Influence of Liver Fibrosis on Hepatic Artery Doppler Resistance Index in Chronic Hepatitis of Viral Origin

Background: Hepatic arterial Doppler sonography is increasingly being used in liver diagnostics. The determinants of the elevation of hepatic artery impedance indexes in chronic liver disease, however, have still not been fully clarified. The aim of the present study was to investigate the relationship between histological alterations and liver circulation in chronic hepatitis. Methods: Hepatic artery resistance index and portal flow velocity were measured using Doppler sonography in 47 patients with chronic hepatitis of viral origin diagnosed at histopathology. The patients were divided into two groups, those with mild and those with severe alterations, in accordance with the various histological parameters of the Knodell scoring system. Results:     

Parameters of Microsomal and Cytosolic Liver Function But Not of Liver Perfusion Predict Portal Vein Velocity in Noncirrhotic Patients with Chronic Hepatitis C

Our aim was to compare color-coded Doppler sonography (CCDS) and quantitative testing of liver function (QTLF) in patients with chronic hepatitis C. In all, 74 patients with chronic hepatitis C and mild fibrosis underwent QTLF, which included aminopyrine breath test (ABT), galactose elimination capacity (GEC), sorbitol clearance (SC), and indocyanine green clearance (ICG). Hepatic artery velocity and resistance index (HA-V, HA-RI) as well as portal vein velocity (PV-V) were measured by CCDS. ABT, GEC, and PV-V were significantly reduced, whereas SCl, ICG, HA-V, and HA-RI showed normal levels. There was a significant correlation between reduction in PV-V only with GEC and ABT. QTLF did not correlate with HA-V and HA-RI. In conclusion, in hepatitis C patients with liver fibrosis, ABT and GEC are decreased significantly, which was paralleled by a reduction of PV-V. Unexpectedly SCl and ICG, the classical hepatic perfusion parameters, do not correlate with the parameters measured by CCDS.     

Doppler measurements: a surrogate marker of liver fibrosis?

OBJECTIVE: The potential diagnostic value of performing Doppler measurements of liver vasculature to assess early stages of liver fibrosis has not been established. Due to the potential clinical impact, this study focused on the correlation between Doppler measurements and histologically proven liver fibrosis. METHODS: Forty-three consecutive patients with chronic viral hepatitis (79% hepatitis C) were enrolled. At the time of liver biopsy, two independent investigators measured maximum and mean blood flow velocity, resistance indices, vessel diameter and blood flow volume in the portal vein, hepatic artery and hepatic veins. All measurements were taken in triplicate. The mean values were correlated to the degree of liver fibrosis using the Ludwig score. RESULTS: Sixty-seven per cent of the patients in our study group had no or only mild fibrosis (Ludwig score stage I or II). Thirty-three per cent showed progressive fibrosis or cirrhosis (Ludwig score stage III or IV). There was a large overlap in the Doppler measurements and findings between the various disease stages. No significant changes of Doppler parameters were detected, even between patients with no or mild fibrosis and patients with severe fibrosis (Ludwig score stage III or IV). CONCLUSIONS: Doppler measurements of the portal vein, hepatic artery and hepatic vein(s) are not a valid surrogate marker of liver fibrosis. Nor are Doppler measurements a useful method to estimate the degree of liver fibrosis.     

Sonographic criteria for the diagnosis of hepatic involvement in hereditary hemorrhagic telangiectasia (HHT)

