胰岛素样生长因子Ⅰ和各型肝病关系的研究

探讨胰岛素样生长因子１（ＩＧＦ－１）在各型肝病患者中的变化规律。用放射免疫法测定２３１例肝病患者及 ６３例正常人的血清 ＩＧＦ－１含量。急性肝炎（６４０．２９± ７３．６０）ｎｇ／ｍｌ，慢性轻度肝炎（５３９．６５± ９６．５５）ｎｇ／ｍｌ，慢性中度肝炎（５１２．６５±６９．５７）ｎｇ／ｍｌ，慢性重度及重症肝炎（３２４．７１±１６３．２７）ｎｇ／ｍｌ，失代偿期肝硬化（１６１．３５±８５．２９）ｎｇ／ｍｌ，原发性肝癌（１６．９１± ９６．５２）ｎｇ／ｍｌ，正常对照（３０２．２６± ８３．２９）ｎｇ／ｍｌ。除慢性重度重症肝炎外；其余各型肝病的ＩＧＦ－１含量与正常比较有显著性差异（Ｐ＜０．０１）。肝硬化及肝癌患者的ＩＧＦ—１水平明显低于正常（Ｐ＜０．０１）。ＩＧＦ－１是在肝脏病变的发展过程中判断肝细胞功能不良的重要指标。检测ＩＧＦ－１对肝病患者尤其是判别肝硬化是否停止进展的预后估计有一定作用。     

检测肝炎患者胆碱脂酶活性的临床价值分析

目的 评估血清胆碱脂酶（CHE）活性变化在判定肝病病程和预后方面的价值。方法 采用全自动生化分析仪检测各种肝炎患者血清CHE的活性。结果 慢性肝炎组、重型肝炎组CHE活性均显著低于正常对照组（P〈0.01）。重型肝炎组（n=68）中存活组（n=40）和死亡组（n=28）CHE分别为3．49±1．23ku／L。和2．88±1．11ku／L，两组比较差异有统计学意义（P＜0.05）。结论 CHE活性检测有助于判定肝病患者的预后。     

失代偿期肝硬化合并胆总管结石患者行十二指肠镜治疗的安全和有效性分析

目的 评价失代偿期肝硬化合并胆总管结石患者行ERCP治疗的安全性和有效性。方法 收集2012年12月至2016年12月在兰州大学第一医院ERCP诊疗技术培训中心经ERCP治疗的失代偿期肝硬化合并胆总管结石的患者79例（肝硬化组）、慢性病毒性肝炎患者92例（慢性病毒性肝炎组）以及无肝病患者随机抽取114例（无肝病组）,对比分析ERCP治疗操作情况、肝功能指标术后改善情况以及并发症情况。结果 肝硬化组ERCP术前凝血酶原时间为（12.9±2.2） s,多于慢性病毒性肝炎组（12.1±1.9） s和无肝病组（11.7±1.4） s,差异有统计学意义（F=21.530,P＜0.001）。术中操作肝硬化组所用时间（58.58±19.40） min,多于慢性病毒性肝炎组（52.53±16.74） min和无肝病组（49.81±14.82） min,差异有统计学意义（F=6.444,P=0.002）。术后各组均无穿孔、死亡的病例。肝硬化组中3例（3.8％）患者行EST后出现十二指肠乳头少量渗血,其中2例为Child-Pugh C级,1例为Child-Pugh B级;1例（1.27％）Child-Pugh C级患者出现食管下段曲张静脉渗血,但该项与其他术中、术后并发症同样,3组间差异均无统计学意义（P＞0.05）。肝硬化组ERCP术前、术后肝功能指标谷草转氨酶（66.0比53.0 IU／L）、谷丙转氨酶（61.0比52.0 IU／L）、γ-谷氨酰转移酶（318.0比231.0 IU／L）、碱性磷酸酶（232.0比210.0 μmol／L）、总胆红素（65.7比56.3 μmol／L）比较,差异均有统计学意义（P＜0.05）,显示肝功能较术前明显改善。结论 Child-Pugh A级、B级失代偿期肝硬化患者行ERCP治疗胆总管结石安全性和有效性良好,对于Child-Pugh C级患者,应尽量在改善肝功能、凝血功能情况后行ERCP。     

