The fornix sign differentiated AD from NC with specificity of 1.0 and sensitivity of .56. It predicted conversion from NC to aMCI with specificity of 1.0 and sensitivity of .67, Protein Tyrosine Kinase inhibitor and from aMCI to AD with specificity of .94 and sensitivity of .83. The fornix sign is a promising predictive imaging sign of AD. “
“The acquisition of literacy during childhood may affect the functional organization of the brain. We studied the effects of illiteracy on neuropsychological

tests and brain glucose metabolism in later life. We recruited 12 illiterate elderly farmers who never attended school and acquired no knowledge of reading or writing. These illiterate subjects were compared with literate subjects in terms of neuropsychological performance and brain glucose metabolism. All subjects were over

65 years and had same socioeconomic environment and normal activities of daily living. Neuropsychological tests indicated that the performance of illiterate subjects was worse than that of literate subjects in all cognitive domains with the exception of forward digit span, tool-use and tool-free gestures, and verbal generation of grocery items. The SPM analysis showed that illiterate subjects had reduced FDG-uptake relative to literate subjects, predominantly in the rostral part of the left superior frontal gyrus and less strikingly NVP-AUY922 in vitro in the left rectal gyrus, right cerebellar declive, and right cerebellar tonsil. In contrast, hypermetabolism was found only in the left precuneus. These results suggest that reading and writing

during childhood is associated with activation of the frontal pole that may play a critical role in complex aspects of human cognition. “
“Limited data exist regarding the long-term clinical and angiographic outcomes of patients with spontaneous cervico-cranial arterial dissection treated with stent placement. To report the Interleukin-2 receptor immediate and long-term clinical and angiographic outcomes of patients who received stent placement for spontaneous cervico-cranial arterial dissection. We reviewed clinical and angiographic data of consecutive patients with spontaneous, cervico-cranial arterial dissection treated with stent placement. Patients with recurrent ischemic symptoms or severe hemodynamic compromise despite maximal medical therapy, or those with compressive symptoms due to expanding pseudoaneurysms were considered for stent placement. Follow-up angiography and intravascular ultrasound (in select patients) was performed to detect in-stent restenosis, intimal flap, thrombus, or persistent pseudoaneurysm. A total of 14 patients were identified, with complete resolution of stenosis achieved in 10 patients immediately post-procedure. Clinical follow-up ranged from 26–900 days, during which there was 1 (7%) TIA, 1 (7%) minor ischemic stroke, and 1 (7%) in hospital death (unrelated to stent placement). Stroke-free survival was 93% at both 1 month and 6 months after the procedure.

2 A multiple cohort model has been developed to predict the effect of chronic hepatitis C infection (HCV+) on public health.3 The model takes into consideration known differences in disease progression related to sex and age at infection. It predicts that 24.8% of the cohort infected between 1970 and 1990 will have cirrhosis by 2010, and 44.9% will progress to cirrhosis by 2030. Eleven percent of the cohort with cirrhosis currently

have hepatic decompensation, and this proportion will increase through 2030. The incidence of HCV-related hepatocellular carcinoma (HCC) is increasing and is forecast to peak in 2019.3 The effect of these projections is already becoming evident. HCV-related ambulatory care visits more than doubled between 1997-1999 and 2003-2005.4 Complications related Roxadustat in vivo to HCV are already the leading cause for liver transplants, BMS-907351 concentration and this

demand is expected to increase, exacerbating the current shortage of available organs.5 The incidence of HCC, much of which is caused by HCV, tripled between 1975 and 2005,6 and HCV-related mortality increased 123% between 1995 and 2004.7 Treatment has the potential to greatly reduce the public health effect of this epidemic. In 2010, it was estimated that based on current treatment practices (i.e., chronic hepatitis C infection [HCV+] was diagnosed in 30% of cases; 25% were treated and 40% responded to treatment), only 1% of cirrhosis cases would be prevented.3 Since then, more effective antiviral therapies have been approved, but more patients need to be diagnosed and treated to fully realize the potential of HCV treatment to reduce HCV-related disease.

