Dosiomics-based prediction of radiation-induced hypothyroidism in nasopharyngeal carcinoma patients

PurposeTo predict the incidence of radiation-induced hypothyroidism (RHT) in nasopharyngeal carcinoma (NPC) patients, dosiomics features based prediction models were established.Materials and methodsA total of 145 NPC patients treated with radiotherapy from January 2012 to January 2015 were included. Dosiomics features of the dose distribution within thyroid gland were extracted. The minimal-redundancy-maximal-relevance (mRMR) criterion was used to rank the extracted features and selected the most relevant features. Machine learning (ML) algorithms including logistic regression (LR), support vector machine (SVM), random forest (RF), and k-nearest neighbor (KNN) were utilized to establish prediction models, respectively. Nested sampling and hyper-tuning methods were adopted to train and validate the prediction models. The dosiomics-based (DO) prediction models were evaluated through comparing with the dose-volume factor-based (DV) models in terms of the area under the receiver operating characteristic (ROC) curve (AUC). The demographics factors (age and gender) were included in both DO model and DV model.ResultsAge, V45 and 37 dosiomics features exhibited significant correlations with RHT in univariate analysis. For prediction performance, DO prediction models exhibited better results with the best AUC value 0.7 while DV prediction models 0.61. In DO prediction models, the AUC values displayed a trend from ascending to descending with the increasing of selected features. The highest AUC value was achieved when the number of selected features was 3. In DV prediction model, similar trend was not observed.ConclusionThis study established a prediction model based on the dosiomics features with better performance than conventional dose-volume factors, leading to early predict the possible RHT among NPC patients who had received radiotherapy and take precaution measures for NPC patients.     

系统性红斑狼疮合并甲状腺功能减退症50例临床分析

目的:分析系统性红斑狼疮合并甲状腺功能减退症50例临床症状和治疗效果.方法:选取2010年6月至2012年6月间于我院接受诊断和治疗的系统性红斑狼疮合并甲状腺功能减退症患者50例作为观察组,同时选取同期入院的单纯系统性红斑狼疮患者50例作为对照组,分析两组临床症状的差异.观察组患者分别给予系统性红斑狼疮合并甲状腺功能减退症联合治疗和甲状腺功能减退症单独治疗,观察比较治疗前后甲状腺功能差异.结果:观察组患者关节病变发病率为64.00％明显高于对照组的22.00％(P＜0.05):观察组患者雷诺现象的发病率为36.00％明显高于对照组的6％(P＜0.05).联合治疗患者治疗后促甲状腺素水平明显低于单独治疗(P＜0.05),联合治疗患者治疗后游离甲状腺素和游离甲状腺三碘原氨酸水平均明显高于单独治疗(p＜0.05).结论:系统性红斑狼疮合并甲状腺功能减退症患者的关节病变和雷诺现象发病率明显较高,联合治疗后甲状腺功能减退症恢复较佳.     

妊娠合并甲状腺功能减退症26例妊娠结局分析

目的：对妊娠合并甲状腺功能减退症进行分析,探讨其对母儿的影响,及孕期筛查甲状腺功能有无意义。方法：对我院26例妊娠合并甲减的临床资料进行回顾性统计分析。结果：26例妊娠合并甲减病例中有1例早产（孕33周）,其余25例患者维持至足月妊娠,其中剖宫产17例（65.38%）,合并妊娠期高血压疾病5例（19.23%）,妊娠期糖尿病3例（11.53%）,羊水胎粪污染3例（11.54%）,新生儿无先天性甲减。经过治疗后甲状腺功能减退孕妇的剖宫产率,糖尿病发生率、高血压疾病发生率、羊水粪染的发生率较对照组增加;但两组妊娠结局差异无统计学意义（P〉0.05）。结论：妊娠合并甲状腺功能减退症孕妇多种妊娠并发症的发病率高于正常孕妇,应加强对妊娠甲减的早期筛查及治疗,可有效降低不良妊娠结局,减少先天性甲低的出生。     

甲状腺功能减退症患者心理健康状况及影响因素分析

目的:研究甲状腺功能减退症患者的心理健康状况及其影响因素,为预防、改善甲减患者心理健康状况提供参考依据。方法:选取2014年1月-2016年1月来我院治疗的226例甲减患者作为甲减组,另从杨浦区多个社区随机抽取同期254例健康者作为健康组,采用SCL-90症状自评量表、社会支持评定量表(SSRS)及一般情况调查问卷对两组研究对象进行调查,采用Logistic回归分析甲减患者的影响因素。结果:两组性别、年龄及职业之间的差异无统计学意义(P0.05),而文化程度、经济收入的差异具有统计学意义(P0.05);甲减组患者强迫症状、抑郁、焦虑、精神病性评分及总分均高于健康组(P0.05);甲减组患者中焦虑、抑郁、人际关系敏感所占比重较高,分别为30.97%,26.11%,26.11%;与健康组相比,甲减组患者SSRS评分中主观支持、客观支持、支持利用度评分及总分均明显降低(P0.05);多因素Logistic回归分析显示社会支持、文化程度为小学、经济收入30000元/年是甲减患者心理健康的影响因素(P0.05)。结论:甲减患者心理状况较差,存在较严重的焦虑和抑郁情况,在治疗同时应注意健康教育和心理关怀,尤其是对收入低、文化程度低或社会支持程度低的患者,应给予及时的心理治疗,可提高患者的生活质量。     

