甲状腺功能亢进性心脏病临床特点及相关危险因素分析

目的:探讨甲状腺功能亢进性心脏病的临床特点及相关危险因素.方法:选取2008年9月至2011年9月收治112例甲状腺功能亢进患者为单纯甲亢组,另选取同期的甲状腺功能亢进性心脏病61例为甲心组.对两组患者性别、年龄、病程、FT3和FT4 进行比较,并采用Logistic回归方法对其危险因素进行分析.结果:①甲心组患者年龄较大,病程较长,FT3和FT4水平较高,与单纯甲亢组比较差异有统计学意义(P＜0.05).②经Logistic回归分析,患者的年龄大、病程长及FT4水平较高为甲状腺功能亢进性心脏病发生的危险因素.结论:对于年龄大、病程长、病情重的甲状腺功能亢进患者应予以充分重视,临床医生应予积极治疗,减少甲状腺功能亢进性心脏病的发病率和死亡率.     

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。     

拉米夫定辅助治疗肺结核合并乙型肝炎的临床观察

目的:探讨拉米夫定辅助治疗对肺结核合并乙型肝炎患者的肝功能的影响和安全性。方法:选择2009年1月至2013年6月在我科门诊就诊或住院的肺结核合并乙型肝炎患者84例,随机均分为对照组与观察组,对照组给予常规治疗措施,观察组在上述基础上加用拉米夫定治疗,检测和比较两组患者治疗前和治疗后6个月相关临床指标及不良反应的发生情况。结果:治疗前,两组患者的总胆红素(TBIL)、丙氨酸转氨酶(ALT)、谷草转氨酶(AST)和HBV-DNA定量结果比较,差异均无统计学意义(均P0.05);治疗6个月后,观察组以上指标均显著低于对照组,差异均具有统计学意义(均P0.05)。两组患者治疗过程中均出现恶心、腹胀、乏力、肝区不适与肝功能损害,观察组以上不良反应的发生率均显著低于对照组,差异具有统计学意义(均P0.05)。结论:在肺结核合并乙型肝炎患者的抗结核药物治疗过程中加用拉米夫定不仅可显著抑制患者肝功能的损害,且安全性性更高。     

SF方案治疗肝硬化的疗效观察

目的：观察SF方案对代偿性乙型肝炎肝硬化患者的治疗作用。方法：代偿性乙肝肝硬化患者63例,分为治疗组33例,对照组30例。治疗组采用SF方案进行治疗,对照组采用常规护肝疗法,疗程为9～12个月,定期监测肝功能指标变化。结果：SF方案对肝硬化有较好的疗效,一是肝脏炎症反应减轻,肝功能恢复,血清ALT、AST、TBiL经治疗后治疗组均显著低于治疗前和同期对照组;二是阻止肝纤维化进展,肝纤维化指标明显好转;三是免疫功能得以改善,外周血CD4／CD8淋巴细胞比值回升,补体C3水平上升;四是抗病毒效果显著,HBVDNA阴转率达54．5％。结论：SF方案有显著改善患者肝功能,恢复患者免疫功能,抑制病毒增殖的作用,可扩大样本量进一步研究。     

同型半胱氨酸及甲状腺功能在他汀致冠心病患者肝功能异常中的研究

目的:研究同型半胱氨酸及甲状腺功能与他汀致冠心病患者肝功能异常的相关性。方法:服用阿托伐他汀钙(20mg,1次/日)后1-3个月肝功能正常组(ALT和AST均正常者)300例;肝功能轻度异常组(ALT或/和AST升高3倍以下者)300例;肝功能重度异常组(ALT或/和AST升高3倍以上者)300例。在转氨酶重度升高组中选取停用他汀药观察组和加用CoQ10(20mg,3次/日)治疗组各100例,对比两组转氨酶下降情况。结果:PCI术后服用他汀类药物治疗1-3个月后出现肝功能异常的冠心病患者,同型半胱氨酸水平升高,甲状腺功能降低;肝功能的异常与年龄及饮酒有相关性。转氨酶重度升高患者中,加用CoQ10治疗组较仅停药组转氨酶显著下降。结论:阿托伐他汀钙引起的冠心病患者同型半胱氨酸水平升高及甲状腺功能下降与肝功能损伤有明显相关性。CoQ10可显著降低转氨酶水平。     

