肝硬化患者体表胃电图表现与血浆胃肠激素的相关性研究

探讨肝硬化患者体表胃电参数的意义、随肝功能Child分级的变化及与血浆胃动素(MTL)、胃泌素(GAS)、血管活性肠肽(VIP)变化的相关性，进一步明晰肝硬化胃肠动力障碍的发病机理及其临床意义。对肝硬化患者进行体表胃电图检查及血浆胃肠激素测定。发现1、肝硬化患者存在胃电节律紊乱，且同时存在胃动过速及胃动过缓；2、主频DF、主功率DP、正常慢波节律N％减少、胃动过缓B％增加随肝功能不良而改变明显。3、胃电节律紊乱与肝硬化血浆胃肠激素水平异常有关，可能是肝硬化胃动力障碍机制中的一个重要因素。同时存在的胃动过速百分比高于对照，与MTL、GAS、VIP无相关性，其机制有待进一步观察研究。     

门脉高压患者空腹胃运动障碍的临床研究

目的：作者应用体表胃电图研究门脉高压患者胃动力障碍发生率及其与肝功能的关系。方法：ＷＣＤＦ型胃肠电分析仪观察３０名肝硬化门脉高压患者和１５名健康人空腹胃肌电活动情况，观察指标包括平均振幅（ＡＰ）、平均过零频率（Ｆ２）、中心频率（Ｆｃ）、主频（Ｆｐ）以及频谱形态。结果：门脉高压组患者胃电节律紊乱率明显高于健康组，其中Ｆ２分别为３７％和５０％；Ｆｐ分别为５７％和４７％；ＣｈｉｌｄＡ组胃窦电节律紊乱率在Ｆｐ、Ｆ２分别为３６％、１８％；ＣｈｉｌｄＢ分别为６０％、３３％；而ＣｈｉｌｄＣ组则１００％有胃窦电节律异常。结论：本研究提示门脉高压患者胃电节律紊乱发生率较正常人明显升高，肝功能对胃电节律有影响。     

门静脉高压性胃病患者的体表胃电图表现

门静脉高压性胃病（PHG）是肝硬化患者最常见的胃黏膜病变。目的：了解PHG患者的胃电图表现。方法：对15例PHG患者行体表胃电图检查，12例健康志愿者作为正常对照。结果：PHG组餐前、餐后主频降低，正常胃电慢波百分比减少，胃动过缓和胃动过速百分比增加，餐后／餐前主功率比降低，与正常对照组相比差异均有统计学意义（P〈0．05）。结论：PHG患者的胃电图表现存在明显异常，可能与其上消化道症状和胃动力紊乱有关。     

功能性消化不良患者胃肌电紊乱的发生率

背景：功能性消化不良（FD）的病理生理机制尚未完全阐明，消化道运动功能异常可能是主要发病机制之一。目的：通过胃电图检查探讨FD患者胃肌电紊乱的发生率，证实胃动力异常在FD发生中的作用。方法：368例FD患者行餐前和餐后体表胃电图榆查，对正常胃慢波百分比和胃电主功率两项参数进行分析。结果：根据正常胃慢波百分比，本组FD患者可分为胃电节律正常组（43．2％）、胃动过缓组（33．2％）、胃动过速组（6．2％）和混合性胃电节律紊乱组（17．4％）。在胃电节律正常的FD患者中，34．0％（54例）存在餐后／餐前胃电主功率比异常。结论：本组71．5％的FD患者存在胃肌电紊乱，证实胃动力异常在FD的发病机制中起有重要作用。     

胃溃疡与十二指肠溃疡胃电图变化的探讨

目的分析胃溃疡与十二指肠溃疡患者胃肌电活动特点,探讨消化性溃疡病患者节律性疼痛、腹胀、反酸等临床症状与胃动力的关系,为消化性溃疡病临床治疗提供客观依据和指导。方法对44例胃溃疡和十二指肠溃疡患者及20例健康志愿者进行胃电图监测,记录主频率,主功比,各频段胃电所占百分比等指标。结果胃溃疡患者多存在胃电失常,以混合节律失常和胃动过缓节律失常为主;而十二指肠溃疡以混合节律及胃动过速失常为主。结论消化性溃疡患者大多有胃动力障碍。胃电图检查结果对其治疗具有一定的指导意义。     

肠易激综合征患者胃运动功能的研究

目的 观察肠易激综合征(IBS)患者的胃运动功能并探讨其在IBS发病中的作用.方法 测定30例腹泻型IBS、46例便秘型IBS患者和30例健康人(对照组)胃固体排空功能,行体表胃电图记录胃电节律变化.结果 与腹泻型患者比较,便秘型患者胃排空延迟的发生率高(P<0.05),二者2 h及6 h胃排空率均明显降低(P<0.01);与对照组比较,IBS患者存在明显的胃电节律紊乱.结论 IBS患者存在胃固体排空障碍及胃电节律紊乱,二者间有一定关系;IBS是一种广泛胃肠道运动障碍性疾病.     