血清总胆汁酸测定在肝病诊断中的应用

血清总胆汁酸(TBA)含量(μmol/L),急性肝炎组28例126.4±116.2>肝癌组43例111.1±101.9>肝硬化组53例72.1±66.9>慢性肝炎组71例39.2±31.7>正常对照组100例5.3±4.1,各疾病组均高于对照组(P<0.01)。急性肝炎、肝硬化和肝癌患者血清TBA异常率达83.1％以上。血清TBA在肝     

阻塞性睡眠呼吸暂停低通气综合征患者呼出气凝集液中过氧化氢浓度

目的测定阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者呼出气凝集液(EBC)中的过氧化氢(H2O2)浓度,观察其改变及与病情程度的相关性。方法收集EBC 42份,其中OSAHS患者32份(吸烟者18份,非吸烟者14份),非OSAHS对照组10份。荧光法测定睡前和晨起EBC中的H2O2浓度。结果OSAHS组患者睡前EBC中H2O2浓度与对照组比较差异无统计学意义(F= 0．01,P=0．99)。晨起EBC中H2O2浓度OSAHS不吸烟组和吸烟组分别为(1．82±1．12)、(1．65±0．89)μmol／L,较对照组(0．71±0．36)μmol／L明显增高(F=5．11,P=0．01)。其浓度亦分别较睡前[(0．87±0．45)、(0．88±0．36)μmol／L]升高(t分别为2．95、3．43,P均<0．01)。对照组睡前[(0．86±0．46)μmol／L]和晨起[(0．71±0．36)μmol／L]差异无统计学意义(t=0．81,P=0．43)。晨起EBC中H2O2浓度与夜间最低血氧饱和度(SpO2min)呈负相关(β=-0．36,P=0．02),晨起与睡前H2O2浓度变化的差值亦与SpO2min呈负相关(β=-0．38,P=0．01)。结论OSAHS患者由于夜间反复出现缺氧-再氧和,呼吸道局部氧应激反应在晨起增加。     

蜂螫伤中毒患者血清肿瘤坏死因子与血浆内皮素的变化及意义

目的探讨肿瘤坏死因子α(TNFα)与内皮素(ET)在蜂螫伤中毒患者中的变化及临床意义。方法将97例蜂螫伤中毒患者分成轻度、中度、重度中毒3组,并根据预后分成死亡组、存活组。另选取35例健康人作为正常对照组,各组均采用放射免疫法检测血清TNFα与血浆ET水平,同时进行对比分析。结果蜂螫伤中毒患者轻度中毒组血清TNFα(1．36±0．37)μg／L与血浆ET (55．20±12．60)ng／L的含量仅轻度升高,与正常对照组[(1．09±0．25)μg／L、(50．90±8．80)ng／L]比较差异无统计学意义(P>0．05);中度、重度组患者血清TNFα(2．82±0．79)μg／L、(4．02±0．93)μg／L与血浆ET水平(139．30±58．80)ng／L、(210．50±86．30)ng／L较正常对照组明显升高(P值均<0．01),中度组患者血清TNFα与血浆ET水平较轻度组为高(P<0．01),重度组患者又较中度组高(P<0．01)。死亡组血清TNFα(4．53±0．89)μg／L与血浆ET(267．50±98．70)ng／L水平高于存活组(2．40±0．82)μg／L、(107．60±57．90)ng／L(P值均<0．01)。蜂螫伤中毒患者血清TNFα与血浆ET水平呈正相关(r=0．62,P<0．01)。结论TNFα与ET可能协同参与了蜂螫伤中毒患者的发病过程。血清TNFα与血浆ET升高越明显,蜂螫伤中毒患者病情越重,病死率就越高。血清TNFα与血浆ET的检测可作为判断病情轻重和预后的一个重要临床指标。应用TNFα与ET拮抗剂或抑制剂对防治蜂螫伤中毒的发生发展、改善预后可能有重要的临床意义。     

