甲状腺机能亢进症合并病毒性肝炎40例回顾性分析

目的 探讨甲状腺机能亢进症(甲亢)合并病毒性肝炎的临床特征及预后。方法 对40例甲亢合并病毒性肝炎病人的临床资料进行回顾性综合分析。结果 85％病人血清总胆红素(SB)升高,SB平均值为454.9±293.2μmol/L重型肝炎发生率为32.5％;病人肝病病情与甲亢病程长短和病情轻重并无显著性差异(P>0.05),但病前使用抗甲状腺药物者SB显著高于未使用抗甲状腺药物者(P<0.01);在综合护肝治疗同时加用小至中等剂量抗甲状腺药治疗后,82.5％病例肝功能恢复、甲亢症状控制。结论 甲亢合并病毒性肝炎黄疸程度深,重型肝炎发生率高,但肝病病情轻重与甲亢病程和病情无显著差异,在加强护肝治疗的基础上同时使用小至中等剂量抗甲状腺药物治疗,可使大部分病例病情恢复。     

53例甲状腺功能亢进症并发肝脏损害临床分析

甲状腺功能亢进症 (以下简称甲亢 )系甲状腺激素分泌过多而引起的一种常见的内分泌疾病。甲状腺激素和肝脏有密切关系 ,在甲亢时可并发各种肝脏损害 ,现将我院 1997年 6月～ 2 0 0 1年 6月的 4年间以肝炎收住入院同时伴有甲亢的 5 3例患者临床资料加以总结 ,对其临床特点做一分析。临床资料一、一般资料5 3例均为住院患者。男 2 9例 ,女 2 4例 ,年龄 2 4～ 65岁 ,平均 42岁。甲亢合并病毒性肝炎 3 8例 ,其中急性肝炎 2 3例 ,慢性肝炎 4例 ,重型肝炎 11例 ;甲亢性肝病 9例 ;抗甲亢药物性肝损害 6例。二、诊断标准(一 )甲亢并发病毒性肝炎　①…     

甲亢131碘治疗剂量修正的探讨

^131碘治疗甲亢，是有效的甲亢治疗方法之一，由于碘盐的普及应用，且甲状腺与碘代谢密切相关，直接关系到^131碘治疗甲亢的剂量及疗效。因此，我们对近10年来1080例甲亢^131碘治疗病人与10年前治疗的620例病人进行回顾性对比分析，探讨碘盐普及后^131碘治疗甲亢对^131碘治疗剂量的影响，以便获得更佳的治疗效果。     

血浆置换治疗甲状腺功能亢进合并戊型病毒性肝炎三例临床分析

甲状腺功能亢进症(简称甲亢)患者较多合并肝损害,包括甲亢性肝损害、病毒性肝损害、药物性肝损害及非酒精性脂肪性肝炎等,症状多较严重,治疗棘手.在其合并病毒性肝损害中,以合并戊型病毒性肝炎(简称戊肝)多见.当甲亢合并严重肝损害时,抗甲状腺药物、手术及131I治疗均有一定的局限性,而血液净化已在治疗中显示一定的价值[1].现对我院2000～2011年收治的12例甲亢合并戊型肝炎患者的临床资料进行回顾性分析,总结其中2例合并重型肝炎及1例胆汁淤积严重患者采用血浆置换治疗的临床疗效.     

甲状腺机能亢进合并病毒性肝炎16例临床分析

我们从1997～2001年共收治甲状腺机能亢进(简称甲亢)合并病毒性肝炎患者16例,现将治疗情况报告如下。 1 临床资料 1.1 一般资料 16例均为1997～2001年收治的甲亢合并病毒性肝炎患者,其中男10例,年龄30～45岁,女6例,年龄30～50岁;先有甲亢病史为1～2年,均未服用抗甲状腺药物,后合并甲型病毒性肝炎7例,合并乙型病毒性肝炎9例;急性黄疽型肝炎11例,亚急性重型肝炎5例。     

