急性胰腺炎合并急性肝损害128例分析

目的:探讨急性胰腺炎(AP)合并肝损害的临床特点及发病机制.方法:对两家医院自2000年1月至2009年11月所收治的176例AP进行回顾性临床分析.结果:176例AP中有128例合并肝损害(占72.72%),重型胰腺炎肝损害程度较轻型胰腺炎肝损害重,差异有显著性,P<0.05.结论:AP合并肝损害发病率较高,其程度与急性胰腺炎病情程度成正相关,其发病机制是炎性破坏因子,多种炎性介质,胆汁淤积,内毒素等多因素结果.因此AP并发肝损时首选积极治疗原发病,同时加强保肝治疗,保护肝脏功能是非常重要的.     

甲亢和亚临床甲亢患者血细胞分析的结果比较

目的探讨甲亢和亚临床甲亢患者的血细胞改变是否存在差异.方法对甲亢患者、亚临床甲亢患者和正常对照者进行血细胞分析,将其主要参数作统计学比较.结果在参数测定值方面,甲亢组WBC、RBC、Hb和PLT这4项参数比亚临床甲亢组和对照组明显降低;亚临床甲亢组Hb和PLT均值比对照组明显降低;在参数检出率方面,与正常对照组比较,甲亢和亚临床甲亢患者WBC≤4.0×109/L、Hb≤110g/L的检出例数明显增多,PLT≤100×109/L增多不明显.结论甲亢患者血细胞分析的几项主要指标比亚临床甲亢患者降低更显著.     

46例甲状腺功能亢进性心脏病临床分析

目的：探讨甲状腺功能亢进性心脏病的防治措施。方法：回顾性分析2003年6月至2009年6月收治的46例甲状腺功能抗进性心脏病患者的临床资料。其中男20例,女26例,年龄15-78岁,病程7月-30年;伴心功能衰竭28例（60.9%）,心房纤颤30例（65.2%）,和病态窦房结综合征1例（2.2%）。结果：46例患者均服用甲状腺药物治疗后,甲亢病情缓解,心力衰竭好转。30例心房纤颤患者中,19例恢复窦性心律,剩余11例平均心室率控制在70-100次/min。结论：甲亢性心脏病治疗的关键在于早期诊断,甲亢病情控制后,绝大部分心脏异常可减轻或消失。     

46 例甲状腺功能亢进性心脏病临床分析

目的:探讨甲状腺功能亢进性心脏病的防治措施。方法:回顾性分析2003年6月至2009年6月收治的46例甲状腺功能抗进性心脏病患者的临床资料。其中男20例,女26例,年龄15-78岁,病程7月-30年;伴心功能衰竭28例(60.9%),心房纤颤30例(65.2%),和病态窦房结综合征1例(2.2%)。结果:46例患者均服用甲状腺药物治疗后,甲亢病情缓解,心力衰竭好转。30例心房纤颤患者中,19例恢复窦性心律,剩余11例平均心室率控制在70-100次/min。结论:甲亢性心脏病治疗的关键在于早期诊断,甲亢病情控制后,绝大部分心脏异常可减轻或消失。     

普萘洛尔治疗桥本病伴发甲亢82例临床疗效观察

目的：探讨普萘洛尔治疗桥本病伴发甲亢82例临床疗效观察。方法：随机选取2010年04月份-2011年05月份因桥本病伴发甲亢就诊于我院的患者82例,随机分为治疗组41例患者（采用普萘洛尔治疗）,对照组41例患者（采用常规治疗）,统计两组患者的甲状腺功能以及影像学改变,并对结果进行统计分析。结果：治疗组总有效率为68.3％,甲状腺功能以及影像学检查结果均明显优于对照组,经统计分析,P〈0．05,差异存在显著性。结论：普萘洛尔治疗桥本病伴发甲亢有效改善甲状腺功能,值得临床普遍使用。     

中西医结合治疗蝮蛇咬伤肝功能损害268例

我院自１９８０～１９９６年共收治蝮蛇咬伤８３４例,其中伴有肝损害２６８例。我们采用保护和改善肝功能的中西医结合治疗方法进行治疗,获得较好疗效,现分析如下。１临床资料２６８例中男１５６例,女１１２例。年龄３～７７岁,平均（３６．４±２３．５）岁。农民１...     

