DYNAMIC CHANGES OF ITO CELLS IN EXPERIMENTAL LIVER CIRRHOSIS OF RAT

That Ho cells in rat liver express desmin was confirmed by immunohistochemical technique. Consequently, changes of desmin-positive cells, lysozyme-positive cells and fibronectin were further studied in experimental cirrhosis of rat. It was found that desmln- positive cells, with the transitional feature between Ito cells and myofibroblasts or fibrobiasts under electron microscope, increased in number and expression of desmin in the necrotic areas as well as in the cellular fibrous septa, but decreased in number in the fibrous septa except those areas closed to the edges of the septa. These results suggested that Ito cells, myofibroblasts and fibroblasts might belong to the same cellular system and play an important role in the pathogenesis of cirrhosis. Meanwhile, it was also noted that changes of both fibronectin and lysozymepositive cells were correlated with those of desmin-positive cells. These provide evidence in vivo that flbronectin and Kupffer cells might exert certain effects on the migration and proliferation of Ito cells in liver cirrhosis.

Immunohistochemical study on expression of epidermal growth factor receptor at hepatocyte nuclei in experimental rat liver cirrhosis

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Thrombospondin-1 expression correlates with angiogenesis in experimental cirrhosis

AIM:To investigate the significance of Thrombospondin-1 (TSP-1) expression and its relationship with angiogenesis during experimental fibrosis. METHODS:Cirrhosis was induced in male Wistar rats by intraperitoneal administration of diethyl nitrosamine (DEN). The serial sections from liver tissues were stained with anti-CD34 and anti-TSP-1 antibodies before being quantitated by light microscopy. RESULTS:Our results showed that of TSP-1 expression gradually increases according to the severity of fibrosis (GroupⅠvs group Ⅱ, Group Ⅲ and Group Ⅳ;Group Ⅱ vs group Ⅲ and group Ⅳ;group Ⅲ vs group Ⅳ, P < 0.05). Moreover, TSP-1 expression was found to be correlated with angiogenesis (P < 0.05). CONCLUSION:The correlative evidence of the link between TSP-1 and fibrosis or angiogenesis provided by this study suggests that besides its role as a strong promoter of transforming growth factor-β1 (TGF-β1), TSP-1 might have an additional role in liver fibrogenesis by stimulating angiogenesis and this protein could be a potential target to prevent fibrogenesis in chronic inflammatory diseases of the liver.

Bone disorders in experimentally induced liver disease in growing rats

AIM： To investigate the change of bone parameters in a new model of experimentally induced liver cirrhosis and hepatocellular carcinoma （HCC） in growing rats. METHODS： Fischer-344 rats （n = 55） were used. Carbon tetrachloride （CCh）, phenobarbital （PB）, and a single diethylnitrosamine （DEN） injection were used. Animals were killed at wk 8 and 16. Bone mineral content, femoral length, cortical index （quotient of cortical thickness and whole diameter） and ultimate bending load （Fmax） of the femora were determined. The results in animals treated with DEN＋PB＋CCh （DPC, n = 21） were com- pared to those in untreated animals （UNT, n = 14） and in control group treated only with DEN＋PB （DP, n = 20）. RESULTS： Fatty liver and cirrhosis developed in each DPC-treated rat at wk 8 and HCC was presented at wk 16. No skeletal changes were found in this group at wk 8, but each parameter was lower （P〈0.05 for each） at wk 16 in comparison to the control group. Neither fatty liver nor cirrhosis was observed in DP-treated animals at any time point. Femoral length and Fmax values were higher （P〈0.05 for both） in DP-treated animals at wk 8 compared to the UNT controls. However, no difference was found at wk 16. CONCLUSION： Experimental liver cirrhosis and HCC are accompanied with inhibited skeletal growth, reduced bone mass, and decreased mechanical resistance in growing rats. Our results are in concordance withthe data of other studies using different animal models. A novel finding is the transiently accelerated skeletal growth and bone strength after a 8-wk long phenobarbital treatment following diethylnitrosamine injection.

