Soluble CD137 is a novel serum marker of liver cirrhosis in patients with hepatitis C and alcohol-associated disease etiology.

Defective T-cell functions play a role in the persistence of HCV infection. Activated T cells express CD137, which costimulates antivirus T-cell responses, and this activity is antagonized by soluble CD137 (sCD137). Here, we show that in sera of 81 patients with chronic HCV, sCD137 levels did not correlate with measures of viral infection, and did not decline after virus eradication using direct-acting antivirals. Thus, serum sCD137 was similar in patients infected with HCV and in uninfected controls. Of note, in HCV patients with liver cirrhosis and patients with mostly alcohol-associated liver cirrhosis, sCD137 was increased. A negative association of sCD137 and albumin existed in both cohorts. sCD137 concentrations were similar in hepatic and portal vein blood excluding the liver as the origin of higher levels. Recombinant sCD137 reduced Th1 and Th2 but not Th17 cell polarization in vitro, and accordingly lowered IFN-γ, TNF, and IL-13 in cell media. Serum sCD137 is associated with inflammatory states, and positively correlated with serum TNF in cirrhotic HCV patients following virus eradication. Our study argues against a role of sCD137 in HCV infection and suggests a function of sCD137 in liver cirrhosis, which yet has to be defined.

Rapid Decline of Serum Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) in Non-Cirrhotic Patients with Chronic Hepatitis C Infection Receiving Direct-Acting Antiviral Therapy.

Direct-acting antivirals (DAAs) efficiently eradicate the hepatitis C virus (HCV). Low-density lipoprotein (LDL) levels increase rapidly upon DAA treatment. Proprotein convertase subtilisin/kexin 9 (PCSK9) induces degradation of the hepatic LDL receptor and thereby elevates serum LDL. The aim of this study was to determine serum PCSK9 concentrations during and after DAA therapy to identify associations with LDL levels. Serum PCSK9 was increased in 82 chronic HCV-infected patients compared to 55 patients not infected with HCV. Serum PCSK9 was low in HCV patients with liver cirrhosis, but patients with HCV-induced liver cirrhosis still exhibited higher serum PCSK9 than patients with non-viral liver cirrhosis. Serum PCSK9 correlated with measures of liver injury and inflammation in cirrhotic HCV patients. In patients without liver cirrhosis, a positive association of serum PCSK9 with viral load existed. Serum PCSK9 was not different between viral genotypes. Serum PCSK9 did not correlate with LDL levels in HCV patients irrespective of cirrhotic status. Serum PCSK9 was reduced, and LDL was increased at four weeks after DAA therapy start in non-cirrhotic HCV patients. Serum PCSK9 and LDL did not change upon DAA treatment in the cirrhotic group. The rapid decline of PCSK9 after the start of DAA therapy in conjunction with raised LDL levels in non-cirrhotic HCV patients shows that these changes are not functionally related.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) levels are not associated with severity of liver disease and are inversely related to cholesterol in a cohort of thirty eight patients with liver cirrhosis.

