原发性干燥综合征死亡原因及相关因素分析

目的 子解原发性干燥综合征（ｐＳＳ）的死亡原因和高危因素。方法 分析１７２例ｐＳＳ患者中９例死亡病例的死亡原因，并通过死亡组与存活组各项资料比较，进行死亡相关单因素分析。结果 死亡９例患者平均存活时间（９．５±６．３）年，总病死率为５．２３％。与ｐＳＳ相关的最常见的死亡原因为肺间质纤维化伴感染，其他还有肝硬化腹水感染、恶性淋巴瘤、颅内出血、肺动脉高压等。９例中与感染有关的有５例。死亡组与存活组的单     

73例乙肝后肝硬化伴发热原因分析

目的分析乙肝后肝硬化的发热原因。方法对73例患者的发热原因进行分析、汇总,同时对患者的发热原因与肝功能情况进行分类。结果乙肝后肝硬化伴发热的原因,以感染为主,占79.45%,感染源以细菌感染为主,占感染性发热的77.59%,其中自发性细菌性腹膜炎占感染性发热原因的58.62%,占所有发热原因的46.58%,肝功能越差发热的发生率越高。结论乙肝后肝硬化容易出现发热,发热以感染性发热为主,肝功能水平与发热有直接关系。     

老年住院患者的尸检研究

老年患者的尸检比年轻人少得多,目前尚无老年住院患者准确的尸检资料。本文旨在深入了解老年住院患者的死亡原因及临床诊断准确率。材料与方法对比分析1969—1983年间死亡的234例老年住院患者(64～103岁,平均84.5岁)的临床与尸检资料。结果 (1)死亡原因:依次为支气管肺炎(33％),充血性心力衰竭(15％),癌肿伴转移(14％),肺栓塞(8％),心肌梗塞(7％),脑血管意外(6％),不明原因(8％);死于其他原因者22例     

氟哌酸预防肝硬化伴胃肠道出血病人细菌感染

胃肠道出血患者构成肝硬化高危感染组群之一。口服非吸收性抗生素预防感染是有效的,但有潜在致病性耐药菌过度生长以及副作用和费用增加等缺点。本研究旨在评估肝硬化伴胃肠道出血病人服用氟哌酸选择性清除肠道菌(SID)预防感染的效果。病人与方法:1989年8月～1991年6月凡因胃肠道出血住院的肝硬化病人均列为研究对象。剔除住院     

肝硬化病因及临床特点分析178例

目的:探讨东北地区肝硬化患者病因及临床特点.方法:选择我院2007-01/2007-10住院确诊的肝硬化患者178例,回顾性分析患者的临床资料和实验室检查结果.结果:178例患者中单纯乙型肝炎病毒感染61例(34.3%),单纯丙型肝炎病毒感染11例(6.2%),乙型与丙型肝炎病毒重叠感染3例(1.7%),单纯饮酒所致肝硬化39例(21.9%),酒精合并肝炎病毒共同损伤所致肝硬化27例(15.2%),其他为原发性胆汁性肝硬化8例(4.5%),不明原因肝硬化29例(16.3%).肝炎病毒感染和酒精中毒所致肝硬化相比,除蜘蛛痣(x2=4.503,P=0.034)外,其他症状和体征的发生率无显著性差异.肝硬化并发症为上消化道出血(42.0%)、原发性肝癌(28.7%)、继发感染(16.1%)和肝性脑病(11.2%).结论:东北地区的肝硬化病因仍然以乙型肝炎病毒感染为主.单纯病毒感染所致肝硬化的临床表现以门脉压力增高为主,酒精中毒则以肝功能损伤为主,肝炎病毒重叠感染及嗜酒与病毒感染并存容易导致肝癌的发生.     

