The duration of cumulative exposure was also extended from 10 to 50 days for clinical efficacy studies. It must be emphasized that GDC-0973 cell line these are requirements not only for new FVIII products but also for

any change in the manufacturing process of licensed products, which in my opinion should be seen as a continuous quality improvement process of any medical product and should occur regularly over time. All in all it can be easily grasped how difficult is to enrol such a large number of rare voluntary patients within a reasonable period of time. This problem is of course much more dramatic for haemophilia B patients with factor IX deficiency, which occurs in males at a rate of 1 in 30 000. It must be emphasized that the focus of current guidelines on FVIII inhibitors does not stem as a new concern, but rather as a shift from the primary safety concern due to viral transmission. The latter may be now viewed as basically solved, because the Selleck BTK inhibitor measures implemented for plasma selection, as well as the two or more inactivation/removal procedures

currently adopted by most manufacturers, are highly effective to optimize the safety of plasma-derived products pertaining to enveloped viruses [8]. Viral inactivation methods are also added to the manufacturing process of recombinant products, even though no transmission of infectious pathogens has ever been documented. Potential transmission of emerging non-enveloped viruses highly resistant to such inactivation methods as heating and solvent/detergent cannot be adequately assessed by means of the clinical studies recommended by regulatory agency (hence the need for long-term post marketing follow-up). However, this

theoretical risk cannot be reduced by an increase in the number of HSP90 recruited patients. A second objection concerns the rationale used by the regulators to select sample size. The recommended number of PTPs is definitely inadequate to establish whether or not new products carry a risk of inhibitor higher than that predicted in this population on the basis of current knowledge on the natural history of this complication [3-6]. Assuming, on the basis of recent epidemiological data [5], an incidence of new inhibitors of 5.5 per 1000 treatment years (95% confidence interval 4.6–6) a huge sample size of more than 14 000 PTPs would be required to have an 80% power to detect a 50% increase in inhibitor incidence, and more than 95 000 patients to demonstrate with a 20% boundary of equivalence that there is no increase in inhibitors (CR Hay, personal communication).

By contrast,

uptake of TBI by the liver was 40% lower in Dmt1liv/liv mice, compared with Dmt1flox/flox mice (Fig. 4B), revealing that hepatocyte DMT1 is partially required for hepatic uptake of iron from plasma transferrin. The effect was specific for the liver because TBI uptake was unaffected in kidneys, pancreas, or hearts of Dmt1liv/liv mice. To determine whether lower hepatic TBI uptake by Dmt1liv/liv mice represents a delay in clearance of plasma TBI, which may resolve at a later time, we measured the percentage of 59Fe in plasma 2 and 24 hours after injection. By 2 hours, the percentage of 59Fe in plasma did not differ between Dmt1flox/flox and Dmt1liv/liv mice (P = 0.11) (Fig. 4C), and by 24 hours, very little 59Fe was detectable in plasma. These data indicate Selleckchem Quizartinib that lower hepatic TBI uptake by Dmt1liv/liv mice does not represent a delay in clearance of plasma TBI. The percentage of 59Fe in the blood and spleen also did

not differ at either time point, suggesting that iron uptake into developing erythroid cells was unaffected in Dmt1liv/liv mice. Although lower hepatic TBI uptake in Dmt1liv/liv mice appears to directly result from inactivation of Dmt1, it is possible that it results from a secondary effect on other proteins implicated in TBI uptake. It is equally possible that the lack of an effect of hepatic Dmt1 inactivation on NTBI uptake is the result of compensatory responses in other proteins involved in NTBI uptake. selleck screening library Therefore, we measured levels Non-specific serine/threonine protein kinase of TfR1, TfR2, and ZIP14, which may also participate in TBI/NTBI uptake.[28, 29] Western blotting analysis revealed that levels of these proteins did not differ between Dmt1flox/flox and Dmt1liv/liv mice (Fig. 5A-C). To determine whether hepatocyte DMT1 is required to maintain iron status during iron deficiency, we compared iron status parameters of

Dmt1flox/flox and Dmt1liv/liv mice that were fed iron-deficient diets. After 3 weeks, mice became iron deficient, as compared to control (Dmt1flox/flox) mice fed a standard diet (Fig. 6A-D). However, no differences were observed between iron-deficient Dmt1flox/flox and Dmt1liv/liv mice. TBI uptake by livers of Dmt1flox/flox mice was higher in iron-deficient animals, compared to controls (36% versus 30%, respectively; P < 0.05) (Fig. 6E). By contrast, TBI uptake by livers of Dmt1liv/liv mice was not higher in iron-deficient animals, compared to controls, suggesting that DMT1 is required for enhanced TBI uptake into an iron-deficient liver. Confocal immunofluorescence (IF) microscopy was used to localize DMT1 in the liver. Human liver was used instead of mouse liver because IF staining of mouse tissue was too weak to allow for reliable localization. In hepatocytes, DMT1 displayed intracellular punctate staining with little, if any, staining of plasma membrane (Supporting Fig.