甲亢甲低患者肝纤维化指标检测的临床意义分析

目的:探讨甲状腺功能亢进(甲亢)、甲状腺功能减低(甲低)与肝纤维化指标的关系及其可能的机制。方法:采用放射免疫分析法(R1A)检测57例甲亢患者、43例甲低患者、39例甲亢治疗后甲状腺激素正常者和50例健康成人的血清Ⅳ型胶原(1V-C)、Ⅲ型前胶原(PCⅢ)、透明质酸(HA)、层粘连蛋白(LN)、T3、T4、FT3、FT4、TSH、TGA、TMA含量。结果:甲亢患者组血清中1V-C、PCⅢ含量比正常对照组及甲低患者组显著性增高(P<0.05);治疗后甲状腺激素下降,1V-C、PCⅢ含量也随之下降(与治疗前比较P<0.01);HA、LN在四组中无显著性差异(P>0.05),在甲亢治疗前后无显著性差异(P>0.05)。各项肝纤维化指标与TGA、TMA的阳性率无关。结论:甲亢患者可有不同程度的肝功能损害,血清中甲状腺激素水平增高时,1V-C、PCⅢ水平也增高,在用1V-C、PCⅢ判断肝纤维化时应注意有无甲状腺疾病特别是甲亢。未发现HA、LN含量与甲状腺激素水平的关系。     

甲亢甲低患者肝纤维化指标检测的临床意义分析

目的：探讨甲状腺功能亢进（甲亢）、甲状腺功能减低（甲低）与肝纤维化指标的关系及其可能的机制。方法：采用放射免疫分析法（R1A）检测57例甲亢患者、43例甲低患者、39例甲亢治疗后甲状腺激素正常者和50例健康成人的血清Ⅳ型胶原（1V-C）、Ⅲ型前胶原（PCⅢ）、透明质酸（HA）、层粘连蛋白（LN）、T3、T4、FT3、FT4、TSH、TGA、TMA含量。结果：甲亢患者组血清中1V-C、PCⅢ含量比正常对照组及甲低患者组显著性增高（P〈0.05）;治疗后甲状腺激素下降,1V-C、PCⅢ含量也随之下降（与治疗前比较P〈0.01）;HA、LN在四组中无显著性差异（P〉0.05）,在甲亢治疗前后无显著性差异（P〉0.05）。各项肝纤维化指标与TGA、TMA的阳性率无关。结论：甲亢患者可有不同程度的肝功能损害,血清中甲状腺激素水平增高时,1V-C、PCⅢ水平也增高,在用1V-C、PCⅢ判断肝纤维化时应注意有无甲状腺疾病特别是甲亢。未发现HA、LN含量与甲状腺激素水平的关系。     

甲巯咪唑联合普萘洛尔治疗甲亢的临床价值分析

目的:探讨甲巯咪唑联合普萘洛尔治疗甲亢患者的临床应用和疗效。方法:选取我院在2010年1月至2013年1月收治的甲状腺功能亢进症(甲亢)患者63例,随机分为观察组和对照组,对照组单用甲巯咪唑治疗,观察组联合应用甲巯咪唑和普萘洛尔,并比较两组疗效。结果:观察组治疗后的FT3、FT4明显降低,TSH明显升高,总有效率为92.9%,均明显优于对照组,P<0.05;且不良反应发生率明显小于对照组,P<0.05。结论:甲巯咪唑联合普萘洛尔治疗甲亢可更好提高治疗效果,降低不良反应,值得临床推广。     

系统性红斑狼疮合并消化道损害32例临床分析

目的：探讨系统性红斑狼疮（SLE）合并消化道损害者的临床特点。方法：回顾性分析32例SLE合并消化道损害的患者,收集整理其临床资料,分析其临床特点。结果：食道受累者7例（21．9％）,胃肠道受累者25例（78．1％）其中假性肠梗阻10例（31．2％）,且以肠梗阻为首发症状的2例均误诊为急腹症收住外科,肾脏受累14例（43．8％）。治疗后,24例好转。4例死亡。结论：以消化道症状为首发表现的SLE极易误诊,特别是以吞咽障碍,肠梗阻为首发症状者最易误诊。对有消化道受损表现同时伴有其它脏器受损者应排除有无SLE可能。SLE消化道损害发生率高,对此应提高认识和警惕。     

