肝硬化患者血钙浓度的临床分析

目的 观察肝硬化患者的血钙浓度,以及肝脏Child-Pugh分级与血钙浓度关系.方法 对190例肝硬化患者进行血钙浓度测定,按Child-Pugh分级标准分为A、B、C级,同时测定健康对照100例血钙浓度.结果 肝硬化代偿期与失代偿期的血清钙浓度明显低于对照组,两者比较差异有统计学意义(P＜0.01);肝硬化失代偿期血钙浓度低于代偿期,差异有统计学意义(P＜0.01).随着Child-Pugh评分的增高,肝硬化程度加重,血钙浓度降低愈加明显,A、B、C级血钙浓度分别为(2.11±0.18) mmol/L、(1.95±0.21 )mmol/L、(1.83±0.20) mmol/L,C级组血钙浓度明显低于A级组和B级组,差异有统计学意义(P＜0.01).结论 血钙浓度与肝硬化患者肝功能损害程度相关.     

血清前白蛋白、胆碱酯酶与肝硬化Child-Pugh分级的关系

测定肝硬化患者血清前白蛋白（PA）含量、胆碱酯酶（CHE）活性及肝功能常规生化指标.结果 肝硬化患者PA含量和CHE活性较正常组显著降低（P＜0.01）.按Child-Pugh分级,PA含量和CHE活性在肝硬化组A级与正常组、B级与A级、C级与B级之间有统计学差异（P＜0.05）;两项指标均随Child-Pugh分级升高而明显降低.提示血清PA含量和CHE活性检测对判断肝硬化程度具有重要的指导意义,可作为肝硬化患者病情诊断和预后判断的指标.     

促红细胞生成素、血小板生成素与肝硬化患者Child-Pugh分级的关系

采用放射免疫法检测肝硬化患者47例和同期门诊健康查体者30例(对照组)的空腹血清促红细胞生成素(EPO)、血小板生成素(TPO)水平.结果肝硬化组血清EPO水平高于对照组(P＜0.01);肝硬化Child-Pugh B级、C级患者血清EPO水平高于Child-Pugh A级,TPO水平低于child-Pugh A级(P＜0.05,＜0.01);肝硬化组血清TPO水平与外周血小板计数之间呈正相关关系(r=0.63,P＜0.01).认为测定肝硬化患者血清EPO、TPO水平可为不同程度肝脏疾病的病理生理研究提供参考,对判断肝病发展具有重要意义.     

骨定量超声检测在肝硬化骨密度诊断中的应用价值

目的探讨骨定量超声检测(QUS)在肝硬化患者骨密度(BMD)诊断中的应用价值,对防治肝硬化骨质疏松(OP)提供诊断依据。方法采用骨定量超声仪分别测量120例肝硬化患者组和120例健康人群对照组的骨质密度;同时抽取空腹血检测血清甲状旁腺素(PTH)、1.25(OH)2D3、血清骨钙素(BGP)、降钙素、血清钙,两组结果进行对照分析。结果肝硬化组骨密度、血清1.25(OH)2D3、骨钙素、血清钙与对照组比较均降低,差异有统计学意义(P0.05);血清甲状旁腺素、降钙素与对照组比较均升高,差异有统计学意义(P0.05)。结论肝硬化患者伴有骨密度减少甚至骨质疏松,骨定量超声可在临床广泛应用于肝硬化患者骨密度减少的检测。     

肝硬化患者血浆二胺氧化酶及内毒素检测的临床意义

探讨肝硬化患者血浆二胺氧化酶(DAO)和内毒素水平的临床意义.方法:以50例肝硬化患者和30例健康体检者为试验组和对照组,用分光光度法检测其外周血中DAO和内毒素的活性.结果:Child-Pugh A、B、C 3组肝硬化患者DAO活性均升高,与对照组比较差异有显著性意义(P＜0.01);Child-Pugh C级组DAO活性低于Child-Pugh B级,两者差异有显著性意义(P＜0.01).Child-Pugh A级组内毒素活性与对照组比较,差异无显著性意义(P＞0.05),Child-Pugh B、C级组与对照组比较,差异有显著性意义(P＜0.01).结论:血浆DAO水平是肠粘膜损伤早期诊断的敏感指标,内毒素血症、肠粘膜屏障衰竭是肝硬化患者病情加重的重要因素,也是治疗的关键之一.     