131碘治疗甲亢二次治疗的原因分析

131^碘治疗甲亢安全、简便、快捷、一次治愈率高，复发率低，已被国内外广泛接受，逐渐成为甲亢治疗的首选方法。我所80年代初开展^131碘治疗甲亢，20年来在实践中不断总结经验，提高诊疗水平，完善治疗方案，一次治愈率不断提高，得到越来越多患者和同行的认可和好评。但仍有一部分患者一次治疗不能完全缓解，需要二次治疗。作者对2001～2002年1409例^131碘治疗病例进行随访和回顾性分析，以期找出二次治疗     

小剂量131碘合并长程抗甲状腺药物治疗甲状腺机能亢进症

放射性碘治疗甲状腺机能亢进症(以下简称甲亢)已有20多年。其缺点为继发性甲状腺机能减退症的发生率在治疗后逐年增高。本文报告自1962年起采用较小剂量放射性碘合并长程抗甲状腺药物治疗165例甲亢的结果。女病人129例(77％),男病人36例(23％)。年龄16～77岁。其中31例在应用抗甲状腺药物1～2年失效后采用本法治疗,134例由于病情较重和年龄较大而用本法治疗。 ~(131)碘剂量:根据有无甲状腺肿、甲状腺最高吸~(131)碘率及病情严重度而定。采用一次剂量者121例(73.4％),余44例(26.6％)采用数次剂量。采用一次~(131)碘治疗的121例中,2～4毫居里39例,5～6毫居里55例,6.5～10毫居里27例。抗甲状腺药物的应用:给予放射性碘48小时后服用抗甲状腺药物,第一个月每日丙基硫脲嘧啶225     

131碘治疗甲状腺功能亢进275例效果观察

甲状腺功能亢进(甲亢)是由于某种原因使机体甲状腺激素分泌增多引起代谢增高，各个系统和组织功能高亢及免疫功能紊乱的综合性症状。目前治疗甲亢的方法主要有放射性^131碘治疗、抗甲状腺药物和外科手术治疗等，其中^131碘治疗以其疗效好、复发低等优点被越来越多的临床医生接受。现将河南省卫生防疫站地病科门诊近两年用     

无机碘对碘~(131)治疗甲亢后的近期作用

甲亢在用碘~(131)治疗后有时加重,一般认为是因为甲状腺放射性坏死因而放出激素的缘故。而无机碘是一种快速但短暂的抗甲状腺药。本文就研究碘~(131)治疗甲亢后立即加用无机碘是否有效的问题。作者对17例甲亢患者在碘~(131)治疗后每天测血清T_3和T_4共9～14天。其中9例在用碘~(131)治疗后48小时开始服碘化钾,每日150毫克;其余8例不加碘化钾。不加碘化钾的     

影响^131I治疗甲亢伴糖尿病疗效因素分析

对72例甲亢伴糖尿病患者,分为：甲亢合并1型DM14例、甲亢合并2型DM46例、甲亢继发DM12例三组;甲亢采用放射性131碘治疗。结果痊愈率30.4%（26/72）,好转率48.6%（35/72）,总有效率84.9%。结论影响疗效的因素不仅与病程、合并症有关,还有①个体对^131I治疗的敏感性与剂量;②糖尿病的疗效;③TPOAb、TRAb可作为判断愈后的参考指标。     

131I治疗非毒性甲状腺肿的临床评价

目的 对^131I治疗非毒性甲状腺肿(NTG)进行临床评价。方法 对35例经临床确诊的NTG患者，采用^131I治疗，随访1年以上，观察临床疗效及近期副作用。结果 35例NTG患者，治愈14例，有效19例，无效2例，甲低15例；治愈率和总有效率分别为40％和94．3％，甲低发生率为42．9％；治疗1年后甲状腺平均缩小60．2％。治疗后除部分患者出现一过性的颈部肿胀及甲亢表现外，未见其他明显的近期不良反应。结论 ^131I治疗NTG疗效肯定、简便、相对安全。对甲状腺肿大明显，甲状腺制剂治疗无效，且不愿接受手术的NTG患者，^131I治疗是值得推荐的方法。     

