亚急性甲状腺炎复发及永久性甲状腺功能减退预测因素的研究进展

亚急性甲状腺炎（subacute thyroiditis,SAT）是一种甲状腺炎性疾病,与病毒感染有关。其不良临床转归,即永久性甲状腺功能减退及复发的发病率似有增高趋势。复发引起的反复发热、颈部疼痛等炎性症状使病人生活质量下降,而且永久性甲状腺功能减退的病人即使终身替代治疗,也难以避免对健康的影响。预防SAT的复发,减少永久性甲状腺功能减退,一直是学者们关注的热点。近几年,探讨SAT不良临床转归的研究涉及甲状腺体积、甲状腺功能相关指标、人类白细胞抗原及治疗因素等方面,且出现了许多具有临床意义的新数据。尤其是2019年至今全球大流行的新型冠状病毒是否与SAT有关,愈发引起人们的重视。因此,该研究将从以上几方面对永久性甲状腺功能减退和复发的可能预测因素作一综述,旨在为临床工作及科研提供参考。     

Pathogenetic aspects of organ-specific autoimmunity

Summary In the last few years a great deal of information on the etiopathogenetic aspects of organ-specific autoimmune diseases (OSADS) has been obtained. It has been shown that genetic factors play an etiologic fundamental role. They are responsible for the dysregulation of the immune system and for the target organ susceptibility which favour the onset of the diseases. Putative environmental factors, such as viral infections, can act as initiating or precipitating events only in genetically predisposed individuals. Immunological mechanisms capable of triggering autoimmune responses have been demonstrated. Data obtained from experimental models and from humans suggest that the ongoing expansion of autoreactive T cells with specificity for autoantigens (AAgs) can be considered as the main immunological event capable of inducing and maintaining the target organ damage. These cells can activate different effector systems, i.e., autoantibody (AAb)-producing B cells, cells with cytotoxic activity, etc., by releasing different combinations of lymphokines. In overt diseases AAbs are directly involved in the pathogenesis of lesions due to autoimmune responses against functional molecules and cellular receptors. The pathogenesis of the common inflammatory destructive lesions of the target organs is more complex and not yet clarified. A large proportion of T cells present in the inflammatory infiltrates are apparently not directed to the AAgs. Most cells display cytolytic activity and may contribute to tissue damage by releasing lymphokines which activate other cells and cascade the process. Vicious cycles, i.e., upregulation of class II and I molecules, alterations of the cytokine network, etc., are supposed to be involved in the maintenance of target organ lesions.     

桥本脑病伴帕金森综合征1例并文献复习

目的加深临床对桥本脑病的认识,提高临床诊出率。方法分析1例临床诊断为桥本脑病患者的临床表现、神经系统体征、实验室检查、电生理、影像学资料及治疗效果。结果患者神经系统表现为认知功能下降、帕金森综合征和癫痫发作,脑脊液IgG合成率增高,头MRI颅内多发病灶,脑电图示慢波增多。糖皮质激素治疗有效。结论桥本脑病临床表现多样,还可伴随帕金森综合征,临床上对脑病患者应想到此病的可能性,避免误诊、漏诊。     

儿童自身免疫性甲状腺疾病的诊治

自身免疫性甲状腺疾病（ATDs）主要包括自身免疫性甲状腺炎（AT）及Graves病（GD），均由T淋巴细胞的浸润及B淋巴细胞产生甲状腺自身免疫性抗体引起甲状腺功能异常。甲状腺功能对儿童的神经系统及生长发育至关重要，因此早期诊治十分必要。本文旨在对儿童自身免疫性甲状腺疾病的病因、诊断及治疗进行探讨。     

Fas/FasL介导的凋亡在桥本病发病机制中的作用

用免疫组织化学法和Westem印迹法在24例桥本病(HT)甲状腺组织中观察到甲状腺细胞Fas表达增高，Fas／FasL介导的细胞凋亡参与HT的发病。     

为我们的儿童而安全补碘

补碘预防碘缺乏性疾病的益处已不言而喻，但也发生甲状腺毒症和引起甲状腺功能减退症（甲减）的甲状腺炎等不良反应。碘致甲状腺炎以前的证据仅来自实验性研究、病理学检查和横断面流行病学调查。本期发表的滕卫平等在中国轻度碘缺乏、超足量碘补充和碘过量摄取地区的3个人群的研究已证实随着较高的碘摄取，甲状腺自身免疫和亚临床甲减的发病率呈轻度、但已有统计学意义的上升。然而，临床甲减的发病率并未见升高。这些发现再次从临床和公共卫生方面消除了人们的疑虑，证实了补碘方案对人类健康会产生巨大的效益而风险甚小。     