肝硬化患者纤溶活性变化与t-PA、PAI的关系

目的探讨肝硬化患者纤溶活性增高与组织纤溶酶原激活物(t-PA)、组织纤溶酶原激活物抑制剂(PAI)的关系.方法根据Child-Pugh分级将确诊为肝硬化的86例患者分为三组,A级组26例,B级组30例,C级组30例.均检测t-PA、PAI、纤维蛋白(原)降解产物(FDP)和D-二聚体.结果三组t-PA抗原随病情严重程度而显著性升高,有显著性差异(P＜0.05);PAI活性三组近似(P＞0.05);纤溶活性高者的t-PA略高于正常纤溶者,且二者PAI近似,均无显著性差异(P＞0.05).结论 t-PA随病情加重而显著性升高,PAI随病情加重变化不大;t-PA、PAI失平衡不是肝硬化患者纤溶活性升高的主要因素.     

肝硬化患者血清总胆汁酸测定的临床意义

目的 探讨肝硬化患者血清总胆汁酸测定的临床意义.方法 75例肝硬化患者Child-Pugh分级,A级28例,B级31例,C级16例,检测血清总胆汁酸水平,与49例正常体检者进行组间比较.结果 肝硬化各级(组)血清总胆汁酸水平均明显高于正常对照组(P<0.01),且其增高程度随Child-Pugh分级差异而不同.结论 总胆汁酸是评价肝硬化患者肝功能的重要指标.与Child-Pugh分级密切相关.     

血清前白蛋白、胆碱酯酶、凝血酶原活动度水平联合Child-Pugh分级对肝硬化患者预后的判断

[目的]探讨血清前白蛋白(PA)、胆碱酯酶(CHE)、凝血酶原活动度(PTA)联合Child-Pugh分级在判断肝硬化患者预后的意义。[方法]将肝硬化组125例患者根据Child-Pugh分级分为3个亚组:Child A级组(50例)、Child B级组(45例)及Child C级组(30例),选取健康体检者40例作为对照组。对所有入选者取静脉血测定血清PA、CHE及PTA水平,并进行腹部彩超检查了解肝、脾、门静脉宽度及腹水情况。[结果]肝硬化组血清PA、CHE及PTA水平均显著低于对照组(P0.01);随着患者肝硬化程度加重,其血清PA、CHE及PTA水平逐渐降低,不同Child-Pugh分级组间比较差异均具有统计学意义(P0.01);肝硬化组中存活患者PA、CHE及PTA水平均明显高于死亡者,差异均具有统计学意义(P0.01)。[结论]肝硬化患者血清PA、CHE、PTA水平与肝功能Child-Pugh分级及预后相关,这些指标的联合对判断肝病损害严重程度及预测患者预后具有较大的临床价值。     

老年肝硬化患者凝血及血小板功能变化与Child-Pugh分级的关系

目的 探讨老年肝硬化患者凝血及血小板指标的变化及其与Child-Pugh分级的关系.方法 肝硬化患者67例,Child-Pugh分级A级21例,B级24例,C级22例;正常对照组22例.全部受试者均检测凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(FIB)、血小板计数(PLT)、血小板压积(PCT)、平均血小板体积(PCV)、血小板体积分布宽度(PDW),并进行对照分析.结果 老年肝硬化组与正常对照组比较,PLT、PCT显著下降(均P＜0.001),MPV、PDW显著升高(均P＜0.001);肝功能B、C 级与A 级比较,C级PLT 和PCT下降显著(均P＜0.01),MPV、PDW显著升高(均P＜0.01);老年肝硬化患者PT、APTT 均较对照组明显延长(均P＜0.001),FIB 明显降低(P＜0.01).结论 老年肝硬化患者存在明显的凝血、血小板异常,且与肝硬化程度密切相关.     