Clinical characteristics of drug-induced liver injury and primary biliary cirrhosis

AIM To summarize and compare the clinical characteristics of drug-induced liver injury(DILI) and primary biliary cirrhosis(PBC).METHODS A total of 124 patients with DILI and 116 patients with PBC treated at Shengjing Hospital Affiliated to China Medical University from 2005 to 2013 were included. Demographic data(sex and age),biochemical indexes(total protein,albumin,alanine aminotransferase,aspartate aminotransferase,total bilirubin,direct bilirubin,indirect bilirubin,alkaline phosphatase,and gamma glutamyltransferase),immunological indexes [immunoglobulin(Ig) A,Ig G,Ig M,antinuclear antibody,anti-smooth muscle antibody,anti-mitochondrial antibody,and anti-mitochondrial antibodies] and pathological findings were compared in PBC patients,untyped DILI patients and patients with different types of DILI(hepatocellular type,cholestatic type and mixed type). RESULTS There were significant differences in age and gender distribution between DILI patients and PBC patients. Biochemical indexes(except ALB),immunological indexes,positive rates of autoantibodies(except SMA),and number of cases of patients with different ANA titers(except the group at a titer of 1:10000)significantly differed between DILI patients and PBC patients. Biochemical indexes,immunological indexes,and positive rate of autoantibodies were not quite similar in different types of DILI. PBC was histologically characterized mainly by edematous degeneration of hepatocytes(n = 30),inflammatory cell infiltration around bile ducts(n = 29),and atypical hyperplasia of small bile ducts(n = 28). DILI manifested mainly as fatty degeneration of hepatocytes(n = 15) and spotty necrosis or loss of hepatocytes(n = 14).CONCLUSION Although DILI and PBC share some similar laboratory tests(biochemical and immunological indexes) and pathological findings,they also show some distinct characteristics,which are helpful to the differential diagnosis of the two diseases.

Regulating effect of Chinese herbal medicine on the peritoneal lymphatic stomata in enhancing ascites absorption of experimental hepatofibrotic mice

AIM: To observe the regulatory effect of Chinese herbal medicine on peritoneal lymphatic stomata and its significance in treating ascites in liver fibrosis model mice. METHODS: Two Chinese herbal composite prescriptions were used separately to treat the carbon tetrachloride-induced mouse model of liver fibrosis. The histo-pathologic changes of the liver sections (HE and VG stainings) were observed. The peritoneal lymphatic stomata was detected by scanning electron microscopy and computer image processing. The changes of urinary volume and sodium ion concentration were measured. RESULTS: In the model group, lots of fibrous tissue formed in liver and extended into the hepatic lobules to separate them incompletely. In the treated and prevention groups, the histo-pathologic changes of liver was rather milder, only showed much less fibrous tissue proliferation in the hepatic lobules. The peritoneal lymphatic stomata enlarged with increased density in the experimental groups (diameter: PA, 3.07 +/- 0.69 microm; PB, 2.82 +/- 0.37 microm; TA, 3.25 +/- 0.82 microm and TB, 2.82 +/- 0.56 microm; density: PA, 7.11 +/- 1.90 stomata.1000 microm(-2); PB, 8.76 +/- 1.45 stomata.1000 microm(-2); TA, 6.55 +/- 1.44 stomata.1000 microm(-2)and TB, 8.76+/-1.79 stomata.1000 microm(-2)), as compared with the model group (diameter: 2.00+/-0.52 microm density: 4.45+/-1.05 stomata.1000 microm(-2)). After treatment, the urinary volume and sodium ion excretion increased in the experimental groups (PA, 231.28+/-41.09 mmol.L(-1); PB, 171.69 +/- 27.48 mmol.L(-1) and TA, 231.44 +/- 34.12 mmol.L(-1)), which were significantly different with those in the model group (129.33 +/- 36.75 mmol.L(-1)). CONCLUSION: Chinese herbal medicine has marked effects in alleviating liver fibrosis, regulating peritoneal lymphatic stomata, improving the drainage of ascites from peritoneal cavity and causing increase of urinary volume and sodium ion excretion to reduce the water and sodium retention, and thus have favorable therapeutic effect in treating ascites.

Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets

Liver fibrosis is a reversible wound-healing process aimed at maintaining organ integrity, and presents as the critical pre-stage of liver cirrhosis, which will eventually progress to hepatocellular carcinoma in the absence of liver transplantation. Fibrosis generally results from chronic hepatic injury caused by various factors, mainly viral infection, schistosomiasis, and alcoholism; however, the exact pathological mechanisms are still unknown. Although numerous drugs have been shown to have antifibrotic activity in vitro and in animal models, none of these drugs have been shown to be efficacious in the clinic. Importantly, hepatic stellate cells(HSCs) play a key role in the initiation, progression, and regression of liver fibrosis by secreting fibrogenic factors that encourage portal fibrocytes, fibroblasts, and bone marrow-derived myofibroblasts to produce collagen and thereby propagate fibrosis. These cells are subject to intricate cross-talk with adjacent cells, resulting in scarring and subsequent liver damage. Thus, an understanding of the molecular mechanisms of liver fibrosis and their relationships with HSCs is essential for the discovery of new therapeutic targets. This comprehensive review outlines the role of HSCs in liver fibrosis and details novel strategies to suppress HSC activity, thereby providing new insights into potential treatments for liver fibrosis.

