me/ir2eb) “
“Contrary to widely held opinion, the headache

disorder we term “migraine” is not clinically stereotyped. The symptoms of a migraine attack may vary dramatically between afflicted individuals, and even in a given individual symptoms SB203580 supplier may be quite different from attack to attack. While on Monday you may experience the severe, one-sided, and throbbing headache (with associated nausea and vomiting) typical of “classical” migraine, Saturday’s migraine attack instead may involve a dull, generalized, and low-intensity headache absent any nausea but accompanied by the visual symptoms known as “aura.” The attacks’ symptoms are quite different – the headaches themselves are quite different – but both attacks are check details “migraine. Not only do the symptoms

of migraine tend to vary from attack to attack, but even within a single attack there may occur a progression of symptoms. Acute migraine is dynamic, both in terms of symptomatology and the biologic process that produces those symptoms; if that process is allowed to progress unchecked for too long, the symptoms it generates can become quite difficult to treat. The concept of stratified care acknowledges the dynamic nature of an evolving migraine attack, and use of a stratified care approach to treatment of acute migraine implies that one selects his/her therapy based upon the headache’s intensity and the presences vs absence of associated symptoms (eg, nausea and vomiting). Very few migraineurs find that a single medication or alternative therapy is effective

for all their migraine headaches. For example, “three aspirin and a cup of coffee” may represent perfectly appropriate (and effective) therapy for early/mild migraine, but this treatment makes little sense if the headache is severe and accompanied by vomiting. For the migraineur’s therapeutic MCE arsenal, it is often ideal to have two or three different therapies available for acute migraine treatment: (1) something for early/mild headache; (2) something for headaches that have escalated despite treatment with #1 or that have escalated rapidly to become moderate to severe (eg, “full-blown” migraine already present upon awakening); and (3) a “rescue” therapy if #2 fails. With this “stratified” approach, you hopefully will find yourself far more capable of controlling your acute migraine attacks. “
“Broad discrepancies in the number of migraine triggers have been reported in several studies. Migraineurs do not seem to recognize easily headache triggers in clinical practice. To evaluate how aware migraineurs are about their headache triggers. We recruited 120 consecutive migraineurs. Each patient was first asked to report spontaneously any migraine trigger. Subsequently, the patient selected from a list of commonly known triggers. Ninety-seven patients (72.

Gli2+ cell counts were associated with fibrosis stage (P = 0.0013); numbers of Gli2+ cells were higher in cases with advanced fibrosis (S3-4) than in cases with no fibrosis (S0, P = 0.004) and cases with mild to moderate fibrosis (S1-2, P = 0.004) (Fig. 2A-D). The number of Gli2+ cells was also significantly associated with the severity of portal inflammation (P = 0.0012, Fig. 2D) XL765 ic50 and tended to be associated with the severity of hepatocyte ballooning (P = 0.073). In the ordinal logistic regression model including portal inflammation grade, fibrosis stage, and gender, portal inflammation and fibrosis showed independent associations with the number of

Gli2+ cells (multiple linear regression model, effect test: P = 0.022 for portal inflammation and P = 0.045 for fibrosis). There were no significant associations between Gli2+ cells and grade of steatosis or lobular inflammation, while a borderline positive association with ballooning grade was noted (P = 0.074). K7+ cell counts were significantly positively selleck kinase inhibitor associated with the severity of portal inflammation (P = 0.0185) and tended to be associated with the severity of hepatocyte ballooning (P = 0.074). In the multiple linear regression model including both grade of portal inflammation and ballooning, portal inflammation, but not hepatocyte ballooning, tended to be associated with the

number of K7+ cells (effect test: P = 0.082 for portal inflammation and P = 0.546 for hepatocyte ballooning). Further, advanced fibrosis (S3-4) tended to be associated with a higher number of K7+ cells versus none to moderate fibrosis (S0-2, P = 0.064). There were no significant associations 上海皓元 between the number of K7+cells and grade of steatosis or lobular inflammation. The percentage of Gli2+ cells among

