甲状腺功能亢进伴发轻度肝功能损害患者的131碘治疗

对 42例甲状腺功能亢进症 (甲亢 )伴发肝功能损害患者口服13 1I治疗并随访 6个月 ,观察治疗前后的肝功能变化 ,证实对这类患者13 1I治疗甲亢是安全和有效的。     

甲巯咪唑治疗甲状腺功能亢进致肝功能损害四例分析

甲巯咪唑是一种临床常用的抗甲状腺药物，其药理作用主要是抑制甲状腺内碘的有机化过程，使酪氨酸碘化和偶联发生障碍，从而抑制甲状腺素的生成。常见的不良反应有粒细胞减少、皮疹和肝功能损害。国内、外关于甲巯咪唑不良反应的新近文献不多。我们于2005年11月至2006年8月收治4例因服用甲巯咪唑导致严重肝功能损害的甲状腺功能亢进（甲亢）患者，现报道如下。     

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     

甲状腺功能亢进致肝功能损害46例临床分析

目的分析甲状腺功能亢进（甲亢）所致肝损害的特点和分布。方法对46例初诊甲状腺功能亢进患者在治疗各阶段进行甲状腺功能、肝功能等检查，并进行对照、分析。结果甲亢患者较正常对照组肝功能异常有显著性差异（P〈0.01），且以Gravers病人为著。积极治疗后肝功能异常能够恢复。结论甲亢患者常伴有肝功能损害．早期检查有助于鉴别是否甲亢药物所致肝损害，积极的抗甲亢及护肝治疗可使肝功能恢复正常。     

甲状腺功能亢进并肝功能损害54例报告

2002年5月～2003年5月,我们对99例初发甲状腺功能亢进症（甲亢）患者的肝功能损害情况进行了观察,现将结果报告如下。     

甲状腺功能亢进合并肝损害临床治疗研究进展

甲状腺功能亢进（hyperthyroidism），简称“甲亢”，是内分泌系统的多发病、常见病，可累及全身多个器官，以心血管系统及神经系统多见，但亦可累及肝脏，引起肝功能异常、肝肿大，甚至发生黄疸、肝硬化等，统称为甲亢合并肝损害。甲状腺功能亢进合并肝损害的发生率国内外文献报道不一，约45％～90％，国外曾报道甲亢死亡病例尸检的资料发现90％的患者合并有肝脏损害，20％的患者伴有黄疸。近年来，甲亢合并肝损害也引起广泛重视，其相关报道也较多，     

甲状腺功能亢进致肝损害

甲状腺功能亢进致肝损害在临床上较为多见,但大多数表现为非特异性损害,容易误诊。本文从临床表现、肝脏病理改变、发病机制、鉴别诊断、治疗措施等方面总结了甲状腺功能亢进致肝损害的研究概况,为临床有效治疗提供参考。     

碘131对老年甲状腺功能亢进患者甲状腺功能及骨密度的影响

目的 分析碘131对老年甲状腺功能亢进(甲亢)患者甲状腺功能及骨密度影响。方法 选取100例老年甲亢患者根据治疗方法均分为两组,基础组给予甲巯咪唑治疗,观察组在基础组基础上联合碘131治疗,对比两组临床疗效、甲状腺功能、骨代谢指标水平及骨密度。结果 观察组临床总有效率明显高于基础组(P<0.05)。两组治疗前甲状腺激素(TSH)、游离甲状腺素(FT4)、游离三碘甲状腺原氨酸(FT3)、β-胶原蛋白(β-CTx)、Ⅰ型前胶原N端肽(PⅠNP)水平及桡骨、腰椎2～3、髋骨骨密度差异均无统计学意义(均P>0.05);治疗后,两组上述指标均较治疗前明显改善,且观察组改善程度明显优于基础组(均P<0.05)。结论 碘131可有效纠正老年甲亢患者甲状腺激素代谢紊乱,缓解突眼等症状,抑制骨代谢,提高骨密度,临床疗效显著。     