Scintigraphy has the potential to replace thyroid stimulating hormone and ultrasonography in hyperthyroidism diagnosis

The value of thyroid scintigraphy in hyperthyroidism diagnosis has long been the subject of debate. Unresolved issue is whether scintigraphy should be performed routinely, selectively, or for all hyperthyroidism patients. So, this study is concerned with the evaluation of thyroid scintigraphy for identifying hyperthyroidism in comparison with thyroid stimulating hormone (TSH) and ultrasound. This is cross sectional study including convenient patients sample (n = 50, 15 males and 35 females) aged (20–50 years) with primary hyperthyroidism and were attending endocrine clinics at King Faisal Specialist Hospital and Research Centre. All patients performed clinical investigations (TSH, ultrasound and thyroid scintigraphy). Among these patients, 96%, 48/50, had positive findings for hyperthyroidism with thyroid SC (95% CI; 96.0–99.5%); 84%, 42/50, had positive findings for hyperthyroidism by US (95% CI; 70.9–92.8%); and 56%, 28/50, had positive findings for hyperthyroidism by TSH measurement (95% CI; 41.3.0–70.0%). There was very good agreement between scintigraphy diagnosis and ultrasonography (kappa score = 0.812 (P < 0.0001), 95% CI (0.77–0.85). In many cases, scintigraphy provides considerably more functioning and anatomic details than ultrasound. In conclusion, these findings bring forth practical aspects of thyroid scintigraphy utilization for hyperthyroidism. By combining functional and anatomical information in one step, scintigraphy provides non-invasive, simple, fast and cost effective hyperthyroidism diagnostic method and has the potential to replace TSH and ultrasonography in hyperthyroidism investigation.     

Expression of new human inorganic pyrophosphatase in thyroid diseases: its intimate association with hyperthyroidism

Inorganic pyrophosphatase (PPase) controls the level of inorganic pyrophosphate produced by biosynthesis of protein, RNA, and DNA. Thus, PPase is essential for life. PPase expression is unclear in the thyroid. We cloned a new human PPase, phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPPase), and established a rabbit polyclonal anti-LHPPase antibody. This is the first study to determine the PPase expression by immunohistochemistry and Western blot. Intranuclear LHPPase expression of thyrocytes was enhanced most prominently in Graves' disease and autonomously functional thyroid nodule. To estimate a regulating factor of subcellular localization of LHPPase, we examined its expression of Graves' disease-derived thyrocytes in vitro with the disease-originated serum. Nuclear expression of LHPPase was lost in cultured thyrocytes even with the serum, while its cytoplasmic expression was retained. The data suggest that increased expression of LHPPase is associated with hyperthyroidism. Intranuclear expression of LHPPase may not be regulated by Graves' disease-derived serum factors.     

两种甲状腺功能亢进症动物模型的对比研究

目的：复制两种甲状腺功能亢进症动物模型,对比研究它们成型性及可持续性的异同,为研究治疗甲亢的药物提供良好的评价载体。方法优甲乐模型：大鼠灌胃给予优甲乐50μg/100 g鼠重共21 d,于末次给药后第1、7、14天分别于眼底取血和接取尿液,检测相关指标;小肠结肠炎耶尔森氏菌模型：大鼠尾静脉注射小肠结肠炎耶尔森氏菌,于第0、5、10、15、20天共注射5次,并于末次注射后第5、15、25天大鼠眼底取血和接取尿液,检测相关指标。结果优甲乐模型：造模后T3、T4、FT3、FT4显著升高,但造模型后1周即恢复正常,尿液代谢的PCA图中显示模型组整体代谢网络偏离空白组,2周后恢复正常;小肠结肠炎耶尔森氏菌模型：造模后第15天和25天时T3和T4升高,第25天时TSH显著升高,尿液代谢的PCA图中模型组偏离空白组,而第15天和25天时未回到空白组位置。结论优甲乐甲亢模型成型性好但恢复迅速,作为药效评价时适合预防给药;而小肠结肠炎耶尔森氏菌甲亢模型成型性好并且持续性较好,作为药效评价时可采取治疗给药方式。     

Effect of hypo- and hyperthyroidism on the function and metabolism of macrophages in rats