the K7+ cells (percentage of Gli2+/K7+ cells) did not show a significant association with the severity of any of the histologic features. Because Hh signaling promotes fibrogenesis, the remaining available liver sections were stained for Vim, a general marker of mesenchymal cells, and α-SMA, a marker of myofibroblasts. The median grades of Vim and αSMA staining were 3 [IQR 1.8, 4.3] (n = 8) and 3 [IQR 1.3, 4.5] (n = 6), respectively. Vim expression was significantly associated with advanced fibrosis (P = 0.038). α-SMA expression showed borderline association with fibrosis and portal inflammation (P = 0.0603). SHh positivity was visualized as three, relatively discrete, patterns: SHh+ ballooned hepatocytes, SHh+ bile ducts and ductules, and SHh+ periportal nonballooned hepatocytes (Fig. 3A-D). SHh+ ballooned hepatocytes, periportal nonballooned hepatocytes, and bile duct/ductular cells were noted in 46.7%, 62.5%, and 86.7% of the cases, respectively. Interestingly, the presence of SHh+ ballooned hepatocytes and SHh+ periportal nonballooned hepatocytes were mutually exclusive (Fig. 3C-E, chi-square test for the presence or absence of these SHh+ patterns, P = 0.03).

Misplacement of knee implants can be responsible for restricted ROM even in patients without arthrofibrosis so this is especially important in haemophilia patients. Patella baja or inferior position of the patella correlates closely with loss of ROM. Other considerations include a balanced flexion and extension gap so the implants have ligament stability without being too tight in flexion or extension. Increasing thickness of the patella by removing too little bone or inserting a patellar

CH5424802 button that is too thick may reduce flexion. This can also occur if the femoral component is placed too anterior. Reduced flexion can also occur if the femoral component is too posterior or too large. Templating the preoperative X-rays will help estimate the proper size of implants but the most critical part is accurate measurement and proper placement at surgery. If at trial reduction some flexion contracture remains, the posterior capsule is released from the distal femur under direct vision. As the capsule is released, the surgeon’s non-dominant hand pushes the posterior capsule away from the femur to protect the popliteal neurovascular structures. The suprapatellar fat covering the anterior distal femur should be

preserved, as it is a barrier to quadriceps adhesion. In patients where it has been selleck chemical replaced by fibrous tissue, restoration of motion is especially challenging. In patients with severe, long-standing flexion contractures serial casting and physical therapy preoperatively may help. Utilizing these methods, it is usually possible to get good, functional ROM at the time of surgery. The problem is keeping it. In patients with inadequate patellar 上海皓元医药股份有限公司 thickness for component fixation, patellectomy is the procedure of choice. This surgery

has been associated with improved ROM in the stiff knee. Most patellectomy patients have an extensor lag for several months that resolves to minimal or no lag. Patients going to surgery with very limited flexion may require quadricepsplasty, which is often associated with an extensor lag for six months or longer. It is important not to overlengthen the extensor mechanism to avoid a permanent extensor lag. The CPM may be useful for 4–6 h during the day, especially prior to physical therapy. It facilitates flexion but is not as helpful for gaining extension as a knee immobilizer, which is recommended at night for patients with a flexion contracture. Use of a towel roll under the ankle periodically during the day also helps gain extension. Residual haemarthrosis will stimulate arthrofibrosis. Postoperative drains are used in all of these patients and left in place until the output is <20cc per shift, usually 48 h.

03) and 0% showed virological

recurrence verus 8/21 (38%) not co-infected (p=0.01). Other possible predictors of recurrence (previous therapies for HCV, patients, grafts and donors conditions at LT, time of HCV-RNA undetectability…) did not show any significance. Nevertheless, at logistic regression the only parameter significantly associated with lower histological recurrence rate was pre-LT HCV-RNA undetectability > 6 months (p=0.02), irrespective of previous therapies for HCV. Graft was lost in 9/50 (18%) patients: graft survival was 86% at 1 year from LT, 81% at 2, 5 and 10 years. 4/50 (8%) patients died: survival was 96% at 1 year from LT, 91% at 2, 5 and 10 years. No significant predictors of mortality and lost of graft were found among HCV-related variables. CONCLUSIONS: In patients with HCV-related liver disease and undetectable HCV-RNA Y-27632 order at LT the HCV recurrence rates are far lower than those observed in HCV-RNA positive patients. The only variable strongly associated with lower HCV recurrence rate seems to be a pre-LT period of HCV-RNA undetectability > 6 months, irrespective of previous therapies for HCV. In our cohort, grafts and patients survival rates after LT are comparable to those observed in patients without an history of HCV infection, and no HCV-re-lated

variable affect these rates. A curious issue is the hypothetical “protective Ibrutinib solubility dmso role” from HCV recurrence that some data suggest for HBV-HCV co-infection. Disclosures: The following people have nothing to disclose: Alessandro Risso, MCE公司 Francesco Tandoi, Silvia Martini, Renato Romagnoli, Mauro Salizzoni Introduction: Treatment of the hepatitis