Hepatic involvement in hereditary hemorrhagic telangiectasia (HHT) is highly variable and may lead to severe clinical symptoms such as heart failure. This controlled, prospective study defined sonographic criteria for hepatic involvement in HHT. Color Doppler sonography and pulsed Doppler sonography were used to study 25 patients with HHT and liver involvement, 20 patients with HHT without liver involvement, 25 patients with cirrhosis, and 25 patients without liver disease. The diagnosis of hepatic manifestation was confirmed by computed tomography and/or angiography. Liver size, parenchymal changes of the liver, vessel diameters, and flow velocities of the portal vein and the hepatic artery were determined. Resistance index (RI) and pulsatility index (PI) were calculated. The diameter of the common hepatic artery was significantly dilated without overlap between HHT patients with liver involvement and the 3 control groups (mean 11.3 +/- 2.8 mm [HHT with liver involvement], 4.6 +/- 0.9 mm [HHT without liver involvement], 4.8 +/- 1.0 mm [cirrhosis], and 4.4 +/- 1.0 mm [healthy controls], P <.001). Doppler parameters of the proper hepatic artery differed significantly (all P <.001). In all patients with HHT and liver involvement, areas with intrahepatic hypervascularization caused by dilated intrahepatic arteries were observed in varying intensity. Cardiac output significantly correlated with the diameter of the common hepatic artery (r = 0.53, P =.007) and the portal vein (r = 0.42, P =.05). In conclusion, the diameter of the common hepatic artery (>7 mm) and intrahepatic hypervascularization are suitable sonographic diagnostic parameters of HHT with high sensitivity and specificity. Dilated diameters of the hepatic feeding vessels are indicators for systemic circulatory distress in these patients.     

Hepatic Blood Flow Changes in Chronic Hepatitis C Measured by Duplex Doppler Color Sonography: Relationship to Histological Features

Our aim was to determine if portal vein andhepatic artery blood flow indices are a noninvasiveindex of severity of liver disease in chronic hepatitisC. The effect of interferon- treatment on liver blood flow was also studied. Liver blood flowmeasurements were recorded by duplex Doppler colorsonography in 39 patients with chronic hepatitis C, 50healthy controls, and a single patient withhepatocellular carcinoma. Doppler perfusion index (DPI)(calculated as the ratio of hepatic artery flow to totalhepatic flow) and the congestive index of the portalvein (area/velocity) were calculated. Liver biopsies were scored for hepatic inflammation andfibrosis. Hepatic arterial flow (415.7 ± 329.1ml/min vs 195.1 ± 103.5 ml/min) and DPI (0.27± 0.14 vs. 0.17 ± 0.06) were elevated inchronic hepatitis C patients compared to controls (P = 0.0002 and0.0003, respectively) while portal vein flow and totalhepatic flow were similar. Portal vein congestive indexwas similar in chronic hepatitis C (0.106 ± 0.05) compared to controls (0.125 ±0.08) P 0.52. Hepatic blood flow indices were notrelated to the grade of hepatic inflammation or thestage of hepatic fibrosis. Twelve weeks of treatmentwith interferon- had no effect on liver blood flow. Inconclusion, patients with chronic hepatitis C haveelevated hepatic artery blood flow. Hepatic blood flowindices have no relationship to the severity ofhistological liver injury in chronic hepatitis C, and theseflow indices are unaffected by a 12-week course ofinterferon-.     

Serum aspartate but not alanine aminotransferase levels help to predict the histological features of chronic hepatitis C viral infections in adults

OBJECTIVES: The aims of this study were to assess the predictive values of age, gender, route of transmission, extent of steatosis, alcohol consumption, and serum aminotransferase values on the histological findings in patients with chronic hepatitis C viral infections. METHODS: We retrospectively reviewed the charts and liver biopsy findings from 79 adult patients with serological evidence of chronic hepatitis C viral infections. RESULTS: The mean (+/- SD) age of the patient population was 43.5 +/- 10.8 yr; 47 patients (60%) were male. The routes of transmission were considered to be parenteral drugs in 44 patients (56%), previous blood transfusions in 25 (32%), and miscellaneous parenteral and nonparenteral routes in 10 (13%). The mean histological activity score of the group as described by Desmet et al. was 3.5 +/- 0.8 (maximum possible score, 18) and the fibrosis score 1.5 +/-0.4 (maximum possible score, 4), indicating relatively mild disease in the majority of cases. The extent of inflammation correlated with fibrosis (r = 0.72). By multivariate stepwise regression analyses, serum aspartate aminotransferase (AST) values emerged as the most important predictive variable of histological activity (r = 0.62). When overall histological activity was further divided into portal inflammation, piecemeal necrosis, and lobular activity, correlations were found between AST values and portal inflammation (r = 0.58) and piecemeal necrosis (r = 0.61) but not lobular activity (r = 0.1). A correlation was also observed between AST values and the extent of hepatic fibrosis (r = 0.64). On the other hand, serum ALT values did not correlate with histological activity but did correlate weakly with the extent of hepatic fibrosis (r = 0.39 and 0.51, respectively). There were no significant correlations between age, gender, route of transmission, steatosis, or alcohol consumption with the extent of histological activity or fibrosis. CONCLUSIONS: Serum AST values correlate well with two of three features of hepatic inflammation and with the extent of hepatic fibrosis. These findings suggest that, among other factors, serum AST values should be considered in decisions regarding the need for liver biopsy and treatment in patients with chronic hepatitis C viral infections.     