血清总胆汁酸测定的意义及其局限性

目的　阐明空腹血清总胆汁酸（TBA）测定的临床意义。方法　收集913例临床资料,用SPSS软件及四格表法进行统计分析。结果　（1）正常人TBA平均（4.0±3.2）μmol/L。肝病组TBA显著高于正常人和非肝病组(P＜0.01)。（2）急性肝炎患者TBA平均为（167.2±132.4）μmol/L,最高达449.5μmol/L,与其他各组相比差异有显著性(P＜0.01),表明TBA是反映急性肝细胞损伤的敏感指标。（3）TBA对肝硬化的敏感性为85.8%,优于其他肝功能试验,TBA是反映肝硬化侧支循环的有价值的指标。（4）TBA对慢性轻度肝炎的敏感性仅为30.5%,不及ALT和总胆红素（TBIL）。（5）TBA水平与病情轻重有一定关系,但与TBIL不完全平行,对病情的判断不如TBIL有价值。结论　TBA特异性高,敏感性尚可,对肝病、特别是急性肝炎和肝硬化有重要诊断价值,但对慢性轻度肝炎的敏感性差,对病情的判断不如TBIL有意义。     

病毒性肝炎患者血浆LPO,VitE及红细胞SOD水平与肝功能的关系

检测45例病毒性肝炎患者血浆LPO,VitE及红细胞SOD水平,发现急性肝炎组、慢活肝组、重症肝炎组及肝硬化组血浆LPO值分别为5.52±2.6、9.67±5.11、18.22±6.81和7.51±5.051mmol/L.均明显高于正常对照组2.77±0.67(P<0.05),重症肝炎组升高最明显。血浆VitE值分别为9.22±3.83、7.81±2.67、6.56±2.64和6.99±2.67μmol/L,均明显低于正常对照组13.95±4.80(P<0.001),重症肝炎组下降最明显。4种肝病红细胞SOD水平与正常对照组比较无明显改变(P>0.05)。LPO增多、VitE减少与肝功能损伤程度一致。     

应用终末期肝病模型评分系统预测血浆置换治疗后重型肝炎患者的预后

目的应用终末期肝病模型(MELD)评分系统预测血浆置换(PE)治疗后重型肝炎患者的预后。方法160例重型肝炎患者随机分为PE组与对照组,应用MELD评分系统对每个患者进行评分,比较两组患者病死率和治疗前后的临床生化指标,探讨与MELD评分的关系。结果MELD分值在30～39的患者PE后总胆红素(TBIL)、凝血酶原时间国际标准化比值(INR)、MELD评分分别为(379．4±40．4)μmol/L、(2．5±0．2)和(30．8±3．8);明显低于治疗前的(509．7±64．6)μmol/L、(3．5±0．3)和(37．3±3．5),差异有统计学意义(P＜0．05)。PE组患者的病死率为50．0%,明显低于对照组的86．7%,差异有统计学意义(P＜0．01)。MELD分值≥40的患者PE后的TBIL、INR及MELD评分分别为(595．6±61．5)μmol/L、(3．8±0．4)、(39．8±3．50),明显低于治疗前的(650．4±66．3)μmol/L、(4．4±0．60)、(45．2±4．2),差异有统计学意义(P＜0．05)。PE组患者病死率为91．2%,与对照组的100%相比,差异无统计学意义(P＞0．05)。结论PE通过降低重型肝炎患者的TBIL、INR、MELD评分,改善肝脏功能。血浆置换可降低MELD分值在30～39之间的重型肝炎患者的病死率,但不能降低MELD分值≥40的患者的病死率。     

各型病毒性肝炎血清氨基酸的研究

自我们采用日立835—50型高速自动氨基酸分析仪对60名正常人的氨基酸组成。与各型病毒性肝炎共计130例进行血清游离氨基酸检测。结果如下:正常人平均数值为163.97μmol/L,BCAA/AAA3.27±0.58;急性肝炎:血中谷、酪氨酸增高为21.83μmol/L,异亮和精氨酸降低为14.06μmol/LBCAA/AAA2.89±0.47;慢迁肝:血中五种氨基酸增高,有酪、谷、胱、赖及组氨酸平均增     