FXIII deficient patients benefit from a plasma concentrate with a long-lasting efficacy and safety record. A phase III clinical trial has recently been completed with a recombinant FXIII which has been proven to be safe and effective in preventing bleeding episodes in patients with congenital FXIII-A subunit deficiency [27]. In future, patients with RBD could take advantage of the many bioengineering as well as alternative strategies (aptamers, RNAi, inhibition

of TFPI, etc.), which are under development for persons with haemophilia [28]. Midori Shima has received honoraria as a consultant for his Fulvestrant active participation in advisory boards of Chugai Pharmaceutical Company, The Chemo-Sero-Therapeutic Research Institute, Bayer, Baxter, Biogen Idec, CSL Behring, Pfizer, Novo Nordisk. He has received research grants from Bayer, Baxter, Pfizer, Novo Nordisk, Chugai Pharmaceutical Company, Japan Blood Products Organization. Cedric Hermans has received honoraria as a consultant or for his active

participation in advisory LY2835219 nmr boards organized by Baxter, Bayer, Pfizer, CAF-DCF, SOBI, Ipsen, LFB, CSL Behring, Novo Nordisk, and Octapharma. He has received research grants or lecture chairs from Baxter, Bayer, Pfizer, CAF-DCF, CSL Behring, Novo Nordisk, Octapharma, and Ipsen. P de Moerloose has received honoraria as a consultant or for his active participation in advisory boards organized by Baxter, Bayer and LFB and has received research grants

or lecture chairs from Baxter, Bayer, CSL Behring, LFB and Novo Nordisk. “
“To compare the use of 740 Mbq (20 mCi) of 153Sm and 185 Mbq (5mCi) of 90Y, both labelling hydroxyapatite (HA), for knee synovectomy in haemophilic patients, 1 year after the intervention. Thirty three men (36 knees) were studied, divided into two groups: 1 – treatment using 740 Mbq of 153Sm-HA: 20 knees of 18 patients, with mean age of 21.4 ± 13.3 years (ranging from 7 to 56 years) and mean Pettersson score of 5.3; 2 – treatment using 185 Mbq of 90Y-HA: 16 knees of 15 patients, with mean age of 26.3 ± 10.3 (ranging from 7 to 51 years) and SPTLC1 mean Pettersson score of 6.3. The following criteria were adopted for the evaluation before and 1 year after synovectomy: reduction in haemarthrosis episodes and pain using a visual analogue scale, as well as improved joint mobility. The occurrence of adverse events in the treatment was also considered. The chi-square, Wilcoxon and Mann–Whitney tests were used with P ≤ 0.05 set as significant. The occurrence of haemarthrosis declined by 65.7% with the use of 153Sm-HA and 82.6% for 90Y-HA, with no statistical difference between the groups (P = 0.632); pain reduction was 42.5% in group 1 and 30.7% in group 2, once again with no statistical difference (P = 0.637). Improvement in joint mobility was not significant for both groups.

Over half are cirrhotic (63%), genotype 1a (56%) and prior non-re-sponders to treatment (52%). We found significant worsening in both IFN-based and IFN-free treated patients from baseline to week-4 in terms physical functioning (-5.9%, p=0.008 and -6.3%, p<0.001 respectively) Selleck Ivacaftor with no significant difference between the groups. The IFN-free group also experienced significant worsening in energy (-8.3%, p=0.009) and pain (-11.7%, p=0.009) from baseline to week-4. The IFN-based group had significant worsening in FSS (mean change:

+1.6, p=0.006) whereas the IFN-free group reported a smaller and non-significant change from baseline (+0.6, p=0.06). In terms of side effects, the IFN-based group experienced increased irritability (+2.0, p=0.009) and itching (+1.0, p=0.009), whereas the IFN-free group reported increased physical tiredness (+1.5, p=0.02). Conclusions: Real world patients treated with IFN-free regimens experience worsened physical symptoms at week-4 of treatment Alectinib solubility dmso similar to the worsening reported by patients treated with IFN-based regimens. Continued enrollment and follow-up may reveal further differences between IFN-based and IFN-free regimens as well as elucidate the role of ribavirin in these reported symptoms. NIH funded (DA031095, DK090317). Disclosures: Kian Bichoupan – Consulting: Janssen Pharmaceuticals, Gilead Sciences

Alyson Harty – Advisory Committees or Review Panels: Gilead; Consulting: Gil-ead, Jannsen, Acaria Pharmacy Jeffrey J. Weiss – Consulting: Vertex; Grant/Research Support: Cephalon Thomas D. Schiano – Advisory Committees or Review Panels: vertex, salix, merck, gilead, pfizer; Grant/Research Support: massbiologics, itherx Douglas Dieterich – Advisory Committees or Review Panels: merck, Idenix, Jans-sen ; Consulting: Gilead, BMS Andrea D. Branch – Grant/Research Support: Kadmon, Gilead, Janssen The following people have nothing to disclose: Jillian Nickerson, Ponni Perum-alswami Background/Aim Hepatitis

C virus (HCV) is a leading cause of hepatocellular carcinoma (HCC) in Japan. We aimed to elucidate the clinical features of chronic hepatitis C patients who develop HCC after achieving a sustained viral response (SVR) to interferon (IFN) therapy. Methods Clinical RVX-208 parameters of 146 patients (mean age: 59 years old, male: 88, female: 58) were evaluated who achieved a SVR from 1991 to 2013 in our hospital. Results Eleven patients (7.5 %) developed HCC within a median follow-up period of 62 months (range12–271 months). Cox regression analysis revealed that the strongest factor predictive of HCC occurrence was higher AST (>50IU/L) level (hazard ratio [HR] 6.51, P=0.024), followed by lower platelet (<17x104 cells/microL) count (HR 4.39, P=0.318), prolonged (<80%) prothrombin time (HR 3.69, P=0.047), higher gamma-GTP(>70IU/L) level HR 3.66, P=0.045) before IFN therapy.

General measures listed BAY 57-1293 for treatment of grade 1 rashes can be employed. If a grade 2 rash progresses despite these measures, it is recommended that telaprevir be discontinued. In a patient with stable grade 2 rash not responding to conservative measures, one could consider temporarily withdrawing ribavirin, as it may be difficult to confidently distinguish rash secondary to telaprevir from that induced by ribavirin or even interferon. Despite the long half-life of ribavirin, it has been reported that withdrawing it for as short as 48 hours may result in resolution of the rash.20 Grade

3 rash (severe) involves more than 50% of the integument or any of the following: vesicles/bullae, any ulceration of mucous membranes, epidermal detachment, targetoid lesion, or palpable purpura. Management of grade 3 rash includes immediate discontinuation of telaprevir, followed by ribavirin/pegylated interferon for nonresolution, and consideration of dermatology consultation. Stevens Johnson Syndrome, toxic epidermal necrolysis syndrome (TENS), erythema multiforme, and drug-related eosinophilia with systemic symptoms

(DRESS) also constitute grade 3 rash, which merit discontinuation of all 3 agents. The DRESS syndrome rash may present with fever, facial edema, hypereosinophilia, and liver www.selleckchem.com/products/PD-0332991.html (elevated liver tests/hepatomegaly) or renal dysfunction.21, 22 Once telaprevir has been discontinued, it should not be restarted. Of note, systemic steroids to allow continued telaprevir dosing should be avoided for rash management, because its impact on rash progression and viral breakthrough have not been assessed. The next most common side effect

is anemia. On average, the addition of telaprevir to PR results in an additional 1 g/dL decline in hemoglobin, in addition to the mean maximal drop of 3 g/dL Reverse transcriptase from pegylated interferon and ribavirin. In phase 3 studies, anemia with hemoglobin <10 g/dL occurred in 36% of patients on telaprevir versus 17% on SOC. The incidence of more severe anemia with a hemoglobin <8.5 g/dL was 14% with telaprevir compared to 5% with SOC. These resulted in dose reduction, interruption or discontinuation of ribavirin in approximately one-third of patients and discontinuation of telaprevir in 4%. The rate of decline of hemoglobin during weeks 1-4 is not any steeper with triple therapy than with SOC. In those receiving telaprevir, however, there is a continued decline between weeks 4 and 8. In theory, anemia of ribavirin should be distinguishable from that of telaprevir by markers of hemolysis. In practice, however, whether such a distinction is going to be helpful in clinical decision making remains uncertain. The most important principle to remember is that telaprevir cannot be dose-reduced or interrupted. Once it is stopped, it should not be restarted.