C virus (HCV) post-liver transplantation has been notoriously difficult. In this population, drug-drug interactions often have serious consequences and immunosuppressant therapy may make viral eradication more difficult. The interferon-free regimen used in the COSMOS study combined two Direct Acting Antivirals (DAAs), sofosbuvir and simeprevir. Early data suggests that it appears safe and effective in non-cirrhotic and cirrhotic individuals. Little data is available on the safety and efficacy of this treatment in patients post-liver transplant. Here we describe our experience using sofosbuvir and simeprevir in patients after liver transplant. Methods: This was an IRB approved retrospective analysis. Thirty-two patients who underwent liver transplantation were started on a 12-week course of sofosbuvir and simeprevir. Two patients were also given ribavirin. Basic laboratory data, viral kinetics, side effects, and changes in immune suppression were recorded. Only patients infected with GT 1a (55%) or 1b (45%) were included. SVR 12 data will be available at time of presentation. Statistics performed using JMP SAS with non-parametric, parametric or multivariate analysis as deemed necessary.

Of note was the much greater degree of ROS production after ovariectomy in transgenic mice than in non-transgenic mice. These results suggested that HCV protein

expression has the potential to increase AZD1208 the sensitivity to oxidative stress in the liver. At least two possibilities may account for the increased sensitivity to oxidative stress in FL-N/35 transgenic mice. One possibility is an additive effect of HCV-induced ROS production on ovariectomy-induced oxidative stress. The HCV core protein has been shown to inhibit mitochondrial electron transport[35] and to induce ROS production.[36] In fact, basal ROS production tended to be higher in transgenic mice than in non-transgenic mice, but was not significantly different. These results suggested that additive HCV-induced ROS production

was unlikely to be the cause of the significantly increased ROS production after ovariectomy in the transgenic mice. The other possibility is HCV-associated attenuation of antioxidant potential against ovariectomy-induced oxidative stress. In this respect, OVX transgenic mice had a lower ratio of BAP to dROM than OVX non-transgenic mice and the expression of SOD2 and GPx1 in the liver was not increased. These results suggest that HCV protein attenuated antioxidant potential against ovariectomy-induced oxidative stress. Proliferator-activated receptor-γ co-activator-1α is required

for the induction see more of many ROS-detoxifying MCE enzymes upon oxidative stress.[26] SIRT3 has been shown to function as a downstream target gene of PGC-1α and mediate the PGC-1α-dependent induction of ROS-detoxifying enzymes.[27] Additionally, AMPK, which is a crucial cellular energy sensor, regulates PGC-1α activity through both modulation of PGC-1α transcription and phosphorylation of the PGC-1α protein.[28, 37] Thus, AMPK/PGC-1α signaling is one of the important pathways that protect cells from oxidative stress through the induction of several key ROS-detoxifying enzymes. Recent evidence indicating that HCV replication inhibits AMPK activity[29] prompted us to investigate whether the antioxidant potential against ovariectomy-induced oxidative stress in FL-N/35 transgenic mice was attenuated through inhibition of this signaling pathway. As expected, upon ovariectomy, AMPK was activated in non-transgenic mice, but not in transgenic mice. This, in turn, led to the lower expression of PGC-1α in the nuclear fraction of the liver in OVX transgenic mice than in OVX non-transgenic mice, resulting in the absence of significant induction of SIRT3 in the mitochondrial fraction of the liver in the OVX transgenic mice. Thus, ROS production in the liver in OVX transgenic mice was increased by attenuation of the antioxidant potential through inhibition of AMPK/PGC-1α signaling.