Doppler Ultrasound of Hepatic Blood Flow for Noninvasive Evaluation of Liver Fibrosis Compared with Liver Biopsy and Transient Elastography

Background

Accurate quantification of liver fibrosis is essential for therapeutic decision-making and follow-up of chronic liver diseases.

Aims

To optimize the quality of non-invasive assessment of liver fibrosis in patients with chronic hepatopathy we compared Doppler ultrasound with liver histology and transient elastography (TE).

Methods

In this prospective observational study, we performed Doppler ultrasound of hepatic blood vessels as well as TE in 125 patients who underwent liver biopsy for diagnostic work-up of hepatopathy. Hepatic venous flow was evaluated by determining resistance index (HVRI) of the right hepatic vein. Doppler and TE results were compared with histological staging, grading and degree of steatosis obtained by liver biopsy.

Results

HVRI showed a high reliability in predicting fibrosis stage FII or higher (AUROC 93.7 %, HVRI < 1.185; sensitivity 89.66 % and specificity 86.32 %) and was superior to TE. Neither steatosis nor inflammation had significant influence on HVRI-based estimation of fibrosis (1.45 ± 0.2; 1.26 ± 0.05; 1.06 ± 0.06; 0.87 ± 0.08; 0.46 ± 0.11 for F0–FIV, respectively). HVRI differed significantly in different stages of fibrosis. In contrast, portal vein and hepatic artery only showed significant changes in higher stages of fibrosis. Hepatic artery resistance index was elevated (0.67–0.74; p < 0.05); portal vein flow maximum and undulation were significantly reduced in higher fibrosis (p < 0.05 and p < 0.01, respectively).

Conclusions

Hepatic blood flow analysis, especially HVRI, provides useful information during assessment of hepatopathy and is a reliable predictor of liver fibrosis stage FII or higher as part of the non-invasive diagnostic work-up and follow-up in chronic liver disease.     

Application of a numerical scoring system for assessment of histological outcome in patients with chronic posttransfusion non-A, non-B hepatitis with or without antibodies to hepatitis C

A numerical scoring system was applied and compared to the conventional histological classification to assess the histological status of liver specimens from 37 patients with chronic posttransfusion non-A, non-B hepatitis followed for 7 to 105 months (mean 35 months). Four histological categories of alterations were assessed and scored: piecemeal necrosis (PMN), fibrosis and cirrhosis, lobular necrosis and portal inflammation. Sequential liver biopsies were obtained from 19 patients. PMN was generally mild but still predictive of progressing fibrosis. Thus, in none of the biopsies from four patients with initial PMN score 0 was there any increase in the fibrosis score in the follow-up biopsy, while in 10/15 (67%) patients with an initial PMN score of greater than or equal to 1 the fibrosis score increased with time (p = 0.033). Lobular necrosis and portal inflammation were not predictive of progressing fibrosis. Judging from the scoring method, 22% of all the 37 patients displayed cirrhosis and 27% bridging fibrosis in the latest liver biopsy performed. Patients with antibodies to hepatitis C did not differ in histological status or outcome from those without antibodies to hepatitis C. It is concluded that the scoring system can be used to monitor the histological long-term follow-up in patients with chronic posttransfusion non-A, non-B hepatitis, and offers a means of predicting the histological outcome.     

