Assessment of thyroid disorders in patients with rosacea: a large case-control study

BackgroundThe frequency of autoimmune diseases and thyroid cancer has been increasingly reported in association with rosacea. However, studies investigating thyroid diseases in rosacea are scarce with conflicting results.ObjectiveTo investigate the relationship between thyroid disorders and rosacea.MethodsA large case-control study on age- and gender-matched 2091 rosacea patients and 9572 controls was conducted. Rosacea patients using the rosacea-specific ICD codes were compiled from the hospital records. Additionally, all participants were evaluated in terms of the presence of hypothyroidism and hyperthyroidism. Conditional logistic regression analysis was used to compute case-control odds ratios (OR) with 95% confidence intervals.ResultsThe analysis comprehended 2091 rosacea patients (1546 female, 545 male; mean 48.73 ± 14.53 years) and 9572 controls (7009 female, 2563 male; mean 48.73 ± 15.1 years). Whereas the rate of hypothyroidism was significantly higher in rosacea patients (OR = 1.3, 95% CI 1.13–1.49, p < 0.001), there was no significant difference in the rate of hyperthyroidism between the groups (OR = 1.12, 95% CI 0.81–1.53, p = 0.497). Stratification for gender revealed a significant association between hypothyroidism and rosacea in females (OR = 1.27, 95% CI 1.1–1.47, p = 0.002) and males (OR = 1.58, 95% CI 1.04–2.4, p = 0.032). The frequency of hypothyroidism in rosacea patients increased towards the age range of 40–49 and then decreased, parallel with the hypothyroidism frequency of the study population.Study limitationsDifferent subtypes and severities of rosacea were not distinguished.ConclusionsHypothyroidism may be a comorbidity of rosacea and investigation for hypothyroidism may be appropriate when evaluating rosacea patients.     

Methimazole-induced hypothyroidism causes cellular damage in the spleen, heart, liver, lung and kidney

It is known that a hypothyroidism-induced hypometabolic state protects against oxidative damage caused by toxins. However, some workers demonstrated that antithyroid drug-induced hypothyroidism can cause cellular damage. Our objective was to determine if methimazole (an antithyroid drug) or hypothyroidism causes cellular damage in the liver, kidney, lung, spleen and heart. Twenty-five male Wistar rats were divided into 5 groups: euthyroid, false thyroidectomy, thyroidectomy-induced hypothyroidism, methimazole-induced hypothyroidism (60 mg/kg), and treatment with methimazole (60 mg/kg) and a T₄ injection (20 μg/kg/d sc). At the end of the treatments (4 weeks for the pharmacological groups and 8 weeks for the surgical groups), the animals were anesthetized with sodium pentobarbital and they were transcardially perfused with 10% formaldehyde. The spleen, heart, liver, lung and kidney were removed and were processed for embedding in paraffin wax. Coronal sections were stained with hematoxylin-eosin. At the end of treatment, animals with both the methimazole- and thyroidectomy-induced hypothyroidism had a significant reduction of serum concentration of thyroid hormones. Only methimazole-induced hypothyroidism causes cellular damage in the kidney, lung, liver, heart, kidney and spleen. In addition, animals treated with methimazole and T₄ showed cellular damage in the lung, spleen and renal medulla with lesser damage in the liver, renal cortex and heart. The thyroidectomy only altered the lung structure. The alterations were prevented by T₄ completely in the heart and partially in the kidney cortex. These results indicate that tissue damage found in hypothyroidism is caused by methimazole.     

Imprinting of maternal thyroid hormones in the offspring

Thyroid hormones (THs) during pregnancy contribute significantly to cellular differentiation and development in several tissues of the offspring, principally the central nervous system (CNS). TH deficiencies, such as hypothyroidism or hypothyroxinemia, are highly frequent during pregnancy worldwide and known to be detrimental for the development of the fetus. The function of CNS in the offspring gestated under TH deficiency will be irreversible impaired, causing low intellectual quotient, attention deficit, and mental retardation. On the other hand, little is known about the effects of TH deficiency in the offspring immune system, being the prevalent notion that the effects are reversible and only for a while will affect the number of B and T cells. Recent studies have shown that maternal hypothyroidism can altered the function of immune system in the offspring, rendering the female offspring more susceptible to suffer autoimmune-inflammatory diseases, such as experimental autoimmune encephalomyelitis (EAE) and to be more resistant to a bacterial infection. In this article we discuss these recent findings, as well as the possible mechanisms underlying these effects and the potential implications for human health.     