重型肝炎患者血清sCR1与肝功能损伤程度的相关性研究

研究重型肝炎患者血清sCR1浓度的变化 ,探讨其临床意义。采用酶联免疫吸附法 ,对 3 0例重型肝炎、46例慢性病毒性肝炎及 3 0例正常人群红细胞研究表明 ,重型肝炎及慢性病毒性肝炎患者血清sCR1浓度均高于正常对照人群 (P <0 0 1) ,但重型肝炎患者血清sCR1浓度升高的幅度明显大于慢性病毒性肝炎患者 (P <0 0 1) ,并与CHE、PT及PTA的变化明显相关。重型肝炎患者血清sCR1浓度的变化与肝功能损伤程度密切相关 ,该指标可作为分析重型肝炎患者病情严重程度、判断病情发展及预后的重要参考指标     

ACUTE EFFECT OF INORGANIC IODIDE AFTER 131I THERAPY FOR HYPERTHYROIDISM

Patients treated with inorganic iodide weeks to years following ¹³¹I therapy for hyperthyroidism do not adapt to its antithyroid effect. To determine whether such adaptation occurs soon after ¹³¹I therapy, serum thyroxine (T4) and triiodothyronine (T3) concentrations were measured daily for 9-14 days following ¹³¹I therapy in seventeen hyperthyroid patients. Nine patients received 150 mg KI daily starting 48 h after ¹³¹I administration; eight received only ¹³¹I. Serum T4 and T3 concentrations did not change significantly in the patients who received only ¹³¹I. In the patients who received ¹³¹I and KI, serum T4 and T3 concentrations fell promptly, reaching nadir values 2-10 days after initiation of iodide, and then increased despite continuation of KI therapy. The mean maximal fall in serum T4 was 34% and in serum T3 42%. These results show that ‘escape’ from the acute antithyroid effect of iodide occurs when it is given immediately after ¹³¹I therapy, thus limiting the utility of iodide as a therapeutic agent at this time. ¹³¹I-iodide is a widely used and effective form of therapy for hyperthyroidism. Reduction in thyroid hormone does not occur within the first weeks after ¹³¹I therapy. Exacerbation of hyperthyroidism may occur shortly after ¹³¹I administration, with frequency ranging from 0 to 11% in several large species (Chapman et al., 1954; Cassidy & Astwood, 1959; Lamberg et al., 1959; Green & Wilson, 1964). Such exacerbations are thought to reflect acute thyroid radiation necrosis and subsequent hormone release, and may limit the use of ¹³¹I therapeutically. Inorganic iodide is a rapidly, but usually transiently, effective antithyroid agent when used alone. No reports are available concerning the efficacy of iodide when given immediately following ¹³¹I therapy. Since some hormone release after ¹³¹I therapy may reflect thyroid destruction, rather than secretion, it is possible iodide might be less effective in this setting. On the other hand, if iodine is effective immediately after ¹³¹I therapy, especially if its action is sustained (as occurs in patients treated with ¹³¹I months or years previously; Hagen et al., 1967; Braverman et al., 1969), it might be a useful adjunct for certain hyperthyroid patients treated with ¹³¹I. This report describes the result of a study of patients so treated.     

Clinical and biochemical changes following 131I therapy for hyperthyroidism in patients not pretreated with antithyroid drugs

BACKGROUND: Radioiodine therapy (131I) for the treatment of hyperthyroidism has been shown to be effective and safe. Despite the extensive experience with radioiodine therapy, the necessity for pretreatment with antithyroid drugs is controversial. Pretreatment is partly based on the concept that antithyroid drugs deplete the thyroidal hormonal stores, thereby reducing the risk of a radioiodine-induced aggravation of hyperthyroidism or thyroid storm. Few data are available on the frequency of clinically significant exacerbations of hyperthyroidism following 131I therapy without prior treatment with antithyroid drugs. The aim of the present study was to determine prospectively the early clinical and biochemical changes after 131I therapy in patients who were not pretreated with antithyroid drugs. METHODS: Patients with Graves' disease (n = 21), toxic multinodular goiter (n = 11) or toxic adenoma (n = 2) were studied before and after 131I therapy. Clinical and biochemical parameters of thyroid function were investigated before and 1, 2, 8, 11, 18 and 25 days after 131I treatment. Patients were given no antithyroid drugs prior to 131I therapy, all patients received beta-blocking agents for symptomatic relief. RESULTS: In 19 of 34 patients, a transient increase in thyroid hormone levels was observed, predominantly in the first week following 131I therapy. None of these patients experienced worsening of thyrotoxic symptoms. This transient increase in thyroid hormone levels was demonstrated in all patients with toxic multinodular goiter, whereas it was found in only six of 21 patients with Graves' disease. This difference could not readily be explained by differences in pretreatment thyroid hormone levels, administered dose or effectively absorbed dose of 131I. CONCLUSIONS: 131I treatment of hyperthyroidism without pretreatment with antithyroid drugs may cause a transient increase in thyroid hormone levels. Clinically significant exacerbations of hyperthyroidism were, however, not observed in our study population. Increased hormone levels following 131I therapy were more often seen in patients with toxic multinodular goiter than in patients with Graves' disease.     