In this article, we focus on barriers to treatment, specifically findings that patients with a history of alcohol abuse are less likely to be treated,8 and that patients who reported any drinking in the 12 months before treatment were less likely to respond to treatment.9 The issue of how to manage HCV in patients with a history of moderate to heavy drinking is a critical one because many patients with HCV have such a history. A national seroprevalence survey found that 48% of HCV+ participants had VAV2 had five or more drinks in a single day during the previous year, and 33% had done so on at least 50 days.1 This study extends previous research in three ways. One, it was conducted in a representative cohort of privately insured members of an integrated health care plan. HCV treatment outcomes have been understudied in insured patients, despite the fact that they represent a large portion of the infected population, and they are likely to have access to resources needed to obtain treatment. Two, it contributes to the limited information available on the relation of alcohol consumption to outcomes of treatment with pegylated interferon-alpha and ribavirin (P/R).

Transduction of B cells by lentiviral vectors encoding FVIII domains that harbour the most common immuno-epitopes has the potential

to diminish antibodies to the protein in HA mice with inhibitors [38]. We initiated an experimental study in HA dogs with inhibitors to canine FVIII (cFVIII) prior to liver-directed gene transfer by AAV-cFVIII. Inhibitor-prone HA dogs from the UNC-Chapel Hill colony or Queen’s University are excellent models for studying tolerance induction, as both colonies have the same mutation found in the majority of the human HA population (inversion of FVIII intron 22) [52,53]. Notably, the most common mutation (∼40% of cases) in severe HA patients is the FVIII intron 22 inversion, which together with rare mutations (large gene deletion and nonsense mutations) phosphatase inhibitor library presents a higher risk for inhibitor formation when compared with patients with FVIII missense mutations. The overall purpose of this strategy is to determine whether an alternative approach, i.e. endogenous liver expression of cFVIII, will lead to the eradication of inhibitors. Because AAV vectors SCH772984 price provide long-term FVIII expression, this strategy has the potential to not only eradicate inhibitor by induction of FVIII-specific immune tolerance but also provide increased therapeutic FVIII levels to ameliorate the disease phenotype. To date,

four HA dogs have been injected with AAV8 expressing B-domain-deleted canine FVIII (BDD-cFVIII) via the peripheral vein. Long-term follow-up of these animals demonstrated that eradication of the inhibitor to cFVIII is feasible in most animals. After inhibitor eradication, repeated challenges with intravenous injections of recombinant BDD-cFVIII did not induce antibody formation to cFVIII and pharmacokinetic studies following

such administration demonstrated normal recovery and half-life of BDD-cFVIIII. In these dogs, the disease phenotype was improved by the persistence of therapeutic levels of cFVIII and a significant reduction in the numbers of spontaneous bleeds. In one animal, AAV-cFVIII induced a strong transient anamnestic response SPTBN5 to the endogenous expressed cFVIII that after 18 months is now <1 BU. Factors such as exposure to xeno-antigens, the nature of the antibody response, or age may influence the outcome of the tolerance induction protocol. Collectively, these data demonstrate the potential of AAV-FVIII gene delivery not only to treat genetic deficiencies such as haemophilia, but also to induce tolerance to the transgene in the setting of pre-existing inhibitory antibodies. Studies on the immune response to FVIII and FIX in haemophilic mice will continue to provide new information relating to immunogenic and tolerance mechanisms. In addition, novel therapeutic approaches will probably require initial evaluation in these animal models.

ID confidence of protein biomarker candidates was

verified by quantitating the percent sequence coverage (percent of the complete protein amino acid sequence where matching peptides for protein ID were found). Statistical analyses were performed using JMP software (SAS Institute Inc., Cary, NC). A total of 85 subjects were included in this study, of which 69 were in the varying spectrum of NAFLD. The NAFLD cohort had several common features of metabolic syndrome including Torin 1 mouse diabetes mellitus, dyslipidemia, hypertension, and obesity. As shown in Table 1, patient clinical characteristics were consistent with what would be expected in the presence or absence of NAFLD.