Carnitine metabolism in patients with chronic liver disease

Carnitine metabolism was studied in 79 patients with chronic liver disease, including 22 patients with noncirrhotic liver disease and 57 patients with different types of cirrhosis (22 patients with hepatitis B- or C-associated cirrhosis, 15 patients with alcohol-induced cirrhosis, 15 patients with primary biliary cirrhosis [PBC], and 5 patients with cryptogenic cirrhosis), and compared with 28 control subjects. In comparison with control subjects, patients with noncirrhotic liver disease showed no change in the plasma carnitine pool, whereas patients with cirrhosis had a 29% increase in the long-chain acylcarnitine concentration. Analysis of subgroups of patients with cirrhosis showed that patients with alcohol-induced cirrhosis had an increase in the total plasma carnitine concentration (67.8 +/- 29.5 vs. 55.2 +/- 9.9 micromol/L in control subjects), resulting from increases in both the short-chain and long-chain acylcarnitine concentration. In this group of patients, the acylcarnitine concentrations showed a close correlation with the total carnitine concentration, and the total carnitine concentration with the serum bilirubin concentration. Urinary excretion of carnitine was not different between patients with noncirrhotic or cirrhotic liver disease and control patients. However, patients with PBC showed an increased urinary excretion of total carnitine (52.5 +/- 40.0 vs. 28.0 +/- 16.7 micromol carnitine/mmol creatinine), resulting from an increase in the fractional excretion of both free carnitine and short-chain acylcarnitine. The current studies show that patients with cirrhosis are normally not carnitine deficient. Patients with alcohol-induced cirrhosis have increased plasma carnitine concentrations, which may result from increased carnitine biosynthesis because of increased skeletal muscle protein turnover. The increase in the fractional carnitine excretion in patients with primary biliary cirrhosis may result from competition of bile acids and/or bilirubin with tubular carnitine reabsorption and/or from a reduced activity of the carnitine transporter located in the proximal tubule.(Hepatology 1997 Jan;25(1):148-53)     

Soluble interleukin 2 receptor in acute viral hepatitis and chronic liver disease

Serum levels of soluble interleukin 2 receptor were determined in patients with acute viral hepatitis and patients with various chronic liver diseases. In addition, the ability of peripheral blood mononuclear cells of patients with alcoholic cirrhosis to generate soluble interleukin 2 receptor following mitogenic stimulation was studied in vitro. Serum soluble interleukin 2 receptor concentrations in all patients with acute viral hepatitis were found to be significantly elevated (1,319 +/- 527 units per ml) during the first week after onset of disease, as compared to healthy control individuals (375 +/- 102 units per ml; p less than 0.0005) and declined toward normal levels during the course of the illness. Similarly, patients suffering from chronic liver disease such as alcoholic liver cirrhosis (1,172 +/- 507 units per ml), primary biliary cirrhosis (619 +/- 190 units per ml) or chronic active HBsAg+ hepatitis (941 +/- 357 units per ml) showed increased serum soluble interleukin 2 receptor concentrations (p less than 0.0005 vs. controls, respectively). In vitro mitogen stimulation of peripheral mononuclear cells derived from patients with alcoholic cirrhosis resulted in a soluble interleukin 2 receptor production not different from that seen in healthy individuals, suggesting that elevated soluble interleukin 2 receptor serum levels seen in this disease are not the result of an increased synthesis by circulating lymphocytes. Due to the ability of soluble interleukin 2 receptor to bind free interleukin 2--thus making it a potential immunoregulatory molecule--its high serum levels could explain some of the immunologic abnormalities observed in acute and chronic liver disease.     