Serum Iron Levels and Hepatic Iron Overload in Nonalcoholic Steatohepatitis and Chronic Viral Hepatitis

Our objective was to determine the effect of serum iron levels and hepatic iron overload on hepatocellular damage in nonalcoholic steatohepatitis (NASH) and to compare this with chronic viral hepatitis. Twenty-five patients who had elevated transaminase levels on at least two occasions, without any evidence of viral and autoimmune hepatitis and diabetes, without a history of significant alcohol use, and with a liver biopsy consistent with NASH were enrolled in the study. Twenty-five patients with chronic viral hepatitis (13 patients with chronic hepatitis C and 12 with chronic hepatitis B) who were not under any antiviral treatment were taken as controls. Metabolic factors were studied in the NASH and chronic hepatitis groups. Biopsy specimens were stained with hematoxylin–eosin, and the grade of steatosis and the stage of fibrosis were evaluated as I, II, or III, I being mild and III being severe. Iron overload in the hepatic tissue was studied by Prussian blue staining. Serum ALT, AST, ALP, GGT, globulin, and ferritin levels were comparable in both steatohepatitis and chronic viral hepatitis groups. However, patients with chronic hepatitis had a lower albumin level and a higher serum iron level, with higher transferrin saturation. Among patients with NASH, mild, moderate, and severe steatosis was found in 7, 10, and 8 patients, respectively. Inflammatory infiltration was grade I in 24 patients and grade III in 1 patient. Fibrosis was mild in 12 patients and 13 patients had no fibrosis. Among patients with chronic viral hepatitis, inflammatory infiltration of grade I was seen in 11 patients, grade II in 11 patients, and grade III in 3 patients. Fibrosis was mild in 9 patients, moderate in 13 patients, and severe in 2 patients; 1 patient had no fibrosis. Compared to patients with NASH, those with chronic viral hepatitis cases had more severe inflammatory infiltration and fibrosis (P < 0.01). While five patients with chronic viral hepatitis had mild iron overload, patients with NASH had no hepatic paranchymal iron overload. Neither NASH nor chronic viral hepatitis revealed a relationship between hepatic iron overload and disease activity. This suggests that the iron overload actually may be a result of hemachromatosis gene mutation. The absence of hepatic parenchymal iron overload in the NASH group and only mild iron accumulation in the chronic hepatitis group may be explained by a lower frequency of the gene mutation in our country.     

人工肝结合~(131)I治疗与内科常规治疗40例甲亢合并重症肝损害疗效的比较

目的:对人工肝结合131I治疗与内科常规治疗甲状腺功能亢进(甲亢)合并重症肝损害患者的临床疗效进行比较.方法:对近6年来我院40例甲亢合并重症肝损害患者的临床表现、实验室检查、治疗方式及预后进行回顾性分析,比较采用人工肝[方式有分子吸附再循环系统(molecula radsorbent recirculating system,MARS)、血浆置换]结合131I与内科常规治疗的疗效和预后.结果:人工肝组有25例患者,20例好转,5例病情恶化,内科常规治疗组共15例患者,6例好转,9例恶化,人工肝组好转率(80%)明显高于内科常规治疗组(40%),人工肝治疗能显著改善患者肝功能、甲状腺功能指标,缩短凝血酶原时间,提高治愈率.结论:甲亢合并重症肝损害病情复杂,治疗棘手,根据病情需要行人工肝治疗,在肝功能改善后行131I能明显改善预后,提高生存率,降低病死率.     