胃食管反流病胃肌电活动的变化

目的 分析描述胃食管反流病(GERD)患者的胃肌电活动特点,探讨胃肌电活动的变化在GERD发病中的作用,以期有助于临床诊疗.方法 对65例GERD患者和30例健康志愿者进行餐前、餐后体表胃电图监测.根据内镜检查结果,把GERD患者分为反流性食管炎(RE)组、非糜烂性反流病(NERD)组,行组间胃电参数比较,随访19例胃电节律异常的GERD患者,观察治疗前后胃电参数的变化.结果 GERD组的主频(DF)正常慢波节律百分比(N%)、餐前餐后功率比(PR)与对照组相比明显降低(P<0.05或0.01).胃电节律紊乱,以胃动过缓为主.经1周治疗后,GERD异常胃电参数明显正常化(P<0.05或0.01).餐前RE组胃电节律异常的发生率(37.5%)显著高于NERD组(12.1%).餐后胃电节律异常的发生率RE组和NERD组分别为71.9%和60.6%,两者没有统计学意义(P>0.05).结论 GERD患者存在餐前、餐后胃肌电活动异常,异常胃电节律以胃动过缓节律为主,胃电图能为GERD诊断提供依据.     

精神心理因素对功能性消化不良患者胃电活动的影响

目的 :探讨在功能性消化不良 (FD)患者中精神心理因素与胃电之间的关系。方法 :对 43例FD患者同时进行精神心理状态测量和体表胃电图检查。结果 :伴焦虑抑郁FD组餐后胃电节律异常的发生率显著高于不伴焦虑抑郁FD组 (39.1 %vs1 0 % )。伴焦虑抑郁FD组发生的胃电节律异常主要是胃电节律过缓和胃电节律紊乱。前者的餐后平均主频不稳定系数显著高于后者 (41 .8± 2 7.4vs32 .6± 2 3 .1 )。结论 :精神心理异常可影响胃电活动 ,产生异常的胃电活动     

窒息对新生儿胃电活动的影响

目的:研究窒息对新生儿胃电活动的影响。方法:研究对象来自我院1998年9月～2000年5月以窒息收住新生儿病房的足月新生儿32例,其中重度窒息20例,轻度窒息12例。对照组:系同期以新生儿生理性黄疸收住院的足月新生儿10例,无消化道症状,吃奶好,二便正常。采用瑞典Synectics公司生产的便携式Digitrapper双电极EGG记录仪进行胃电图检查,用计算机运行频谱分析数据。结果:窒息组与对照组比较,餐前胃动过缓显著增加,正常节律百分比、胃动过速明显降低,差别有显著意义(P<0.01和P<0.05)。餐后胃动过缓也有增加,差别有显著意义(P<0.01)。餐后正常节律百分比、胃动过速也有降低但差别无显著性意义。重度窒息组与轻度窒息组比较,前者餐前胃动过缓明显增加,正常节律百分比明显降低,差别有显著意义(P<0.01)。两者餐前胃动过速及餐后各项指标比较均无显著差异(P>0.05)。结论:(1)窒息新生儿存在明显胃电节律紊乱。临床多表现为拒奶、喂养不耐受。呕吐和腹胀等消化道症状;(2)体表胃电图与胃肌电活动的相关性较好,可用来研究窒息新生儿的胃电活动,进而研究新生儿消化道动力;(3)窒息组胃电提示异常者,曾试用普瑞博思0.2mg/(kg·次)治疗能改善临床症状,但尚缺乏胃电图观察,有待进一步胃电图研究。     