肝硬化患者凝血、抗凝及纤溶指标的变化与Child-Pugh分级的关系

目的 探讨肝硬化患者凝血、抗凝及纤溶指标的变化及其与Child-Pugh分级的关系。 方法肝硬化患者43例,Child-Pugh分级A级13例,B级15例,C级15例。正常对照组16例,男11例,女5例。均检测凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(Fib)、凝血因子Ⅱ、Ⅴ、Ⅶ、Ⅷ、Ⅸ、Ⅹ、血管性假性血友病因子(vWF)、抗凝血酶-Ⅲ(AT-Ⅲ)、蛋白-C(PC)、D-二聚体(D-d)、组织纤溶酶原激活物(t-PA)抗原和组织纤溶酶原激活物抑制剂(PAI)。 结果 PT、APTT随病情加重而显著延长,F值分别为32.828和18.743,P值均<0.01;Fib随病情加重逐渐降低,F=4.747,P<0.01。凝血因子Ⅱ、Ⅴ、Ⅶ、Ⅸ、Ⅹ随病情加重活性逐渐降低,F值分别为43.129、12.677、36.405、9.380和21.988,P值均<0.01。Ⅷ、vWF因子随病情加重活性逐渐增高,F值分别为16.672和14.657,P值均<0.01。AT-Ⅲ、PC随病情加重活性逐渐降低,F值分别为22.602和15.430,P值均<0.01。D-d、t-PA抗原随病情加重逐渐增高,F=5.957,P<0.05。PAI活性正常对照组和3组患者检测结果近似,差异无统计学意义。 结论 肝硬化患者存在明显的凝血、抗凝血以及纤溶机制的异常,且与肝硬化程度密切相关。在防治肝硬化患者出血时,不仅要纠正患者的凝血因子异常,还要给予一定的抗纤溶治疗。     

慢性肝病患者骨代谢变化的临床意义

为探讨慢性乙型肝炎（下称慢乙肝），乙肝肝硬化（下称肝硬化）与骨代谢的关系，分别对32例慢乙肝，32例肝硬化和31例对照组患者进行了骨钙素（BGP），甲状旁腺激素M（PTHM），血钙，血磷及尺桡骨骨密度（BMD）检测。结果显示，肝硬化组血清BGP水平较肝炎组和对照组明显降低（P＜0．05，＜0．01），血清PTHM水平较肝炎组及对照组升高（P＜0．05，＜0．05），两肝病组血钙水平较对照组明显下降（P均＜0．001），BMD较对照组降低（P＜0．001，＜0．01）；肝硬化组和肝炎组BGP均与BMD呈正相关。提示慢性病毒性肝病可出现调钙激素异常变化，且其骨质疏松随肝病加重而呈加重趋势。     

乙型肝炎肝硬化肝性骨营养不良的临床研究

目的探讨乙型肝炎肝硬化与肝性骨营养不良和骨质疏松的关系。方法收集自2008年3月~2009年3月在我院住院的乙型肝炎肝硬化患者43例,健康对照组21例,采用双能X线骨密度仪测定股骨颈、尺桡骨骨密度,空腹抽血测定血钙、血磷、甲状旁腺素、降钙素、白细胞介素-6。结果肝硬化组骨质疏松发生率显著高于对照组（P=0.003）;两组股骨颈骨密度[（-0.860±0.705）g/cm2vs（0.125±0.715）g/cm2,P〈0.001]、尺桡骨骨密度[（-0.702±0.666）g/cm2vs（0.279±0.709）g/cm2,P〈0.001）]、血钙[（2.151±0.168）mmol/Lvs（2.336±0.170）mmol/L,P〈0.001）]比较,肝硬化组显著低于对照组;血磷[（1.051±0.077）mmol/Lvs（0.961±0.069）mmol/L,P〈0.001）]、甲状旁腺素[（412.674±22.779）ng/Lvs（386.000±30.223）ng/L,P〈0.001）]、降钙素[（45.358±3.900）pg/Lvs（30.667±3.120）pg/L,P〈0.001）]、IL-6[（41.795±14.988）pg/mlvs（4.077±1.555）pg/mL,P〈0.001]比较,肝硬化组显著高于对照组;肝硬化组股骨颈骨密度与IL-6呈负相关。结论肝性骨营养不良是乙型肝炎肝硬化严重并发症之一,以骨质疏松为常见表现,应监测骨密度预防肝性骨营养不良。     