Clinical significance of serum procalcitonin levels in patients with acute or chronic liver disease

OBJECTIVE: To evaluate the diagnostic value of serum procalcitonin levels in patients with acute or chronic liver disease, with or without bacterial infections and to correlate the results with the clinical outcome and the laboratory findings for these patients. METHODS: One hundred and six consecutive hospitalized patients with liver disease were evaluated for procalcitonin levels on admission. Fifteen of them (14.2%) had acute alcoholic hepatitis on cirrhotic background (group A), 20 (18.9%) had alcoholic cirrhosis without hepatitis and/or bacterial infection (group B), 16 (15.1%) had decompensated cirrhosis with proved bacterial infection (group C), 42 (39.6%) had uncomplicated viral hepatitis-related cirrhosis (group D) and 13 (12.3%) had acute icteric viral hepatitis (group E). Serum procalcitonin levels were measured using an immunoluminometric assay. Statistical analysis was based on Student's t-test and the non-parametric Kruskall-Wallis test (P<0.05). RESULTS: Serum procalcitonin levels were significantly higher in cirrhotic patients with bacterial infection (9.80+/-16.80 ng/ml) than in those without bacterial infection (0.21+/-0.13 ng/ml, P=0.001), whereas they were within normal range (<0.5 ng/ml) in all patients with uncomplicated cirrhosis, irrespective of the cause of cirrhosis. Seven of 15 group A patients (46.2%) and 4/13 group E patients (30.8%), all of them cirrhotics, had procalcitonin levels higher than 0.5 ng/ml on admission, without established bacterial infection. CONCLUSION: Serum procalcitonin levels remain below the threshold of 0.5 ng/ml in all patients with uncomplicated cirrhosis, irrespective of the cause of the disease, while they are significantly elevated when bacterial infection complicates the course of the disease. A significant proportion of patients with acute alcoholic hepatitis on a cirrhotic background as well as of patients with acute on chronic viral hepatitis, without bacterial infection, exhibit serum procalcitonin levels above 0.5 ng/ml, suggesting that this cut-off value is probably not enough to discriminate between patients with or without bacterial infection within these subgroups of patients with liver disease.     

Serum thrombopoietin levels in patients with chronic hepatitis and liver cirrhosis,and its relationship with circulating thrombocyte counts

BACKGROUND/AIMS: Thrombocytopenia in chronic liver diseases may be related to deficient production of thrombopoietin. The aim of this study was to measure serum thrombopoietin levels and to examine the relationship between serum thrombopoietin concentration, circulating platelet counts and clinical stage of the disease in patients with chronic hepatitis and liver cirrhosis. METHODOLOGY: The study included 18 patients with chronic hepatitis, 48 with liver cirrhosis and 27 healthy volunteers. Serum thrombopoietin levels were measured by enzyme-linked immunosorbent assay. Additionally, serum albumin levels, prothrombin time, circulating platelet counts and spleen volume index were determined. RESULTS: Mean serum thrombopoietin level (100.96 +/- 41.67 pg/mL) in the chronic hepatitis group was similar to that of the healthy group (97.60 +/- 43.99 pg/mL), however serum thrombopoietin levels in patients with liver cirrhosis (69.60 +/- 30.23 pg/mL) were lower than patients with chronic hepatitis and controls (p < 0.05 for both). In patients with liver cirrhosis, serum thrombopoietin levels were found to be decreased as the disease progressed (80.99 +/- 24.85 pg/mL in patients at Child-Pugh stage A, 67.92 +/- 39.37 in patients at stage B and 57.62 +/- 21.09 pg/mL in patients at stage C). Cirrhotic patients had increased prothrombin time (17.12 +/- 3.52 sec) and spleen volume index (94.38 +/- 26.48 cm2), and decreased serum albumin level (3.11 +/- 0.56 g/dL) and platelet counts (102,368 +/- 30,653/mm3) when compared to both chronic hepatitis and control groups. Thrombocytopenia was found in 31 (65%) of the patients with liver cirrhosis. In patients with liver cirrhosis, while there was a positive correlation between serum thrombopoietin and albumin levels (r = 0.36, p = 0.004), no correlation was found between platelet counts and serum thrombopoietin level, and spleen volume index. CONCLUSIONS: The findings reveal that serum thrombopoietin levels are normal in patients with chronic hepatitis, but in patients with liver cirrhosis, serum thrombopoietin levels decrease, as degree of cirrhosis progresses. The impaired production of thrombopoietin may contribute to the development of thrombocytopenia in advanced stage of liver disease.     