5A,B), while the apical transporter Mrp4 was down-regulated (Fig. 5D). Immunoblots confirmed the up-regulation of Ostα and Ostβ in Tph1−/− relative to WT kidney (Fig. 6A,B). The nonsignificant down-regulation of Asbt in Tph1−/− kidneys (Fig. 5C) could not be confirmed on the protein level. Instead, Asbt protein was similarly expressed in WT and Tph1−/− mice (Fig. 6A) and was Gefitinib mouse reduced by BDL relative

to sham-operated animals (Fig. 6B). To examine whether the observed expression changes may be associated with an altered bile salt regulation by the kidney, we measured urinary levels of bile salts at 3 days of BDL (Fig. 6C). Urinary bile salts were significantly reduced in Tph1−/− relative to WT mice. We next examined whether serotonin reloading by injection of the serotonin precursor see more 5-HTP can reverse the renal changes observed in Tph1−/− mice. The increased expression of Osta and Ostb genes was reduced by serotonin reloading of Tph1−/− mice (Fig. 7A). Expression levels of other transporters (Mrp2, Mrp3, and

Mrp4) were not affected by serotonin reloading (data not shown). Immunoblots on Tph1−/− kidneys demonstrated a reduction in Ostα and Ostβ, but no change in Asbt protein by serotonin (Fig. 7B,C). Immunohistochemical staining confirmed basolateral Ostβ down-regulation in serotonin-reloaded Tph1−/− kidney (Supporting Fig. 7). Finally, the lowered level of urinary bile salts in Tph1−/− were increased following reloading (Fig. CYTH4 7D). Taken together, these results indicate a relationship between increased plasma

bile salts, elevated levels of the Ostα·Ostβ transporter in the kidney, and a reduced urinary excretion of bile salts in serotonin-depleted mice. We hence conclude that serotonin affects bile salt homeostasis in acute cholestasis by controlling renal transporter expression in mice. Serotonin is a monoamine neurotransmitter regulating mood, appetite, sleep, and cognitive activities in the central nervous system. A significant amount of serotonin is also stored in the gut and platelets.30 We have shown that serotonin is important in liver regeneration, nonalcoholic steatohepatitis, and repair after ischemic injury.10, 11, 31 Here, we demonstrate that endogenous serotonin ameliorates liver injury in cholestatic mice. Lack of serotonin increases liver injury and bile salt levels in liver and circulation. Unexpectedly, serotonin appears to affect bile salt pools through adaptive regulation of renal rather than hepatic bile transporters. Cholestasis induced by BDL in the mouse is characterized by a series of phases; it includes an acute phase, an immune reaction, and fibrotic changes.32 Here, we focus on the acute phase at 3 days of BDL, where liver injury is maximal as determined in an initial time course experiment. At this time point, hepatic necrosis was exacerbated in serotonin-deficient Tph1−/− mice relative to WT mice and correlated with higher bile salt levels.

Initially

described in 1876 by von Kupffer as liver Sternzellen (“star-shaped cells”) and then by Ito as vitamin-A storing cells, HSCs have since been well characterized, and much is known about their molecular and cellular biology.1 However, the exact developmental origin of HSCs remains unknown, and until recently we have lacked the capabilities to observe stellate cell activation in vivo. Moreover, we have been unable to discover novel chemical and genetic factors that regulate stellate cell development and activation. In the current issue of HEPATOLOGY, Yin et al.2 describe a novel cell population in the zebrafish liver that exhibits all the hallmarks of HSCs in mammals, from their morphology, to their capacity to store fat and vitamin A, to their expression profile and activation in response to injury. How can this newly discovered cell type in the Selleckchem Staurosporine zebrafish help us understand HSC regulation and improve patient outcomes? HSC, hepatic stellate cell. Over the past two decades,