There were five patients in the NAFLD group with methotrexate use, three in the simple steatosis and two in the NASH group. Findings from the global serum protein analysis are summarized in Table 2. Of the 1,738 proteins that were identified, 183 had multiple unique amino acid sequences identified and high peptide ID confidence (priority 1), and there was a significant change observed (q < 0.05) in the protein expression level between any two patient groups for 72 of these proteins (Table 2). The significant changes Ganetespib cell line observed between groups are further described in a pairwise fashion in Table 3. Of the priority 1

proteins identified, there were 21 significant changes in protein levels observed between simple steatosis and NASH F3/F4 groups and 9 significant changes between NASH and NASH F3/F4 groups. It is important to note that no serum proteins had significant differential expression Histamine H2 receptor when the simple steatosis and NASH groups were compared. A comprehensive list of all 56 priority 1 proteins with a significant change >14% (1.14-fold) among any two patient groups (q < 0.05), sorted by fold change, is shown in Supporting Table 1. Protein identification numbers, mean protein intensity (log2) for each patient group, and a description of protein function is listed. Biological functions of these proteins are summarized in Table 4. The function of two proteins, 13 kDa protein and 11 kDa protein, is unknown. Of the 72 proteins with significant differential expression (q < 0.05) identified as priority 1, 27 had expression levels that differed by at least 30% (1.30-fold change). Of these 27 proteins, six patterns of protein expression changes among the four patient groups were noted: (1) decreased in all stages of NAFLD; (2) increased in all stages of NAFLD; (3) decreased in NASH F3/F4 only; (4) increased in NASH F3/F4 only; (5) decreased with progression of NAFLD; and (6) increased with progression of NAFLD.

1α-hydroxylase, 25-hydroxyvitamin-D 1α-hydroxylase; 1α,25(OH)2D, 1α,25-dihydroxyvitamin D; 24-hydroxylase, Selleck Vadimezan 25-hydroxyvitamin-D 24-hydroxylase; 25(OH)D, 25-hydroxyvitamin D; HCV, hepatitis C virus; IFNα, interferon-α; ISG, interferon-stimulated gene; SVR, sustained viral response; TLR3, Toll-like receptor 3; RIG-I, retinoic acid-inducible gene I; VDR, vitamin D receptor. Vitamin D3 was purchased from Sigma Chemical (St. Louis,

MO). Calcitriol was obtained from Teva Pharmaceutical Industries (Israel). Virus assays were carried out with the intergenotypic HJ3-5 chimeric HCV virus.25 Virus stocks were produced in FT3-7 cells.26 Huh-7.5 cells were used for all assays and were cultured as described.25 Total RNA was extracted from cells using the guanidine isothiocyanate method.27 RNA samples were treated with DNaseI (Ambion, Cambridgeshire, UK). Total RNA (1 μg) was subjected to reverse transcription (RT) using the High Capacity cDNA Reverse Transcription Kit (Applied Biosystems, Foster City, CA). Real-time RT-PCR assays were performed in the ABI 7000 sequence device (Applied Biosystems), using TaqMan click here gene expression assays essentially as described.28 For measurement of HCV expression, 20-μL reactions were prepared in a 96-well

format, using 1 μL of the template cDNA, 10 μL of 2× TaqMan Universal PCR Master (Applied Biosystems), 10 pmol of forward primer HCV-F (nucleotides [nt] 130-146), and reverse primer HCV-R (nt 272-290) (AF139594) for the HCV nontranslated region, and 5 pmol of an HCV-specific TaqMan probe. Assay-on-Demand Gene Expression Products (Applied Biosystems) were Thalidomide used for the measurement of IFN-β (Hs02621180_s1), GAPDH (Hs99999905_m1) CYP27B1 (Hs00168017_m1), CYP24A1 (Hs001679999_m1), and VDR (Hs00172113_m1). Results are expressed as the ratio of the target gene messenger RNA (mRNA) and GAPDH