Steatosis and chronic hepatitis C: analysis of fibrosis and stellate cell activation

BACKGROUND/AIMS: Steatosis is a frequent histological finding in chronic hepatitis C and is associated with increased hepatic fibrosis. METHODS: We studied 80 patients with untreated chronic hepatitis C to determine whether steatosis contributes to fibrosis through a steatohepatitis-like pathway. RESULTS: Fine sinusoidal and/or central vein fibrosis was present in 52 patients (65%). This was typically located in acinar zone 3 and had a chicken-wire appearance similar to that seen in steatohepatitis. A statistically significant relationship was found between subsinusoidal fibrosis and age (r(s) = 0.33, P = 0.003) and grade of steatosis (r(s) = 0.35, P = 0.001). Mean body mass index was higher in patients with focal (28.4 +/- 4.7 kg/m2) or extensive (29.6 +/- 5.9 kg/m2) subsinusoidal fibrosis than in those patients with no subsinusoidal fibrosis (25.5 +/- 3.7 kg/m2). The extent of alpha-smooth muscle actin staining (as a marker of stellate cell activation) correlated with the degree of portal inflammation and the stage of portal fibrosis, but not with the grade of hepatic steatosis. CONCLUSIONS: These findings suggest that in hepatitis C infection, host factors, particularly adiposity, contribute to both steatosis and acinar fibrosis. The implication of these observations is that weight reduction may provide an important therapeutic strategy for patients with chronic hepatitis C.     

Hepatic iron accumulation may be associated with insulin resistance in patients with chronic hepatitis C

Background/Aim: Insulin resistance and hepatic iron overload are frequently demonstrated in hepatitis C virus (HCV)-related liver diseases. We investigated the relationship between insulin resistance and hepatic iron deposition in patients with chronic HCV infection. Methods: Insulin resistance was evaluated using the homeostasis model assessments for insulin resistance (HOMA-IR) in 56 non-diabetic non-obese patients with biopsy proven chronic hepatitis C. The relationship between insulin resistance and serum ferritin levels or the grade of hepatic iron deposition was assessed. Results: The levels of plasma immunoreactive insulin (IRI) and HOMA-IR were significantly correlated with serum ferritin levels and the grade of hepatic iron deposition (P = 0.003).Although IRI and HOMA-IR increased in parallel with the development of hepatic fibrosis, insulin resistance (HOMA-IR > 2) was observed in 11 (26.2%) of 42 patients even without severe fibrosis (F0-2). Among patients without severe fibrosis, IRI and HOMA-IR were significantly higher in patients with iron deposits than in those without iron deposits. Conclusion: Hepatic iron overload may be associated with insulin resistance in patients with chronic hepatitis C, especially in patients with mild to moderate fibrosis.     

慢性肝病肝纤维化程度的非侵入性诊断

探讨慢性肝病患者肝纤维化的非侵入性诊断、灵敏度等。对80例慢性肝病患者进行彩色多普勒超声 检查,检测肝动脉收缩期最大流速／门静脉流速比值(A／P)、肝动脉阻力指数(RI),并同时测定血透明质酸(HA)、凝 血酶原指数。肝硬化患者A／P、RI、HA水平显著高于慢性肝病和正常对照组,P<0．05;凝血酶原指数显著低于慢 性肝病和正常对照组,P<0．05。A／P、RI、HA、凝血酶原指数对慢性肝病肝纤维化程度的非侵入性诊断有一定的指 导意义。     

Association of hepatic iron deposition and serum iron indices with hepatic inflammation and fibrosis stage in nonalcoholic fatty liver disease]