非手术与手术治疗肝硬化并脾功能亢进患者肝功能损害的对比观察

目的对比观察非手术与手术治疗肝硬化并脾功能亢进患者肝功能损害的临床疗效和安全性。方法将58例肝硬化并脾功能亢进患者分为非手术组（34例）和手术组（24例）。并对两组患者治疗前后临床表现、肝功能[丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、总胆红素（TBil）、直接胆红素（DBil）]和不良反应进行比较,探讨非手术与手术治疗肝硬化脾功能亢进患者肝功能损害的疗效和安全性。结果两组治疗后1周和2周时,ALT和AST均显著降低（P〈0．01,P〈0．05）;与非手术组比较,手术组治疗后1周和2周时,ALT、AST降低显著优于非手术组（P〈0．01,P〈0．05）。两种治疗方法均能改善患者的临床症状,缓解并发症,且手术治疗较非手术治疗不良反应少。结论手术和非手术治疗均能显著改善肝硬化并脾功能亢进患者肝功能损害,且手术治疗改善肝功能疗效显著,不良反应较少,安全性较好。     

甲状腺功能亢进合并肝脏损害46例临床分析

甲状腺功能亢进症（简称甲亢）是内分泌系统的常见病、多发病，常累及全身多个器官。最多见的是对心血管和神经系统的损害。但在临床工作中也不乏甲亢性肝损害，表现为肝肿大、肝功能异常等，严重者甚至发生黄疽及肝硬化。本文对1995年1月～2004年12月间收治的甲亢性肝损害46例临床资料进行分析，现报告如下。     

Thyroid uptake of liquid versus capsule 131I tracers in hyperthyroid patients treated with liquid 131I.

The amount of 131I used to treat hyperthyroid patients is based in part on the 24-hour thyroid uptake of a diagnostic amount of radioiodine (tracer). We compared the 24-hour uptake of an 131I tracer administered in liquid or capsule form to the 24-hour uptake of 131I therapy administered as liquid. Sixty-five hyperthyroid patients with Graves' disease were evaluated and subsequently treated with radioiodine. The liquid group (45 patients) received a liquid 131I tracer (1.85 MBq [0.05 mCi]) and the capsule group (20 patients) received a capsule 131I tracer (1.63 MBq [0.044 mCi]). Probe calibration factors were the same for the liquid and capsule 131I standards. All patients received therapeutic amounts of 131I [114.7-1106.3 MBq [3.1-29.9 mCi]) in liquid form. Therapy uptakes were obtained using the same collimated uptake probe modified with a calibrated lead shield to attenuate the high photon flux. The mean therapeutic uptake was the same for both groups (58%). The mean diagnostic uptake for the capsule group, however, was less than the mean diagnostic uptake for the liquid group (44% vs. 63%). The mean diagnostic uptake for the capsule group was significantly lower than the mean therapeutic uptake for this group (44% vs. 58%), whereas the mean diagnostic and therapeutic uptakes were similar for the group receiving a liquid tracer (63% vs. 58%). In conclusion, diagnostic uptakes performed with a liquid tracer more accurately predicted liquid therapy uptakes than diagnostic uptakes performed with a capsule tracer. This raises concern about the bioavailability of 131I in capsule form and has implications for determining the amount of 131I to administer for therapy. Patients whose 131I therapy was based on the uptake of a capsule tracer received a higher than intended amount of radiation to the thyroid gland.     

甲状腺功能亢进症初诊患者肝功能异常的临床分析

探讨甲状腺功能亢进症(甲亢)初诊患者肝功能异常的发生率、临床特点及相关因素。将428例甲亢患者根据肝功能是否异常分为两组,分析其临床表现、肝功能指标与血清甲状腺激素水平以及甲状腺自身抗体的水平的关系。初诊甲亢患者肝功能异常的发生率为30．1％,肝功能损害最常见的是碱性磷酸酶(ALP)、丙氨酸氨基转移酶(ALT)增高,其甲状腺激素水平显著高于无肝功能异常者。而TSH、甲状腺微粒体抗体(TMA)、甲状腺球蛋白抗体(TGA)则无明显差异。甲亢初诊患者合并肝功能异常较常见,肝功能损害以ALP、ALT增高为最常见,且与甲状腺激素水平关系密切。     