乙型肝炎肝硬化骨代谢异常的临床研究

目的探讨乙型肝炎肝硬化患者骨代谢异常的发病机制。方法用NM-300单光子骨密度测量系统检测61例乙型肝炎肝硬化患者的骨密度，空腹抽血检测血清钙调节激素：1，25二羟维生素D3[1，25（OH）2D3]、甲状旁腺素（PTH）、降钙素（CT）、骨钙素（BGP），白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、肿瘤坏死因子α（TNF α）、尿骨胶原交联（Corsslaps），并与30名健康者对照。结果肝硬化组尺骨密度、桡骨密度、尺桡密度均较对照组明显降低。肝硬化组血清1，25（OH）2D3、BGP水平较对照组明显降低，其中骨质疏松（OP）组较无骨质疏松（NOP）组降低更明显，尿Crosslaps水平肝硬化组较对照组明显升高，其中OP组较NOP升高更明显。血清1，25（OH）2D3、BGP水平与尺桡密度呈正相关。OP组尿Crosslaps水平与尺桡密度呈负相关，而NOP组尿Crosslaps水平与尺桡密度无相关关系。肝硬化组血清IL-1β、IL-6、TNF α水平较对照组明显升高。血清IL-1β、IL-6、TNF α水平肝硬化OP组较NOP组显著升高。肝硬化组IL-1β、IL-6、TNF α水平与尺桡密度呈负相关，其中OP组较NOP组相关性更明显。结论乙型肝炎肝硬化患者存在着骨形成减少和骨破坏过多两种因素，从而引起肝性骨病，在骨形成减弱的过程中1，25（OH）2D3起了主要作用，在骨吸收增强的过程中IL-1β、IL-6、TNF α起到了重要的作用。     

A slight decrease in renal function further impairs bone mineral density in primary hyperparathyroidism

BACKGROUND: The impairment of renal function can affect the clinical presentation of primary hyperparathyroidism (PHPT), increasing cardiovascular morbidity, fracture rate, and the risk of mortality. AIM: The aim of the study was to assess the differences in bone status in a series of consecutive patients affected by PHPT without overt renal failure at diagnosis grouped according to creatinine clearance (Ccr). METHODS: A total of 161 consecutive patients with PHPT were studied. They were divided into two groups based on Ccr. Group A had Ccr 70 ml/min or less (n = 49), and group B had Ccr greater than 70 ml/min (n = 112). PTH, total and ionized serum calcium; urinary calcium and phosphate; serum 25-hydroxyvitamin D3; serum and urinary bone markers; lumbar, forearm, and femoral bone mineral density (BMD) were evaluated. RESULTS: Patients in group A were older than those in group B (P < 0.0001). PTH levels did not differ in the two groups, whereas both urinary calcium and phosphorus were lower in group A than group B (P < 0.01). Lower BMD was evident in group A at lumbar spine (P < 0.002), forearm (P < 0.0001), and femur (P < 0.01). In asymptomatic PHPT, those with Ccr 70 ml/min or less had lower forearm BMD than patients with higher Ccr (P < 0.00001). When adjusting for age and body mass index in PHPT, BMD at each site persisted being lower (P < 0.05) in group A than group B. In all PHPT subjects, Ccr (beta = 0.29, P < 0.0005), age (beta = -0.27, P < 0.00001), and PTH levels (beta = -0.27, P < 0.0005) were all independently associated with forearm BMD. CONCLUSIONS: In PHPT a slight decrease in renal function is associated with more severe BMD decrease, independent of age, body mass index, and PTH levels. This association is also present in asymptomatic PHPT and strengthens the National Institutes of Health recommendations for surgery in patients with mild PHPT.     

Relationships between bone mineral density, serum vitamin D metabolites and calcium:phosphorus intake in healthy perimenopausal women