亚急性甲状腺炎11例误诊手术临床分析

目的探讨亚急性甲状腺炎误诊外科手术的原因。方法回顾性分析错误地行甲状腺部分或大部分切除术的11例亚急性甲状腺炎临床资料。结果医生对亚急性甲状腺炎的认识不足及其伴发甲状腺结节是导致该病误诊、误治的主要原因。绝大多数病例术前可以明确诊断而避免不必要的手术。结论临床工作中可进一步降低亚急性甲状腺炎的误诊。     

碘过量对实验性自身免疫性甲状腺炎大鼠骨代谢的影响

目的 探讨碘过量对实验性自身免疫性甲状腺炎(EAT)大鼠骨代谢的影响.方法 雌性Lewis大鼠36只,体质量为(131±15)g,按体质量随机分为3组:对照组、EAT组和EAT+高碘组,每组12只.以不同含碘量(0.9、0.9、18.0 mg/kg)的饲料喂养各组大鼠,并用猪甲状腺球蛋白(pTG)和完全弗氏佐剂(CFA)对EAT组和EAT+高碘组大鼠进行免疫以建立EAT模型.2周后观察大鼠甲状腺病理改变,测定血清甲状腺自身抗体[甲状腺球蛋白抗体(TGAb)、甲状腺微粒体抗体(TMAb)]和甲状腺激素[三碘甲腺原氨酸(T3)、甲状腺素(T4)]以及骨代谢相关指标[骨钙素(BGP)、抗酒石酸盐酸性磷酸酶(TRAP)、Ⅰ型前胶原羧基末端前肽(PICP)、Ⅰ型胶原羧基吡啶并啉交联肽(ICTP)、胰岛素样生长因子-1(IGF-1)、护骨素(OPG)、核因子κB受体活化因子配体(RANKL)]水平.结果 EAT组和EAT+高碘组大鼠甲状腺组织均呈现炎细胞浸润,局部滤泡结构破坏,其中EAT+高碘组以甲状腺滤泡扩张、融合为主.EAT组和EAT+高碘组大鼠血清TGAb、TMAb、T3和T4水平[(63.01±12.36)%、(60.62±11.24)%,(3.78±1.43)、(125.12±16.00)pmol/L和(75.00±15.44)%、(72.15±15.00)%,(3.69±0.91)、(149.40±20.67)pmol/L]高于对照组[(4.47±1.04)%、(5.73±1.01)%,(0.75±0.12)、(76.91±9.30)pmol/L,P均＜0.05],EAT+高碘组大鼠血清TGAb、TMAb和T4水平较EAT组升高(P均＜0.05).EAT组大鼠血清BGP、PICP和IGF-1水平[(1.70±0.31)、(11.31±1.52)μg/L,(0.31±0.06)mg/L]较对照组[(8.60±0.33)、(14.28±3.10)μg/L,(1.16±0.02)mg/L]降低(P均＜0.05),血清TRAP、ICTP、OPG和RANKL水平[(19.88±3.60)ng/L,(2.43±0.82)、(22.36±2.80)、(1.35±0.23)μg/L]较对照组[(14.57±3.56)ng/L,(0.50±0.20)、(1.61±0.34)、(0.10±0.02)μg/L]升高(P均＜0.05);与EAT组比较,EAT+高碘组大鼠血清PICP和OPG水平[(8.03±1.84)、(16.80±3.79)μg/L]明显降低(P均＜0.05).结论 EAT时大鼠的破骨细胞分化与成熟增强,导致骨吸收增强.碘过量可抑制EAT大鼠成骨细胞和破骨细胞活性,呈现低转化型骨质疏松.