系统性红斑狼疮487例住院患者发热的病因及相关分析

目的 探讨系统性红斑狼疮(SLE)发热的病因,活动性发热与感染性发热的临床特点以及对糖皮质激素治疗的反应.方法 回顾性分析2002年1月至2007年5月SLE伴发热的住院患者的临床表现、实验室检查和治疗情况等.结果 共有487例SLE住院患者伴发热,其病因为:感染265例、疾病活动206例、活动合并感染8例、肿瘤4例,其他4例.常见的感染部位主要为:呼吸道61.3%,皮肤黏膜10.9%,中枢神经系统9.1%.常见的病原体主要为:细菌77.4%,真菌13.5%,病毒7.8%.大部分SIN活动性发热患者(81.0%)在给予相当于泼尼松剂量≤100 mg/d治疗1～5 d后体温可恢复正常.通过对照研究,补体C3、C4、CH50下降.贫血,淋巴细胞增多,免疫球蛋白水平升高,抗双链DNA(dsDNA)抗体、抗核抗体(ANA)滴度升高,SLE疾病活动指数(SLEDAI)积分高与活动性发热相关;原发病病程长,发病年龄大,血清C反应蛋白(CRP)升高,白细胞与中性粒细胞增多,整个病程中糖皮质激素累积剂量高,以及发热前6个月曾接受免疫抑制剂治疗与感染性发热相关.结论 感染和疾病活动是导致SLE住院患者发热的主要原因.两者的临床特点以及对糖皮质激素治疗的反应不尽相同,慎重并正确地应用糖皮质激素与免疫抑制剂治疗是改善SLE发热患者预后的关键.     

肺结核化疗中发热原因分析

目的分析肺结核患者在使用抗结核化学药物治疗过程中出现发热的原因。方法对2003—2006年在抗结核治疗中出现发热的112例住院病人进行回顾性分析。结果112例病人共出现发热140例次,总结发热原因可分为6大类,按照所占比例依次为:非结核性感染、结核性发热、药物反应、支气管镜检查术后、合并肺外结核和其他合并症。院内获得性感染占非结核性感染例数的98%。结核性发热与低蛋白血症有一定相关性。结论以院内获得性感染为主的非结核性感染是所有发热原因中最多见者,其次要警惕药物热和合并肺外结核。     

143例肝硬化死亡患者的感染特征及中医证型特点分析

目的:探究肝硬化死亡患者的感染特征及中医证型特点。方法:回顾性分析2017年1月-2021年12月上海中医药大学附属曙光医院肝病科143例肝硬化伴或不伴感染的死亡患者的病例资料，包括肝硬化病因、中医证型、实验室指标、并发症、感染部位及感染病原体等，并计算Child-Turcotte-Pugh(CTP)评分、终末期肝病血清钠模型(MELD-Na)评分。计量资料两组间比较采用独立样本t检验或Mann-Whitney U秩和检验，计数资料组间比较采用χ²检验或Fisher精确概率法。结果:143例患者肝硬化病因以乙型病毒性肝炎为主，酒精性肝病、自身免疫性肝病、血吸虫感染位列其后。肝硬化相关并发症发生率：腹腔积液(85.31%)、原发性肝癌(57.34%)、慢加急性肝衰竭(54.55%)、急性肾损伤(50.35%)、胸腔积液(45.45%)、肝性脑病(42.66%)、门静脉血栓(39.16%)、门脉高压相关消化道出血(32.87%)等。直接死亡原因为多脏器功能衰竭、循环衰竭、中枢性呼吸循环衰竭及呼吸衰竭。感染发生率为72.73%,感染部位包括肺部、腹腔、尿路、皮肤/软组织...     

云南省239例艾滋病病例分析

目的 探索云南省艾滋病病人的临床特点和就医行为,为艾滋病病人的临床治疗和关怀提供基础资料。方法 对1990～1998年云南省在医务人员随访和病人就诊过程中诊断及报告的239例AIDS病人的流行病学资料进行统计分析。结果 84％的AIDS病人通过共用针具静脉吸毒而感染,临床表现以发热(70％)、肺部感染(60％)和腹泻(49％)为主,病人从发现感染到发病的平均时间为3年,55.2％的病人在出现机会性感染后一年内死亡,病人就诊率低,94％的病人在家中死亡。结论 胃肠道和肺部感染为云南省AIDS病人的主要临床谱,艾滋病病人的就诊率低,病例报告存在医院的漏诊和漏报,应继续加强对病例报告的管理和对AIDS病人的关怀力度。     

