一个遗传性出血性毛细血管扩张症家系的临床和基因诊断

目的：探讨一个遗传性出血性毛细血管扩张症(hereditary hemorrhagic telangiectasia,HHT)家系的临床特征 及基因诊断的可行性。方法：收集先证者及家系成员的病史资料并进行临床诊断。同时,对先证者进行致病基因突 变检测;鉴定出可能致病性变异后,对家系成员进行特定致病基因突变检测及基因诊断。结果：该家系中4代有5例 个体以鼻衄为突出临床表现。先证者临床诊断为HHT;2例在世家系成员为临床疑诊个体。ENG(endoglin)基因5'非编 码区c.1-127C>T突变见于先证者和2例临床疑诊个体,未见于其他家系成员;综合临床与基因突变分析2例临床疑诊个 体确诊为HHT。结论：HHT临床表现个体差异大,ENG基因c.1-127C>T突变是此HHT家系的可能致病性变异。临床 与基因诊断相结合可提高HHT的诊治水平。     

Clinical phenotypes, ALK1 gene mutation and level of related plasma proteins in Chinese hereditary hemorrhagic telangiectasia

Background We determined the diagnosis of hereditary hemorrhagic telangiectasis (HHT) in a suspected HHT family, identified ALK1 gene mutation and established a gene diagnosis method of HHT. The level of related plasma proteins (transforming growth factor β and thrombomodulin ) were also analyzed,Methods Bleeding history and family history were collected; Dilatant nasal mucosal capillaries in proband were observed under nasal cavity endoscope; exons 3, 7, 8 of ALK1 gene in proband and her family members were amplified with polymerase chain reaction (PCR), and the PCR products were analyzed. Using enzyme-linked immunosorbent assay (ELISA), plasma TGF-β1 and TGF-β2.concentrations were measured. Plasma thrombomodulin (TM) level was detected by Westem blotting.Results Of all family members, four had epstaxis, two had evident telangiectases on skin or mucosa. Gene screening results showed that C to T substitution at position 1231 in exon 8 of ALK1gene (CGG→TGG) existed in proband,her affected brother and their father. The mutation did not exist in proband‘s sister-in-law and nephew. Plasma TGF-β1 concentrations in the affected HHT was 20538, 17194, 13131 pg/ml, while that of normal control and unaffected family members was 15950,20297, 12836 pg/ml, respectively. Plasma TGF-β2. in HHT patients was 14502, 9550, 10592 and that of normal controls 8579, 20297, 7680 pg/ml respectively. Level of plasma TM was in HHT subjects significantly lower than in normal subjects.Conclusions Chinese HHT individuals have mutant ALK1 gene, a C1231 T variation on exon 8 of ALK1 is responsible for HHT clinical phenotypes in this family. ALK1 gene analysis, together with special clinical phenotypes and family history, provides a reliable method in diagnosing HHT. In affected HHT subjects, plasma TGFβ levels were not obviously different from those of normal subject;while plasma TM concentration was significantly lower than that in normal subjects. The significance and mechanism remain to be elucidated.     

Coinheritance of hereditary spherocytosis and reversibility of cirrhosis in a young female patient with hereditary hemochromatosis

Here we report a 33-years-old woman with hereditary spherocytosis and hemochromatosis due to homozygosity for the C282Y mutation of the HFE gene. The coinheritance of both conditions led to severe iron overload and liver cirrhosis at young age. The patient was treated by repeated phlebotomy, and reversibility of cirrhosis was documented by transient elastography. This report discusses the pathophysiology of iron accumulation in patients with hemolytic anemia combined with HFE C282Y homozygosity. The case indicates that patients with hematological disorders characterized by increased erythropoetic activity should be screened for HFE mutations.     