mRNA threshold values. Analysis of the ISG MxA expression level was performed by SYBR Green I dye (Applied Biosystems) using MxA-specific primers as published29 and GAPDH as the internal control gene (primers: GAPDHS 5′-GAAGGTGAAGGTCGGA GTC-3′ and GAPDHAS 5′-GAAGATGGTGATGG GATTTC-3′) using the ABI 7000 (Applied Biosystems) detection system. The level of calcitriol in the supernatants was determined by specific 1α,25-dihydroxyvitamin D enzyme-linked immunosorbent assay (ELISA) kit following extraction with monoclonal anti-1α,25-dihydroxyvitamin D antibody according to the manufacturer’s instructions (Immunodiagnostic Systems, Boldon, UK). Huh-7.5 cells were pretreated with vitamin D3, calcitriol, or the vehicle ethanol (ethanol concentration did not exceed 0.015%) for 3 hours before infection with the HJ3-5 virus at a multiplicity of infection (moi) of 0.1-0.01.

On a positive note, the modifications have not been associated with any adverse events and, in animal studies, have been associated

with reduced levels of antibody production. Indeed, it has previously been observed that PEGylation of molecules tends to reduce immunogenicity [113]. However, the combination with other molecules has produced some alterations in the way the FVIII behaves in standard assays of FVIII activity. Whilst this has sometimes been similar to the discrepancies already seen with concentrates and B-domain-deleted products, the discrepancies are somewhat reagent- and product-dependent which may result in problems limiting selleck chemicals their widespread use [109]. The initial trials with PEGylated FVIII molecules have not demonstrated any adverse events of concern, but these were single injections into PTPs. Use of PEG in other circumstances has generally been for limited courses of treatment. There is therefore a possible concern regarding PEG accumulation when patients receive repeated injections for many years. This is particularly relevant in view of the fact that PEG is a non-physiological molecule with no specific degradation or excretion pathway [113]. In general it appears that, after administration, PEG is either taken up by macrophages or follows the pathway of the molecule to which it has been BMN 673 purchase linked. In very high doses over

periods of 6–12 months, modest degrees of vacuolation have been seen in animal models. It has been calculated that for some of the modified FVIII Forskolin in vitro molecules described above, a 60 IU kg−1 dose will constitute a 4 μg kg−1 load of PEG which

equates to approximately 20 mg per year for an adult on prophylaxis. However, the doses required to produce the vacuolation changes noted above are approximately four orders of magnitude greater than this, and in any event were not associated with any functional toxicity. Large doses of other PEGylated molecules have been given over 6-month periods without any toxicity. Moreover, although there is no specific pathway, it appears that PEG can be broken down by cytochrome enzymes and some of it will appear in the urine [113]. Overall, it seems unlikely that significant PEG toxicity will be encountered using these modified FVIII molecules but it will undoubtedly be a subject for postmarketing monitoring. The relatively modest prolongation of half-life achieved with the agents to date means that it will be necessary to prioritize frequency, trough levels and costs when they become available for use. In current prophylactic regimens the principal concern centres on the trough level of FVIII. In particular, the critical factor in reducing bleed frequency is the time spent below 0.01 IU mL−1, which is known to be a major determinant of bleed frequency [114]. The peak level achieved may also be important for individuals taking part in physical activity where a period of higher FVIII level is desirable.