以皮肤瘙痒为首发症状的原发性胆汁性肝硬化临床误诊分析

目的分析以皮肤瘙痒为首发症状的原发性胆汁性肝硬化(PBC)患者早期误诊的原因及防范措施。方法选取2022年5月至2023年11月收治早期误诊为皮肤瘙痒症的以皮肤瘙痒为首发症状的PBC患者,分析其临床资料。结果3例中2例为中老年女性,1例为中年男性,均以皮肤瘙痒为首发症状就诊,并伴全身乏力,均未查肝功能,初诊为皮肤瘙痒症,予对症治疗未见明显好转。后经详细查体、多次查肝功能、腹部彩超和(或)肝脏CT,并行血清抗线粒体抗体(AMA)检测阳性,确诊为PBC。误诊时间13 d~4年半。确诊后予以熊去氧胆酸等药物治疗,肝功能恢复正常,症状好转或消失。结论PBC早期症状常不典型,当接诊以皮肤瘙痒为主要症状伴乏力、黄疸和肝功能损伤无或较轻患者时,应多次动态观察肝功能指标变化,行血清AMA检测,必要时行肝穿刺病理学检查,多可确诊。此外,接诊医生应加强对本病的认识,熟知引起肝功能损伤的病因,仔细鉴别,认真查体,尤其应重视男性患者发病的可能,提高警惕性。

Safe upper limit of intermittent hepatic inflow occlusion for liver resection in cirrhotic rats

AIM: To evaluate the effects of varying ischemic durations on cirrhotic liver and to determine the safe upper limit of repeated intermittent hepatic inflow occlusion. METHODS: Hepatic ischemia in cirrhotic rats was induced by clamping the common pedicle of left and median lobes after non-ischemic lobes resection. The cirrhotic rats were divided into six groups according to the duration and form of vascular clamping: sham occlusion (SO), intermittent occlusion for 10 (IO-10), 15(IO-15), 20(IO-20) and 30(IO-30) minutes with 5 minutes of reflow and continuous occlusion for 60 minutes (CO-60). All animals received a total duration of 60 minutes of hepatic inflow occlusion. Liver viability was investigated in relation of hepatic adenylate energy charge (EC). Triphenyltetrazollum chloride (TTC) reduction activities were assayed to qualitatively evaluate the degree of irreversible hepatocellular injury. The biochemical and morphological changes were also assessed and a 7-day mortality was observed. RESULTS: At 60 minutes after reperfusion following a total of 60 minutes of hepatic inflow occlusion, EC values in IO-10 (0.749 +/- 0.012) and IO-15 (0.699 +/- 0.002) groups were rapidly restored to that in SO group (0.748 +/- 0.016), TTC reduction activities remained in high levels (0.144 +/- 0.002 mg/mg protein, 0.139 +/- 0.003 mg/mg protein and 0.121 +/- 0.003 mg/mg protein in SO, IO-10 and IO-15 groups, respectively). But in IO-20 and IO-30 groups, EC levels were partly restored (0.457 +/- 0.023 and 0.534 +/- 0.027) accompanying with a significantly decreased TTC reduction activities (0.070 +/- 0.005 mg/mg protein and 0.061 +/- 0.003 mg/mg protein). No recovery in EC values (0.228 +/- 0.004) and a progressive decrease in TTC reduction activities (0.033 +/- 0.002 mg/mg protein) were shown in CO-60 group. Although not significantly different, the activities of the serum aspartate aminotransferase (AST) on the third postoperative day (POD(3)) and POD(7) and of the serum alanine aminotransferase (ALT) on POD(3) in CO-60 group remained higher than that in intermittent occlusion groups. Moreover, a 60% animal mortality rate and more severe morphological alterations were also shown in CO-60 group. CONCLUSION: Hepatic inflow occlusion during 60 minutes for liver resection in cirrhotic rats resulted in less hepatocellular injury when occlusion was intermittent rather than continuous. Each period of 15 minutes was the safe upper limit of repeated intermittent vascular occlusion that the cirrhotic liver could tolerate without undergoing irreversible hepatocellular injury.