75例老年肺结核死亡分析

本文报告我院30年来60岁以上因肺结核住院死亡75例,其中男64例(85％),女11例(15％),男:女=5.8:1。分析表明,死亡原因以呼吸衰竭、心衰、全身衰竭多见。病型以Ⅲ型多见(72％),Ⅳ型次之(22％)。合并症共32种,以肺内感染为最多(62％),     

Latent hepatic cirrhosis

Among 513 cases of hepatic cirrhosis reviewed, 95 (18%) were found to have latent hepatic cirrhosis (of unknown cause in most cases). Identifiable causes included chronic alcoholism and, in rare instances, chronic ulcerative colitis and hemochromatosis. There were no well-documented cases of latent posthepatitic cirrhosis. Latent hepatic cirrhosis occurred most often in patients of advanced age. The body weight was usually normal or above normal. Splenomegaly appeared to be the single most important clinical sign. The liver was usually granular. The cirrhosis was of the portal type, characterized by normal or above-normal liver weights, fatty changes, and the absence of histologic signs indicating a specific cause. We concluded that latent hepatic cirrhosis may represent either the preclinical phase of an active, usually alcoholic, cirrhosis or, more often, a slowly progressing cirrhotic process of unknown cause, closely associated with advanced age.Supported in part by a grant from the Irwin Strasburger Memorial Medical Foundation, NY.     

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.     

原发性肝癌合并与不合并肝硬化患者年龄及乙型肝炎病毒血清学特点比较

目的探讨原发性肝癌（PHC）合并肝硬化与无肝硬化患者年龄及HBV血清学特点。方法回顾性分析经影像学检查及甲胎蛋白（AFP）测定诊断为PHC的患者547例,分为有肝硬化和无肝硬化两组,统计分析并比较其年龄分布及HBV血清学标记的特点。结果合并肝硬化与无肝硬化患者分别为265例及282例,两组伴HBV感染者分别为221例、256例。合并肝硬化的肝癌患者男女比例为7.83∶1;60岁以下的男性肝癌患者年龄分布无明显差异,无肝硬化的男性肝癌患者60岁以上比例明显高于有肝硬化者（P〈0.005）。合并肝硬化的男性肝癌患者HBV感染率40岁以下年龄组最高（96.67%）,而HBeAg血清学转换率以40～60岁年龄段最高（89.47%）;无肝硬化者HBV感染率40～60岁年龄段最高（90.43%）,但HBeAg血清学转换率最低（80%）。结论合并肝硬化的PHC患者中,男性占大多数,而且早年HBV感染率高;无肝硬化的PHC患者中,老年人占多数;HBeAg血清学转换率高的人群肝癌发病率相对较高。     

Fatal liver failure in haemophiliacs with HIV-induced immunodeficiency: observation of six patients

We observed six cases of haemophiliacs with HIV-induced immunodeficiency who died from fatal liver failure despite the absence of evident cirrhosis. They all had the infection with hepatitis viruses (two patients with hepatitis B and D viruses and four patients with hepatitis C virus) and their CD4 counts were severely decreased. They were much younger than cirrhotic haemophiliacs without HIV. Their serum levels of hyaluronic acid and type IV collagen were lower than those in haemophiliacs with cirrhosis, and were normal. No patients had experienced symptoms or concomitant diseases characteristic of cirrhosis, such as ascites, jaundice, oesophageal/gastric varices or hepatocellular carcinoma, except for one case who had a history of mild ascites. The characteristics of this liver failure were different from liver failure resulting from cirrhosis caused by chronic hepatitis, which suggests liver failure that is specific to patients with immunodeficiency. This kind of liver failure can be a factor threatening survival in patients with HIV infection and with hepatitis virus co-infection in an immunodeficient state.     

Hepatitis B antigen in liver cirrhosis and hepatocellular carcinoma.

