97 × 140 cm with no crossing of layers EUS-FNA (GF-UCT-140-AL5,

97 × 1.40 cm with no crossing of layers. EUS-FNA (GF-UCT-140-AL5, Olympus, Tokyo, Japan) was performed initially with 3 passes using the 19 G ProCore buy CP-690550 needle (Cook Medical Inc, Limerick Ireland). Decision was made to switch to 25 G needle (Cook Medical Inc, Limerick Ireland) as only blood was seen on the smears from the core needle and 2 extra passes performed. The procedure was uneventful. Eight hours after procedure, patient presented with sudden onset epigastric pain. Physical examination was unremarkable. Blood investigation showed raised amylase and lipase

at 302 U/L (33–126) and more than 400 U/L (14–40) respectively. Pain resolved with 75 mg of diclofenac sodium given via intramuscular route. Results: Abdominal computer tomography was performed four days later, and showed stranding of the fat adjacent to the SMT suggestive of inflammation. The histologic later showed benign yield of acinar and ductal epithelial cells, the cores of tissue shows lobules of pancreatic parenchyma composed of acinar cells and occasional ducts and fibrous stroma. The features are consistent with diagnosis of benign pancreatic tissue and pancreatic heterotropia.

Conclusion: Pancreatic heterotopia is presence of pancreatic tissue outside of its usual location, without structural or vascular continuity with pancreas proper. Similar to the pancreas proper, Temozolomide clinical trial acute pancreatitis can also occur in patients with pancreatic heterotopia undergoing EUS-FNA. Key Word(s): 1. Ectopic pancreas; 2. FNA; 3. Ultrasound; 4. Endoscopic; Presenting Author: GANG LI Additional

Authors: HUI-ZHEN FAN, PING XIE, JIAN-WEN SHENG, GU-PING ZHONG Corresponding Author: GANG LI Affiliations: Jiangxi Yichun People’s Hospital Objective: To evaluate the relationship between adenomyomatosis of the gallbladder (GBA) and the postcholecystectomy diarrhoea (PCD). Methods: 33 patients of cholecystectomy with pathologically proved GBA were included in this study. The mean age was 51.2 years old, and male (n = 15), female (n = 17), diffuse type (n = 12), localized type (n = 3), associated with cholecystolithiasis (n = 2), cholecystitis PTK6 (n = 8) and gallbladder polyps (n = 5). 55 cholecystectomy patients (the mean age: 53.4,) were as the control group with male 26 cases, female 29 cases, cholecystolithiasis 27 cases, cholecystitis 16 cases and gallbladder polyps 12 cases, which were not proved GBA by pathology. This study analyzed the preoperative gallbladder contraction function, gallbladder sonography and the postoperative follow-up of 6 months to 12 months with gastrointestinal symptom rating scale (GSRS). Diagnostic Criteria of the postcholecystectomy diarrhoea (PCD): patients with a history of cholecystectomy, preoperative didn’t have a diarrhea history, but postoperative had, the routine examination was normal. Results: There was the statistically significant difference in two groups’ thickness of gallbladder wall, the observation group (0.3–1.

97 × 140 cm with no crossing of layers EUS-FNA (GF-UCT-140-AL5,

97 × 1.40 cm with no crossing of layers. EUS-FNA (GF-UCT-140-AL5, Olympus, Tokyo, Japan) was performed initially with 3 passes using the 19 G ProCore Fluorouracil nmr needle (Cook Medical Inc, Limerick Ireland). Decision was made to switch to 25 G needle (Cook Medical Inc, Limerick Ireland) as only blood was seen on the smears from the core needle and 2 extra passes performed. The procedure was uneventful. Eight hours after procedure, patient presented with sudden onset epigastric pain. Physical examination was unremarkable. Blood investigation showed raised amylase and lipase

at 302 U/L (33–126) and more than 400 U/L (14–40) respectively. Pain resolved with 75 mg of diclofenac sodium given via intramuscular route. Results: Abdominal computer tomography was performed four days later, and showed stranding of the fat adjacent to the SMT suggestive of inflammation. The histologic later showed benign yield of acinar and ductal epithelial cells, the cores of tissue shows lobules of pancreatic parenchyma composed of acinar cells and occasional ducts and fibrous stroma. The features are consistent with diagnosis of benign pancreatic tissue and pancreatic heterotropia.