BACKGROUND: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is of particular importance in cholesterol metabolism with high levels contributing to hypercholesterolemia. Cholesterol and sphingolipids are low in patients with liver cirrhosis. Purpose of this study was to find associations of plasma PCSK9 with circulating cholesterol and sphingolipid species and measures of liver disease severity in patients with liver cirrhosis. METHODS: PCSK9 protein levels were determined by ELISA in systemic vein (SVP), hepatic vein (HVP) and portal vein plasma of patients with mostly alcoholic liver cirrhosis. PCSK9 and LDL-receptor protein expression were analysed in cirrhotic and non-cirrhotic liver tissues. RESULTS: Serum PCSK9 was reduced in patients with liver cirrhosis in comparison to non-cirrhotic patients. In liver cirrhosis, plasma PCSK9 was not correlated with Child-Pugh score, Model for End-Stage Liver Disease score, bilirubin or aminotransferases. A negative association of SVP PCSK9 with albumin existed. PCSK9 protein in the liver did not change with fibrosis stage and was even positively correlated with LDL-receptor protein levels. Ascites volume and variceal size were not related to PCSK9 levels. Along the same line, transjugular intrahepatic shunt to lower portal pressure did not affect PCSK9 concentrations in the three blood compartments. Serum cholesterol, sphingomyelin and ceramide levels did not correlate with PCSK9. Stratifying patients by high versus low PCSK9 levels using the median as cut-off, several cholesteryl ester species were even low in the subgroup with high PCSK9 levels. A few sphingomyelin species were also reduced in the patients with PCSK9 levels above the median. PCSK9 is highly expressed in the liver but systemic, portal and hepatic vein levels were similar. PCSK9 was not correlated with the inflammatory proteins C-reactive protein, IL-6, galectin-3, resistin or pentraxin 3. Of note, HVP PCSK9 was positively associated with HVP chemerin and negatively with HVP adiponectin levels. CONCLUSIONS: In the cohort of patients with liver cirrhosis mostly secondary to alcohol consumption high PCSK9 was associated with low levels of certain cholesteryl ester and sphingomyelin species. Positive correlations of PCSK9 and LDL-receptor protein in the liver of patients with chronic liver injury are consistent with these findings.

Serum Adiponectin Levels Do Not Distinguish Primary from Metastatic Liver Tumors.

BACKGROUND/AIM: Adiponectin protects from metabolic disease and cancer. Accordingly, serum adiponectin was reduced in patients with colorectal cancer (CRC). This hepatoprotective factor was definitely increased in hepatocellular carcinoma (HCC). CRC metastases to the liver are common and the aim of the present study was to evaluate whether serum adiponectin discriminates primary from secondary liver cancers. MATERIALS AND METHODS: Adiponectin was measured by ELISA in the serum of 36 patients with colorectal liver metastases, 32 patients with HCC and 49 patients without cancer. RESULTS: Serum adiponectin levels were higher in cancer than non-tumor patients. Adiponectin was not related to TNM stage in HCC nor to the levels of serum tumor markers. Moreover, hepatic inflammation and liver fibrosis were not correlated with serum adiponectin levels. Metabolic diseases are associated with low adiponectin and a higher risk of cancer. In HCC, but not in CRC serum, adiponectin was increased in patients with hypertension and hyperuricemia. In this cohort, adiponectin positively correlated with chemerin, an adipokine supposed to contribute to metabolic disturbances. CONCLUSION: Serum adiponectin cannot discriminate primary from secondary liver tumors.

Serum Chemerin Does Not Differentiate Colorectal Liver Metastases from Hepatocellular Carcinoma.

The chemoattractant adipokine chemerin is related to the metabolic syndrome, which is a risk factor for different cancers. Recent studies provide evidence that chemerin is an important molecule in colorectal cancer (CRC) and hepatocellular carcinoma (HCC). Serum chemerin is high in CRC patients and low in HCC patients and may serve as a differential diagnostic marker for HCC and liver metastases from CRC. To this end, serum chemerin was measured in 36 patients with CRC metastases, 32 patients with HCC and 49 non-tumor patients by ELISA. Chemerin serum protein levels were, however, similar in the three cohorts. Serum chemerin was higher in hypertensive than normotensive tumor patients but not controls. Cancer patients with hypercholesterolemia or hyperuricemia also had increased serum chemerin. When patients with these comorbidities were excluded from the calculation, chemerin was higher in CRC than HCC patients but did not differ from controls. Chemerin did not correlate with the tumor markers carcinoembryonic antigen, carbohydrate antigen 19-9 and alpha-fetoprotein in both cohorts and was not changed with tumor-node-metastasis stage in HCC. Chemerin was not associated with hepatic fat, liver inflammation and fibrosis. To conclude, systemic chemerin did not discriminate between CRC metastases and HCC. Comorbidities among tumor patients were linked with elevated systemic chemerin.