OBJECTIVES: To determine the relationships between serum vitamin D metabolites, bone mass, and dietary calcium and phosphorus in a cohort of 510 healthy Danish perimenopausal women. DESIGN: A population-based cross-sectional study. SUBJECTS: A total of 510 healthy women aged 45-58 years, with amenorrhoea for 3-24 months. None of the women was using hormone replacement therapy. MEASUREMENTS: Measurements of total bone mineral content and regional bone mineral density were performed by dual-energy X-ray absorptiometry. Analyses of serum levels of 25-OHD and 1,25-(OH)2D, intact PTH, ionized calcium and phosphate, as well as biochemical markers of bone turnover in blood and urine. Assessment of calcium and phosphorus intake using dietary records. RESULTS: A consistent inverse relationship between serum 1,25-(OH)2D and bone mineral content/ density was found in whole-body mineral content (P = 0.001), spine (P = 0.005) and femoral neck (P<0.05). There was a positive relationship between levels of 1,25-(OH)2D and biochemical bone markers, indicating that high levels of 1,25-(OH)2D are accompanied by increased bone turnover. The dietary calcium:phosphorus ratio was inversely related to serum 1,25-(OH)2D (P = 0.04) and positively related to bone mineral density (P<0.0005). No relationships could be detected between levels of PTH, serum ionized calcium and phosphate, and serum vitamin D metabolites. CONCLUSION: Within normal physiological range, elevated levels of 1,25-(OH)2D were associated with decreased bone mineral density and content, reduced calcium:phosphorus ratio in the diet and increased bone turnover.     

Parathyroid hormone gene polymorphisms in primary hyperparathyroidism

OBJECTIVE: Genetic contributions to bone mineral density (BMD) and bone turnover are well known. In the present study, we analysed the relationship between restriction fragment length polymorphisms of the PTH gene and the development of primary hyperparathyroidism (pHPT) as well as its severity. PATIENTS: Seventy-nine pHPT patients and 104 age-matched healthy controls were analysed. DESIGN AND MEASUREMENTS: PTH genotypes were determined by polymerase chain reaction and BstB I or Dra II restriction fragment length polymorphisms. The presence and absence of BstB I or Dra II restriction sites of the PTH gene were indicated by B and b or D and d, respectively. BMD levels at the lumbar spine and at the radius were measured in all subjects. Serum levels of calcium, phosphorus, alkaline phosphatase and intact PTH were measured in pHPT patients. RESULTS: There were no differences in the frequencies of these PTH genotypes between pHPT patients and controls. In control subjects, lumbar BMD was significantly higher in BB genotype than in Bb/bb genotypes. In pHPT patients, there was no difference of BMD between BB and Bb/bb genotypes. In pHPT patients, serum calcium level was significantly higher in those with the BB genotype than Bb/bb genotypes. On the other hand, there was no association between Dra II polymorphism and BMD in both controls and pHPT patients, but serum intact PTH level was significantly higher in DD genotype than Dd/dd genotype in pHPT patients. Moreover, serum levels of ALP and intact PTH were significantly higher in the PTH BBDD haplotype, compared to those in haplotypes other than BBDD. CONCLUSIONS: The present study suggests that the BstB I polymorphism of PTH gene is closely related to bone mineral density and that PTH gene polymorphisms do not seem to affect the development of primary hyperparathyroidism but may relate to the severity of primary hyperparathyroidism.     

Effects of pregnancy and lactation on bone mineral density, and their relation to the serum calcium, phosphorus, calcitonin and parathyroid hormone levels in rats

The aim of this study was to evaluate the net changes in bone mineral density (BMD) during the reproductive cycle, and their relation with changes in serum calcium (Ca), phosphorus (P), PTH and calcitonin levels in rats. Twenty-seven female Wistar rats were included in this study. They were divided into three groups as pregnant, lactating and control groups. BMDs of lumbar vertebrates, femoral and tibial bones, and Ca, P, calcitonin and PTH levels were measured at the end of pregnancy, at the end of lactation and in nulliparous controls. In the pregnant group, the BMDs of rats were significantly higher in lumbar vertebrates, femoral and tibia bones than those of the control group (p<0.05). Their PTH and Ca levels were significantly lower than the control group (p<0.05). However, no statistically significant difference was found regarding P and calcitonin levels when compared to those of the control group. In the lactating group, the BMDs were significantly lower in lumbar vertebrates, femoral and tibia bones than those seen in the control and pregnant groups (p<0.05). Ca and PTH levels were significantly higher in lactating rats than in those of pregnant rats (p<0.005). Normal pregnancy increases BMD in rats, whereas lactation decreases it. Change in PTH levels is supposed to contribute to the mineralization and demineralization of the skeleton during pregnancy and lactation, respectively.     