Effect of 131 I treatment on the calcitonin response to calcium infusion in hyperthyroid patients

OBJECTIVE The objective was to evaluate the effect of ¹³¹I treatment for hyperthyroidism on calcitonin secretion by thyroid C-cells. DESIGN Determination of basal calcitonin levels and calcitonin secretory reserve before and aiter ¹³¹I administration. PATIENTS Seventeen hyperthyroid patients (15 female, two male) were studied before, and 2 months after ¹³¹I treatment, and 12 of these patients were restudied 8 months after ¹³¹I treatment. MEASUREMENTS Calcitonin response was assessed by measuring basal and post calcium infusion calcitonin levels. Basal TSH, T3, and T4 levels were also determined at each study. RESULTS The rise of plasma calcium resulted in statistically significant increase of plasma calcitonin levels before ¹³¹I treatment (10.9·2.4 pmol/l), while this response was significantly diminished 2 and 8 months after treatment (2.6·0.7 and 1.6·0.3 pmol/l, respectively). No correlation was found between the calcitonin response and age or plasma TSH. CONCLUSION Our results demonstrate that ¹³¹I treatment for hyperthyroidism may seriously damage thyroid C-cells and cause calcitonin deficiency.     

Complement levels in patients with hepatic dysfunction

Total hemolytic complement activity and serum complement protein concentrations were compared in 17 hospitalized patients with normal hepatic function and 16 patients with liver disease due to alcohol (15 patients) or acetaminophen toxicity (one patient). In contrast to the control patients, individuals with hepatic dysfunction had decreased total CH₅₀ levels and low concentrations of total C3, C4, C5, factor B, and the regulatory proteins factor I and beta-1H. These patients also had increased C4d/C4 ratios, indicating classical pathway activation. The level of complement deficiency appears to correlate with either prolongation of the prothrombin time or depression of serum albumin concentration. These results indicate that patients with hepatic disease have severe complement depletion that is probably multifactorial in origin. This impairment in complement function will contribute to the impaired antibacterial host defense of the patient with chronic hepatic disease.This research was supported in part by the Veterans Administration Research Service. Dr. Ellison has a Research Associate career development award from the Veterans Administration.     

Thyroid dysfunction (TD) among chronic hepatitis C patients with mild and severe hepatic fibrosis

Background: Thyroid dysfunction (TD) is associated to chronic hepatitis C (HCV) and interferon (IFN) therapy. The prevalence of TD at baseline and during IFN therapy among stages of hepatic fibrosis is unknown.Goals: To examine the frequency of TD at baseline and during Peg-IFN therapy among patients with severe and mild fibrosis.Study: 100 patients were treated with Peg-IFN and divided in 2 groups (50 each), according to liver histology; Metavir 0-2 (mild fibrosis) and Metavir 3-4 (severe fibrosis). Baseline TD was defined as history of TD, or abnormal thyroid stimulating hormone (TSH) or antiperoxidase thyroid auto-antibodies (TPO-Ab). Frequency of TD during therapy was defined as TD that required treatment.Results: 20% in the severe fibrosis group and 10% in the mild fibrosis group, had TD at baseline. Most of the cases, 31.4% were female as compared to 6.25% males. During therapy, 24% of patients in the severe fibrosis group, compared to 12% in the mild fibrosis, had TD. Most patients had biochemical hypothyroidism, and 66% were female, compared to 33.33 % male. TPO-Ab predicted TD during therapy in 50% of cases while those negative only had 16.6% TD during IFN therapy.Conclusions: Patients with severe fibrosis have more TD events at baseline and during treatment with Peg IFN alfa-2a. Patients with more hepatic fibrosis require careful attention to diagnose and manage TD. More research in the immune mechanisms of hepatic fibrosis progression and autoimmune complications is needed.