[Impact of abdominal ultrasound on the identification of the site of infection in the emergency department - Analysis whether it makes sense to perform abdominal ultrasound examination for the identfication of the site of infection if medical history and clinical examination do not indicate an abdominal focus.] / Bedeutung der Abdomen-Sonografie zur Infektfokussuche in der Notaufnahme.

Introduction A very high number of patients presenting in emergency departments suffer from an unknown infection or rather fever. If diagnostic imaging is necessary ultrasound can be performed. Whether ultrasound is superior to medical history and clinical examination considering the significantly enhanced technology in recent years and hence has to be performed in patients without abdominal symptoms with non-obvious focus cannot be answered by review of the literature. The objective of this study was to evaluate the relevance of abdominal ultrasound in the determination of the site of infection and to analyse whether an abdominal ultrasound for the identification of the source of infection is dispensable in patients in whom history and clinical examination do not indicate an abdominal focus. Methods All patients undergoing an ultrasound between 2013/04 and 2013/07 in the emergency department of the university hospital of Regensburg were retrospectively analysed. 500 abdominal ultrasound examinations were performed for identifying an abdominal site of infection. These cases were analysed whether medical history and clinical examination were indicating an abdominal focus. Furthermore, on the basis of patient record and medical report the result of the performed ultrasound, final diagnosis, clinical parameters (lab results, fever) were retrospectively analysed. Results Based on the medical report in 208 (41.6 %) of the 500 reviewed cases there has been an abdominal focus. In 122 of these patients (59.0 %) abdominal ultrasound identified the abdominal focus correctly. In 206 patients (99.0 %) medical history and in 152 patients (73.1 %) clinical examination indicated an abdominal focus. A subgroup analysis regarding immunocompromised patients revealed that in 25 of 38 patients (65.8 %) an abdominal focus was determined via abdominal ultrasound. In patients with unremarkable medical history and clinical examination (23 examinations) no abdominal focus could be found via abdominal ultrasound. Discussion An urgent examination of the abdomen via ultrasound is dispensable in patients in whom history (provided complete history) and clinical examination (i.e. particularly no immunosuppression) do not indicate an abdominal focus.

Diagnostic Value of Systemic Cholesteryl Ester/Free Cholesterol Ratio in Hepatocellular Carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) most commonly occurs in the setting of liver cirrhosis which is characterized by low serum lipids. We hypothesized that composition of lipoproteins and consequently lipid species ratios are mostly unchanged in patients with cirrhosis compared to controls. This approach may be appropriate to identify lipid ratios altered in HCC irrespective of liver dysfunction. PATIENTS AND METHODS: Lipids were measured in serum of 21 patients with HCC, 41 patients with liver cirrhosis and 22 controls. Ratios of lipids known to be changed in HCC tissues were calculated. RESULTS: Ratios of polyunsaturated to mono-unsaturated lysophosphatidylcholine, ceramide/sphingomyelin and cholesteryl ester/free cholesterol were changed in HCC compared to both control cohorts. The latter was most suited to diagnosing HCC. Systemic ratios of these lipid classes were not associated with fibrosis, staging or grade in patients with HCC. CONCLUSION: The cholesteryl ester/free cholesterol ratio is comparable in controls and patients with cirrhosis, but is specifically increased in patients with HCC.

Hepatic chemerin mRNA expression is reduced in human nonalcoholic steatohepatitis.