Iron and liver fibrosis: Mechanistic and clinical aspects

Liver fibrosis is characterised by excessive deposition of extracellular matrix that interrupts normal liver functionality. It is a pathological stage in several untreated chronic liver diseases such as the iron overload syndrome hereditary haemochromatosis, viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis and diabetes. Interestingly, regardless of the aetiology, iron-loading is frequently observed in chronic liver diseases. Excess iron can feed the Fenton reaction to generate unquenchable amounts of free radicals that cause grave cellular and tissue damage and thereby contribute to fibrosis. Moreover, excess iron can induce fibrosis-promoting signals in the parenchymal and non-parenchymal cells, which accelerate disease progression and exacerbate liver pathology. Fibrosis regression is achievable following treatment, but if untreated or unsuccessful, it can progress to the irreversible cirrhotic stage leading to organ failure and hepatocellular carcinoma, where resection or transplantation remain the only curative options. Therefore,understanding the role of iron in liver fibrosis is extremely essential as it can help in formulating iron-related diagnostic, prognostic and treatment strategies. These can be implemented in isolation or in combination with the current approaches to prepone detection, and halt or decelerate fibrosis progression before it reaches the irreparable stage. Thus, this review narrates the role of iron in liver fibrosis. It examines the underlying mechanisms by which excess iron can facilitate fibrotic responses. It describes the role of iron in various clinical pathologies and lastly,highlights the significance and potential of iron-related proteins in the diagnosis and therapeutics of liver fibrosis.

Study of heteroserum-induced rat liver fibrosis model and its mechanism

AIM To investigate the morphological changes in the process of heteroserum induced rat liver fibrosis and the mechanism of fibrogenesis of this model. METHODS A model of heteroserum induced rat liver fibrosis was established by intraperitoneal injection of porcine serum. In addition to the observation of the morphological changes of this model, the infiltration of eosinophils and mast cells were measured quantitatively and the deposition of IgG and complement C 3 was detected by immunofluorescence. RESULTS The rat liver fibrosis was induced successfully at the end of the 8th week after the injection of heteroserum. Besides the increase of hepatic stellate cells (HSC) during the process of liver fibrosis, proliferation and activation of primary mesenchyma cells (PMCs) were also found. In the early stage, the infiltration of eosinophils and mast cells was significantly increased and the deposition of IgG and complement C 3 was positive in the portal tracts and septa, while gradually reduced after the injection was stopped. CONCLUSIONS This model is suitable for the research on liver fibrogenesis; the pathogenesis of this model may be related with the allergen induced late phase reaction (LPR) caused by the injection of heteroserum, and the HSCs and the PMCs are important sources of ECM producing cells.

Psychosocial stress and liver disease status

"Psychosocial stress" is an increasingly common concept in the challenging and highly-demanding modern society of today. Organic response to stress implicates two major components of the stress system, namely the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Stress is anamnestically reported by patients during the course of disease, usually accompanied by a decline in their overall health status. As the mechanisms involving glucocorticoids and catecholamines have been deciphered, and their actions on immune cell function deeper understood, it has become clear that stress has an impact on hepatic inflam-matory response. An increasing number of articles have approached the link between psychosocial stress and the negative evolution of hepatic diseases. This article reviews a number of studies on both human populations and animal models performed in recent years, all linking stress, mainly of psychosocial nature, and the evolution of three important liver-related pathological entities: viral hepatitis, cirrhosis and hepatocellular carcinoma.

肝硬化再代偿:现状与挑战

传统上,从代偿性肝硬化到失代偿性肝硬化的进展被认为是疾病自然史中的一个不可逆转点,然而,随着潜在病因的抑制、治愈与疾病消退,越来越多的新证据挑战了这一观点,“肝硬化再代偿”的观点逐渐被接受。近年来,关于肝硬化再代偿具体可行的定义及患者的临床特征引发国内外学者的不断探索。本文通过总结近期国内外对“肝硬化再代偿”的研究,整合已有观点并梳理研究证据,指出现阶段再代偿领域面临的挑战主要包括缺乏深层次的临床与基础研究、需定义非酒精性脂肪性肝病背景下的再代偿,以及面临的伦理方面的问题,为该领域未来的研究提供了新的探索方向。

原发性胆汁性胆管炎诊治——病理是否必需?