The effect of thyroid hormones on monocyte migration, phagocytic capacity and hydrogen peroxide production by macrophages and the effect of these hormones on glutamine and glucose metabolism was investigated. The experiments were performed on resident, thioglycollate- and BCG-stimulated cells from hypo- and hyperthyroid rats. High plasma levels of thyroid hormones suppressed the migration of monocytes and hydrogen peroxide production, whereas hypothyuroidism did not affect cell migration but rasied the phagocytic capacity and the hydrogen peroxide production. Hyperthyroidism increased the activities of glutaminase and hexokinase and the rates of decarboxylation of [U-¹⁴C]-glutamine and [U-¹⁴C]-glucose in inflammatory and activated cells. Hypothyroidism stimulated glucose metabolism and had only a slight effect on glutaminolysis. The activity of the TCA cycle was, however, diminished in the presence of high plasma levels of thyroid hormones and enhanced by the hypothyroid state. These findings suggest that the functional changes observed are more likely to be related to the activity of the TCA cycle rather than to glutaminolysis and glycolysis.     

Pathway analysis of liver metabolism under stressed condition

Pathway analysis is a useful tool which reveals important metabolic network properties. However, the big challenge is to propose an objective function for estimating active pathways, which represent the actual state of network. In order to provide weight values for all possible pathways within the metabolic network, this study presents different approaches, considering the structural and physiological properties of the metabolic network, aiming at a unique decomposition of the flux vector into pathways. These methods were used to analyze the hepatic metabolism considering available data sets obtained from the perfused livers of fasted rats receiving burn injury. Utilizing unique decomposition techniques and different fluxes revealed that higher weights were always attributed to short pathways. Specific pathways, including pyruvate, glutamate and oxaloacetate pools, and urea production from arginine, were found to be important or essential in all methods and experimental conditions. Moreover the pathways, including serine production from glycine and conversion between acetoacetate and B—OH-butyrate, were assigned higher weights. Pathway analysis was also used to identify the main sources for the production of certain products in the hepatic metabolic network to gain a better understanding of the effects of burn injury on liver metabolism.     

Effect of experimental and cold exposure induced hyperthyroidism on H2O2 production and susceptibility to oxidative stress of rat liver mitochondria

To investigate the iodothyronine role in liver responses to cold, we examined metabolic and oxidative mitochondrial changes in cold-exposed, T3-treated, and T4-treated rats, which exhibit different T4 serum levels. All treatments increased mitochondrial respiration which reached the highest and lowest values after T3 and cold treatment, respectively. The T3- and T4-induced changes agreed with the respective increases in Complex IV activities, while those elicited by cold were inconsistent with increased activities of respiratory complexes. Mitochondrial capacity to produce H2O2 was the highest in T3-treated rats, whereas it was similar in T4-treated and cold-exposed rats. The effects of respiratory inhibitors suggested that T3 and T4 mainly increase the mitochondrial content of autoxidizable electron carrier of Complex I and Complex III, respectively. The indices of oxidative modifications of proteins exhibited increases consistent with the treatment effects on H2O2 production. The increases in indices of lipid peroxidation were also dependent on changes in lipid composition. The increased protein damage in treatment groups was confirmed using immunoblotting analysis, which also showed oxidative damage in a 133 kDa fraction, which was not expressed in T3-treated rats. Antioxidant levels were not related to the extent of oxidative damage as only mitochondrial GSH levels decreased in T3-treated rats. Mitochondrial susceptibility to in vitro oxidative challenge and Ca2+-induced swelling was increased by all treatments, but was the highest in T3-treated rats. In the whole, our results indicate T3 as main responsible for the changes in the mitochondrial population associated with cold exposure. However, a significant role is also played by T4, which appears to acts mainly modulating T3 effects, but also inducing some effects different from the T3 ones.     

Hepatoprotective effects of Arctium lappa Linne on liver injuries induced by chronic ethanol consumption and potentiated by carbon tetrachloride