维持性血液透析患者静脉补铁的治疗

目的探讨规律血液透析患者予以静脉补铁后铁的状况及血红蛋白水平的变化。方法选择70例稳定血透患者,维持性血液透析2、3次/周。所有患者血红蛋白(Hb)<80g/L,红细胞压积(Hct)<27%,铁蛋白(SF)<500μg/L,转铁蛋白饱和度(TSAT)<30%,Kt/V均<1.2,皮下注射促红细胞生成素(EPO)100～150单位/kg·周。将上述病人随机分为两组(口服组1和静脉组1),分别采用静脉输注右旋糖酐氢氧化铁和口服多糖铁复合物进行补铁治疗,检测治疗前后的血清铁指标和红细胞相关指标。将口服治疗组未达标者进一步分为两组,继续上述方法治疗。结果静脉补铁可使Hb、Hct、SF和TSAT迅速升高,治疗前后差异有显著性(P<0.001)。口服铁剂无效的病人静脉应用铁剂76.9%仍然有效。静脉铁剂治疗后Hb/Hct达标患者,EPO用量减少(与起始剂量相比,P<0.001)。结论纠正肾性贫血时静脉应用铁剂安全可靠,疗效优于口服铁剂,并且可以减少EPO用量。     

静脉补铁和口服补铁对肾性贫血的治疗比较

目的　比较静脉和口服补铁对血液透析患者铁缺乏和贫血的治疗效果。方法　选择 41例维持性血液透析患者 ,平均透析时间 10 .3± 8.8个月 ,每周透析 2～ 3次。试验前检查每位患者的血红蛋白、血球压积、RBC、血清铁(SI)、血清铁蛋白 (SF)、转铁蛋白 (Tf)、转铁蛋白受体 (sTfR)、前白蛋白 (Pro Alb)和C反应蛋白 (CRP)。HCT <3 3 %作为贫血的指标 ,将患者随机分入静脉补铁组和口服补铁组 ,静脉补铁组 19例。给予枸橼酸铁 5 0mg透析后输入 ,共 10次 ,口服补铁组 2 2例 ,给予硫酸亚铁 60 0mg/d。两组病人都给予促红细胞生成素 60 0 0U/周 ,6周后两组重复检查上述指标。结果　试验结束时静脉补铁组各铁参数指标明显高于口服补铁组 ,Tf(2 .2 1± 0 .77vs1.75± 0 .2 5g/L ,P <0 .0 0 1) ;sTfR(1.2 2±0 .68vs 0 .78± 0 .19mg/L ,P <0 .0 1) ;SF(4 96.13± 3 0 6.5 7vs2 79.2± 2 0 6μg/L ,P <0 .0 0 1) ,SI(14 1.6± 5 8.7vs60 .6± 19.1μg/dl,P<0 .0 0 0 1) ;静脉补铁组贫血改善较口服组好 ,HCT上升值 (0 .0 5 4± 0 .0 5 0vs0 .0 3 7± 0 .0 40 )和Hb上升值 (13 .8± 14 .9vs6.9± 9.1P <0 .0 0 1)有明显差异 ;将两组病人治疗前后血红蛋白、血球压积的变化值 ,与治疗前后各铁参数变化值作相关分析 ,发现转     

静脉注射蔗糖铁与口服多糖铁复合物治疗肾性贫血的临床疗效比较分析

目的探讨静脉注射蔗糖铁与口服多糖铁复合物对肾性贫血患者的治疗效果。方法选取我院维持性血液透析患者50例,随机分为静脉注射蔗糖铁组(治疗组)和口服多糖铁复合物组(对照组),两组均同时皮下注射重组人促红细胞生成素(EPO),观察患者治疗8周前后血红蛋白(Hb)、红细胞压积(Hct)、血清铁蛋白(SF)上升幅度情况。结果经8周治疗后,治疗组及对照组血红蛋白(Hb)、红细胞压积(Hct)、血清铁蛋白(SF)均有上升,但治疗组上升幅度优于对照组,差异有统计学意义(P<0.05)。结论静脉注射蔗糖铁治疗肾性贫血较口服多糖铁复合物治疗肾性贫血效果显著。     

蔗糖铁注射液治疗维持性血液透析患者肾性贫血的疗效与安全性观察

目的比较静脉应用蔗糖铁（简称静脉组）与口服多糖铁复合物（简称口服组）治疗使用促红细胞生成素（EPO）的维持性血液透析（MHD）患者肾性贫血的疗效与安全性。方法采用同期随机对照研究。结果治疗后血红蛋白（Hb）、血细胞比容（HCT）、血清铁蛋白（SF）、血清转铁蛋白饱和度（TSAT）两组均有升高,静脉组比口服组升高差异有统计学意义（P〈0．05）,且上升速度快于口服组;静脉组不良反应少于口服组（P〈0．05）;治疗前后两组肝功能、C反应蛋白（CRP）等生化指标差异无统计学意义。结论静脉用蔗糖铁治疗MHD患者的肾性贫血安全有效。     