Prevention of glucocorticoid induced osteoporosis with alendronate or alfacalcidol: relations of change in bone mineral density, bone markers, and calcium homeostasis

OBJECTIVE: To explore the relation of changes in measures of bone turnover and changes in bone mineral density (BMD) of the lumbar spine and total hip over 18 months in a double-blinded, randomized trial, comparing the effect of alfacalcidol (101 patients) versus alendronate (100 patients) on BMD in patients who recently started treatment with glucocorticoids for various rheumatic diseases. METHODS: Associations between changes in serum procollagen type I C-propeptide (P1CP), fasting urine N-terminal telopeptide of type I collagen (NTx), serum calcium, parathyroid hormone (PTH), osteocalcin, and change from baseline in BMD over 18 months were explored with regression and correlation analyses. RESULTS: In both treatment groups, there was a statistically significant decrease in NTx. In the alfacalcidol group there was also a significant increase in P1CP and osteocalcin, in contrast to the alendronate group, but BMD in the alfacalcidol decreased versus an increase in the alendronate group (p < 0.001). In neither treatment group were changes in biochemical measures correlated with the change in BMD, with the exception of a negative correlation in the alendronate group between changes in total hip BMD and NTx. Use of alendronate resulted in an increased PTH in 27 patients, but the increase in BMD of these patients was not statistically significantly different compared to patients taking alendronate with normal PTH levels. CONCLUSION: Changes in BMD were not associated with changes in bone measures, with the exception of NTx in the alendronate group. For the patient taking glucocorticoids in clinical practice, the value of serial assessment of bone markers is low; changes in markers are no substitute for changes in BMD. ClinicalTrials.gov number: NCT00138983.     

Pathogenesis of osteoporosis in liver cirrhosis

BACKGROUND/AIMS: Osteoporosis has been recognized in patients with liver cirrhosis, although the prevalence and the exact mechanisms vary considerably in the literature. We have studied the prevalence of bone disease in cirrhotic patients, the pathogenesis and the relation to the etiology and the severity of liver failure. METHODOLOGY: The study included 83 hospitalized patients with various types of cirrhosis, where 25 healthy individuals served as controls. Patients were classified according to Child-Pugh's stages as follows: Child A: 49, Child B: 20, Child C: 14. Serum levels of iPTH, 250HD, LH, FSH, SHBG, testosterone, estradiol, IGF-I, osteocalcin and urine levels of cross-linked N-telopeptides of collagen type 1 (NTX) were measured in all patients. Bone mineral density (BMD) was measured by DEXA at the spine of both patients and controls. RESULTS: The prevalence of osteoporosis was higher in patients (26/83) 31.3% than in controls (4/25) 16%. Osteopenia was positively related with the elevated levels of crosslinked N-telopeptides (p=0.048). There were no differences in BMD between the types of cirrhosis. BMD was found to be significantly lower in Child B and C male patients than in Child A (p=0.043). Patients' groups B, and C had lower testosterone levels with a trend to contribute to the low BMD (p=0.15). 250HD and IGF-1 were significantly lower in decompensated cirrhosis (p<0.002), but did not correlate with BMD. CONCLUSIONS: Cirrhosis is a major cause of osteoporosis and the degree of osteopenia is related to the severity and not the etiology of the liver disease. The biochemical markers of bone remodeling suggest a high-turnover osteoporosis in cirrhosis.     

肝炎肝硬化的骨钙素、甲状旁腺素、降钙素的变化及其临床意义

目的：为了解肝硬化骨病的形成机理。方法：本文采用放射免疫法对３５例肝炎肝硬化的血清进行了骨钙素、甲状旁腺素（ＰＴＨ）及降钙素（Ｃａｌｃｉｔｏｎｉｎ）的测定。结果：肝硬化患者的骨钙素（Ｇａｌ）明显高于正常对照（Ｐ＜０．０１），ＰＴＨ也高于正常，血钙低于正常，但均无统计学意义（Ｐ＜０．０５），各激素与血清白蛋白、凝血酶原时间及总胆红素之间无明显相关。按Ｃｈｉｌｄ分级，Ｃ级患者的Ｇａｌ及ＰＴＨ明显高于Ａ级及Ｂ级患者，而血钙浓度低于Ａ级及Ｂ级。结论：肝硬化对骨病的产生与所测三种激素的代谢紊乱有密切关系，由于钙离子吸收不良所致的低钙血症在致肝硬化骨病中可能起着相当重要的作用