BACKGROUND/AIMS: Nonalcoholic steatohepatitis can develop from nonalcoholic fatty liver and progress to severe liver disease such as cirrhosis. The mechanism determining the progression from fatty liver to steatohepatitis is unknown. Iron is suspected to enhance hepatic damage associated with nonalcoholic fatty liver disease (NAFLD). The aims of this study were to evaluate the relationship of serum iron indices and hepatic iron deposition with hepatic fibrosis or inflammation, and to assess whether the increased hepatic iron deposition is an independent predictor of progression to liver injury. METHODS: The biochemical and histopathological data of thirty-nine patients with NAFLD were analyzed. Liver biopsy findings were graded according to the method described by Brunt, et al. Hepatic iron concentration was available in 29 of 39 patients. RESULTS: The mean hepatic iron concentration and hepatic iron indices were 1,349+/-1,188 microg/g dry weight and 0.9+/-0.7 microg/g/age. Serum ferritin and body mass indices were associated with hepatic inflammation (p=0.001, p=0.006) and fibrosis (p=0.005, p=0.013). Hepatic iron concentration and hepatic iron index were not associated with hepatic inflammation and fibrosis. Multivariate analysis did not identify serum ferritin or body mass index as an independent predictor of liver injury. CONCLUSIONS: Hepatic iron deposition shows no association with the degree of hepatic inflammation or fibrosis. Hepatic iron is not an independent predictor of hepatic injury in patients with NAFLD.     

Hepatic arterial pulsatility index in cirrhosis: correlation with portal pressure.

BACKGROUND/AIMS: Determination of the pulsatility index by means of duplex sonography provides the opportunity to evaluate the vascular resistance of the hepatic artery noninvasively. The aim of this study was to investigate the relationship between the hepatic arterial pulsatility index and the hepatic venous pressure gradient in cirrhosis. METHODS: In 50 patients with cirrhosis, hepatic venous pressure gradient was determined in the fasting state. Immediately thereafter, hepatic arterial pulsatility index and portal blood flow velocity were measured by duplex sonography with no knowledge of hepatic venous pressure values. In addition, the duplex parameters were determined in 20 controls. RESULTS: Hepatic arterial pulsatility index was significantly higher in patients with cirrhosis than in controls (0.92+/-0.1 vs. 1.14+/-0.18; p<0.001) and directly correlated with the hepatic venous pressure gradient (r = 0.7; p<0.001). Furthermore, weak correlations were found between hepatic arterial pulsatility index and Child-Pugh score (r = 0.49; p<0.01) and between portal blood flow velocity and hepatic venous pressure gradient (r = -0.48; p<0.01). CONCLUSION: In cirrhosis the hepatic arterial vascular resistance seems to increase parallel to the rise of the portal pressure. Therefore, duplex sonographic determination of the hepatic arterial pulsatility index may contribute to the noninvasive evaluation of portal hypertension.     

Clinical, virological, and pathological significance of hepatic bile duct injuries in Chinese patients with chronic hepatitis C

Purpose. Hepatic bile duct injuries are characteristic histological findings in patients with chronic hepatitis C virus (HCV) infection. However, the pathogenesis and clinical significance of this phenomenon remain unclear. The aims of this study were to evaluate the prevalence and clinical significance of hepatic bile duct injuries in Chinese patients with chronic hepatitis C. Methods. One hundred and seventeen Chinese patients with chronic hepatitis C were enrolled. Clinical, biochemical, immunological (serum autoantibodies and cryoglobulinemia), histological, and virological data (serum HCV RNA titer and HCV genotype) were compared between patients with and without hepatic bile duct injuries. Results. Eighty-three (71%) of the 117 patients with chronic hepatitis C had hepatic bile duct injuries. Patients with hepatic bile duct injuries had a significantly higher frequency of HCV genotype 1b; a higher mean serum globulin level; significantly higher mean scores for histological periportal necro-inflammation, portal inflammation, and fibrosis; and more severe portal lymphoid aggregation/follicles when compared with patients without hepatic bile duct injuries (P < 0.05, all). No significant differences in the presence of serum autoantibodies, cryoglobulinemia, mean serum HCV RNA titer, or response to interferon treatment were noted between the two groups. Multivariate logistic regression analysis showed that HCV genotype 1b infection, portal inflammation, and lymphoid aggregation/follicles were significant independent predictors associated with hepatic bile duct injuries. Conclusions. The presence of hepatic bile duct injuries in Chinese patients with chronic hepatitis C was significantly correlated with HCV genotype 1b infection, and the patients with these injuries had more severe portal inflammation and formation of lymphoid aggregates/follicles. Received: September 8, 2000 / Accepted: January 26, 2001     

Performance of Doppler ultrasound in the prediction of severe portal hypertension in hepatitis C virus-related chronic liver disease.