甲状腺机能亢进和减退患者的胃电图改变初探

目的通过胃电图(EGG)检查,观察32例甲状腺机能亢进(甲亢)病人,29名甲状腺机能减退(甲减)病人及30名正常健康人餐前和餐后30min的体表胃电频谱变化。结果3组内餐后胃电图主频(DF)、平均幅值(AP)、正常慢波百分比(N%)与餐前相比均有显著增加(P<0.01)。甲亢组主频和平均幅值与对照组相比,无显著差异(P>0.05),甲减组平均幅值与正常慢波百分比较对照组差异显著(P<0.01)。结论甲亢组食欲亢进在胃电图上无特殊反映,表现为主频正常,胃电节律正常,振幅亦无明显升高。甲减组食欲减退可能与胃动过缓,胃电节律紊乱增多有关。     

Ultrasound liver elastography beyond liver fibrosis assessment

Several guidelines have indicated that liver stiffness(LS) assessed by means of shear wave elastography(SWE) can safely replace liver biopsy in several clinical scenarios, particularly in patients with chronic viral hepatitis. However, an increase of LS may be due to some other clinical conditions not related to fibrosis,such as liver inflammation, acute hepatitis, obstructive cholestasis, liver congestion, infiltrative liver diseases. This review analyzes the role that SWE can play in cases of liver congestion due to right-sided heart failure, congenital heart diseases or valvular diseases. In patients with heart failure LS seems directly influenced by central venous pressure and can be used as a prognostic marker to predict cardiac events. The potential role of LS in evaluating liver disease beyond the stage of liver fibrosis has been investigated also in the hepatic sinusoidal obstruction syndrome(SOS) and in the Budd-Chiari syndrome. In the hepatic SOS, an increase of LS is observed some days before the clinical manifestations;therefore, it could allow an early diagnosis to timely start an effective treatment.Moreover, it has been reported that patients that were successfully treated showed a LS decrease, that reached pre-transplantation value within two to four weeks. It has been reported that, in patients with Budd-Chiari syndrome, LS values can be used to monitor short and long-term outcome after angioplasty.     

Recurrent nonviral liver disease following liver transplantation

Recurrent disease after liver transplantation is well recognized and remains a potential cause of premature graft loss. The rates of recurrence are difficult to establish because of the lack of consistency in diagnostic criteria and approaches to diagnosis. Owing to the fact that recurrent parenchymal disease may occur in the presence of normal liver tests, those centers that use protocol biopsies will report greater rates of recurrence. It is important to recognize that rates of recurrence vary according to indication and show little correlation with rates of graft loss from recurrent disease. Recurrance rates are greatest for primary sclerosing cholangitis and autoimmune hepatitis, and low reccurrance rates are reported for alcoholic liver disease and recurrent primary biliary cirrhosis. The impact of recurrent nonalcoholic fatty liver disease is not yet clear. Patients and clinicians need to be aware of the possibility of recurrent disease in the differential diagnosis of abnormal liver tests, and management stategies may require alteration to reduce the impact of disease recurrence on outcome. Finally, an understanding of which diseases do recur after transplantation and identification of the risk factors may lead to a better understanding of the pathogenetic mechanisms of these conditions.     

脂肪性肝病与原发性肝癌

脂肪性肝病是隐原性肝硬化的主要原因之一,其经过肝硬化进展至原发性肝癌的过程已被认可,但是近年来越来越多的研究证实脂肪性肝病本身存在有促肿瘤形成的机制,它可以不经过肝硬化而直接进展成原发性肝癌,两者之间的具体机制还未明确.此文就脂肪性肝病向原发性肝癌进展的可能机制作一综述.     

Auxiliary liver transplantation for acute liver failure

BACKGROUND: In patients with acute liver failure (ALF) who fulfil criteria, liver transplantation is the only effective treatment which can substitute metabolic and excretory function of the liver. Auxiliary liver transplantation was developed because a significant minority of patients with ALF who fulfil transplant criteria can have a complete morphological and functional recovery of their liver. The favourable outcome reported in European series using auxiliary partial orthotopic liver transplantation (APOLT), the greater experience as well as the lessons from split liver and from living related donors have revived interest in this approach. In selected patients aged <40 years without haemodynamic instability, the use of ABO-compatible, non-steatotic grafts harvested from young donors with normal liver function can restore liver function and prevent the occurrence of irreversible brain damage. In the majority of cases the auxiliary graft is a right graft which is placed orthotopically after a right hepatectomy in the recipient. After standard immunosuppression, the recovery of the native liver is assessed by biopsies, hepatobiliary scintigraphy and computed tomography. When, on the basis of histological, scintigraphical and morphological data, there is evidence of sufficient regeneration of the native liver, immunosuppression can be discontinued progressively. Complete regeneration of the native liver can be observed in >50% of patients, who can be withdrawn from immunosuppression. Therefore the advantages of auxiliary transplantation seem to balance favourably with the potential inconvenience of this technique in selected patients.     