BACKGROUND: Chemerin is associated with insulin resistance and is expressed in the liver. Nonalcoholic fatty liver disease (NAFLD) is related to impaired insulin sensitivity, but studies evaluating hepatic and serum chemerin in NAFLD resulted in discordant data. MATERIALS AND METHODS: Chemerin mRNA was determined in the liver tissue obtained from 33 controls and 76 NAFLD patients. Chemerin serum levels were measured in a different cohort of patients with ultrasound-diagnosed NAFLD and the respective controls. Hepatic stellate cells and hepatocytes were exposed to selected metabolites and nuclear receptor agonists to study the regulation of chemerin. Effect of recombinant chemerin on hepatocyte released proteins was analysed. RESULTS: Hepatic chemerin expression was not related to BMI, gender, type 2 diabetes and hypertension. Chemerin mRNA did not correlate with steatosis and was negatively associated with inflammation, fibrosis and nonalcoholic steatohepatitis (NASH) score. Patients with NASH had lower chemerin mRNA compared to those with borderline NASH and controls. Factors with a role in NASH mostly did not regulate chemerin in the liver cells. Of note, liver X receptor agonist reduced chemerin protein. Serum chemerin was not changed in NAFLD. Levels positively correlated with age, waist-to-hip ratio, systolic blood pressure, serum FGF21 and lipocalin 2, and negatively with transferrin saturation. Chemerin induced FGF21 in supernatants of primary human hepatocytes. Hepcidin, a major regulator of iron homoeostasis and lipocalin 2, were not regulated by chemerin. CONCLUSION: Chemerin mRNA is reduced in the liver of NASH patients, and liver X receptor seems to have a role herein.

Circulating lipocalin 2 is neither related to liver steatosis in patients with non-alcoholic fatty liver disease nor to residual liver function in cirrhosis.

Lipocalin 2 (LCN2) is induced in the injured liver and associated with inflammation. Aim of the present study was to evaluate whether serum LCN2 is a non-invasive marker to assess hepatic steatosis in patients with non-alcoholic fatty liver disease (NAFLD) or residual liver function in patients with liver cirrhosis. Therefore, LCN2 was measured by ELISA in serum of 32 randomly selected patients without fatty liver (controls), 24 patients with ultrasound diagnosed NAFLD and 42 patients with liver cirrhosis mainly due to alcohol. Systemic LCN2 was comparable in patients with liver steatosis, those with liver cirrhosis and controls. LCN2 negatively correlated with bilirubin in both cohorts. In cirrhosis, LCN2 was not associated with more advanced liver injury defined by the CHILD-PUGH score and model for end-stage liver disease score. Resistin but not C-reactive protein or chemerin positively correlated with LCN2. LCN2 levels were not increased in patients with ascites or patients with esophageal varices. Consequently, reduction of portal pressure by transjugular intrahepatic portosystemic shunt did not affect LCN2 levels. Hepatic venous blood (HVS), portal venous blood and systemic venous blood levels of LCN2 were similar. HVS LCN2 was unchanged in patients with end-stage liver cirrhosis compared to those with well-compensated disease arguing against increased hepatic release. Current data exclude that serum LCN2 is of any value as steatosis marker in patients with NAFLD and indicator of liver function in patients with alcoholic liver cirrhosis.

Comparison between quantitative assessment of bowel wall vascularization by contrast-enhanced ultrasound and results of histopathological scoring in ulcerative colitis.

PURPOSE: In ulcerative colitis (UC), endoscopic methods are preferred for assessment of extent and activity of disease. Due to the invasive nature of endoscopical examinations, replacement by other, reliable imaging procedures would be helpful. Contrast-enhanced ultrasound (CEUS) in combination with perfusion assessment using a specific quantification software might be such a new diagnostic tool. Thus, we compared the findings of CEUS with the results of endoscopically taken specimens applying a histopathological scoring system. METHODS: We prospectively evaluated 15 patients with proven UC undergoing endoscopy. CEUS was performed and the quantification software Qontrast® applied to obtain contrast-enhanced sonographic perfusion maps. Moreover, in each patient C-reactive protein (CRP) was measured and taken biopsies were assessed using an advanced scoring system. Four patients had to be excluded from final analysis. RESULTS: There was a trend to higher Peak (%) values with increasing histological inflammation. Furthermore, a strong negative correlation between the ratio TTP (s)/Peak (%) (Spearman's correlation r = -0.761, p < 0.01) was found. There was no significant relationship between CRP and histopathological scoring or CEUS parameters, respectively. CONCLUSION: Quantitative evaluation with CEUS, particularly the calculation of the ratio TTP (s)/Peak (%), provides a simple method for assessment of inflammatory activity in UC.