原发性胆汁性胆管炎(PBC)是一种慢性肝内胆汁淤积性疾病。本文归纳了PBC病理组织学特征、病理检查在PBC的诊断和治疗中的作用,对病理在分期预后、不典型PBC的诊断、重叠综合征诊断、熊去氧胆酸UDCA应答不佳原因分析和鉴别疾病或排除其他合并疾病等中的作用进行综述,提高临床医生对病理检查对PBC作用的认识。

不明原因肝硬化的病理诊断思路

肝硬化是各类慢性肝病发展的终末阶段,常见的病因包括慢性病毒性肝炎、非酒精性脂肪性肝病、自身免疫性肝病、遗传代谢性肝病等。明确病因诊断是对因治疗的重要前提。“不明原因”肝硬化指经过常规病史询问、体格检查及辅助检查后无法明确病因的肝硬化。此时,肝组织病理学检查既是肝硬化诊断的“金标准”,也是探究肝硬化病因的重要依据。通过对肝纤维化模式、炎症损伤类型及伴随病理改变等进行评估,同时结合相关病史、体征、实验室检查及影像学检查结果综合分析,有助于不明原因肝硬化的病因诊断。本文将对不明原因肝硬化的病理特征及诊断思路进行综述。

马齿苋多糖抗CCl4诱导的小鼠慢性肝纤维化作用

目的:研究马齿苋多糖(Purslane polysaccharide,POP)对小鼠慢性肝纤维化的逆转作用。方法:采用四氯化碳(CCl4)诱导的小鼠肝纤维化模型,分别灌胃给予不同剂量的POP(25、50、100 mg·kg^(-1))、2.5 mg·kg^(-1)的联苯双酯或等体积的生理盐水治疗6周。HE染色观察肝组织形态,电镜观察肝细胞结构变化,定量PCR(qPCR)方法检测肝组织中胶原蛋白(Collagen)Ⅰ和Ⅲ、α-平滑肌动蛋白(Alpha smooth muscle actin,α-SMA)、转化生长因子β1(Transforming growth factor,TGF-β1)、Smad4的mRNA表达,ELISA方法检测透明质酸(Hyaluronic acid,HA)、层黏连蛋LN(Laminin,LN)和Ⅲ型前胶原-N(Procollagen typeⅢ-N,PⅢNP)等肝纤维化相关蛋白含量,Western blot方法检测α-SMA蛋白表达。结果:(1)模型组小鼠表现为肝组织脂肪变性,空泡,脉管区炎性细胞浸润,肝细胞变性坏死,纤维增生;不同剂量POP组肝组织炎症浸润不同程度改善,肝索排列规律;(2)模型组肝细胞结构不清,细胞核增大,常染色质数量异常增加,线粒体和内质网等细胞器代偿性增多,脊增多或断裂,有少许空泡;与模型组相比,POP给药组和联苯双酯组上述状态减轻;(3)模型组α-SMA、TGF-β1、Smad4、CollagenⅢ的mRNA表达增高,POP治疗组以上基因表达呈剂量依赖性下降;(4)模型组LN、HA、PⅢNP和α-SMA含量升高,POP治疗后以上相关蛋白随剂量表达下降。结论:POP可缓解CCl4诱导的小鼠肝纤维化,其机制可能与POP抑制TGF-β1/Smad信号通路,进而下调胶原蛋白的表达有关。