Conclusion: Pancreatic heterotopia is presence of pancreatic tissue outside of its usual location, without structural or vascular continuity with pancreas proper. Similar to the pancreas proper, Selleck MAPK Inhibitor Library acute pancreatitis can also occur in patients with pancreatic heterotopia undergoing EUS-FNA. Key Word(s): 1. Ectopic pancreas; 2. FNA; 3. Ultrasound; 4. Endoscopic; Presenting Author: GANG LI Additional

Authors: HUI-ZHEN FAN, PING XIE, JIAN-WEN SHENG, GU-PING ZHONG Corresponding Author: GANG LI Affiliations: Jiangxi Yichun People’s Hospital Objective: To evaluate the relationship between adenomyomatosis of the gallbladder (GBA) and the postcholecystectomy diarrhoea (PCD). Methods: 33 patients of cholecystectomy with pathologically proved GBA were included in this study. The mean age was 51.2 years old, and male (n = 15), female (n = 17), diffuse type (n = 12), localized type (n = 3), associated with cholecystolithiasis (n = 2), cholecystitis Parvulin (n = 8) and gallbladder polyps (n = 5). 55 cholecystectomy patients (the mean age: 53.4,) were as the control group with male 26 cases, female 29 cases, cholecystolithiasis 27 cases, cholecystitis 16 cases and gallbladder polyps 12 cases, which were not proved GBA by pathology. This study analyzed the preoperative gallbladder contraction function, gallbladder sonography and the postoperative follow-up of 6 months to 12 months with gastrointestinal symptom rating scale (GSRS). Diagnostic Criteria of the postcholecystectomy diarrhoea (PCD): patients with a history of cholecystectomy, preoperative didn’t have a diarrhea history, but postoperative had, the routine examination was normal. Results: There was the statistically significant difference in two groups’ thickness of gallbladder wall, the observation group (0.3–1.

This was followed by a provider-administered survey regarding pai

This was followed by a provider-administered survey regarding pain directionality. Survey questions were designed to allow the patient to express pain directionality utilizing simple written and pictorial representations of pain (Fig. 1). The design of the questions and diagrams were similar to those utilized by Jakubowski et al.[3] The survey classified migraine pain directionality as “exploding alone, imploding alone, ocular alone, or mixed (ie, combination of any 2 types or all 3 types).” Patients were given a paper survey with

the pictorial representations listed first followed by the written question, “Is your headache pain pushing in or pushing out of your head or is it located within your eye socket (ocular).” After the patient completed the written survey, the clinician conducted a scripted interview from which headache directionality, interattack variability in headache directionality and intra-attack variability in headache AZD6244 cost directionality were determined (Fig. 2). The clinician was blinded to the patient self-assignments of headache directionality. Summary statistics were used to describe selleck chemicals the study sample. Mean ± standard deviation was reported for continuous variables, and percentage/frequency count was computed for nominal variables. For comparison between groups, Kruskal–Wallis test and Pearson’s chi-square

test (or Fisher’s exact test, if applicable) were applied. If the overall test was significant, pairwise comparison was performed using Bonferroni adjustment. Using a 2-sided test, a P value < .05 for overall test was considered statistically significant. Kappa coefficients were calculated to determine concordance between the different methods of assigning headaches to 1 of 4 pain directionalities: imploding ± ocular, exploding ± ocular, ocular, or imploding and exploding. Kappa coefficients were considered