遗传性非息肉病性大肠癌30例临床病理特点与诊治分析

目的：探讨遗传性非息肉病性大肠癌（hereditary nonpolyposis colorectal cancer,HNPCC）的临床病理及分子病理特征,提高对该病的认识和诊疗水平。方法：回顾性分析中南大学湘雅医院普通外科诊治的30例HNPCC病人,以同期在该院治疗的散发性结直肠癌25例为对照组。比较其发病年龄、肿瘤部位、病理类型、治疗方法及预后。采用免疫组织化学检测两组病人错配修复基因（mismatch repair genes,MMR）MLH1和 MSH2 表达缺失率。结果：与对照组相比,HNPCC组的发病年龄早,近段大肠癌比例高,易于合并多发癌,肿瘤高分化类型所占比例高（P＜0.05）。MLH1和 MSH2 表达缺失率高于对照组（P＜0.05）。HNPCC组中1/3的病人接受了大肠次全切除术,预后与散发大肠癌相当（P＞0.05）。结论：HNPCC具有发病早,易合并多发癌的特点,结合MMR的检测可提高诊断的准确率。彻底手术和密切随访可取得好的效果。     

静脉与口服补铁治疗尿毒症患者肾性贫血的效果观察

目的 观察对比静脉与口服补铁治疗尿毒症患者肾性贫血的效果.方法 选取2019年1月～2020年7月本院收治的尿毒症肾性贫血患者60例开展本研究,回顾病例,根据不同的治疗措施将60例患者分为对照组与观察组,每组各30例.前者采用口服右旋糖酐铁分散片治疗,后者采用静脉补蔗糖铁治疗,治疗8周后,对比两组患者血常规及铁代谢指标...     

静脉滴注蔗糖铁治疗缺铁性贫血的有效性与安全性分析

目的 探讨对缺铁性贫血患者采用静脉滴注蔗糖铁治疗的有效性与安全性.方法 选择2018年6月至2020年2月在我院进行治疗的80例缺铁性贫血患者随机分成对照组和观察组,每组各40例.对照组采用口服铁剂用药,观察组采用静脉滴注蔗糖铁,记录患者治疗前后血红蛋白(Hb)、血清铁蛋白水平(SF)、治疗时间、治疗后不良反应总发生率...     

静脉铁剂对维持性血液透析患者微炎症反应和氧化应激状态的影响

目的 观察静脉铁剂对维持性血液透析（MHD）患者微炎症反应和氧化应激状态的影响.方法 检测48例病情稳定、透析时间3个月以上、行静脉补铁的肾性贫血MHD患者补铁前,补铁1、3、5、7及10周血清超敏C反应蛋白（hs-CRP）、肿瘤坏死因子-α（TNF-α）、白介素-6（IL-6）、脂质过氧化物丙二醛（MDA）及谷胱甘肽过氧化物酶（GSH-px）水平,评价经静脉补铁对MHD患者并发症发生的诱导作用.结果 补铁1周后,hs-CRP、TNF-α、IL-6及MDA升高,GSH-px降低（均P＜0.01）.3周后,hs-CRP、TNF-α、IL-6及MDA仍上升,至5周时达最高峰,而GSH-px在5周时达最低水平,但与1周时差异均无统计学意义（均P＞0.05）.与5周比较,补铁7周后hs-CRP、TNF-α、IL-6及GSH-px有所降低,MDA继续升高,但各组间差异无统计学意义（均P＞0.05）.补铁10周后各指标逐渐恢复,但与7周时差异均无统计学意义（均P＞ 0.05）.结论 静脉补铁早期就可促进MHD患者微炎症反应,并加重其氧化应激,但在中后期逐渐减弱而趋于稳定.     

贫血病人维持性透析中静脉补铁的治疗及相关护理

目的 通过静脉给予蔗糖铁 (维乐福),使患者体内有充足的铁储备,从而提高基因重组红细胞生成素(rHuEPO)的治疗效果.方法 62例血液透析病人静脉使用蔗糖铁,每次100 mg,每周2～次,总剂量1 000 mg.治疗前后检测血红蛋白,血细胞比容,血清铁蛋白(SF),运铁蛋白地和度(TSAT),血清总铁结合力(TIBC)及CRP.结果 经过静脉铁剂的治疗,两组病人的Hb和Hct均有不同的程度的升高(P<0.01),两组血清铁蛋白和转铁蛋白饱和度均较治疗前升高(P<0.01);在透析患者补铁时给予相应的护理干预,可及时发现过敏反应和延迟反应的发生并及时处理.结论 透析病人补铁治疗有助于改善病人的肾性贫血,良好的护理可以确保补铁治疗的顺利进行.     