Ⅱ型糖尿病患者血糖对肝功能和血脂的影响及其意义

目的:探讨II型糖尿病患者血糖浓度对患者肝功能及血脂指标的影响及其意义。方法:选取某三级甲等医院内分泌科已确诊为II型糖尿病患者408例,根据空腹血糖浓度(FPG)分为三组:(A组,FPG8.0 mmol/L;B组,8.0≤FPG11.0 mmol/L;C组,FPG≥11 mmol/L),检测三组患者的肝功能指标及血脂指标,进而对其肝功能损害及血脂的异常情况进行分析,其数据结果应用统计学软件SPSS 17.0处理。结果:与A组及B组相比较,C组患者肝功能损伤更为严重,表现为:肝酶显著升高(P0.05);胆红素显著升高(P0.05);球蛋白显著升高(P0.05);总胆固醇、甘油三酯水平异常(P0.05)。其结果均有统计学意义。结论:II型糖尿病患者随着其血糖浓度升高可造成肝功能损伤及血脂异常,血糖监测及控制对糖尿病患者的身体健康状况具有重要意义。     

眼镜蛇咬伤患者早期肝肾功能、心肌酶的变化

目的观察眼镜蛇咬伤患者早期肝、肾功能及心肌酶的改变,以探讨其临床意义。方法对30例眼镜蛇咬伤患者入院时即抽取静脉血2.0 ml,分离血清,按常规方法行肝、肾功能及心肌酶的测定,并与健康体检者进行比较。结果与对照组比较,眼镜蛇咬伤患者早期肝功能及心肌酶指标显著升高(P0.05);肾功能检测结果差异无显著性(P0.05)。结论通过对眼镜蛇咬伤患者肝、肾功能及心肌酶的测定,了解患者肝脏、肾脏、心肌损害程度,对指导临床治疗具有一定意义。     

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。     

Serum digoxin in patients with thyroid disease.

Serum digoxin concentrations were measured by radioimmunoassay in 17 hyperthyroid and 16 hypothyroid patients after a seven-day course of oral digoxin. The significantly higher levels of serum digoxin in patients with hypothyroidism and lower levels in those with hyperthyroidism were closely related to the measured changes of glomerular filtration rate and digoxin serum half time in these two groups. Differences in serum digoxin concentration contribute to the altered sensitivity to digoxin shown by patients with thyroid disease.     

Influence of hyper‐ and hypothyroidism on lipid peroxidation,unsaturation of phospholipids,glutathione system and oxidative damage to nuclear and mitochondrial DNA in mice skeletal muscle

While the biochemical literature on free radical metabolism is extensive, there is little information on the endocrine control of tissue oxidative stress, and in the case of thyroid hormones it is mainly limited to liver tissue and to short-term effects on a few selected biochemical parameters. In this investigation, chronic hypothyroidism and hyperthyroidism were successfully induced in mice, and various oxidative-stress-related parameters were studied in skeletal muscle. In vivo and in vitro lipid peroxidation significantly increased in hyperthyroidism and did not change in the hypothyroid state. The fatty acid composition of the major phospholipid classes was affected by thyroid hormones, leading to a significant decrease in total fatty acid unsaturation both in hypothyroid and hyperthyroid muscle in phosphatidylcholine and phosphatidylethanolamine fractions. In cardiolipin, however, the double bond content significantly increased as a function of thyroid status, leading to a 2.7 fold increase in the peroxidizability index from euthyroid to hyperthyroid muscle. Cardiolipin content was also directly and significantly related to thyroid state across the three groups. Glutathione system was not modified by thyroid state. The oxidative damage marker 8-oxo-7,8-dihydro-2'-deoxyguanosine did not change in mitochondrial DNA, and decreased in genomic DNA both in hypothyroid and hyperthyroid muscle. The results indicate that chronic alterations in thyroid status specially affect oxidative damage to lipids in skeletal muscle, with a probably stronger effect on mitochondrial membranes, whereas the cytosolic redox potential and DNA are better protected possibly due to homeostatic compensatory reactions on the long-term.     