高氯酸盐对女性甲状腺功能的影响调查

目的探讨高氯酸盐对从事烟花爆竹制造职业女性甲状腺功能的影响。方法选择我市2010年1月～2011年1月某烟花爆竹工厂女性员工65例为暴露组，另选择同时期体检的正常女性35例为对照组。比较两组甲状腺功能异常症状出现人数及甲状腺相关激素水平。结果暴露组人群尿液中的高氯酸盐浓度显著高于对照组。暴露组出现疲乏感、便秘、记忆力减退、头晕耳鸣、皮肤干燥、水肿、手脚麻木、骨关节不灵活、小腿肌肉痉挛疼痛、腹胀症状的人数均高于对照组。暴露组FT，水平低于对照组。两组的一般情况对人群甲状腺相关激素水平无明显影响。结论高氯酸盐暴露可能会影响育龄女性甲状腺的功能。因此，我们要对暴露于高氯酸盐环境中的人群进行必要的预防和宣教，帮助她们降低危害。     

冠心病合并甲状腺功能减退症冠状动脉搭桥术围术期治疗

目的:分析总结冠心病合并甲状腺功能减退症外科治疗围术期处理方法。方法:回顾性分析20例冠心病合并甲状腺功能减退患者外科治疗围术期临床资料。结果:全组患者手术效果良好,19例患者经治疗后痊愈出院,围术期死亡1例。术前甲减确诊者均服用左旋甲状腺素片,剂量为12.5～200μg/d,平均(85±11.9)μg/d,(1.15±0.14)μg/kg,术后3d内服用剂量为25～200μg/d,平均(113±11.3)μg/d,(1.56±0.13)μg/kg;术前漏诊6例,术后确诊后立即行激素替代治疗,左旋甲状腺素片最大剂量为250μg/d,最小剂量为75μg/d,平均179.17μg/d,(2.38±0.66)μg/kg;术后机械通气时间14～146 h,平均(38±21)h,ICU停留时间16～67 h,平均(35±14.5)h;术后使用2～5μg.kg-1.min-1多巴胺改善心功能,其中使用肾上腺素维持心功能者4例,剂量在0.02～0.08μg.kg-1.min-1,行IABP辅助治疗者1例,5 d后顺利撤除。结论:冠心病合并甲状腺功能减退症外科治疗增加患者术后机械通气时间、ICU停留时间,术后恢复较甲状腺功能正常者慢,积极有效的围术期处理,术后并发症的发生率、围术期病死率并无明显增高,可安全耐受手术。     

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。     

Absence of inferior vena cava as a rare cause of deep venous thrombosis complicated by liver and lung embolism

Congenital anomalies of the inferior vena cava such as absence or atresia are uncommon vascular defects and result from aberrant development during embryogenesis. We report a case of a young female patient affected by proximal deep venous thrombosis (DVT) complicated by liver and pulmonary embolism; subsequent extensive evaluation revealed the congenital absence of infrarenal inferior vena cava, with emboli probably occurring through collateral veins. Accordingly, in young patients with idiopathic DVT of the lower extremities and pelvic veins, the presence of inferior vena cava abnormalities should always be considered and investigated, together with classic coagulation factors, as a factor predisposing to thromboembolic complications.     