硫辛酸预处理对腹膜透析患者静脉铁剂治疗诱导的氧化应激反应的影响

目的 观察硫辛酸预处理对持续性不卧床腹膜透析(CAPD)患者接受静脉铁剂治疗诱导的急性氧化应激反应的影响.方法 40例CAPD患者先后接受单纯静脉铁剂治疗(Fe组)和先给予硫辛酸静脉滴注后的静脉铁剂治疗(Lipoic+Fe组),两次治疗间隔8周以上;分别于静脉铁剂滴注前(0时点)和滴注后10、60、120、240 min时点采集血样,可见光分光光度计测定血清超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性及血清丙二醛(MDA)水平.以20名健康志愿者作为正常对照组.结果 与正常对照组相比,Fe组和Lipoic+Fe组0时点血清SOD和GSH-Px活性降低,MDA水平升高(P<0.05).Fe组和Lipoic+Fe组静脉补铁后,血清SOD和GSH-Px活性下降,MDA水平升高,分别于60 min时点达到谷值或峰值.Lipoic+Fe组各时点血清SOD和GSH-Px活性均显著高于Fe组(P<0.05),MDA水平均显著低于Fe组(P<0.05).结论 静脉补铁可使CAPD患者的氧化应激状态急性加重;预防性应用硫辛酸可在一定程度上减轻静脉铁剂诱导的氧化应激反应.     

硫辛酸预处理对腹膜透析患者静脉铁剂治疗诱导的氧化应激反应的影响

目的观察硫辛酸预处理对持续性不卧床腹膜透析（CAPD）患者接受静脉铁剂治疗诱导的急性氧化应激反应的影响。方法 40例CAPD患者先后接受单纯静脉铁剂治疗（Fe组）和先给予硫辛酸静脉滴注后的静脉铁剂治疗（Lipoic＋Fe组）,两次治疗间隔8周以上;分别于静脉铁剂滴注前（0时点）和滴注后10、60、120、240min时点采集血样,可见光分光光度计测定血清超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）活性及血清丙二醛（MDA）水平。以20名健康志愿者作为正常对照组。结果与正常对照组相比,Fe组和Lipoic＋Fe组0时点血清SOD和GSH-Px活性降低,MDA水平升高（P〈0.05）。Fe组和Lipoic＋Fe组静脉补铁后,血清SOD和GSH-Px活性下降,MDA水平升高,分别于60min时点达到谷值或峰值。Lipoic＋Fe组各时点血清SOD和GSH-Px活性均显著高于Fe组（P〈0.05）,MDA水平均显著低于Fe组（P〈0.05）。结论静脉补铁可使CAPD患者的氧化应激状态急性加重;预防性应用硫辛酸可在一定程度上减轻静脉铁剂诱导的氧化应激反应。     

A study of haematological and bone marrow changes in symptomatic patients with human immune deficiency virus infection with special mention of functional iron deficiency,anaemia of critically ill and haemophagocytic lymphohistiocytosis

Background

Haematological abnormalities are among the most common complications of HIV. These involve all lineages of blood cells. Bone marrow studies form integral part of complete workup of the HIV positive patients specially when they present as case of pyrexia of unknown origin (PUO), refractory anaemia and pancytopenia.

Method

55 HIV infected symptomatic patient requiring bone marrow examination were included in the study. Relevant clinical history, baseline haematological investigations including full blood count, CD4 cell counts using flow cytometry were recorded.