Soluble CD163 is not increased in visceral fat and steatotic liver and is even suppressed by free fatty acids in vitro.

Visceral fat differs from subcutaneous fat by higher local inflammation and increased release of IL-6 and free fatty acids (FFA) which contribute to hepatic steatosis. IL-6 has been shown to upregulate the monocyte/macrophage specific receptor CD163 whose soluble form, sCD163, is increased in inflammatory diseases. Here, it was analyzed whether CD163 and sCD163 are differentially expressed in the human fat depots and fatty liver. CD163 mRNA and protein were similarly expressed in paired samples of human visceral and subcutaneous fat, and comparable levels in portal venous and systemic venous blood of liver-healthy controls indicate that release of sCD163 from visceral adipose tissue was not increased. CD163 was also similarly expressed in steatotic liver when compared to non-steatotic tissues and sCD163 was almost equal in the respective sera. Concentrations of sCD163 were not affected when passing the liver excluding substantial hepatic removal/release of this protein. A high concentration of IL-6 upregulated CD163 protein while physiological doses had no effect. However, sCD163 was not increased by any of the IL-6 doses tested. FFA even modestly decreased CD163 and sCD163. The anti-inflammatory mediators fenofibrate, pioglitazone, and eicosapentaenoic acid (EPA) did not influence sCD163 levels while CD163 was reduced by EPA. These data suggest that in humans neither visceral fat nor fatty liver are major sources of sCD163.

Elevated systemic monocyte chemoattractrant protein-1 in hepatic steatosis without significant hepatic inflammation.

Non-alcoholic fatty liver disease (NAFLD) is strongly associated with obesity and the metabolic syndrome. It encompasses a clinico-pathologic spectrum of conditions ranging from simple steatosis to nonalcoholic steatohepatitis (NASH). The latter develops upon pro-inflammatory cell infiltration and is widely considered as the first relevant pathophysiological step in NAFLD-progression. The chemokine monocyte chemoattractant protein 1 (MCP-1) plays an important role in the progression of hepatic inflammation and fibrosis, and both increased hepatic expression and circulating serum levels have been described in NASH. Here, we aimed to investigate MCP-1 expression in simple hepatic steatosis. Upon feeding a high-fat diet mice developed hepatic steatosis in the absence of significant hepatic inflammation, but elevated hepatic MCP-1 expression compared to control mice fed a standard chow. Interestingly, high-fat diet fed mice had significantly higher MCP-1 serum levels, and MCP-1 mRNA expression was significantly increased in visceral adipose tissue. Furthermore, MCP-1 serum levels were also elevated in patients with ultrasound-diagnosed NAFLD and correlated with the body-mass index and fasting glucose. In conclusion, our data indicate both the liver and adipose tissue as cellular sources of elevated circulating MCP-1 levels already in the early phase of hepatic steatosis. Since MCP-1 derived from visceral adipose tissue reaches the liver via portal circulation at high concentrations it may significantly contribute to the progression of simple steatosis to NASH.

Comparison of high-resolution ultrasound and MR-enterography in patients with inflammatory bowel disease.