Her younger sister (III.16) developed liver disease in her early teens and died of cirrhosis at age 19 (Fig. 1). A first cousin (III.1) died of liver disease at age 6 and her sister, a 32-year-old reportedly healthy Ibrutinib in vitro woman (III.5), had self-limited jaundice and abdominal swelling as a child that fully resolved by age 9. On physical examination the proband had jaundice, multiple echymoses, splenomegaly, and mild pedal edema. Laboratory evaluation revealed mildly elevated levels of aspartate aminotransferase (AST) (67 IU/L, normal range: 13-40 IU/L),

alanine aminotransferase (ALT) (50 IU/L, normal range: 10-40 IU/L), alkaline phosphatase (ALKP) (153 IU/L, normal range: 38-126 IU/L), and a normal GGT level (14 IU/L, normal range: 4-63 IU/L). Her serum bilirubin was 1.8 mg/dL (normal range: 0.2-1.3 mg/dL) with a direct bilirubin of 1.3 mg/dL (normal range: 0.0-0.3 mg/dL). Her prothrombin time and international normalized ratio (INR) was increased (2.0, normal range: 0.8-1.2) and serum albumin level was reduced (3 g/dL, normal range: 3.4-5.4 g/dL). Abdominal computerized tomography (CT) showed a small nodular liver, numerous splenic and gastroesophageal varices, and marked splenomegaly (spleen span of 24 cm). Liver biopsy revealed extensive bridging fibrosis with abnormal ducts encircling parenchymal nodules. Laboratory evaluation was negative for Wilson’s disease, hemochromatosis, and α1 anti-trypsin deficiency as well as for viral or autoimmune

hepatitis. She denied any history of alcohol abuse. Blood samples were collected from the 13 family members who were available for study (Fig. JNK inhibitor molecular weight 1). The proband’s parents (II.10 and II.11) were first cousins and two of her paternal uncles (II.2 and II.4) married first cousins. Two brothers (II.4 and II.10) had married two sisters (II.5 and II.11). The

32-year-old offspring of a paternal uncle (III.5) had been diagnosed with liver disease in childhood but was subsequently asymptomatic and had normal serum levels of hepatic enzymes (AST = 21 IU/L, ALT = 30 IU/L, ALKP = 67 IU/L) and bilirubin (total, 0.9 mg/dL; direct, 0.3 mg/dL) at the time of this study. The inheritance pattern of liver disease in the family was most consistent with an autosomal recessive disorder. Given the high level of consanguinity Nintedanib (BIBF 1120) in the family, we hypothesized that the affected family members were homozygous for a mutation inherited identical-by-descent from a common ancestor. Genotype analysis revealed extensive homozygosity in all three family members, including single regions encompassing 63% and 78% of chromosomes 10 and 19, respectively, in the affected first cousin (III.5). We focused on those runs of homozygosity (ROH) that were >3 Mb because regions of this length are uncommon in the general population22 (Fig. 2). Candidate regions were further refined by identifying those ROHs that were shared by both affected patients but not by the unaffected family member. The resulting candidate regions totaled 36.5 Mb or 1.

2% for flat- and 4.2% for protruded-type. This was significantly higher in the depressed-type lesions. The rate of adenomatous component was 6.2%, 50.8% and 55.7%, respectively. This was significantly lower in depressed-type

lesions, and suggested that they emerge directly from the normal epithelium without going through the adenoma stage. Conclusion: Depressed-type colorectal carcinomas are small, but invade massively. They had higher risks of vessel permeation, tumor budding and nodal metastasis than flat- and protruded-types. Furthermore, they had a lower rate of adenomatous component, suggesting that they are “de novo” carcinomas. For their rapid growth and malignant nature, whether or not they are depressed-type Rapamycin is very important in the diagnosis of colorectal neoplasms. Key Word(s): 1. cororectal carcinoma; Presenting Author: XIAOHUI GUAN Additional Authors: XIAOYING LI, XIAO HAN, LIPING AN Corresponding Author: XIAOHUI GUAN Affiliations: Affiliated Hospital of Beihua University; College of Pharmacy of Beihua University Poziotinib Objective: Polyclonal antibody preparation of ASPP1 and research ASPP1 and expression in the colon cancer tissue, study the expression and the colon cancer tissue differentiation degree, infiltration depth,

lymph node metastasis, to clarify the role of ASPP1 in knot bowel cancer. The role of bowel cancer. Methods: According Branched chain aminotransferase to bioinformatics software analysis of ASPP1 protein secondary structure, antigenicity and hydrophilicity, hydrophobicity, physical and chemical properties by homology search, antibody design consideration of other factors, to design a polypeptide, preparation of polyclonal antibody. Using the ELISA and Western blot and immunohistochemistry method to measure its titer and specificity. Using immunohistochemical