Plasma nitrites/nitrates in HCV infection and hepatocellular carcinoma

OBJECTIVE: Nitric oxide (NO) is produced in response to inflammatory and mitogenic stimuli and may have a role in carcinogenesis. However, the role of NO in hepatitis C-associated hepatocellular carcinoma (HCC) is unclear. In this study, we investigated the potential role of NO in HCC complicating hepatitis C virus (HCV) infection. METHOD: We measured plasma nitrites/nitrates as being representative for NO release in blood of patients with chronic hepatitis C without cirrhosis (n = 20), cirrhosis of different aetiologies (n = 30) including HCV, HCC (n = 22) and in healthy controls (n = 8), by an enzyme-linked immunosorbent assay. RESULTS: Plasma NO levels in patients with chronic hepatitis C without cirrhosis (32.3+/-8.94 micromol/l) were not significantly different from those in healthy control subjects (35.5+/-15.12 micromol/l). Also, there were no statistical differences between plasma NO levels in patients on alpha-interferon (alpha-IFN) therapy (n = 10) (31.60+/-10.55 micromol/l) and in non-treated patients (n = 10) (33.00+/-7.51 micromol/l) within the group of chronic hepatitis C. Plasma NO levels in patients with cirrhosis (42.36+/-26.86 micromol/l) were significantly higher than those with chronic hepatitis C (P < 0.001). The cause of cirrhosis had no effect on plasma NO levels. Plasma NO levels in patients with HCC (49.40+/-49.11 micromol/l) were significantly higher than those with liver cirrhosis (P < 0.03). No significant correlation was found between plasma NO and serum ALT (alanine aminotransferase) levels. There were positive correlations between plasma NO levels and alkaline phosphatase (r = 0.528) (P = 0.0001), bilirubin (r = 0.244) (P = 0.039) and GGT (gamma glutamyltransferase) (r = 0.255) (P = 0.030). CONCLUSION: The results of this study demonstrate that patients with chronic hepatitis C without cirrhosis have the same plasma NO levels as controls, and that alpha-IFN therapy had no effect on NO production in these patients. However, patients with HCC have elevated plasma NO levels compared with patients with cirrhosis. These data support the concept that NO is elevated in cirrhosis and HCC, but HCV infection does not appear to be responsible for the increase of NO in these patients. The severity of liver disease may be an important factor.     

Lamivudine treatment for decompensated cirrhosis resulting from chronic hepatitis B

The prognosis of decompensated cirrhosis resulting from chronic hepatitis B is poor, and the benefits of treatment with interferon are outweighed by serious side effects and by the risk of fatal exacerbation of disease activity. Lamivudine rapidly reduces hepatitis B virus (HBV)-DNA in serum to undetectable levels. We have treated 35 patients with chronic hepatitis B and decompensated cirrhosis with lamivudine 100 mg or 150 mg orally once daily. Pretreatment, all were positive for HBV-DNA in serum. Ten had Child-Pugh class B and 25 had Child-Pugh class C liver disease. Seven patients underwent liver transplantation within 6 months of treatment initiation, 5 patients died within 6 months, and 23 patients were treated for at least 6 months (mean = 19 months). In a majority of these 23 cases, there was a slow but marked improvement in liver function, which was most apparent after 9 months of treatment, with a decrease in serum bilirubin from 67 +/- 13 to 30 +/- 4 micromol/L (P <.05, baseline vs. 9 months), an increase in serum albumin from 27 +/- 1 to 34 +/- 1g/L (P <.05), and a decrease in Child-Pugh score from 10.3 +/- 0.4 to 7.5 +/- 0.5 (P <.05). Three patients developed resistance to lamivudine because of a mutation in the YMDD motif, but liver function did not deteriorate. We conclude that inhibition of viral replication with lamivudine results in a significant improvement of liver function in patients with decompensated HBV cirrhosis, but the long-term benefits remain uncertain.     