新疆地区少数民族与汉族甲状腺疾病患者的临床特征比较

目的：比较新疆地区少数民族与汉族甲状腺疾病的患病情况和临床类型特点。方法：选择本院2009 年1月至2011 年12 月收治的312 例被确诊为甲状腺疾病的患者,统计分析其临床资料如民族、年龄、性别、病程间的分布。结果：新疆地区少数民族和汉族8 种常见甲状腺疾病如甲状腺瘤、甲亢、单纯性甲状腺肿、亚急性甲状腺炎、桥本氏病、毒性甲亢、甲减和结节性甲状腺肿的发病率比较均无统计学差异（P〉0.05）。少数民族和汉族男性和女性间常见甲状腺疾病的发病率比较均无显著性差异（P〉0.05）,但少数民族男女性患者和汉族男女性间常见甲状腺疾病的发病率比较的差异均有统计学意义（P〈0.05）。少数民族与汉族甲状腺功能减退症患者的发病年龄、病程以及居住地分布均无显著性差异（P〉0.05）。结论：新疆地区各少数民族几种常见甲状腺疾病发病情况与汉族比较无显著性差异。     

Effect of disorders of thyroid function on phenazone pharmacokinetics

Phenazone elimination test, as a marker of metabolic efficiency of the liver, was carried out in 11 hypothyroid patients. 20 hyperthyroid patients, 10 persons after hyperthyroidism treatment and in 20 healthy persons as a control group. In hyperthyroid patients the acceleration, and in hypothyroid patients the delay of phenazone elimination, in comparison with a control group was observed. Moreover, the impairment of phenazone gastrointestinal absorption was shown in hypothyroid patients and in persons after hyperthyroidism treatment. Similar alterations may be expected in persons with thyroid dysfunctions to whom the drugs with pharmacokinetic properties similar to phenazone are administered.     

Plasma atrial natriuretic peptide, plasma renin activity and aldosterone during treatment of hyperthyroidism due to Graves' disease

Plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA) and aldosterone were consecutively measured during methimazole treatment in patients with hyperthyroidism due to Graves' disease. ANP values of untreated hyperthyroid patients varied greatly from patient to patient, but decreased progressively with a decrease of serum thyroid hormone concentration during methimazole treatment. PRA was elevated in hyperthyroid patients but less aldosterone was secreted as evidenced by lower aldosterone/PRA ratio in these patients than in normal subjects and in hypertensive patients treated with thiazide. In addition, aldosterone/PRA ratio increased progressively with a decrease of ANP during methimazole treatment. The data indicated that ANP secretion was increased and ANP thus secreted depressed aldosterone secretion in hyperthyroid patients. Propranolol depressed pulse rate but failed to affect ANP secretion. It is suggested that thyroid hormone specifically acts on myocytes to stimulate ANP secretion but physiologic significance of such increased ANP secretion remains to be solved.     

Serum and tissue coenzyme Q9 in rats with thyroid dysfunctions

Serum and tissue CoQ9 levels were determined in hypothyroid, euthyroid and hyperthyroid rats. A significant negative correlation was demonstrated between serum FT4 or T3 and CoQ9 in rats with various states of thyroid functions. Liver CoQ9 was significantly increased in rats rendered mildly hyperthyroid. There was a significant positive correlation between serum FT4 or T3 and liver CoQ9. While liver CoQ9 did not significantly change in severely hyperthyroid animals, liver mitochondrial CoQ9 showed a significant positive correlation with serum T3. Kidney and heart CoQ9 levels did not significantly change in hyperthyroid rats, but those in hypothyroid rats showed a tendency to increase. It was suggested that the synthesis of CoQ9 was increased in the liver in hyperthyroidism.     