Arctium lappa Linne (burdock) is a perennial herb which is popularly cultivated as a vegetable. In order to evaluate its hepatoprotective effects, a group of rats (n = 10) was fed a liquid ethanol diet (4 g of absolute ethanol/ 80 ml of liquid basal diet) for 28 days and another group (n = 10) received a single intraperitoneal injection of 0.5 ml/kg carbon tetrachloride (CCl(4)) in order to potentiate the liver damage on the 21st day (1 day before the beginning of A. lappa treatment). Control group rats were given a liquid basal diet which did not contain absolute ethanol. When 300 mg/kg A. lappa was administered orally 3 times per day in both the 1-day and 7-day treatment groups, some biochemical and histopathological parameters were significantly altered, both in the ethanol group and the groups receiving ethanol supplemented with CCl(4). A. lappa significantly improved various pathological and biochemical parameters which were worsened by ethanol plus CCl(4)-induced liver damage, such as the ethanol plus CCl(4)-induced decreases in total cytochrome P-450 content and NADPH-cytochrome c reductase activity, increases in serum triglyceride levels and lipid peroxidation (the deleterious peroxidative and toxic malondialdehyde metabolite may be produced in quantity) and elevation of serum transaminase levels. It could even restore the glutathione content and affect the histopathological lesions. These results tended to imply that the hepatotoxicity induced by ethanol and potentiated by CCl(4) could be alleviated with 1 and 7 days of A. lappa treatment. The hepatoprotective mechanism of A. lappa could be attributed, at least in part, to its antioxidative activity, which decreases the oxidative stress of hepatocytes, or to other unknown protective mechanism(s).     

肺炎克雷伯菌致肝脓肿侵袭综合征3例临床分析及文献复习

为提高对肺炎克雷伯菌感染所致肝脓肿侵袭综合征的临床表现及其危害的认识,回顾性分析3例确诊为肺炎克雷伯菌感染所致肝脓肿患者的临床经过、治疗反应及转归。结果发现3例患者均有肝外播散性病灶,符合肝脓肿侵袭综合征的临床特征。这3例患者为社区获得性感染,均有肝脓肿,其中2例合并眼内炎并造成失明,1例合并腰椎感染、腹主动脉感染及感染性心内膜炎。2例有糖尿病病史,1例免疫正常。结合文献复习,发现肺炎克雷伯菌感染引起肝脓肿及肝外播散性病灶,临床上称为肝脓肿侵袭综合征,大多由高毒力肺炎克雷伯菌引起,好发于糖尿病及免疫缺陷人群,也可发生于免疫正常人群,治疗困难,临床危害严重,需引起重视。     

Melatonin prevents oxidant damage in various tissues of rats with hyperthyroidism

Impairment of thyroid functions brings about pathological changes in different organs of body. Findings of in vivo and in vitro studies indicate that thyroid hormones have a considerable impact on oxidative stress. Melatonin reduces oxidative damage through its free radical eliminating and direct anti-oxidant effects. The present study was undertaken to determine how a 3-week period of intraperitoneal melatonin administration affected oxidative damage caused in experimental hyperthyroidism in rat. The experimental animals were divided into 3 groups (control, hyperthyroidism, hyperthyroidism+melatonin). Malondialdehyde (MDA) and glutathione (GSH) levels were determined in different tissues. MDA levels in cerebral, liver and cardiac tissues in hyperthyroidism group were significantly higher than those in control and hyperthyroidism+melatonin supplemented groups (p<0.001). The highest GSH levels were observed in the group that was administered melatonin in addition to having hyperthyroidism (p<0.001). These results show that hyperthyroidism increased oxidative damage in cerebral, hepatic and cardiac tissues of rat. Melatonin supplementation may also suppress oxidative damage.     

Involvement of JNK regulation in oxidative stress-mediated murine liver injury by microcystin-LR

Microcystin-LR (MC-LR) produced by cyanobacteria in diverse water systems is a potent specific hepatotoxin and has been documented to induce various liver diseases via oxidative stress. However, the underlying mechanisms are largely unknown. In the current study, we investigated the molecular events involved in the oxidative liver injury by MC-LR. Our results demonstrated that MC-LR induced liver injury in mice through a series of steps that began with the production of reactive oxygen species (ROS), which stimulated the sustained activation of JNK and its downstream targets, AP-1 and Bid. Furthermore, the mitochondrial proteomic analysis indicated that JNK activation affected some crucial enzymes of energy metabolism, led to mitochondria dysfunction, which contributed to hepatocyte apoptosis and oxidative liver injury by MC-LR. Our results reveal significant insights into the mechanisms of liver injury induced by microcystins, and serve as a framework for deciphering the role of JNK in oxidative stress-associated liver diseases. Yinna Wei and Dan Weng equally contributed to this work. D. Owen Young—An international exchange student from USA.