新生早期甲状腺功能减退大鼠心肌甲状腺激素受体mRNA表达的实验研究

目的探讨新生早期甲状腺功能减退（简称甲减）对大鼠心肌发育过程中甲状腺激素受体（TR）各亚型mRNA表达的影响。方法Wistar雌鼠从怀孕15d开始每天经胃灌注1％丙硫氧嘧啶2．5ml，复制甲减仔鼠动物模型，分别于各时间点称体质量后处死仔鼠，取心脏。放射免疫分析法（RIA）动态监测各组大鼠血清FT3、FT4水平，FQ—PCR方法检测各组心肌TR各亚型mRNA的表达差异。结果与对照组比较，甲减大鼠心肌TRα1 mRNA表达量在出生后0、21、45d分别下调90％、15％、36％（tod=8．33，t21d=2．58，t45d=3．25，P〈0．05），表达峰值于生后2周延迟出现。甲减大鼠心肌TRα2 mRNA表达量在出生后0、14、21、45d分别上调22％、72％、82％、36％（t0d=3．89，t14d=11．88，t21d=13．90，t45d=6．19，P〈0．05），表达峰值于生后2周延迟出现。甲减大鼠心肌TRβ1 mRNA表达量在出生后0、14、21、45d分别下调75％、62％、68％、60％（t0d=38．96，t14d=5．22，t21d=17．23，t45d=5．43，P〈0．05），表达变化趋势与对照组一致。结论新生早期甲减大鼠心肌上TR mRNA的异常表达可能与甲减性心脏病的发病机制密切相关。     

Cardiac electrolytes and water in thyroparathyroidectomized rat

The effect of thyroparathyroidectomy (TPTX) on myocardial extracellular space (ECS), water and electrolytes was studied in young, female, Sprague-Dawley rats. Eight weeks after TPTX the ventricular ECS, measured in vivo with [³⁵S]sulfate, was found to be 0.219 ± 0.004 (g H₂O/g tissue as compared to 0.177 ± 0.006 in euthyroid control rats. Measurement of ECS in the same ventricular tissue of TPTX rat by a morphometric procedure confirmed the increase: 0.209 ± 0.004 (cm³/cm³). This increase in ECS was only relative to the size of the cellular compartment, for the absolute volume of the ECS in the ventricular myocardium fell. Thus, the relative expansion of the ECS at the expense of the cellular compartment appears to be due to a greater sensitivity of the parenchyma to the inhibitory effects of hypothyroidism on growth. This finding is compatible with a decrease in cellular size of the hearts of hypothyroid rats; a compartmental shift in water from the cellular to the extracellular compartment need not be postulated. Most or all of the enlargement of ECS is due to an expansion of the interstitial compartment. No changes in tissue water content were detected. Plasma concentrations of potassium, calcium and magnesium declined, whereas the concentrations of sodium and chloride remained constant. Depending on whether the electrolytes are predominantly intracellular or extracellular, tissue electrolyte contents showed alterations appropriate to the relative changes in compartmental volumes. Assuming homogeneous distributions of the electrolytes throughout the ECS, the calculated cellular concentrations slightly increased for sodium and potassium, decreased for magnesium, and remained unchanged for calcium and chloride.     

442例Graves病131I治疗后晚发甲减相关因素分析

目的 回顾分析Graves' disease(GD)131I治疗后永久性甲状腺功能减退(晚发甲减)的相关因素.方法 依据摄131I率公式并结合临床经验确定131 I剂量,一次给药,门诊治疗GD患者442例,其中男性128例(29.0％),女性314例(71.0％).一次治疗未愈或复发者,相隔3个月以上同法重复治疗,直至治愈.结束治疗后随访疗效1年以上,并根据是否发生晚发甲减分成甲减组和非甲减组,然后分析两组患者相关因素的差异及临床意义.结果 ①晚发甲减231例(52.3％),包括男性56例(43.8％)和女性175例(55.7％)(x2=4.7639,P＜0.05).②两组事先抗甲状腺药物(antithyroid drugs,ATD)治疗时间分别为43.6±42.0月和64.6±50.1月(t=3.0290,P＜0.01);治疗前ATD停药时间分别为27.2±25.3周和18.7±16.4周(t=2.7709,P＜0.01).③两组的年龄、病程、摄131I率、治疗前激素和自身抗体水平、甲状腺质量和质地、治疗次数、首次和累计治疗剂量等,均无统计学差异(t=0.2592 ～1.2363,P＞0.05).结论 晚发甲减与性别和ATD有一定关系,与年龄、病程、摄131I率、激素和自身抗体水平、甲状腺大小和质地、1311I剂量等未见明显相关,提示患者内在规律的自然转归是晚发甲减主要原因,因此临床应用131I剂量不必过于保守.