Abstract：

Objective To explore the effect of iodine excess on bone metabolism in experimental autoimmune thyroiditis (EAT) rats. Methods We selected 36 female Lewis rats with body weight of (131 ± 15)g,and divided them into 3 groups randomly: control group, EAT group and EAT + high iodine group, assuring 12 rats in every group. These rats were fed fodder with different concentration of iodine(0.9,0.9, 18.0 mg/kg), and rats in EAT group and EAT + high iodine group were immunized with pig thyroglobulin(pTG) and complete Freund's adjuvant(CFA) to create EAT model. After two weeks, the pathological changes of the thyroid tissues were observed,and the serum thyroid autoantibody[thyroglobulin antibody(TGAb) and thyroid microsomal antibody(TMAb)], the thyroid hormone levels[triiodo thyronine(T3) and thyrine(T4)] and some relevant data of bone metabolism[bone gla protein (BGP), tartrate-resistant acid phosphatase (TRAP), C-terminal propeptide of type Ⅰ procollagen (PICP),C-terminal telopeptide of type Ⅰ collagen (ICTP), insulin-like growth factor- 1 ( IGF- 1 ), osteoprotegerin (OPG) and receptor activator of NF-κB ligand (RANKL)] were measured. Results Inflammatory cell infiltration and local follicular structural damage were observed in the thyroid tissues of EAT rats in EAT group and EAT + high iodine group, and the pathological changes of EAT + high iodine group were mainly thyroid follicular expansion and integration. The level of serum TGAb, TMAb, T3 and T4 of EAT rats in EAT group and EAT + high iodine group[ (63.01 ± 12.36)%, (60.62 ± 11.24)%, (3.78 ± 1.43), (125.12 ± 16.00)pmol/L and (75.00 ± 15.44)%,(72.15 ± 15.00)%, (3.69 ± 0.91 ), (149.40 ± 20.67)pmol/L] were higher than those of the control group[ (4.47 ±1.04)%, (5.73 ± 1.01 )%, (0.75 ± 0.12), (76.91 ± 9.30)pmol/L, all P ＜ 0.05], and the level of serum TGAb,TMAb and T4 of EAT rats in EAT + high iodine group were higher than those of the EAT group(all P ＜ 0.05).The level of serum BGP, PICP and IGF- 1 in EAT group[ ( 1.70 ± 0.31 ), ( 11.31 ± 1.52) μg/L, (0.31 ± 0.06 ) mg/L]were lower than those of the control group[ (8.60 ± 0.33), (14.28 ± 3.10)μg/L, (1.16 ± 0.02)mg/L, all P ＜0.05], and the level of serum TRAP, ICTP, OPG and RANKL[ ( 19.88 ± 3.60)ng/L, (2.43 ± 0.82), (22.36 ± 2.80),( 1.35 ± 0.23 )μg/L] were higher than those of the control group[ ( 14.57 ± 3.56)ng/L, (0.50 ± 0.20), (1.61 ± 0.34),(0.10 ± 0.02)μg/L, all P ＜ 0.05]; compared with EAT group, the level of PCIP and OPG in EAT + high iodine group [ (8.03 ± 1.84), ( 16.80 ± 3.79)μg/L] were obviously decreased(all P ＜ 0.05). Conclusions The reinforcement of differentiation and maturation of osteoblast in the EAT rats results in the increasing of bone resorption. The activity of osteoblast and osteoclast of the EAT rats are inhibited by excessive iodine, showing a low conversion-type osteoporosis.     

Endocrine disorders during the first year after autologous stem-cell transplant

BACKGROUND: Frequent endocrine disorders have been reported after allogeneic stem-cell transplant, but data on adult survivors of autologous transplants are still scarce. METHODS: In this prospective study we investigated early (at 3 months) and late (at 12 months) endocrine dysfunctions in 95 consecutive autologous stem-cell transplant recipients (47 men and 48 women) aged 16 to 55 years. The functions of the hypothalamic-pituitary-gonadal/thyroid/adrenal/somatotroph axis were evaluated. RESULTS: Three months after the transplant, insulin-like growth factor-1 values were below the normal range in 53 patients (56%); 37 of 40 women (93%) of reproductive age experienced precocious ovarian failure; 39 of 46 men (85%) showed high follicular stimulating hormone, and 17 men (37%) showed low testosterone levels. Adrenal insufficiency occurred in 28 patients (30%) during the peritransplant period after corticosteroid withdrawal. Transient subclinical hyperthyroidism was found in 15 patients (16%). Transient "low T(3)" syndrome was revealed in 29 patients (31%). Twelve months after the transplant, insulin-like growth factor-1 values were still low in 36 patients (38%). Menstrual cycles resumed in four women; follicular stimulating hormone, luteinizing hormone, and estradiol levels improved in 10 patients. Testosterone was low in only two men (4%). Seminal analysis revealed azoospermia in 32 (91%) of 35 men examined. Subclinical hypothyroidism was found in 11 patients (12%); eight of them had previously received radiotherapy for the upper half of the body. CONCLUSION: This study documents frequent endocrine disorders during the first year after autologous stem-cell transplant. Despite a tendency to improve, in more than half of the cases, the complications persisted for more than 1 year. Therefore, to diagnose and correct early and late endocrine dysfunctions, endocrine screening is required during the first year in all patients undergoing autografting.