Smad inhibitor weak if less than 0.41, moderate if between 0.41 and 0.60, and strong if 0.61 or greater.[9] Analyses were conducted using SAS 9.2 (SAS Institute, Inc., Cary, NC, USA). One hundred ninety-eight female patients between the ages of 18 years and 77 years were included in the study. Mean age was 48 ± 12.4 years, and median age was 50 years. Race was self-reported as white by 88%, Asian/Pacific Islander by 4%, African American by 3%, and Other by 5%. Highest level of education was graduated college or higher by 65.5%, some college or technical school by 31%, graduated high school by 4%, and grade 11 or less by 1%. There were no differences in age, race, or highest level of education when comparing subjects with different headache directionality. Ninety-five percent (n = 188) of patients in the study reported episodic migraine (<45 headache days in 90), while 5% (n = 10) reported chronic migraine (>45 headache days in 90 days). According to patient selection of pictures that best represented their pain directionality, 14.

1 and Supporting Information Table 1) Interestingly, the express

1 and Supporting Information Table 1). Interestingly, the expression levels of FGF8, FGF17, and FGF18 were considerably lower in healthy livers versus the tumor surrounding this stemmed

mostly from heavily diseased organs containing numerous cirrhotic (premalignant) nodules (Supporting Information Mitomycin C price Table 2). The FGF8, FGF17, and FGF18 protein contents of HCC were analyzed by immunohistochemistry. The extent and intensity of the stains were comparable to the transcript levels; this is exemplified by representative cases in Fig. 1 and Supporting Information Table 4. The positive immunostains of human HCC were most prominent in the malignant hepatocytes (Fig. 1C). Furthermore, recently established hepatocarcinoma cell lines expressed FGF8, FGF17, and FGF18 at mRNA levels close to those in HCC (Fig.

2 and Supporting Information Table 2). These findings suggest that the epithelial compartment in HCC is the major source of the elevated levels of the FGF8 subfamily. The four FGF8 isoforms as well as FGF17 and FGF18 bind with considerable affinity to FGFR2, FGFR3, and FGFR4.19 We applied primers for qRT-PCR to detect all important splice variants of these receptors and found many HCC cases with elevated mRNA levels in comparison with selleckchem the surrounding tissue (Fig. 1A and Supporting Information Table 1). Accordingly, 56% of the investigated HCC cases showed at least 2-fold up-regulation of one or more FGFRs. The immunostaining of FGFR2, FGFR3, and FGFR4 occurred predominantly in the epithelial HCC cells and matched the transcript levels well (Fig. 1C and Supporting Information

Table 4). In conclusion, 82% of the studied HCC cases showed up-regulation of at least one FGF8 subfamily member and/or one FGFR. In every third tumor, the enhanced expression of at least one FGF and SPTLC1 one FGFR coincided. Rapidly growing tumors such as HCC often suffer from an insufficient blood supply. Therefore, we asked whether the up-regulation of FGFs in HCC may be a response to a lack of serum and insufficient oxygen. When HCC-1.2, HepG2, and Hep3B cells were either serum-starved or kept under the hypoxia-mimetic drug deferoxamine mesylate, the transcript levels of FGF8, FGF17, and FGF18 were increased up to 40-fold within 48 hours above the already notable levels of controls (Fig. 2A,B and Supporting Information Table 2). Similar increases were obtained when the cells were kept under 1% oxygen (Supporting Information Fig. 1). Immunoblotting revealed that the up-regulated FGF18 mRNA in the serum-starved cells was paralleled not by an increased intracellular protein level (not shown) but instead by an elevated secretion of this growth factor to the culture supernatant. We estimated that 5 × 105 cells released at least 2 ng of FGF18 per mL of the medium when they were kept serum-free for 48 hours (Fig. 2C and Supporting Information Fig. 2). We asked whether the elevated production of FGF8 subfamily members due to a shortage of serum and oxygen confers any advantage to HCC-1.