AIM: To compare the results of high-resolution ultrasound (HR-US) and magnetic resonance enterography (MRE) examinations in patients with inflammatory bowel disease (IBD). METHODS: The reports of 250 consecutive cases with known IBD, who had an MRE and HR-US examination, were retrospectively analyzed. Using a patient-based approach we evaluated morphological disease features such as affected bowel wall, stenosis, abscess and fistula. The comparison between the two modalities was based on the hypothesis, that any pathological change described in any imaging modality was a true finding, as no further standard of reference was available for complete assessment. RESULTS: Two hundred and fifty examinations representing 207 different patients were evaluated. Both modalities assessed similar bowel wall changes in 65% of the examinations, with more US findings in 11% and more MRE findings in 15%. When the reports were analyzed with regard to "bowel wall inflammation", US reported more findings in 2%, while MRE reported more findings in 53%. Stenoses were assessed to be identical in 8%, while US found more in 3% and MRE in 29% (P < 0.01). For abscess detection, US showed more findings in 2% (n = 4) while MRE detected more in 6% (n = 16). US detected more fistulas in 1% (n = 2), while MRE detected more in 13% (n = 32) (P < 0.001). The most common reason for no detected pathology by US was a difficult to assess anatomical region (lesser pelvis, n = 72). CONCLUSION: US can miss clinically relevant pathological changes in patients with IBD mostly due to difficulty in assessing certain anatomical regions.

Lipid accumulation impairs adiponectin-mediated induction of activin A by increasing TGFbeta in primary human hepatocytes.

Fatty liver is commonly detected in obesity and has been identified as a risk factor for the progression of hepatic fibrosis in a wide range of liver diseases. Transforming growth factor beta (TGFß) and activin A, both members of the TGFß superfamiliy, are central regulators in liver fibrosis and regeneration, and the effect of hepatocyte lipid accumulation on the release of these proteins was studied. Primary human hepatocytes (PHH) were incubated with palmitic acid or oleic acid to increase lipid storage. Whereas activin A and its natural inhibitor follistatin were not affected, TGFß was 2-fold increased. The hepatoprotective adipokine adiponectin dose-dependently induced activin A while lowering follistatin but did not alter TGFß. Activin A was markedly reduced in hepatocyte cell lines compared to PHH and was not induced upon adiponectin incubation demonstrating significant differences of primary and transformed cells. In free fatty acid (FFA)-incubated PHH adiponectin-mediated induction of activin A was impaired. Inhibition of TGFß receptors ALK4/5 and blockage of SMAD3 phosphorylation rescued activin A synthesis in FFA and in TGFß incubated cells suggesting that FFA inhibit adiponectin activity by inducing TGFß. To evaluate whether serum levels of activin A and its antagonist are altered in patients with hepatic steatosis, both proteins were measured in the serum of patients with sonographically diagnosed fatty liver and age- and BMI-matched controls. Systemic adiponectin was significantly reduced in patients with fatty liver but activin A and follistatin were not altered. In summary the current data demonstrate that lipid accumulation in hepatocytes induces TGFß which impairs adiponectin bioactivity, and thereby may contribute to liver injury.

Clinical feature and bowel ultrasound in Crohn's disease - does additional information from magnetic resonance imaging affect therapeutic approach and when does extended diagnostic investigation make sense?

BACKGROUND/AIMS: Some suggest MRI to be superior to ultrasound in Crohn's disease. We analyzed how often MR enterography (MRE) following a routine ultrasound leads to a change in therapeutic decision. MATERIAL AND METHODS: We retrospectively evaluated 47 patients with Crohn's disease undergoing routine ultrasound examination. Actual medical history, complete blood count, C-reactive protein (CRP), and sonographic findings were assessed independently by two specialists who retrospectively provided a therapeutic proposal. Additionally, all patients received MRE. Thereafter, the specialists had to provide a new therapeutic concept regarding all the available information. RESULTS: Evaluation of the rectum was not successful by ultrasound, but MRE gave good results. Only 1 of 7 abscesses was identified sonographically. Three of the abscesses missed at sonography were localized in the perirectal/perianal region. MRE detected more inflamed bowel segments, but ultrasound assessment of anatomically fixed bowel parts showed good recognition by MRE. With increasing CRP values, we found more positive results of ultrasound and MRE. Therapeutic change was suggested in only 18 patients. CONCLUSIONS: Ultrasound should be performed by an experienced examiner, and a proctological examination should be added. MRE is justified in cases of discrepancy between clinical findings and the results of diagnostic ultrasound and, moreover, if Crohn's lesions are suspected at sites proximal to the terminal or neoterminal ileum.