人脐带间充质干细胞经不同移植途径治疗肝硬化大鼠模型的效果比较

目的探讨人脐带间充质干细胞(hUC-MSC)制剂(冷冻细胞制剂和新鲜细胞制剂)通过两种给药途径(门静脉/尾静脉)移植对肝硬化模型大鼠的治疗效果。方法70只SPF级健康雄性SD大鼠随机分为正常组(n=13,予以普通自来水及普通鼠粮喂养)和肝硬化模型组(n=57,给予CCl4/橄榄油溶液混合液,皮下多点注射造模)。第8周观察两组大鼠的生长状况,取正常组及肝硬化模型组小鼠各3只行组织病理学检查,明确肝硬化形成。选取50只肝硬化模型组大鼠按随机数字表法分为模型组、门静脉(新鲜细胞制剂)组、门静脉(冷冻细胞制剂)组、尾静脉(新鲜细胞制剂)组、尾静脉(冷冻细胞制剂)组,每组10只。分别取新鲜或冷冻hUC-MSC制剂通过门静脉或尾静脉途径移植。给药4周后,比较各组大鼠肝功能指标、肝纤维化程度变化。计量资料两组间比较采用成组t检验;多组间比较采用单因素方差分析,进一步两两比较采用LSD-t检验。结果造模第8周时,肝硬化模型组大鼠肝脏形成多个大小不等的假小叶,符合肝硬化诊断标准,ALT、AST、TBil、ALP水平相较于正常组均明显升高(P值均<0.001),肝硬化大鼠造模成功。第12周时5组大鼠ALT、AST、TBil、ALP水平比较差异均有统计学意义(F值分别为232.00、177.10、112.30、121.70,P值均<0.001)。进一步两两比较结果显示,模型组ALT、AST、TBil、ALP水平均显著高于正常组(P值均<0.01);门静脉(新鲜细胞制剂)组、门静脉(冷冻细胞制剂)组、尾静脉(新鲜细胞制剂)组、尾静脉(冷冻细胞制剂)组ALT、AST、TBil、ALP水平均显著低于模型组(P值均<0.01)。结论hUC-MSC移植4周可改善肝硬化模型大鼠肝功能和肝纤维化程度,细胞制剂的不同、给药途径的不同对治疗结果无明显影响。

40例特发性非肝硬化性门静脉高压的临床与病理特点分析

目的 了解特发性非肝硬化性门静脉高压(idiopathic non-cirrhosis portal hypertension,INCPH)的临床与病理特点,为临床医生的诊断提供帮助。方法 回顾性分析2019年8月1日—2022年7月31日福建医科大学孟超肝胆医院收治并确诊有INCPH的40例患者,并随机抽取同期住院并确诊有乙型肝炎肝硬化失代偿期的40例患者作为对照,对两组患者的性别、年龄、症状、肝功能、凝血功能、血常规、门静脉高压表现等进行比较。另外,40例INCPH患者均进行彩超引导下肝穿刺活检术,对相关病理结果进行归纳分析。结果 两组的性别分布、脾大及肝性脑病的发生率比较,差异无统计学意义(P> 0.05)。INCPH患者的平均年龄为(41.05±14.35)岁,乙型肝炎肝硬化失代偿期患者的平均年龄为(58.55±13.65)岁,两组数据差异有统计学意义(P <0.001)。INCPH患者的肝功能异常发生率、凝血功能障碍发生率、血红蛋白(hemoglobin,Hb)及血小板降低发生率、腹腔积液发生率、食管静脉曲张发生率均显著低于乙型肝炎肝硬化失代偿期患者(P <0.05)。在就诊原因方面,INCPH患者以体检发现肝硬化及发现肝功能异常为主,发生率分别为35.0%、27.5%;而乙型肝炎肝硬化失代偿期患者以乏力、食少、黄疸、腹胀为主,发生率分别为72.5%、52.5%、45.0%、30.0%,两者差异有统计学意义(P<0.05)。在病理表现方面,40例INCPH患者均无假小叶形成,其中,小叶间静脉疝者30例,肝窦扩张者21例,中央静脉扩张者11例,汇管区多血管化者13例,小叶间静脉闭塞者9例,小叶间静脉狭窄者13例,小叶间静脉扩张者28例。结论INCPH的临床症状轻微,多为体检发现肝硬化或肝功能异常,但其病理未见假小叶形成,且有特殊表现,临床上对于病因不明的肝硬化患者可行肝穿刺活检协助诊断。

22例血色病铁过载患者临床与病理特点分析

目的研究血色病患者铁过载的临床和肝脏病理特点,总结血色病的治疗方法,提高临床医生对于铁过载疾病的认识。方法回顾性分析2012年1月—2022年12月在解放军总医院第五医学中心诊断为血色病的住院患者的病历资料,总结其临床与肝脏病理特点。结果血色病患者中符合铁过载诊断标准的共22例,其中原发性血色病7例,继发性血色病15例。患者临床症状以乏力、腹胀、皮肤色素沉着等为主,最常见的合并症是贫血和肝硬化。患者的血清铁蛋白、血清铁、铁饱和度较正常值升高,原发性血色病患者的这些指标均高于继发性血色病。肝脏病理表现出明显的铁沉积和纤维化,炎症活动度为轻中度;影像学表现出肝脾增大和铁过载。治疗主要采取静脉放血和铁螯合药物治疗,对其余合并症均采取标准治疗,最终21例患者好转,1例治疗无效。结论铁过载造成肝脏的慢性炎症性损伤,可伴有肝硬化,经过消除病因等治疗后预后较好。