1 and Supporting Information Table 1) Interestingly, the express

1 and Supporting Information Table 1). Interestingly, the expression levels of FGF8, FGF17, and FGF18 were considerably lower in healthy livers versus the tumor surrounding this stemmed

mostly from heavily diseased organs containing numerous cirrhotic (premalignant) nodules (Supporting Information selleck Table 2). The FGF8, FGF17, and FGF18 protein contents of HCC were analyzed by immunohistochemistry. The extent and intensity of the stains were comparable to the transcript levels; this is exemplified by representative cases in Fig. 1 and Supporting Information Table 4. The positive immunostains of human HCC were most prominent in the malignant hepatocytes (Fig. 1C). Furthermore, recently established hepatocarcinoma cell lines expressed FGF8, FGF17, and FGF18 at mRNA levels close to those in HCC (Fig.

2 and Supporting Information Table 2). These findings suggest that the epithelial compartment in HCC is the major source of the elevated levels of the FGF8 subfamily. The four FGF8 isoforms as well as FGF17 and FGF18 bind with considerable affinity to FGFR2, FGFR3, and FGFR4.19 We applied primers for qRT-PCR to detect all important splice variants of these receptors and found many HCC cases with elevated mRNA levels in comparison with Carfilzomib in vivo the surrounding tissue (Fig. 1A and Supporting Information Table 1). Accordingly, 56% of the investigated HCC cases showed at least 2-fold up-regulation of one or more FGFRs. The immunostaining of FGFR2, FGFR3, and FGFR4 occurred predominantly in the epithelial HCC cells and matched the transcript levels well (Fig. 1C and Supporting Information

Table 4). In conclusion, 82% of the studied HCC cases showed up-regulation of at least one FGF8 subfamily member and/or one FGFR. In every third tumor, the enhanced expression of at least one FGF and Tolmetin one FGFR coincided. Rapidly growing tumors such as HCC often suffer from an insufficient blood supply. Therefore, we asked whether the up-regulation of FGFs in HCC may be a response to a lack of serum and insufficient oxygen. When HCC-1.2, HepG2, and Hep3B cells were either serum-starved or kept under the hypoxia-mimetic drug deferoxamine mesylate, the transcript levels of FGF8, FGF17, and FGF18 were increased up to 40-fold within 48 hours above the already notable levels of controls (Fig. 2A,B and Supporting Information Table 2). Similar increases were obtained when the cells were kept under 1% oxygen (Supporting Information Fig. 1). Immunoblotting revealed that the up-regulated FGF18 mRNA in the serum-starved cells was paralleled not by an increased intracellular protein level (not shown) but instead by an elevated secretion of this growth factor to the culture supernatant. We estimated that 5 × 105 cells released at least 2 ng of FGF18 per mL of the medium when they were kept serum-free for 48 hours (Fig. 2C and Supporting Information Fig. 2). We asked whether the elevated production of FGF8 subfamily members due to a shortage of serum and oxygen confers any advantage to HCC-1.

Postoperative

complications of the donors were graded acc

Postoperative

complications of the donors were graded according to the Clavien classification. Staurosporine mouse Results: There were 45 donors (7%) with Gilbert’s syndrom in a mean age of 33 years. The control group consist of 99 donors by a mean age of 32 years. All patients received the right lobe of their donor. There were no intraoperative complications. The comparison of the two groups have shown that there are no significant differences in age, remnant ratio, intra- or postoperative complications, AST-, ALT-, INR- levels, hospital stay or survival. However the postoperative bilirubin levels at day 1-7, the maximal peak bilirubin level and the level one and six month after transplantation are significantly higher in donors with Gilbert’s syndrome compared to non-Gilbert’s donors (Table 1). There were no donor death in our series. Conclusion: Although ABT-199 cost the bilirubin levels are significantly higher in donor with Gilbert’s syndrome compared to non-Gilbert’s group, the results do not show any clinical importance. Based on the results of our study we can conclude that donor with Gilbert’s syndrome can be accepted safely for living donor liver transplantation without increased risk. p:0.000, student T test, for all Disclosures: The following people have nothing to disclose:

Murat Akyildiz, Gokhan Gungor, Necdet Guler, Arzu Oezcelik, Tonguc Utku Yilmaz, Onur Yaprak, Yalcin Erdogan, Murat Dayangac, Yildiray Yuzer, Yaman Tokat Purpose: Laparoscopic liver resection (LLR) has been shown to be safe and efficacious

in the management of liver masses in adults, however, little literature Pyruvate dehydrogenase lipoamide kinase isozyme 1 exists describing the feasibility of and approaches to LLR in children. Additionally, the indications for LLR have typically excluded large lesions (>5 cm) and masses in the posterior and superior segments of the liver, due to technical limitations. We present our experience with LLR for liver lesions in the pediatric population, including large tumors, masses in difficult locations, and major hepatic resection. Methods: After IRB approval, we retrospectively reviewed LLR patients treated at our institution from 2009 – 2012. Data collected included demographics, clinical presentations, radio-graphic studies, intraoperative details, and postoperative complications and outcomes. Results: Six LLR procedures were performed in children (2 males, 4 females) presenting between 5 – 21 years of age. Maximal tumor diameter ranged from 3.1 – 10 cm (mean, 5.7 cm). Indications for resection included enlarging mass and/or right upper quadrant pain. Operative approaches included pure laparoscopy (n = 3) and hand-assisted laparoscopy (n = 3). Laparoscopic ultrasound was utilized in all patients to delineate resection margins and major intrahepatic vasculature. Techniques utilized for parenchymal transection included electrocautery, Harmonic scalpel, CUSA ultrasonic dissection, and endoscopic surgical staplers.

Postoperative

complications of the donors were graded acc

Postoperative

complications of the donors were graded according to the Clavien classification. www.selleckchem.com/Akt.html Results: There were 45 donors (7%) with Gilbert’s syndrom in a mean age of 33 years. The control group consist of 99 donors by a mean age of 32 years. All patients received the right lobe of their donor. There were no intraoperative complications. The comparison of the two groups have shown that there are no significant differences in age, remnant ratio, intra- or postoperative complications, AST-, ALT-, INR- levels, hospital stay or survival. However the postoperative bilirubin levels at day 1-7, the maximal peak bilirubin level and the level one and six month after transplantation are significantly higher in donors with Gilbert’s syndrome compared to non-Gilbert’s donors (Table 1). There were no donor death in our series. Conclusion: Although BVD-523 concentration the bilirubin levels are significantly higher in donor with Gilbert’s syndrome compared to non-Gilbert’s group, the results do not show any clinical importance. Based on the results of our study we can conclude that donor with Gilbert’s syndrome can be accepted safely for living donor liver transplantation without increased risk. p:0.000, student T test, for all Disclosures: The following people have nothing to disclose:

Murat Akyildiz, Gokhan Gungor, Necdet Guler, Arzu Oezcelik, Tonguc Utku Yilmaz, Onur Yaprak, Yalcin Erdogan, Murat Dayangac, Yildiray Yuzer, Yaman Tokat Purpose: Laparoscopic liver resection (LLR) has been shown to be safe and efficacious