[19] Activating Notch also promotes epithelial-to-mesenchymal transition in kidney cells,[20] stimulates expansion of cardiac progenitors at the expense of MFs,[21] and promotes an epithelial-to-mesenchymal transition process that enhances the stem-like properties of cancer stem cells.[22] Notch signaling is critical for biliary morphogenesis during development.[23-25] As mentioned earlier, the fate of adult liver progenitors is also directed by Notch: Increasing selleckchem Notch signaling promotes differentiation along the biliary lineage, whereas suppressing

the Notch pathway shifts progenitors toward an hepatocytic fate.[2] Deregulated Notch signaling has been implicated in the pathogenesis of hepatocellular carcinoma and cholangiocarcinoma.[26, 27] Despite growing evidence for Notch pathway involvement in liver cancer and fibrosis, it is unclear how Notch interfaces with other key signaling pathways that have been implicated in those disorders, or how Notch signaling in one type of liver cell (e.g., MFs) might influence the accumulation of other types of liver cells (e.g., epithelial progenitors) that are required for adult liver repair. In this study, we evaluated the

hypothesis that Notch pathway activation in HSCs stimulates them to become (and remain) MFs through a mechanism that involves an epithelial-to-mesenchymal–like transition requiring cross-talk with canonical (i.e., TGF-β-independent) Hedgehog signaling. Full methods are available in the Supporting Information. Male C57BL/6 mice selleck and Smotm2Amc/J (Smoothened [Smo]/flox) mice were obtained from The Jackson Laboratory (Bar Harbor, ME).[28] Smo/flox mice were crossed with α-SMA-Cre-ERT2

transgenic mice[29] to generate double-transgenic (DTG) mice in which treatment with tamoxifen induces conditional deletion of Smo in α-SMA-positive cells.[9] Mice (8-12 weeks old) were subjected to bile duct ligation (BDL) or sham surgery for 14 days. Other 8-10-week-old wild-type (WT) mice were fed with a high-fat diet (HFD) and given intraperitoneal injection of either vehicle (olive oil) or CCl4 (1 μL/g body weight, prediluted 1:3 in olive oil) twice per week for 2 weeks and sacrificed 72 hours after last CCl4 injection.[30] Animal experiments fulfilled 上海皓元 National Institutes of Health (Bethesda, MD) and Duke University Institutional Animal Care and Use Committee (Durham, NC) requirements for humane animal care. Formalin-fixed, paraffin-embedded livers were prepared for immunohistochemistry (IHC).[9] Protocols and antibodies used are listed in the Supporting Information. Quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and immunoblottings were performed as previously described.[31] Primary HSCs were isolated from C57BL/6 mice using standard approaches. Purity of the preparations was rigorously analyzed as previously described.

60 ± 0.43 to 1.00 ± 0.36, P < 0.05) was observed 1 month after resection. Patients with consistent CTC7.5 <2 had lower recurrence rates than those with values consistently ≥2 (15.5% versus 87.50%, P < 0.001). EpCAM+ CTCs displayed cancer stem cell biomarkers (CD133 and ABCG2), epithelial-mesenchymal transition, Wnt pathway activation, high tumorigenic potential, and low apoptotic propensity. Conclusion: selleck inhibitor Stem cell–like phenotypes are observed in EpCAM+ CTCs, and a preoperative CTC7.5 of ≥2 is a novel predictor for tumor recurrence in HCC patients after surgery, especially in patient subgroups with AFP levels of ≤400 ng/mL or low tumor recurrence

risk. EpCAM+ CTCs may serve Selleckchem SB525334 as a real-time parameter for monitoring treatment response and a therapeutic target in HCC recurrence. (HEPATOLOGY 2013) Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies worldwide, and associated morbidity and mortality rates have escalated in recent years.1 Despite improvements in surveillance and clinical treatment strategies, the prognosis of HCC remains very poor due to high incidence of recurrence and

metastasis.2 Traditional clinicopathological parameters such as tumor morphology, histopathological features, and tumor staging system offer limited information for predicting postoperative recurrence and fail to monitor the therapeutic response in a real-time MCE公司 manner.3 Therefore, it is imperative to develop novel approaches for discriminating high-risk factors of recurrent patients and continuous surveillance of antitumor treatment response. The spread of circulating tumor cells (CTCs) in the blood plays a major role in the initiation of metastases and tumor recurrence after surgery.3 Recent studies have reported that stem cell markers are frequently overexpressed in CTCs of metastatic breast cancer.4 In addition, clinical observations and animal model studies indicate that although thousands of tumor cells disseminate into the circulation, only a small population with stem cell–like properties survives migration

to establish secondary colonies.5, 6 Therefore, CTCs with stem cell properties might be potential sources for cancer relapse and distant metastasis, consistent with the cancer stem cell (CSC) hypothesis.7 AFP, alpha-fetoprotein; AUC, area under the curve; BCLC, Barcelona Clinical Liver Cancer; CI, confidence interval; CK, cytokeratin; CSC, cancer stem cell; CTC, circulating tumor cell; DAPI, 4′,6-diamidino-2-phenylindole; EpCAM+, epithelial cell adhesion molecule–positive; HCC, hepatocellular carcinoma; mRNA, messenger RNA; NOD/SCID, nonobese diabetic/severe combined immunodeficiency; qRT-PCR, quantitative real-time polymerase chain reaction; ROC, receiver operating characteristic; TACE, transcatheter arterial chemoembolization; TTR, time to recurrence.