Postmortem diagnosis of liver cirrhosis was made over a one-year period in 43 cases, 18 of which also exhibited hepatocellular carcinoma. Blood samples taken from these and 120 other patients who died from other diseases were tested for hepatitis-B antigen (HB-Ag) and its antibodies (HB-AB) by counter-electrophoresis. The types of cirrhosis found were classified on the basis of morphological characteristics and available etiological data. The greater part of controls had had cardiovascular diseases and 32 had had non-hepatic carcinoma. Age limits were similar in the cirrhotic and control groups. HB-Ag was detected in 5 of the 25 subjects with macronodular cirrhosis and in one alcoholic patient among 18 subjects with other types of cirrhosis. The possibility of a coincidental HB virus infection existed in the alcoholic case and in one case of macronodular cirrhosis. Only one patient with liver carcinoma had HB-Ag. Among the 120 controls, HB-Ag and HB-AB were found in a one case. Microscopic lesions did not seem to be related specifically to the presence of HB-Ag in the cirrhotic livers.     

Clinical implications of hepatogenous diabetes in liver cirrhosis

BACKGROUND: Hepatogenous diabetes is a common complication of liver cirrhosis. The aim of the present study was to examine the clinical and therapeutic implications and the prognostic significance of hepatogenous diabetes in patients with liver cirrhosis. METHODS: The prospective cohort study was conducted in 52 patients with histologically confirmed liver cirrhosis (44% Child A, 37% Child B, 19% Child C). The examination included a history, determination of basal C-peptide and glycosylated hemoglobin (HbA(1c)) and, in some cases, a 3 h oral glucose tolerance test with 100 g glucose. Patients were also examined for signs of diabetic retinopathy and information on the further course of illness was obtained. RESULTS: Seventy-one percent of patients with liver cirrhosis had manifest diabetes, 25% had impaired glucose tolerance and only 4% had normal glucose tolerance. In most cases, the hepatogenous diabetes was clinically asymptomatic. Sixteen percent of patients with hepatogenous diabetes had a family history of diabetes; only 8% had retinopathic complications. Within 5.6 +/- 4.5 years after diagnosis of liver cirrhosis, 52% of the diabetics had died, mainly of complications of the cirrhosis. There were no diabetes-associated or cardiovascular deaths. CONCLUSIONS: Hepatogenous diabetes differs from type 2 diabetes in that there is less often a positive family history and that the cardiovascular and retinopathic risk is low. The prognosis of cirrhotic patients with diabetes is more likely to be negatively affected by the underlying hepatic disease and its complications than by the diabetes. Antihyperglycemic treatment of hepatogenous diabetes should always be carefully weighed up in each individual case.     

Liver abscess in patients with cirrhosis of the liver: a 12-year experience

Purpose. Liver abscess is rare in patients with cirrhosis of the liver. The aim of this retrospective study was to investigate the incidence, clinical presentation, causal pathogens, and outcome of liver abscess in cirrhotic patients. Methods. We collected 21 liver abscess specimens (from 14 male patients and 7 female patients; Child A: B: C, 4: 7: 10) from 22 731 admissions of 6450 cirrhotic patients, from 1986 through 1998. Results. The common clinical symptoms and signs included fever, chills, and abdominal tenderness. The major predisposing factors were biliary tract disease (52%) and diabetes mellitus (48%). The diagnosis rate with abdominal ultrasonography was 79%. Gram-negative aerobes were the predominant pathogens (Klebsiella pneumoniae, 66.7%; Escherichia coli, 23.8%), and occurred in 80% and 69% of blood and pus cultures, respectively, while 38% of cases showed polymicrobial pathogens. The location of the abscess was predominantly in the right lobe (71.4%), and 47.6% of patients had multiple abscesses. Six patients died (all with Child C cirrhosis). The overall mortality rate was 28.6% (6/21). Conclusions. The incidence of liver abscess in the cirrhotic patients was low, at 0.09% (21/22 731 admissions). The clinical presentations and pathogens were not different from those in noncirrhotic patients, except that in our cirrhotic patients, there was no significant difference in mortality between those with monomicrobial and those with polymicrobial abscess; nor was there a significant difference in mortality between those with single and those with multiple abscesses. The Child C patients were the high-risk group. Received: November 6, 2000 / Accepted: February 2, 2001     