Abnormal concentrations of esterified carnitine in bile: a feature of pediatric acute liver failure with poor prognosis

The etiology of acute liver failure in children is unknown in a large number of cases. Defects in fatty acid oxidation have been shown to lead to severe liver injury. This retrospective analysis examined the bile acylcarnitine profiles of 27 children with acute liver failure who underwent liver transplantation or died. Results were compared with 758 postmortem samples from individuals without acute liver failure. Cumulative amounts of free carnitine, medium- or long-chain species in excess of the 95th percentile of the control group were considered abnormal. Fourteen samples had normal profiles. Three had markedly elevated concentrations of free carnitine, whereas ten showed elevations in medium- or long-chain species. The relative risk of death was 2.86 (95% confidence interval, 1.08-7.54, P = .01) in the 10 children with elevated concentrations of medium- or long-chain species compared with those with normal analyses. Overall, medium- and long-chain acylcarnitines were increased in those patients who died compared with survivors, (dead vs. alive; medium-chain, 187 +/- 74 vs. 32 +/- 12 micromol/L, P = .008; long-chain, 146 +/- 74 vs. 15 +/- 8 micromol/L, mean +/- standard error of the mean, P = .018). These studies describe biliary free and esterified carnitine profiles in children with acute liver failure. In conclusion, the findings raise the hypothesis that abnormalities in fatty acid oxidation may predispose to a worse outcome in acute liver failure.     

Thrombocytopenia associated with liver cirrhosis and hepatitis C viral infection: role of thrombopoietin

BACKGROUND/AIMS: Thrombocytopenia in chronic liver diseases has traditionally been considered a consequence of platelet pooling and destruction in spleen. We tried to evaluate the influence of thrombopoietin, the physiological regulator of thrombopoiesis, on the origin of this thrombocytopenia. METHODOLOGY: We determined serum thrombopoietin levels by ELISA in thrombocytopenic patients with liver cirrhosis (n = 32) and with chronic hepatitis C viral infection (n = 23). A group of 43 healthy subjects was used as a control. RESULTS: Liver cirrhosis patients presented slightly, but not significantly, lower serum thrombopoietin levels (104 +/- 56 pg/mL) than controls (121 +/- 58 pg/mL) or patients infected with chronic hepatitis C virus (125 +/- 40 pg/mL). No correlations were found between serum thrombopoietin concentrations and liver tests or hematological parameters. CONCLUSIONS: We conclude that low thrombopoietin production may play a role, along with hypersplenism, in the development of thrombocytopenia in patients with liver cirrhosis. Normal thrombopoietin levels exclude a defect in thrombopoietin production as a possible etiology for the thrombocytopenia in patients with chronic hepatitis C viral infection. However, a direct viral megakaryocyte infection or an immune mechanism could explain this thrombocytopenia, according to the thrombopoietin levels detected.     

A clinical evaluation of serum alpha-1-antichymotrypsin levels in liver disease and cancers

The serum levels of alpha-1-antichymotrypsin (ACT) were studied in 168 patients with various liver diseases and cancers in conjunction with other liver function tests, serum sialic acid, AFP and CEA. The ACT levels in acute viral hepatitis and chronic hepatitis were not significantly altered compared with the normal level (220 +/- 40 microgram/ml), although the level was slightly increased or decreased temporarily during the acute phase of the former. In liver cirrhosis, the mean level was significantly lower than the normal in spite of the absence of signs of hepatic decompensation (168 +/- 51 microgram/ml, p less than 0.001). In contrast to cirrhosis, the levels were increased to various extents in 65% of cases with hepatoma, in spite of the association of liver cirrhosis in the majority of them. Much higher levels were observed in all cases of metastatic liver cancers and cancers of the pancreas and the biliary tract. The elevations were observed even in cases without the increase of AFP or CEA. Both in cirrhosis and cancers, ACT levels were not correlated with any of serum bilirubin and serum enzyme activities, but were positively correlated with the levels of plasma fibrinogen and serum sialic acid. The measurement of serum ACT level can be taken advantage of for the diagnosis and monitoring of liver cirrhosis and liver cancers, particularly of hepatoma without AFP elevation.