Sp method in 30 cases of colon cancer tissue and 15 cases of normal colon tissue expression of ASPP1 and determine the expression of ASPP1 and colon tissue differentiation degree, infiltration depth, lymph node metastasis and clinical pathological features of relations. Results: Successfully predicted its antigenicity analysis; Preparation of polyclonal antibody against people ASPP1; By using ELISA and Western blot and immunohistochemistry staining method confirmed the high antibody titer, the specificity is strong. ASPP1 in carcinoma tissue of high, medium and low differentiation degree of expression of the lower level of differentiation, the less the expression. The infiltration depth, and presence of expression there was no significant difference in lymph node metastasis. ASPP1 in colon cancer and normal colon tissues was no significant difference (p > 0.05). Conclusion: Using bioinformatics software to predict ASPP1 antigenicity, and successful preparation of the high specificity of ASPP1 polyclonal antibody.

Among them, 10 patients had HBsAg reduction by greater than 1 log IU/mL

at the second visit (Fig. 2). The baseline HBV DNA, HBsAg, ratio of HBsAg/HBV DNA, and ALT levels had no relationship with chance of greater HBsAg reduction at subsequent follow-up (Table 4). In general, an HBsAg reduction of greater than 1 log IU/mL could reflect a better viral control. The reduction in HBV DNA among patients with greater HBsAg reduction (median 2.30, range 0.04-6.59, log IU/mL) was more dramatic than that among patients with HBsAg reduction <1 log IU/mL (median 0.58, range −3.50 to 5.53, log IU/mL; P < 0.001). Patients with greater HBsAg reduction also tend to have lower HBsAg/HBV DNA from the second to the last visit. Three patients (two in Tamoxifen mw Group 2 and one in Group 4) developed hepatocellular carcinoma; all of them had HBsAg reduction <1 log IU/mL. A good immune control was most obvious among patients who were negative for HBeAg while having an HBsAg NVP-BKM120 nmr reduction of >1 log IU/mL (Table 5). There was a trend, though not statistically significant, of higher proportion of low HBV DNA and HBsAg loss among patients who underwent HBeAg seroconversion (Group 3) if they had HBsAg reduction by >1 log IU/mL. Among HbeAg-negative patients (Group 4 and Group 5), HBsAg reduction >1 log IU/mL was associated with higher chance of HBsAg loss and better viral suppression.

Among nine patients who experienced HBsAg loss, eight had HBsAg reduction by >1 log IU/mL at the last visit. The remaining patient had HBsAg level lower than 0.5 IU/mL at the first visit and had undetectable HBsAg (<0.05 IU/mL) starting the second visit. Twenty patients had a total of 27 hepatitis flares (12 HBeAg-positive, 14 HBeAg-negative, and one with absent HBeAg result) during the follow-up period. The ALT levels at the visits before flare, during flare, and after flare were 53 (24-185) IU/L, 330 (214-1066) IU/L, and 46