非酒精性脂肪性肝病与肝硬化

非酒精性脂肪性肝病（Nonalcoholic fatty liver disease, NAFLD）发病与胰岛素抵抗（Insulin resistance, IR） 和遗传易感性密切相关,病理学改变与酒精性肝病（Alcoholic liver disease, ALD）相似,但无过量饮酒史^[1]。在此要强调NAFL与NASH的不同,NAFL是指病理活检显示肝脏脂肪变性,但是不具有肝纤维化或气球样变性的肝细胞损伤。NASH指在肝脏脂肪变基础上出现气球样肝细胞损伤伴或不伴肝纤维化^[2],NASH发生肝纤维化、肝硬化、肝细胞癌风险明显增高,而NAFL则很低^[2],NASH是NAFL发生肝硬化的必经阶段^[3]。     

中国肝癌肝移植的现状与展望

肝癌行肝移植治疗的指征、效果和相关问题一直存在争论,国际上已经有数个通用的肝癌肝移植标准,如Milan标准、Pittsburgh标准、UCSF标准等等,中国的移植学家们也在纷纷探讨适合中国的肝癌肝移植标准.本文收集并分析近年来国内外的文献,结合本移植中心460例肝移植的病例,对肝癌的分期标准、晚期肝癌行肝移植的指征进行了探讨,笔者认为影响我国肝癌肝移植的主要因素有:供肝的来源、术后乙肝及肿瘤的复发及相关社会因素等.     

Chronic liver diseases as liver tumor precursors

Liver cancer is a major global health problem and hepatocellular carcinoma (HCC) accounts for 75% of all liver carcinoma. HCC occurs more often in men than in women and mostly in people 50 to 60 years old. The disease is more common in parts of sub-Saharan Africa and Asia than in North and South America and Europe. Nevertheless its incidence increased over the past 4 decades in some Western countries. Worldwide, liver carcinoma is the 5th most common cancer and 3rd most common cause of cancer mortality (behind only lung and colorectal cancer) with approximately 680,000 annual deaths. Unlike most of the other malignancies, HCC almost entirely develops in the context of inflammation and organ injury and is related to cirrhosis in about 85% of the cases. Among underlying etiologies of liver cirrhosis, most frequent are viral infection and toxic substances, mostly alcohol. The main HCC risk factor in Eastern Asia and Africa is hepatitis B virus infection. Hepatitis C virus infection is the main risk factor in Western countries. Hereditary hemochromatosis is not a very frequent cause of liver cirrhosis, but these patients are at higher risk for HCC compared with other etiologies of cirrhosis. Aflatoxins, cancer-causing substances made by a type of plant mold, can play a role in some countries in Asia and Africa, and can have a synergistic effect with hepatitis B infection.     

Fatty liver in liver transplantation and surgery

Steatosis of the liver is common in Western countries, affecting about 25% of donors for liver transplantation and 20% of patients undergoing liver resection. Transplantation of livers with severe steatosis (> 60%) is associated with a high risk of primary nonfunction, and these livers should not be used for organ donation. In contrast, transplantation with livers containing mild steatosis (< 30%) yields results similar to those of transplantation performed with nonfatty livers. The outcome of livers with moderate steatosis (30 to 60%) are varying, and the use of these organs depends on the existence of additional risk factors. Similarly, liver resection in patients with steatosis is associated with a risk of postoperative mortality when compared with patients with nonfatty livers (14% versus 2%). Although hepatic steatosis is an important risk factor for surgery, little is known about the mechanisms of injury. In animal experiments, steatosis is associated with decreased ATP production and a disturbance of sinusoidal flow. Further contributing factors may include Kupffer cell dysfunction and leukocyte adhesion. Fatty hepatocytes have reduced tolerance against ischemic injury with a predominant necrotic form of cell death. In addition, the ability of hepatocytes to regenerate after major tissue loss is impaired in the steatotic liver. Very few protective strategies are known. Ischemic preconditioning and intermittent clamping protect the human liver against prolonged periods of ischemia. These techniques appear to be particularly protective in the steatotic liver. New insights into the mechanisms of liver failure in steatotic organs are needed to decrease the risk of surgery and increase the pool of organ donors.