Hepatic steatosis causes induction of the chemokine RANTES in the absence of significant hepatic inflammation.

Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum ranging from simple steatosis to cirrhosis. Hepatocellular lipid accumulation is a hallmark of both nonalcoholic steatosis and steatohepatitis (NASH). The latter develops upon pro-inflammatory cell infiltration and is widely considered as the first relevant pathophysiological step in NAFLD-progression. The chemokine CCL5/RANTES plays an important role in the progression of hepatic inflammation and fibrosis. We here aimed to investigate its expression in NAFLD. Incubation of primary human hepatocytes with palmitic acid induced a dose-dependent lipid accumulation, and corresponding dose-dependent RANTES induction in vitro. Furthermore, we observed significantly elevated hepatic RANTES expression in a dietary model of NAFLD, in which mice were fed a high-fat diet for 12 weeks. This diet induced significant hepatic steatosis but only minimal inflammation. In contrast to the liver, RANTES expression was not induced in visceral adipose tissue of the group fed with high-fat diet. Finally, RANTES serum levels were elevated in patients with ultrasound-diagnosed NAFLD. In conclusion, our data indicate hepatocytes as cellular source of elevated hepatic as well as circulating RANTES levels in response to hepatic steatosis. Noteworthy, upregulation of RANTES in response to lipid accumulation occurs in the absence of relevant inflammation, which further indicates that hepatic steatosis per se has pathophysiological relevance and should not be considered as benign.

Prevalence of ultrasound-diagnosed non-alcoholic fatty liver disease in a hospital cohort and its association with anthropometric, biochemical and sonographic characteristics.

UNLABELLED: Non-alcoholic fatty liver disease (NAFLD) is considered as the most common liver disease in Western countries with still rising prevalence due to a lifestyle favoring the development of the metabolic syndrome. AIM: To investigate the prevalence of ultrasound-diagnosed NAFLD in patients with referral for sonographic examination of the abdomen, and to determine risk factors. METHODS: After exclusion of patients with known liver disease or risk factors for secondary NAFLD, a total of 155 arbitrarily selected patients (mean age 53.6±17.4 years; 52.6% male) from the interdisciplinary ultrasound department of a German University Hospital were included in this prospective study. Each patient underwent a standardized ultrasound, anthropometric and biochemical examination. RESULTS: The prevalence of ultrasound-diagnosed NAFLD was 40.0%. NAFLD-patients had significantly higher body mass index (BMI) and waist-to-hip ratio, higher rates of reported hypertension and diabetes mellitus, and lower HDL cholesterol serum levels. Furthermore, NAFLD-patients revealed significantly higher serum ALT levels (23.2±22.1 U/l vs. 15.0±8.2 U/l; p=0.001), lower AST/ALT ratio (1.76±0.79 vs. 2.11±0.94; p=0.019), and notably, decreased flow in the portal vein (22.9±6.3 cm/s vs. 26.7±10.5 cm/s; p=0.011). Multivariate analysis revealed BMI (odds ratio (OR): 14.05; 95% Confidence interval (CI): 3.3-59.8), AST/ALT ratio (OR: 0.39; CI: 0.18-0.82), and HDL-C (OR: 4.33; CI: 1.6-11.9) as independent risk factors. CONCLUSIONS: Ultrasound-diagnosed NAFLD is frequent in patients with referral for ultrasound examination of the abdomen, and our findings further support that NAFLD is the hepatic manifestation of the metabolic syndrome with obesity being the most important risk factor.

[Congress of the German Society of Internal Medicine 2009: evaluation of the poster exhibition]. / Kongress der Deutschen Gesellschaft für Innere Medizin 2009: Evaluation der Posterausstellung.