PURPOSE: To evaluate the correlation between hepatic vein pressure gradient measurement and Doppler ultrasonography (DUS) in patients with chronic liver disease (CLD). PATIENTS AND METHODS: Sixty-six patients with fibrotic to cirrhotic hepatitis C virus-related CLD, were consecutively included upon referral to our haemodynamic laboratory. Superior mesenteric artery pulsatility index (SMA-PI), right interlobar renal and intraparenchymal splenic artery resistance indices, were determined, followed by hepatic venous pressure gradient (HVPG) measurement. RESULTS: A correlation was found between HVPG and intraparenchymal splenic artery resistance index (SA-RI) (r=0.50, P<0.0001), SMA-PI (r=-0,48, P<0.0001), right interlobar renal artery resistance index (RRA-RI) (r=0.51, P<0.0001) in the whole patient population. However, dividing patients according to the presence/absence of severe portal hypertension (i.e. HVPG > or =12 mmHg), a correlation between HVPG and intraparenchymal SA-RI (r=0.70, P<0.0001), SMA-PI (r=-0.49, P=0.02), RRA-RI (r=0.66, P=0.0002) was observed only for HVPG values <12 mmHg. HVPG but not DUS correlated with the presence of esophageal varices (P<0.0001). CONCLUSIONS: Superior mesenteric artery pulsatility index, intraparenchymal splenic and right interlobar renal artery resistance indices do not adequately predict severe portal hypertension.     

Splanchnic Hemodynamics in Idiopathic Portal Hypertension: Comparison with Chronic Persistent Hepatitis

A comparative study of splanchnic hemodynamics was made in 12 patients with idiopathic portal hypertension and in eight patients with chronic persistent hepatitis, but without portal hypertension, who served as the control. Venous pressures were measured by portal and hepatic vein catheterizations, blood flow by the pulsed Doppler flowmeter, and organ volume by computed tomography. Splenic artery blood flow was 788 +/- 242 ml/min in idiopathic portal hypertension and about four times that in chronic persistent hepatitis (215 +/- 42 ml/min), whereas there was no difference in superior mesenteric artery blood flow between the former and the latter (408 +/- 142 vs. 389 +/- 32 ml/min). Spleen volume in idiopathic portal hypertension was six times that in chronic persistent hepatitis, and splenic artery blood flow showed a significant linear correlation with spleen volume in idiopathic portal hypertension (r = 0.71, p less than 0.02). The sum of splenic artery blood flow and superior mesenteric artery blood flow in idiopathic portal hypertension was 1195 +/- 294 ml/min, twice that in chronic persistent hepatitis (603 +/- 109 ml/min). Portal vascular resistance and intrahepatic portal vascular resistance were three times and four times those in chronic persistent hepatitis, respectively. These results indicate that both increased intrahepatic portal vascular resistance and increased splenic artery blood flow may play roles in the development of portal hypertension in idiopathic portal hypertension.     

Chronic hepatitis C and superimposed nonalcoholic fatty liver disease.

BACKGROUND/AIMS: Hepatitis C and nonalcoholic fatty liver disease (NAFL) are the two most common forms of liver disease in the United States. Recently, obesity and its associated risk factors have been suggested to enhance HCV-related fibrosis. The aim of this study was to assess the impact of hepatic steatosis, steatohepatitis, and its associated risk factors on HCV-related fibrosis. METHODS: Patients with untreated, biopsy-proven, chronic hepatitis C (6/97-3/99) were included. Clinical and demographic data at the time of liver biopsy were obtained from chart review and verified by telephone survey. One hepatopathologist reviewed all pathologic specimens, using the modified histological activity index score and the Ishak staging for fibrosis and a NAFL pathologic protocol. RESULTS: One hundred and seventy patients with hepatitis C were included [age: 48.7+/-9.33 (years), body mass index (BMI): 28.1+/-5.7 (kg/m2) and type 2 diabetes mellitus (DM): 14%]. Of these, 77 (45.3%) had no or mild fibrosis and 93 (54.7%) had advanced fibrosis. Hepatic steatosis was seen in 90 (52.9%) patients. The grade of steatosis was associated with markers of obesity only. Age (p=0.002), type 2 DM (p=0.04), and superimposed steatohepatitis (p=0.047) were independently associated with advanced fibrosis. Superimposed nonalcoholic steatohepatitis (NASH) was seen in 17 (10%) patients. Patients with superimposed NASH were mostly obese (76.5%), males (62%) with 16% having type 2 diabetes and a BMI 33.8+/-7.12. CONCLUSION: In patients with chronic hepatitis C, type 2 DM and superimposed steatohepatitis are independently associated with advanced fibrosis.     