Interferon beta 1a-induced severe autoimmune hepatitis in patients with multiple sclerosis: report of two cases and review of the literature

Type I interferons are potent cytokines that possess antiviral, immunomodulating and antiproliferative actions. The development of autoimmune hepatitis is a well recognized complication of treatment with alpha IFN in patients with chronic viral hepatitis. Yet, the occurrence in patients under treatment with beta IFN for other indications is controversial and its occurrence often underestimated. We report two cases of severe acute autoimmune hepatitis in two patients undergoing therapy with IFN beta 1a for multiple sclerosis who recovered under early immunosuppressive therapy.     

Methimazole, but not betamethasone, prevents 131I treatment-induced rises in thyrotropin receptor autoantibodies in hyperthyroid Graves' disease

The effects of methimazole or betamethasone therapy on the TSH receptor antibody response to radioiodine therapy were compared in a prospective randomized study of 60 patients with hyperthyroidism due to Graves' disease. The patients were followed for 1 yr after treatment with 131I. Twenty-three patients received 131I alone, 17 were treated with methimazole for 2 months before and 3 months after 131I therapy, and 20 patients were treated with betamethasone for 3 weeks before and 4 weeks after 131I therapy. 131I induced a transient rise in the mean serum level of TSH receptor autoantibodies, measured as TSH binding inhibitory immunoglobulin (TBII), but in patients receiving methimazole treatment, no such rise occurred. In the betamethasone-treated patients, TBII increased similarly to that in patients treated with 131I alone. In addition, in patients given betamethasone, there was an early decrease in total serum immunoglobulin G, which persisted throughout the follow-up period. In the other 2 groups, no changes in total immunoglobulin G were found. The results demonstrate that in hyperthyroid Graves' disease, TBII production is influenced by therapy. Methimazole abolished the 131I-induced increase in TBII, whereas betamethasone did not have such an inhibitory effect.     

小剂量~(131)碘治疗儿童Graves病42例疗效观察

目的　探讨小剂量 1 31 碘 (1 31 I)治疗儿童 Graves病的疗效。方法　 1 31 I剂量降至常规计算用量的 1/2～ 2 /3,1次顿服 ,3个月为 1个疗程 ,进行疗效复查 ,总剂量 37～ 185 MBq。结果　 4 2例患儿中 ,痊愈 38例 ,治愈率为 90 .5 % ;显效 2例 ,占 4 .8% ;无效 1例 ,占 2 .4 % ;1例出现早发甲状腺功能低下 (甲低 ) ,经治疗后恢复。治愈总疗程 1～ 3个 ,时间 3～ 9个月。痊愈病例中 ,服药 1个疗程治愈 17人 (44 .8% ) ,2个疗程治愈 16人 (42 .1% ) ,3个疗程治愈 5人 (13.1% ) ,观察 3～ 5年 ,38例治愈患者中未出现甲状腺功能亢进症复发或晚发甲低。结论　小剂量 1 31 I是治疗儿童 Graves病安全、有效的方法。     

干扰素治疗慢性丙型肝炎发生甲状腺功能异常的分析

目的：探讨干扰素治疗慢性丙型肝炎患者后发生甲状腺功能异常的情况及相关因素的分析。方法回顾性分析206例慢性丙型肝炎患者,观察89例干扰素治疗前和117例治疗后甲状腺功能的异常情况及其影响因素,Logistic分析发生甲状腺功能异常的危险因素。结果干扰素治疗前的89例患者中,有23例合并甲状腺功能异常,其中甲状腺功能减退症7例,甲状腺功能亢进症2例,亚临床甲状腺功能减退症14例;干扰素治疗后的117例患者中,有17例发生甲状腺功能异常,其中甲状腺功能减退4例,为桥本甲状腺炎2例和非自身免疫性甲状腺功能减退2例;甲状腺功能亢进1例;亚临床甲状腺功能减退症12例。多元Logistic回归分析显示,女性（OR＝5．828）、体内预存抗甲状腺自身抗体（OR＝35．393）是慢性丙型肝炎患者使用干扰素治疗后诱发甲状腺疾病的独立危险因素。结论干扰素治疗慢性丙型肝炎可导致甲状腺功能异常的发生;对体内预存大量抗甲状腺过氧化物酶抗体的女性,要监测甲状腺功能,定期复查。