in the management of liver masses in adults, however, little literature DCLK1 exists describing the feasibility of and approaches to LLR in children. Additionally, the indications for LLR have typically excluded large lesions (>5 cm) and masses in the posterior and superior segments of the liver, due to technical limitations. We present our experience with LLR for liver lesions in the pediatric population, including large tumors, masses in difficult locations, and major hepatic resection. Methods: After IRB approval, we retrospectively reviewed LLR patients treated at our institution from 2009 – 2012. Data collected included demographics, clinical presentations, radio-graphic studies, intraoperative details, and postoperative complications and outcomes. Results: Six LLR procedures were performed in children (2 males, 4 females) presenting between 5 – 21 years of age. Maximal tumor diameter ranged from 3.1 – 10 cm (mean, 5.7 cm). Indications for resection included enlarging mass and/or right upper quadrant pain. Operative approaches included pure laparoscopy (n = 3) and hand-assisted laparoscopy (n = 3). Laparoscopic ultrasound was utilized in all patients to delineate resection margins and major intrahepatic vasculature. Techniques utilized for parenchymal transection included electrocautery, Harmonic scalpel, CUSA ultrasonic dissection, and endoscopic surgical staplers.

The parallel findings also extend to the dilated sinusoids and pe

The parallel findings also extend to the dilated sinusoids and peliotic changes, which are regular features of HCA and FNH. Arterial sprouts, described in Ang-1 transgenic mice, might well represent the equivalent of the single arteries

that are regularly found in HCA. The large dystrophic vessels with robust myointimal thickening that characterize FNH are, however, not found in HCA. These differences indicate a preponderance of the myofibroblast BMN 673 price recruitment effect of Ang-1 in FNH, whereas in HCA, up-regulation of Ang-1 seems to be predominantly stimulating vascular remodeling. These variable effects of Ang-1 could be due to the difference in the magnitude of Ang-1 enhancement, although the etiological context in which Ang-1 exerts its effects is probably similar if not more important. BMS-907351 research buy The etiological

context of FNH is a liver already affected by vascular injury that possibly has stimulated reparative mechanisms to restore vascular integrity and triggered recruitment of vascular SMCs. Of note is the fact that the nodular lesions resembling human FNH in the hepatic Ang-1 transgenic mice were also preceded by an obliterative vascular lesion.14 It remains to be elucidated whether the early stage of vascular injury itself provokes Ang-1 overexpression in FNH. HCA is

a primary neoplastic lesion and lacks a primary vascular anomaly such as that in FNH. As such, in HCA, the vascular integrity is not jeopardized, and recruitment of myofibroblasts to stabilize vessels is less stimulated; this is compatible with the less prominent increase in Ang-1 observed in HCA. The emphasis of Ang-1 overexpression in HCA seems to lie in the induction of vascular remodeling. Whether these vascular changes represent angiogenesis effective at providing neoplastic growth with its increasing vascular demands is yet unclear. The single arteries observed in HCA are also regularly else found in HCC, and in our previous study, we also found increased Ang-1 in human HCC.8 However, studies on the expression of Ang-1 in tumor models have reported variable results in different types of tumors, including the induction of tumor angiogenesis in astrocytomas, glioblastomas, and cervical cancer but a decrease in angiogenesis in colorectal cancer and liver metastases of colorectal cancer (reviewed by Shim et al.26). In conclusion, we have demonstrated increased expression of the angiogenic growth factor Ang-1 in FNH and HCA with maintenance of the expression of its receptor Tie-2, which potentially underlies the development of the dysmorphic vascular features in these two lesions.

The parallel findings also extend to the dilated sinusoids and pe

The parallel findings also extend to the dilated sinusoids and peliotic changes, which are regular features of HCA and FNH. Arterial sprouts, described in Ang-1 transgenic mice, might well represent the equivalent of the single arteries

that are regularly found in HCA. The large dystrophic vessels with robust myointimal thickening that characterize FNH are, however, not found in HCA. These differences indicate a preponderance of the myofibroblast this website recruitment effect of Ang-1 in FNH, whereas in HCA, up-regulation of Ang-1 seems to be predominantly stimulating vascular remodeling. These variable effects of Ang-1 could be due to the difference in the magnitude of Ang-1 enhancement, although the etiological context in which Ang-1 exerts its effects is probably similar if not more important. Daporinad solubility dmso The etiological