Results

Median ANC values in males were found to be significantly lower than females (p = 0.046). CD4 cell count statistically significantly correlated with age, TLC, ANC & platelet count. Anaemia was present in 45 patients and out of which 66.66% patients had normocytic normochromic anaemia. Iron deficiency anaemia was present in (37.77%) patients and anaemia of chronic disease in (62.22%) patients. 2 patients had anaemia of the critically ill.Two patients had non-Hodgkin's lymphoma (NHL) and showed lymphoma deposit in the bone marrow. Gelatinous degeneration was seen in 3 patients. Ill formed epithelioid cell granulomas were seen in 7 cases, and 2 cases were positive for acid fast bacilli (AFB). Haemophagocytosis was seen in 8 cases; two cases later diagnosed as a case of infection induced HLH. Leishmania donovani (LD) bodies seen in 2 cases.

Conclusions

Bone marrow study is an important investigation in HIV infected symptomatic patients with peripheral haematological abnormalities.     

遗传性非息肉病性大肠癌和家族性腺瘤性息肉病腺瘤的预防性干预治疗

目的 探索非甾体抗炎药（NSAID）消退遗传性非息肉病性大肠癌（HNPCC）和家族性腺瘤性息肉病（FAP）结直肠腺瘤的有效性和安全性。方法6例HNPCC患者,口服赛来昔布400mg／d。18例符合FAP临床诊断的患者按照随机数字表随机分为2组：赛来昔布400mg组（8例,口服赛来昔布400mg／d）,赛来昔布200mg组（10例,口服赛来昔布200mg,／d）,服药观察24个月。另外4例FAP患者不愿接受赛来昔布治疗,改服肠溶阿司匹林80mg／d（阿司匹林组）。FAP患者以息肉数目描述治疗效果,HNPCC患者按照息肉级别描述治疗后息肉的变化。由专人负责肠镜复查,第1年每3个月复查肠镜1次,第2年每6个月复查肠镜1次。结果两种剂量的赛来昔布均有消退FAP结肠腺瘤作用,服药9个月后400mg组腺瘤消退的比率为86．69％（280／323）,200mg组腺瘤消退比率为51．81％（129／249）,两组比率的差异有统计学意义。4例FAP患者服用80mg肠溶阿司匹林9个月后,37．89％（36／95）的腺瘤消退,5例HNPCC腺瘤患者治疗9个月后腺瘤消失。无论是FAP还是HNPCC结肠腺瘤,服用大剂量（400mg）药物,时间超过6个月时,14例患者中有7例发生不良反应;当减少药物剂量或换用阿司匹林后,不良反应均可逆转。赛来昔布200mg组,治疗期间无不良反应发生。结论NASID是FAP和HNPCC腺瘤干预性治疗的有效药物;赛来昔布400mg／d疗效好,但不良反应较大,国人可先以200mg／d长期治疗或400mg／d治疗6个月后以200mg／d维持;肠溶阿司匹林也有类似效果。     

Novel mutation and polymorphism of PRSS1 gene in the Chinese patients with hereditary pancreatitis and chronic pancreatitis

Background Mutations in the cationic trypsinogen gene （PRSS1） have been detected in patients with hereditary pancreatitis （HP）. This study investigated the prevalence of the R122H （c.365G〉A）, A121T （c.361 G〉A） and D162D （c.488 C〉T） mutations or polymorphisms in the common, non-hereditary forms of chronic pancreatitis and in an HP family.
Methods DNA was prepared from blood samples of 54 patients with chronic pancreatitis （35 alcoholic, 17 idiopathic and 2 hereditary） and 120 normal controls. The PRSS1 genes were amplified by polymerase chain reaction （PCR） and their products were analyzed by sequencing and related clinical data were also collected.
Results A new polymorphism （c.488 C〉T） of PRSS1 was found in 25 patients with chronic pancreatitis （including one affected member of the HP family） and six members of the normal controls. The C/T genotype was significantly increased in chronic pancreatitis （OR： 16.379, 95% CI： 5.7522-52.3663）, the frequency of c.488 C〉T change was in according with the Hardy-Weinberg equilibrium, but it doesn＇t affect the clinical phenotype. The commonly reported change of R122H （c.365G〉A） was not detected in any of the study subjects, c.361 G〉A was found in 2 affected members and one unaffected carrier in an HP family. One of the affected members of an HP family had c.361 G〉A mutation and polymorphism （c.488 C〉T） in the PRSS1 gene at the same time. The patient＇s clinical values （C3, C4, CA19-9 and HbA1c） were higher than those of the other patients with chronic pancreatitis. The two patients with HP developed diabetes mellitus and their father died with pancreatic cancer.
Conclusion A new polymorphism （c.488 C〉T） in the PRSS1 gene is associated with chronic pancreatitis, but it did not affect the clinical phenotype while the A121T （c.361 G〉A） mutation in the gene shows a significant correlation in the patients with HP.     