BACKGROUND AND PURPOSE: The presentation of scientific posters gives young scientists the opportunity to present their data in the setting of a medical congress. In preparation of the organization of the 116th Congress of the German Society of Internal Medicine (DGIM) 2010, the authors evaluated the poster rounds at the 115th Congress of the DGIM 2009 by using a questionnaire that was given to poster presenters, poster chairmen, and visitors. The authors sought to receive an instructive criticism for the organization in 2010. METHODS: Distribution of questionnaires containing ten questions with preformulated response options and an additional field for further comments to all presenters, chairmen, and visitors of the poster rounds during the 115th Congress of the DGIM (April 2009). RESULTS: 159 questionnaires were returned and evaluated. Almost all respondents quoted the poster presentation as being important for their scientific work (98%). In general, they were satisfied with the discussion at the poster rounds (83%). The amount of posters within one round was criticized by 41%, as was the inadequate adherence to time constraints and time frame and room conditions themselves. CONCLUSION: The poster exhibition of the 115th Congress of the DGIM 2009 was evaluated positively by most of the respondents to the survey. Nevertheless, helpful hints were retrieved as how to further improve poster rounds. They should be respected when planning the exhibition at the congress in 2010.

To eat or not to eat? Effect of fasting prior to abdominal sonography examinations on the quality of imaging under routine conditions: A randomized, examiner-blinded trial.

OBJECTIVE: Although often recommended, it is unclear whether fasting enhances the imaging quality of abdominal sonography examinations. The aim of this study was to produce experimental evidence of the effect of fasting on the imaging quality of abdominal organs. MATERIAL AND METHODS: Formally consenting medical inpatients who underwent elective abdominal sonography examinations at a university medical center were randomized to either a fasting or a non-fasting preparation. Blinded examiners evaluated the imaging quality of 11 anatomical regions. The primary end-point was the proportion of completely evaluable patients for each region. In secondary analyses, values of an imaging index reflecting the mean imaging quality of all regions (range 0-1) were compared. RESULTS. Of 280 screened patients, 102 (36%) met the exclusion criteria and 35 (13%) declined participation. Of the 143 randomized patients, 130 (91%) were included in the primary analyses (66 fasting, 64 non-fasting). The proportion of completely evaluable patients did not differ significantly for any of the 11 regions, but a large nominal difference occurred for the gallbladder (45/66 (73%) fasting versus 34/64 (56%) non-fasting patients, p=0.051). The median (range) imaging index was 0.57 (0.14-0.95) for fasting and 0.43 (0.00-1.00) for non-fasting subjects (p =0.078). A significant (p=0.002) difference favoring fasting was detected in the post-hoc subgroup analyses for male patients. CONCLUSIONS: For examinations of the gallbladder and for male patients, fasting might improve the sonographic imaging quality to some extent. Overall, no significant improvement in the imaging quality of abdominal organs was reached with a fasting preparation.

Transabdominal ultrasound with echoenhancement by contrast media in the diagnosis of hepatocellular carcinoma.

According to the European Association for the Study of the Liver (EASL) and the American Association for the Study of Liver Diseases (AASLD), ultrasound (US) is the recommended tool for surveillance of patients at risk of developing hepatocellular carcinoma (HCC). Larger HCCs can be diagnosed with a high accuracy by conventional US. However, the differentiation of smaller malignant lesions in cirrhotic livers can be improved by contrast-enhanced ultrasound (CEUS). Second-generation contrast agents consisting of microbubbles enable us to visualize specific tumor vascularization patterns. With CEUS, it is not only possible to detect and characterize HCC nodules, but to control the effects of ablation techniques of HCC as well, evaluating the former lesion with respect to complete necrosis or residual viable tumor. Limitations of CEUS are its inability to characterize lesions distant to the applicator. Moreover, so far the use of contrast agents in US did not result in increased sensitivity in the detection of small HCCs (<1 cm). Thus, there is currently no indication to use contrast agents to increase the detection rate of HCC in patients undergoing US surveillance.