1).1,2 According to the report of the 18th follow-up survey, 3-, 5- and 10-year survival rates for TACE (including chemolipiodolization)

used to treat HCC were all poor, at 43.2%, 24.1% and 6.6%, respectively.9 These PLX-4720 datasheet outcomes are due to the inclusion of patients in poor condition with hepatic reserve or tumor stage that contraindicates hepatic resection or RFA. The same Japanese follow-up survey of outcomes for TACE as initial therapy for Child–Pugh class A patients with a single tumor found that 1-, 3- and 5-year survival rates were good, at 93%, 73% and 52%, respectively.35,38 Transcatheter arterial chemoembolization is performed as initial treatment in 31.7% of cases,9 but is the most frequently used treatment for recurrence, and it is no exaggeration to say that most HCC patients undergo this therapy at some point (Fig. 2). TACE is periodically repeated in Europe and the USA, but this situation rarely arises in Japan. selleck compound When one to three intrahepatic lesions are present, TACE is followed by additional RFA with the aim of improving local control. With the advent of sorafenib, definitions of TACE failure/refractory HCC have

now been proposed to prevent liver dysfunction from decreasing after excursively repeating TACE and to maintain opportunities to administrate sorafenib.1 SORAFENIB WAS APPROVED as a molecular-targeted drug for the treatment of HCC in Japan from May 2009. This agent was approved based on the results MCE公司 of two randomized control trials from outside of Japan39,40 and a phase I clinical trial carried out in Japan.41 However, studies continued after sorafenib entered the market due to a lack of experience with administration in Japan. A safety alert was initially issued due to early deaths resulting from liver failure and hepatic encephalopathy, but it has since been used correctly. The median survival period in Japan is 11.0 months and the response rate is 4%, almost the same outcomes as those of the SHARP trial, but reports to date have shown a tendency

for a greater number of side-effects, including hand–foot skin reaction, diarrhea, hypertension, loss of appetite and fatigue.42 Sorafenib is used to treat Child–Pugh class A patients who have extrahepatic lesions or multiple intrahepatic lesions who are unable to undergo TACE or HAIC, and patients with vascular invasion.1 Measures taken in Japan to reduce side-effects include a low initial dose of 400 mg/day,42 but drug effectiveness at half dose has yet to be fully investigated. Sorafenib has also not been compared with HAIC, which was already being performed in Japan, and there is debate on its positioning in the treatment of advanced intrahepatic cancer. A study is currently underway to verify the effects of combining sorafenib therapy and HAIC.

The present study aimed to evaluate the safety and validity of endoscopic hemostasis for lower gastrointestinal bleeding in elderly individuals aged more than 70 years. Methods: We reviewed the cases of 36 patients with lower gastrointestinal bleeding who underwent endoscopic hemostasis at our hospital between April 2009 and February 2014. Results: The mean age was 76.2 years (70–91 years). Nineteen patients were men, and 17 were women. Five patients

were using an antiplatelet selleck products agent. Seven patients were using an anticoagulant agent (including heparin injection). Three patients were using a combination of both agents. The cause of bleeding was ulcer induced by endoscopic mucosal resection in 12 cases, ulcer induced by endoscopic submucosal dissection in 6, anastomosis site of colon resection in 5, colon diverticulum in 4, radiation proctitis in 4, hemorrhagic rectal ulcer in 3, biopsy for advanced colorectal cancer in 1, and vascular ectasia in 1. The methods of treatment were as follows:

clipping in 27 cases, argon plasma coagulation in 6, hemostatic forceps in 5, and temporary snare in 1. All patients find more who underwent endoscopic therapy achieved hemostasis. There were no serious complications such as perioperative death or complications requiring emergency surgery. Conclusion: Endoscopic hemostasis is a safe and effective treatment for lower gastrointestinal bleeding in the elderly. Key Word(s): 1. lower gastrointestinal bleeding endoscopic therapy Presenting Author: YULI PRAMANA TRIYANTA Additional Authors: Na Corresponding Author: YULI PRAMANA TRIYANTA Affiliations: PGI PEGI Objective: Endoscopic schlerotherapy and endoscopic ligation were accepted in the treatment of esophageal varices bleeding in patients with liver cirrhosis. Endoscopic ligation seem to be superior than endoscopic schlerotherapy. Primary prevention must be performed if the criteria are concluded, and the secondary prevention must be

performed to prevent variceal rebleeding. According to the guideline Endoscopic ligation is the first choice, if ligation was difficult because of continued bleeding or this technique is not available, endoscopic variceal sclerotherapy should be performed. Methods: Cases report. Case 1. A women get serial variceal ligation. MCE公司 At the last endoscopic evaluation, there was esophageal varices lining between cicatrix, it is difficult to perform ligation, so schlerotherapy must be choosed. Case 2. A man with liver cirrhosis and the shape of the varix is wide and look like a fan, schlerotherapy was done. Case 3. A man with liver cirrhosis and has esophageal varices continue to the gastroesophageal varices, it’s better schlerotherapy. Results: Beside variceal size and tension of variceal wall, others condition of varix itself must be mentioned. The type of esophageal varix is important. The varix look like pipe, it’s better to perform ligation.

Demographics, presence of metabolic syndrome, alcohol use, laboratory data and clinical progression of liver disease were compared between the two groups using Student T-test, with statistical significance defined as p<0.05. Degree of fibrosis was assessed using FIB-4 and APRI, which were calculated

at time of HCV diagnosis and five years later. Cirrhosis was defined as evidence of nodularity by imaging. Results: The average age for the total population was 54.5 years, 52% were white, 94% male, and 78% overweight or obese (average BMI 29). No difference in tobacco use, or cholesterol levels was noted between the two groups. There were differences in alcohol consumption (p-value 0.013) and metabolic syndrome GSK3235025 chemical structure (p-value < 0.001) between the two cohorts. Five years after cohort entry, the cholecystectomy cohort was found to have increased rates of hepatic fibrosis, development of cirrhosis, ascites, hepatic encephalopathy, and death compared DZNeP price to the non- cholecystectomy cohort (Table 1). Importantly, absolute change in APRI (0.73) in the cholecystectomy cohort was different than then non-cholecystectomy cohort (0.36) (p-value 0.03). Conclusions: Cholecystectomy in patients with chronic HCV may be associated with increased rate of fibrosis, development of cirrhosis, ascites, hepatic encephalopathy and death compared to non-responder HCV patients. Disclosures: The following people have nothing to disclose: Donald J. Martin,

Rick A. Weideman, Terri Crook, Geri Brown Background: Liver-related deaths represent MCE公司 the leading cause of mortality among patients with HIV/HCV coinfection, and are mainly related to complications of fibrosis and portal hypertension (PHT). However, biomarkers for prediction of fibrosis progression and the degree of PHT in patients with HIV/HCV coinfection are currently not available. Thus, we assessed the value of extracellular matrix (ECM) degraded fragments in peripheral blood as biomarkers for fibrosis and PHT in HIV/

HCV coinfection. Methods: Fifty-eight patients (67% male, mean age: 36.5 years) with HIV/HCV coinfection were included in this study. Hepatic venous pressure gradient (HVPG) was measured in forty-three patients. The fibrosis stage was determined using the FIB4-Score. ECM degraded products (C4M, MMP-2/9 degraded type IV collagen; C5M, MMP-2/9 degraded type V collagen; PRO-C3, neoepitope specific propeptide of type III collagen formation) were measured in peripheral blood by ELISA PRO-C3 Results: HVPG showed strong and significant correlations with FIB4-Score (rs=0.628; p=7*10-7). PRO-C3 significantly correlated with HVPG (rs=0.354; p=0.02), alanine aminotransferase (rs=0.30; p=0.038), as well as with FIB4-Score (rs=0.3230; p=0.035). C4M and C5M levels were higher in patients with PHT. Conclusion: PRO-C3-levels reflecting true type III collagen formationcorrelated to hepatic injury, liver fibrosis stage, and PHT in HIV/HCV-co-infected patients.