context of FNH is a liver already affected by vascular injury that possibly has stimulated reparative mechanisms to restore vascular integrity and triggered recruitment of vascular SMCs. Of note is the fact that the nodular lesions resembling human FNH in the hepatic Ang-1 transgenic mice were also preceded by an obliterative vascular lesion.14 It remains to be elucidated whether the early stage of vascular injury itself provokes Ang-1 overexpression in FNH. HCA is

a primary neoplastic lesion and lacks a primary vascular anomaly such as that in FNH. As such, in HCA, the vascular integrity is not jeopardized, and recruitment of myofibroblasts to stabilize vessels is less stimulated; this is compatible with the less prominent increase in Ang-1 observed in HCA. The emphasis of Ang-1 overexpression in HCA seems to lie in the induction of vascular remodeling. Whether these vascular changes represent angiogenesis effective at providing neoplastic growth with its increasing vascular demands is yet unclear. The single arteries observed in HCA are also regularly selleck kinase inhibitor found in HCC, and in our previous study, we also found increased Ang-1 in human HCC.8 However, studies on the expression of Ang-1 in tumor models have reported variable results in different types of tumors, including the induction of tumor angiogenesis in astrocytomas, glioblastomas, and cervical cancer but a decrease in angiogenesis in colorectal cancer and liver metastases of colorectal cancer (reviewed by Shim et al.26). In conclusion, we have demonstrated increased expression of the angiogenic growth factor Ang-1 in FNH and HCA with maintenance of the expression of its receptor Tie-2, which potentially underlies the development of the dysmorphic vascular features in these two lesions.

Differences in categorical measures across ordinal groups (ie,

Differences in categorical measures across ordinal groups (i.e., PI3K inhibitor drugs educational attainment and iron scores) were assessed using a Jonckeere-Terpstra test, or the exact equivalent. Continuous measures were summarized as medians and interquartile ranges with differences in group distributions assessed using a Wilcoxon rank sum test (for comparison of two groups) or a Kruskal-Wallis test (for comparison

of more than two groups). To assess whether changes in lipid profile measures significantly differed from baseline, a Wilcoxon sign rank test was used. Associations between the proportion of PEG-IFN and ribavirin taken with changes in serum selleck chemical lipids were assessed using Spearman’s correlation analyses. For all statistical tests, P < 0.05 was considered statistically significant. To evaluate factors associated with SVR, a relative risk model was employed with a robust variance

estimator.38 In regression models, TG, HDLc, and TC were transformed to the natural logarithm scale to achieve normality. All continuous predictors were centered. The relationships between baseline and 24-week changes during treatment in lipid profile measures and the probability of SVR were graphically assessed using smoothing spline plots. Due to different patterns observed by gender, smoothing spline plots for HDLc were examined separately for males and females. Two types of multivariable models of SVR were constructed using a stepwise approach. One type of multivariable model (models 1 and 2) allowed Farnesyltransferase pretreatment characteristics and the amount of PEG-IFN taken during the first 24 weeks as eligible predictors. Model 2 allowed as additional eligible predictors the baseline lipid profile measures. A second type of multivariable model (model 3) also

adjusted for body weight changes and allowed for the inclusion of variables representing baseline and changes in lipid profile measures during the first 24 weeks of therapy as eligible predictors. To compare the prediction of multivariable models, differences in area under the receiver operating curves (AUROCs) were assessed using a nonparametric method.39 Baseline characteristics of the 330 participants are shown in Table 1. AAs did not significantly differ from CAs by age, gender, employment status, health risk behaviors (smoking status and weekly alcohol consumption), viral level, aspartate aminotransferase, international normalized ratio, white blood cell count, platelet count, percent iron/total iron-binding capacity, Ishak fibrosis, total histological activity index score, steatosis, TG, HDLc, or TC. Compared with CAs, a larger percentage of AAs had health insurance coverage (87% versus 78%, P = 0.