Ultrasonographic splanchnic arterial flow measurement in severe acute pancreatitis

INTRODUCTION: Duplex ultrasonographic technology is now capable of detecting flow signals in the various splanchnic vessels and calculating the concomitant flow velocities using fast-Fourier transformation. AIM: To use Doppler sonography to investigate how splanchnic hemodynamics vary during the early stage of severe acute pancreatitis. METHODOLOGY: Six patients with severe acute pancreatitis (age, 59.0 +/- 6.57 years; four men, two women) and seven with mild to moderate acute pancreatitis (age, 60.1 +/- 7.41 years; five men, two women) were examined with Doppler sonography immediately after disease onset. The maximum velocity, minimum velocity, mean velocity, pulsatility index, and resistive index were determined from the Doppler spectra from the proper hepatic artery, celiac artery, and superior mesenteric artery. We also examined 15 healthy subjects (age, 59.3 +/- 4.60 years; 10 men, five women) as controls. RESULTS: The maximum velocity of the proper hepatic artery in patients with severe acute pancreatitis was significantly higher than that in patients with mild to moderate acute pancreatitis (p = 0.011) and in control subjects (p = 0.0047). Similarly, significant increases in both the minimum velocity and the mean velocity of the proper hepatic artery were observed in patients with severe acute pancreatitis. Neither pulsatility index nor resistive index of the proper hepatic artery showed a significant difference among the three groups. There were no significant differences among the three groups with respect to the flow velocity of the superior mesenteric artery. In contrast, the pulsatility index of the superior mesenteric artery in patients with severe acute pancreatitis was significantly lower than that in patients with mild to moderate acute pancreatitis (p = 0.0058) or in control subjects (p = 0.0024). For patients with acute pancreatitis, a significant inverse correlation was obtained between the maximum velocity of the proper hepatic artery and the pulsatility index of the superior mesenteric artery (r = -0.658, p = 0.0145). CONCLUSION: The increase in the hepatic arterial flow velocity and the decrease in the superior mesenteric arterial pulsatility index may represent early events of the severe type of acute pancreatitis.     

IFN-γ治疗20例慢性乙型肝炎肝纤维化患者肝组织学变化

目的采用重组人IFN-γ治疗20例慢性乙型肝炎肝纤维化患者,通过治疗前后肝组织活检,观察其组织病理学的变化。方法20例慢性乙型肝炎患者,肝纤维化分期在2～4期。采用重组人IFN-γ肌注,开始3月每日一次,其后6月隔日1次,每次100万U,疗程为9个月。组织病理学观察包括HE染色和天狼红染色。使用肝纤维化半定量计分方案评价治疗前后肝纤维化程度变化。另测治疗前后血清肝纤维化指标,包括血清透明质酸、Ⅳ型胶原、Ⅲ型前胶原、层粘蛋白等四项指标。结果20例患者经IFN-γ治疗9月后,其肝纤维化计分由治疗前的11.24±5.34下降为治疗后的8.67±4.16（P＜0.01）;治疗后的炎症计分由治疗前的12.78±5.19下降为治疗后的6.57±2.95（P＜0.01）。结论IFN-γ能较好改善慢性乙型肝炎肝纤维化患者的肝纤维化程度,证明其有良好的抗肝纤维化治疗效果。