zebrafish have been established as an excellent model to study early development and organogenesis. The embryos are transparent, allowing for direct visualization of in vivo processes, and they develop rapidly, so that they harbor differentiated hepatocytes by 3 days of life.3, 4 Zebrafish are equally amenable to forward genetic and chemical genetic screening approaches. Despite several hundreds of millions of years of divergent evolution, the zebrafish gastrointestinal tract and PF-02341066 datasheet liver are remarkably similar to those GBA3 of mammals, both in their cellular organization and in the molecular signals governing organ development, growth, regeneration, and malignant transformation.5, 6 Using transgenic zebrafish lines, as well as by in situ hybridization and immunocytological methods, hepatocytes, biliary epithelial cells and endothelial cells can be identified with specific markers.3, 7 Yin et al. describe the discovery

of HSCs as a novel cell type in the zebrafish liver. Their study made use of recently generated transgenic reporter fish, which highlight the expression of the bHLH transcription factor hand2 (heart and neural crest derivates expressed transcript 2). This gene, expressed early in the lateral plate mesoderm, had been described previously by the authors as an essential factor for gut looping and laterality during early endoderm development.8 The authors demonstrate the morphological similarity to mammalian HSCs, with a star-shaped appearance and cellular processes that lie in close proximity to endothelial cells, expressing desmin and glial fibrillary acidic protein. The authors further elucidate the developmental origin of this cell type in the mesoderm, which had been shown via lineage-tracing experiments to be the source of HSCs in mouse liver.9 More importantly, Yin et al.

The latter hypothesis requires more investigation, which is also the case for understanding the optimal dosing required to allow this potential benefit of prophylaxis to occur. For most

of the other debated non-genetic factors, the impact on the immunological outcome is, to date, not supported by the literature. Because the factors are often interrelated, it is also difficult to identify the relative contribution of each. This is also reflected by the results of the survey carried out among the EHTSB members, in which the impact of the majority of the factors was extremely variable; a pattern also recently reported in a survey by van den Berg and Chalmers [68]. The genetic profile of the patient will have a major impact on the immunological outcome and must be considered. This has not been done in the current literature. As haemophilia is a rare disease, and inhibitors develop in a minority of patients,

the statistical power of see more studies addressing these issues will, by definition, be limited. In light of the complexity of the aetiology of inhibitor development, future research should be directed at the identification of early immunological markers of high risk patients. In 2007, the EMEA [8] produced a report that defined many of the variables that should be considered when evaluating the literature on inhibitor formation. Unfortunately, several of these variables have not been included in a substantial second number of published studies, which will indeed influence the accuracy, validity and interpretation of the data. For example, the type of assay used to measure and to identify the inhibitor. The Nijmegen modification of the Bethesda assay was considered the ‘gold standard’ with a cut-off point of >0.6 BU. In addition, confirmatory tests on a second, separately drawn sample within a month should be performed. As seen in the tables, however,

these requirements are frequently not adhered to by studies published in the current literature. Moreover, the previous exposure to factor concentrates will be of major importance. According to the EMEA report, PUPs should be defined as those patients who have never been exposed to clotting factor products. Frequently, inhibitor studies involve patients who are considered to be MTPs. This term was considered inappropriate and these patients should instead be defined as previously treated patients (PTPs). This will have an impact on the interpretation of inhibitor incidence in each cohort described. It was also suggested that the number of EDs should be utilized as parameters to categorize risk rather than rely on the categories of PUP or MTP. In the case of factor concentrate immunogenicity, it was agreed that PTPs was the optimal group to study to limit the impact of confounding factors.

0%, and 46.4% versus 50.6%, respectively). When evaluating the combined effect of CD151, MMP9, and MVD on the prognosis of HCC, we classified patients into three subgroups according

to their CD151, MMP9, and MVD-CD34 density: group I had high expression of all three markers, group II had high expression of one or two 3-Methyladenine research buy of the three markers, and group III had low expression of all three markers. We found that the 3-, 5-, and 7-year OS in group I was 50.9%, 39.1%, and 30.0%, respectively, significantly lower than the OS for groups II and III (Fig. 6A). The 3-, 5-, and 7-year cumulative recurrence rates in group I were 58.2%, 63.6%, and 64.5%, respectively, which were significantly higher than those for groups II and III (Fig. 6B). Individual clinicopathological features that showed significance by univariate analysis were adopted as covariates in a multivariate Cox proportional hazards model, and then combined variables were further analyzed. Multivariate Cox proportional hazards analysis also showed that overexpression of CD151, MMP9, and MVD together was independent of other prognostic markers (large size, microvascular invasion, and multiple tumors) for both OS (P < 0.001) and cumulative recurrence (Table 1; P < 0.001). Traditionally, tetraspanin