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。     

Individual plasma ghrelin changes in the same patients in hyperthyroid,hypothyroid and euthyroid state

Ghrelin is a multifunctional peptide of widespread expression. Since it has been shown to influence energy homeostatis, its potential role in thyroid dysfunction may have clinical significance. In this study, plasma ghrelin changes have been analyzed in the same patients in three different thyroid states for the first time. The study group consisted of 16 patients who had been diagnosed with hyperthyroidism, were treated with radioiodine, developed hypothyroidism after treatment, and finally became euthyroid on l-thyroxine substitution. In the initial state of hyperthyroidism plasma ghrelin levels correlated negatively with fT₃ and fT₄. In hypothyroidism ghrelin concentration increased significantly (p < 0.05). Although the mean value of plasma ghrelin tended to decrease in the euthyroid state, the individual difference between hypothyroidism and euthyroidism was not significant. Plasma ghrelin in euthyroidism was still significantly higher than in hyperthyroidism (p < 0.05), and correlated positively with ghrelin levels in hyperthyroidism and hypothyroidism. In our opinion, plasma ghrelin fluctuations may reflect metabolic changes in patients with thyroid dysfunction. Moreover, it cannot be excluded that in thyroid disorders ghrelin acts as a compensatory factor, helping to balance metabolic disturbances.     

P-glycoprotein polymorphism in hypo- and hyper-thyroidism patients

P-glycoprotein (Pgp) is encoded by the multidrug resistance gene (MDR1) in humans and is the product of MDR1. It is expressed in various tissues and is related to drug distribution in intestinal erythrocytes, capillary endotel of brain, proximal tubules cells of kidneys and liver canalicular cells. Expression of Pgp is affected by Pgp polymorphism, and exon 26 C3435T polymorphism is the most common one. It has been thought that expression of Pgp is high in C-allele subjects and this situation is responsible for the resistance against some drugs and substances. Pgp may have a role in the distribution of thyroid hormones, drugs used for hypo- and hyperthyroidism and the resistance occurred. For this purpose possible relationship between T and C alleles and frequency of Pgp polymorphism as well as thyroid hormone distribution in patients with hypo- and hyperthyroidism was investigated. Thirty five hyperthyroidism patients diagnosed as Graves’ disease, 78 hypothyroidism patients diagnosed as Hashimoto’s thyroiditis and 100 healthy volunteers were included in the study. According to the results obtained no statistically significant difference was found in Pgp C3435T polymorphism between hypo- and hyperthyroidism patients. In addition, the serum free T3 levels of hyperthyroidism patients with C alleles was higher than those of subjects with T alleles. No statistically significant difference was seen in the CC, CT and TT genotype frequencies between the patients and control groups. In conclusion, it seems that Pgp polymorphism is not a predictor factor for the occurrence of hypo- and hyperthyroidism. There is a significant relationship between Pgp and the elevated serum free T3 levels of hyperthyroidism patients, and further research will help understand this situation.     

Hypothyroidism provides resistance to kidney mitochondria against the injury induced by renal ischemia-reperfusion

Massive Ca(2+) accumulation in mitochondria, plus the stimulating effect of an inducing agent, i.e., oxidative stress, induces the so-called permeability transition, which is characterized by the opening of a nonspecific pore. This work was aimed at studying the influence of thyroid hormone on the opening of such a nonspecific pore in kidney mitochondria, as induced by an oxidative stress. To meet this objective, membrane permeability transition was examined in mitochondria isolated from kidney of euthyroid and hypothyroid rats, after a period of ischemia/reperfusion. It was found that mitochondria from hypothyroid rats were able to retain accumulated Ca(2+) to sustain a transmembrane potential after Ca(2+) addition, as well as to maintain matrix NAD(+) and membrane cytochrome c content. The protective effect of hypothyroidism was clearly opposed to that occurring in ischemic reperfused mitochondria from euthyroid rats. Our findings demonstrate that these mitochondria were unable to preserve selective membrane permeability, except when cyclosporin A was added. It is proposed that the protection is conferred by the low content of cardiolipin found in the inner membrane. This phospholipid is required to switch adenine nucleotide translocase from specific carrier to a non-specific pore.