survival based on bead size (100-300, 300-500, 500-700, and 700-900 μm), number of vials, doxorubicin dose, and degree of stasis.RESULTS:In total, 206 patients underwent 343 treatments. The use of all four bead sizes was similar based on Child-Pugh class and Okuda stage, with a significantly higher use (50%) of beads of size 100-300 μm in patients with portal vein thrombosis (P=0.05). Significant differences were seen for the number of median treatments, median doxorubicin dose, lobar infusion), and degree of complete stasis. The rate of adverse events was higher for larger beads than for smaller beads (28% vs. 16%; P=0.02).CONCLUSIONS:Bead size and dose may vary according to disease distribution. Smaller beads offer the opportunity for repeated treatments, a larger cumulative dose delivery, a lesser degree of complete stasis, and fewer adverse events.
Background/Aims Several studies suggested that serum cystatin C (CysC) is more useful than serum creatinine (Cr) for the assessment of renal function in patients with liver cirrhosis. This study evaluated the clinical significance of CysC in patients with cirrhotic ascites and normal Cr level. Methods We enrolled patients with cirrhotic ascites and a normal serum Cr level (<1.2 mg/dL). GFR was measured by 99mTc-DTPA renal scan. Serum Cr, CysC, and Cr clearance (CCr) were measured on the same day. Significant renal impairment and severe renal impairment were defined as GFR <60 mL/min and GFR <30 mL/min, respectively. Results Eighty-nine patients with cirrhotic ascites were enrolled in the study (63 men and 26 women; age, 55±11 years). Forty-seven (52.8%) and 42 (47.2%) patients were in Child-Pugh grade B and C, respectively. Serum Cr and CysC levels and GFR were 0.8±0.2 mg/dL, 1.1±0.3 mg/L, and 73.4±25.5 mL/min, respectively. Significant and severe renal impairment were noted in 28 (31.5%) and 2 (2.2%) patients, respectively. GFR was well correlated with serum Cr, CysC, and e-GFRMDRD, while it was not correlated with e-GFRC&G. In multivariate analysis, only CysC was significantly correlated with GFR (β, 45.620; 95% CI, 23.042-68.198; P<0.001). Serum CysC level was the only independent predictor for significant renal impairment. Conclusions Significant renal dysfunction was not rare in patients with cirrhotic ascites, even their serum Cr level is normal. Serum CysC is a useful marker for detecting significant renal dysfunction in these patients.
Background/Aims Recent outbreak of hepatitis A in Korea is clearly related to the epidemiological shift of hepatitis A virus (HAV). However, nationwide seroprevalence data have been limited. This study estimated the nationwide, age- and area-adjusted anti-HAV prevalence from 2005 to 2009. Methods Retrospective analysis of the results of total anti-HAV test in 25,140 cases which were requested by 1,699 medical institutions throughout the nation to Seoul Clinical Laboratory from Jan. 1 2005 to Dec. 31 2009 was performed. The estimated seroprevalence was adjusted by area and age of the standard population based on the 2005 Census data from Korea National Statistical Office. Results The area-adjusted anti-HAV prevalence in the children younger than 10 years were 33.4% in 2005 and 69.9% in 2009. The most susceptible age groups to HAV infection during the last 5 years were teenagers and the young adults in their age of twenties. The area-adjusted seroprevalence in 2009 were 11.9% in the age group of 20-29 years, 23.4% in the age group of 10-19 years, 48.4% in the age group of 30-39 years. The population in 40-49 years showed geographically different seroprevalence with the lowest rate in Seoul (80%). Conclusions The most susceptible age group to HAV infection is 10-29 years, while the young children less than 10 years showed about 70% seropositivity. The changing seroepidemiology should be monitored continuously for the proper vaccination and patient care.
This is a case report of a 68-year-old man with hepatocellular carcinoma (HCC) accompanied by hereditary hemorrhagic telangiectasia (HHT), also known as Osler-Weber-Rendu disease, and hepatic vascular malformation. HHT is an autosomal dominant disorder of the fibrovascular tissue that is characterized by recurrent epistaxis, mucocutaneous telangiectasias, and visceral arteriovenous malformations. HHT is caused by mutation of the genes involved in the signaling pathway of transforming growth factor-β, which plays an important role in the formation of vascular endothelia. Hepatic involvement has been reported as occurring in 30-73% of patients with HHT. However, symptomatic liver involvement is quite rare, and the representative clinical presentations of HHT in hepatic involvement are high-output heart failure, portal hypertension, nodular regenerative hyperplasia, and symptoms of biliary ischemia. Some cases of HCC in association with HHT have been reported, but are very rare. We present herein the characteristic radiologic and genetic findings of HHT that was diagnosed during the evaluation and treatment of HCC.
Background/Aims Cross-sectional studies have documented that 2-10% of patients who are chronically infected with hepatitis C virus (HCV) are also positive for hepatitis B virus (HBV) surface antigen (HBsAg). Data related to HCV-HBV coinfection are lacking in Korea. This study evaluated the clinical characteristics, the treatment efficacy of peginterferon alfa plus ribavirin, and the changes induced by such treatment in HBV status in chronic hepatitis C (CHC) patients coinfected with HBV. Methods Eighteen (2.37%) HBsAg-positive CHC patients were selected from among the 758 subjects from the K(G)yeonggi-Incheon Peginterferon alfa and ribavirin in chronic hepatitis C Treatment (KIPECT) study, which evaluated the treatment efficacy and safety of peginterferon alfa plus ribavirin in CHC patients. Data on changes in the status of HBV infections were obtained. Results HCV genotype 1b was the most common (44%). The overall sustained virologic response rate was 72% in all patients, and 60% and 87.5% in genotypes 1 and 2, respectively. Two of the 18 patients were positive for HBeAg, and 15 had baseline HBV DNA level of less than 2,000 IU/mL. Two of the three whose levels exceeded this threshold showed no detectable DNA after treatment. After the completion of treatment, serum HBV DNA levels were increased in the two patients whose baseline HBV DNA levels were less than 2,000 IU/mL. Conclusions The prevalence of HBV coinfection in CHC patients was 2.37% and most of the patients were inactive carriers. The treatment efficacy was similar to that of HCV mono-infection. Reactivation of HBV replication was observed in some patients after CHC treatment.