CD151 may activate Rac and Cdc42 by facilitating the integrins selleckchem and growth factor receptor signals or redistribute integrins by endocytosis and/or trafficking, with the end result being the promotion of motility and metastasis of tumor cells.4, 35, 36 In the present

study, we consistently observed that overexpression of CD151 facilitated tumor-associated neoangiogenesis in HCC and apparently did so by engaging MMP9 as an agent via the PI3K/Akt/GSK-3β/Snail signal, and thus it promoted the progression of HCC. An earlier study reported that homophilic interactions of tetraspanin CD151 up-regulated the expression of MMP9 in human melanoma (MelJuSo) cells through the FAK/p38/MAPK/JNK/c-Jun pathway.17 In contrast to the results with MelJuSo cells,17 we found that overexpression of check details CD151 in HCC cells up-regulated the expression of MMP9 by facilitating the PI3K/Akt/GSK-3β/Snail signal in HCC cells. One of the reasons for this inconsistency may reside in the special structural and functional characteristics of the tetraspanins.4 These proteins can assemble themselves into complexes consisting of a core structure surrounded by other specific proteins. This complex formation provides a great deal of variability, which in turn allows for specificity and functional differences to occur in different cell types.4, 37 Tetraspanin complexes can also present different functional profiles at different cell development stages, even though they may share several common components.4, 35 To our knowledge, the present study is the first to clearly demonstrate that overexpression of CD151 promotes MMP9 expression via the PI3K/Akt/GSK-3β/Snail cascade.

Conclusion: It is critical for the rehabilitation of patients with mild acute pancreatitis to observe and analyze

the causes of serum amylase unfalling and Epigenetics inhibitor take effective measures to deal with. Key Word(s): 1. acute pancreatitis; 2. serum amylase; 3. analysis; 4. treatment; Presenting Author: CHENWEN JING Additional Authors: TANGGUO DU Corresponding Author: TANGGUO DU Affiliations: guangxi medical university Objective: To investigate the relationship between AOPP and severity of AP by detecting serum levels of AOPP in patients with AP, combination the results of serum interleukin -6(IL-6), indicators which associated with disease severity and clinical datas. Methods: Fifty-eight patients who were diagnosed acute pancreatitis in our hospital from November 2010 to September 2012 were collected[18 cases with severe acute pancreatitis (SAP) and

40 cases with mild acute pancreatitis (MAP)]. Serum levels of AOPP and IL-6 were dectected by enzymelinked immunosorbent assay (ELISA) within 24 hours. Blood samples were sent to the laboratory to dectect blood routine, liver function, renal function, blood calcium, blood glucose and actate dehydrogenase. APACHE II scores, Ranson scores, CTSI scores, BISAP scores and Glasgow scores were also determined. Results: ① Serum levels of WBC, GLU, LDH in SAP group were higher than MAP group (P < 0.05). ALB and check details blood calcium in SAP group was lower than MAP group (P < 0.05). ② Serum levels of BUN, Cr, blood amylase were no significant difference between SAP FDA approved Drug Library clinical trial group and MAP group (P > 0.05). ③ In SAP group and MAP group, APACHE II scores were (5.00 ± 3.67) and (3.39 ± 2.91), Ranson scores were (2.04 ± 1.46) and (1.33 ± 1.21), CTSI scores were (5.87 ± 1.46) and (1.20 ± 1.26), BISAP scores were (1.52 ± 0.80) and (0.86 ± 0.76), Glasgow scores were (2.61 ± 1.20) and (1.24 ± 1.12), respectively, and SAP group was higher than MAP group (P < 0.05). ④ Serum levels of AOPP in

SAP group and MAP group were (38.1156 ± 11.67)ng/ml and (29.40 ± 14.19)ng/ml, respectively, and SAP group was higher than MAP group (P < 0.05). Serum levels of IL-6 in SAP group and MAP group were (211.01 ± 107.98)pg/ml and (129.72 ± 56.53)pg/ml, respectively, and SAP group was higher than MAP group (P < 0.05). ⑤ There are relations between AOPP and WBC, GLU (P < 0.05), but no relations with LDH, blood calcium, ALB, BUN, Cr and blood amylase (P > 0.05). Conclusion: Serum levels of AOPP may be associated with the severity of AP; AOPP may be associated with the process of inflammatory response in the occurrence and development of AP; AOPP and indicators which associated with disease severity may be used as markers to estimate the severity in AP. Key Word(s): 1. acute pancreatitis; 2. AOPP; 3.