(24-128) IU/L, respectively. There was a significant increase in HBV DNA level at hepatitis flare (from 5.27 ± 1.89 log IU/mL to 6.79 ± 1.09 log IU/mL; P < 0.001) but the HBsAg level remained relatively static (from 3.32 ± 1.17 log IU/mL to 3.28 ± 0.98 log IU/mL; P = 0.72) (Fig. 1C). The HBsAg/HBV DNA ratio decreased from 0.68 ± 0.34 before flare to 0.48 ± 0.14 at ALT flare (P < 0.001) and increased back to 0.74 Carnitine palmitoyltransferase II ± 0.33 after flare (P < 0.001). Overall, with the 585 samples from 49 HBeAg-positive and 68 HBeAg-negative patients at five time points of assessment, the HBsAg levels had moderate correlation with HBV DNA (r = 0.61, P < 0.001). The correlation of HBsAg with HBV DNA was higher in the 176 HBeAg-positive samples (r = 0.66, P < 0.001) than that in the 409 HBeAg-negative samples (r = 0.41, P < 0.001; Fig. 3). Based on an 8-year follow-up of patients at different stages of chronic HBV infection, we found that serum HBsAg quantification was closely related to the HBeAg status and HBV DNA levels.

3% were female. Etiology of liver fibrosis were 46.9% HBV, 15.6% HCV and 37.5% miscellanous. Results of Spearman rank test

level of hyaluronic acid (r = 0.436; p = 0.014), YKL-40 (r = 0.43; p = 0.014), Type IV collagen (r = 0.509; p = 0.003), laminin (r = 0.733; p = 0.001). Double linear regression test with stepwise method on all of the determinant factors show that the most significant determinant factor was type IV collagen (r = 0.463; p < 0.001). Conclusion: There was significant positive correlation between serum extracellular matrix (hyaluronic acid, laminin, YKL-40, type IV collagen) and liver stiffness in liver fibrosis patients. The most significant determinant factor was type IV collagen. Key Word(s): 1. liver stiffness; 2. liver fibrosis; 3. serum extracellular matrix (hyaluronic acid, laminin, Ykl-40, Type Iv collagen)

Presenting Author: XIU QING WEI Additional Authors: JIN TAO, ZUOFU WEN, BIN WU Corresponding Author: XIUQING WEI Affiliations: The Third Affiliated Hospital of Sun learn more Yat-Sen University; Third Affiliated Hospital, Sun Yat-Sen University; The Third Affiliated Hospital of Sun Yat-Sen Unive Objective: To introduce an uncommon cause of anorexia and jaundice. Methods: The medical course of a rare patient with anorexia and jaundice was presented in brief. Results: A 65-year-old woman was admitted to our hospital because of fatigue, anorexia and food avoidance during the past 6 months and jaundice for one month. Serum level of AST, ALT, total bilirubin and direct bilirubin tuclazepam were elevated at 174 U/L, 89 U/L , 163.9 umol/L and 117.9 umol/L respectively. Testes for serum cortisol level at the following time points: 0 am 76.67 nmol/L, 8 am 42.12 nmol/L,

4 pm 74.23 nmol/L, and ACTH was markedly low at 1.23 pmol/L. Hormones on other pituitary axes were within normal range. The patient responded quickly to hydrocortision and all the symptoms relieved totally one month later. Conclusion: Addision’s disease can be presented as hepatitis and anorexia in some rare cases. Key Word(s): 1. Addision’s disease; 2. hepatitis Presenting Author: MUSTOKO NEGORO WIBOWO Additional Authors: ARITANTRI DAMAYANI, PAULUS KUSNANTO, TRIYANTA YULI PRAMANA, TANTORO HARMONO Corresponding Author: MUSTOKO NEGORO WIBOWO Affiliations: Fk Uns – Dr Moewardi Hospital, Fk Uns – Dr Moewardi Hospital, Fk Uns – Dr Moewardi Hospital, Fk Uns – Dr Moewardi Hospital Objective: The aim of our study was to evaluate a possible correlation between HBV DNA, HCV RNA viral load and liver fibrosis assessed by Fibroscan among chronically infected subject Methods: Restrospective analysis of 64 patients with hepatitis B and hepatitis C undergoing Fibroscan in Dr. Moewardi Hospital Surakarta from January 2012 to March 2014. Statical analysis with Chi Square Test. Exclusion criteria were the presence of diabetes mellitus, advanced cancer and pregnancy.