Factors predicting the course of diabetes mellitus in hyperthyroid patients

The relationship between changes in glucose tolerance with treatment of hyperthyroidism and various factors that might be relevant to carbohydrate metabolism were investigated in 64 hyperthyroid patients with abnormal glucose tolerance, including 35 cases with fasting plasma glucose (FPG) levels of 140 mg/dl or more. All patients had diffuse toxic goiter. After correction of the hyperthyroidism, glucose intolerance improved in almost all cases, even in cases with fasting hyperglycemia, but diabetes mellitus in patients with FPG above 140 mg/dl and/or delta IRI/delta PG X 30' during a 50-g oral glucose tolerance test below 0.10, persisted. Patients who showed diabetic glucose tolerance even after remission from thyroid dysfunction had significantly lower delta IRI/delta PG X 30' values and a higher incidence of family histories of diabetes mellitus than those not showing diabetic glucose tolerance. There were no significant differences in serum T3 and T4 levels between these two groups of patients. The findings suggest that predisposition to diabetes may be an important factor in persistent glucose intolerance in the hyperthyroidism of Graves' disease. The FPG and delta IRI/delta PG X 30' values may be useful in predicting which patients with hyperthyroidism will have permanent diabetes.     

Cardiovascular events in thyroid disease: a population based, prospective study

No consensus exists whether subclinical thyroid disease should be treated or just observed. Untreated overt thyroid disease is associated with increased risk of cardiovascular disease, and this study was conducted to assess the risk of cardiovascular events in subclinical thyroid disease. The population-based prospective study was conducted in Denmark. A total of 609 subjects from general practice aged 50 years or above with normal left ventricular function were examined. During a median of 5 years of follow-up, major cardiovascular events were documented. In subjects with abnormal TSH at baseline, information about potential thyroid treatment during follow-up was obtained from case reports and mailings. At baseline, 549 (90.7%) were euthyroid (TSH 0.40-4.00?mU/l), 31 (5.1%) were subclinical hypothyroid (TSH>4.00?mU/l), and 25 (4.1%) were subclinical hyperthyroid (TSH<0.40?mU/l). 1 overt hyperthyroid and 3 overt hypothyroid participants were excluded from the analyses. At baseline, the levels of NT-proBNP were inversely associated with the levels of TSH; the lower the levels of TSH, the higher the NT-proBNP concentration. During follow-up, 88 participants died, 81 had a major cardiovascular event, and 28 had a stroke. The incidence of stroke was increased among subjects with subclinical hyperthyroidism, HR 3.39 (95% CI 1.15-10.00, p=0.027) after adjusting for sex, age, and atrial fibrillation. Subclinical hypothyroidism was not related with any of the outcome measurements. Subclinical hyperthyroidism seems to be a risk factor of developing major cardiovascular events, especially stroke in older adults from the general population with normal left ventricular function.     

Raised plasma glutathione S-transferase values in hyperthyroidism and in hypothyroid patients receiving thyroxine replacement: evidence for hepatic damage.

Using plasma glutathione S-transferase measurements hepatocellular integrity was assessed in groups of hyperthyroid and hypothyroid patients before and after treatment. Ten of 14 hyperthyroid patients had clearly raised plasma glutathione S-transferase values at presentation and in each patient treatment with either iodine-131 or carbimazole resulted in a significant fall in glutathione S-transferase. The eight hypothyroid patients had normal glutathione S-transferase values at presentation and all showed a significant increase in these after thyroxine replacement therapy. In three of these patients in whom standard doses of replacement therapy were associated with a raised free thyroxine (T4) concentration but normal total and free triiodothyronine (T3) values glutathione S-transferase was increased. Similar though less consistent changes were seen in the results of standard chemical tests of liver function. It is concluded that hyperthyroidism may produce subclinical liver damage in a high proportion of patients and that this resolves with effective treatment. More important, the data suggest that hypothyroid patients receiving thyroxine replacement therapy may have similar subclinical liver damage. Patients receiving thyroxine should be monitored by the measurement of free, not total hormone concentrations, and in those in whom free T4 is raised the dose of thyroxine should be reduced. It would also be expedient to include periodic biochemical assessment of liver function in patients receiving thyroxine.