Hepatitis B and C virus infection as risk factors for liver cirrhosis and cirrhotic hepatocellular carcinoma: a case-control study

To investigate whether hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are risk factors for liver cirrhosis and hepatocellular carcinoma (HCC), a case-control study of 102 cirrhotic HCC patients, 102 sex-matched and age-matched patients with liver cirrhosis, and 102 matched patients with non-hepatic disease controls was performed. The prevalences of hepatitis B surface antigen (HBsAg) and antibody to HCV (anti-HCV) in HCC (70.5%, 39.2%) and liver cirrhosis (74.5%, 27.4%) were higher than controls (16.6%, 10.5%) (P = 0.0001). In HBsAg-negative patients, the prevalence of anti-HCV in cirrhotic HCC (66.6%) and liver cirrhosis (46.1%) was higher than in controls (10.5%; P = 0.0001). There was no such difference in HBsAg-positive patients. Multivariate analysis revealed that both HBsAg and anti-HCV were important risk factors for HCC (odds ratio, 6.52 and 4.59, respectively) and liver cirrhosis (odds ratio, 4.22 and 2.29, respectively). There was no difference in odds ratio when HCC and liver cirrhosis were compared. Our result implies that both HBV and HCV are independent risk factors for cirrhotic HCC and liver cirrhosis in Taiwan.     

Complications of Partial Splenic Embolization in Cirrhotic Patients

In recent years, partial splenic embolization (PSE) has been widely used in patients with cirrhosis and hypersplenism caused by portal hypertension. We investigated the complications associated with PSE cases seen in our hospital. Seventeen cases of liver cirrhosis that had undergone PSE were examined to investigate the complications associated with it. Mean infarcted area of the spleen was 66.2%. Leukocyte and platelet counts in 16 of 17 patients were seen to improve after PSE and persisted for at least one year. The most frequent side effects were abdominal pain (82.4%) and fever (94.1%). Severe side effects were seen in two of those 17 patients. One patient died from acute on chronic liver failure. The other patients contracted bacterial peritonitis and splenic abscess and needed drainage of splenic abscess before recovery. These two cases were in Child-Pugh class B. In conclusions, PSE is a useful treatment for patients with cirrhosis and hypersplenism caused by portal hypertension. However, the possibility of severe complications, especially in patients with noncompensated cirrhosis, should be kept in mind.     

Bacteremia in patients with cirrhosis of the liver.

Infections are frequent in patients with liver cirrhosis, as their defenses against infectious agents are altered. But bacteremia occurring in cirrhotic patients has seldom been reported in the literature. From 1981 to 1986, we collected 197 cases with 228 episodes of bacteremia for this retrospective study. The incidence of bacteremia in cirrhotic patients was 8.8%; no significant difference was noted between cirrhotic patients with variant etiologies of HBV(+), HBV(-) and alcohol. But the incidence increased with the severity of the disease (1%, 4.8%, 17.1% in Child's A, B, C groups, respectively). Gram-negative bacteria were the predominant microorganisms of bacteremia (75.6%). Among them, Escherichia coli, Klebsiella pneumoniae and Aeromonas hydrophilia were the three most commonly detected microorganisms. Gram-positive bacterias were detected in 21.2% of patients with bacteremia, with predominance of the Streptococcus group and Staphylococcus aureus. In about 26.3% of cases the infectious sources were the same by bacteria cultures as from blood. The most common sources were spontaneous bacterial peritonitis, urinary tract infection, pneumonia and biliary tree infection. In cirrhotic patients with and without bacteremia, the mortality rate increased significantly in the bacteremia group (54.8% vs 23.2%, P less than 0.05). By Child's classification, the mortality of patients with classes B and C increased significantly after onset of bacteremia. There was no significant difference in mortality between bacteremic patients in the HBV(+), HBV(-) and alcohol groups. In conclusion, bacteremia is a severe complication of liver cirrhosis and a sign of a poor prognosis.