122例营养性缺铁性贫血的病因及疗效分析

目的:探讨6月龄至3岁婴幼儿营养性缺铁性贫血(NIDA)的发病原因及铁剂治疗的疗效。方法:总结122例NIDA患儿发病原因,并给予硫酸亚铁口服治疗,重度贫血还给予输血治疗,对临床疗效进行分析。结果:依据贫血程度区分:轻度42例,中度66例,重度14例。未规律添加辅食、挑食与婴幼儿NIDA关系最密切。全部患儿经3到4周的针对性治疗,贫血均得以纠正。结论:NIDA仍是目前严重的婴幼儿期营养缺乏性疾病,应重视母孕期的营养,及时规范添加辅食,及早治疗慢性腹泻等疾病,对婴幼儿贫血早发现、早规范治疗。     

Clinical features and hMSH2/hMLH1 germ-line mutations in Chinese patients with hereditary nonpolyposis colorectal cancer

Background At least five mismatch repair （MMR） genes, including hMSH2, hMLH1, hPMS, hPMS2, and hMSH6/GTBP, are associated with hereditary nonpolyposis colorectal cancer （HNPCC）. More than 90% of families with HNPCC harbor the hMSH2and hMLH1 gene mutations. We have analyzed the clinical features of HNPCC among Chinese patients and report the results of screening for mutations in the hMSH2 and hMLH1 genes.
Methods The data concerning gender, site of colorectal cancer （CRC）, age at diagnosis, history of synchronous and/or metachronous colorectal cancer, instance of extracolonic cancers, and histopathology of tumors for 126 patients from 28 independent families with HNPCC were collected. Fifteen of the families met the Amsterdam I criteria, and 13 met the Japanese clinical criteria for diagnosis. Genomic DNA was extracted from the peripheral lymphocytes. Polymerase chain reaction （PCR） and denaturing high-performance liquid chromatography （DHPLC） were used to screen the coding region of the hMSH2 and hMLH1 genes. Samples showing abnormal DHPLC profiles were sequenced.
Results One hundred and seventy malignant neoplasms were found in the 126 patients, of whom 23 had multiple cancers. Ninety-eight of the patients （77.8%） had colorectal cancers, with an average age at onset of 45.9 years and a right-sided predominance. Eight hMSH2 or hMLH1 gene sequence variations were found in 12 families, and a germ-line G204X nonsense mutation in the third exon of hMSH2 was found, representing the first mutation in an MMR gene ever found in people of Chinese Mongolian ethnicity.
Conclusions HNPCC is a typical autosomally dominant hereditary disease, characterized by early onset, a predominance of proximal colorectal cancer, and multiple synchronous and metachronous colorectal cancers. DHPLC is a powerful tool for detecting mutations in the hMSH2 and hMLH1 genes, Mutations in the first nine exons of the hMLH1 gene were more common in Chinese patients.     

血清铁和血清铁蛋白与病毒性肝炎患者肝纤维化指标的关系

目的 研究血清铁和血清铁蛋白与病毒性肝炎患者血清肝纤维化指标（透明质酸、层黏蛋白、人Ⅲ型前胶原、Ⅳ型胶原）的关系。方法 采用1s快速肝穿刺法对39例病毒性肝炎患者和30例病毒标志物阴性对照组取肝组织标本，行HE和铁染色后镜检；同时分别应用原子吸收光谱法、放射免疫法和酶联免疫法检测患者的血清铁、血清铁蛋白、肝纤维化指标。结果 对照组和病毒性肝炎患者比较，血清铁、血清铁蛋白测定值差异显著（P〈0．05）；病毒性肝炎患者肝纤维化指标测定值与对照组间有显著性差异（P〈0．05）。血清铁及血清铁蛋白与Ⅳ型胶原具有统计学上的相关性（血清铁r=0．614，P=0．026；血清铁蛋白r=0．549，P=0．019）。病毒性肝炎患者多合并有肝铁过载，肝功能损害程度严重的患者肝组织有明显铁颗粒沉积。结论 血清铁、血清铁蛋白测定值可以作为病毒性肝炎患者铁过载的重要指标。