Clinical and biochemical characteristic features of metastatic cancer to the sella turcica: an analytical review

Background and objectives

Sellar metastasis is uncommon and poorly characterized as published data include small series of subjects. This study’s goal is to identify unique features that differentiate this entity from other sellar masses such as pituitary macroadenomas.

Methods

Published cases of pathologically-confirmed sellar metastasis along with our experience in such patients over a 6-years period were reviewed (total = 129). As a control group, we reviewed similar data on 55 patients with pituitary macroadenomas managed over the same time-period. Presenting symptoms, pituitary dysfunction were analyzed using univariate, multivariate and receiver operating characteristic (ROC) analyses.

Results

Sellar metastasis has equal gender distribution with a median patient-age of 56 years. The most common primary malignancy was breast cancer (29 %) in women and lung cancer (30 %) in men. Sellar metastasis was the first manifestation of cancer in over 40 % of patients. Common presenting symptoms included headaches, visual field deficits, abnormal eye motility and diabetes insipidus. These symptoms were less frequent among patients with pituitary macroadenomas. Univariate regression analyses showed that headaches, abnormal eye motility, visual field deficits and diabetes insipidus were each predictive of metastatic disease. ROC analysis combining all 4 features revealed an AUC of 0.953 with a sensitivity of 0.818 and a specificity of 0.935. Using the multivariate regression, abnormal eye motility and/or diabetes insipidus independently predicted metastatic disease.

Conclusions

Sellar metastasis should be suspected in patients presenting with sellar masses, abnormal eye motility and/or diabetes insipidus even those without known malignancy since pituitary metastasis can often be the first manifestation of cancer.     

心脏介入术前患者焦虑抑郁两种测量方法的研究

目的 将脑功能指标客观定量测量与目前临床广泛应用的9项病例健康问卷（PHQ-9）、7 项广泛性焦虑（GAD-7）、躯体化症状自评量表（SSS）三种量表联合应用对患者焦虑抑郁的评估结果进行对比,为心脏康复患者筛查、术后患者焦虑、抑郁的评估提供一种新的客观定量评测手段。方法 采取知情同意、自主填写问卷的方法对阜外医院心内科随机选取的31例拟行冠状动脉支架置入手术前患者进行PHQ-9、GAD-7、SSS的评估。根据量表评分结果将患者分为有焦虑抑郁组和无焦虑抑郁组两组,分别对两组患者的脑功能指标进行测量[1-2],分析两组患者的脑功能指标是否存在显著差异,并分析两种测量结果的一致性。结果 根据主观量表PHQ-9、GAD-7[3]总分进行分组,共分为两组：焦虑抑郁组13例（41.94%,PHQ-9≥5分或GAD-7≥5分）,无焦虑抑郁组18例（58.06%,PHQ-9<5分且GAD-7<5分）。焦虑抑郁组脑指标内专注为39.00±9.89,无焦虑抑郁组脑指标内专注为22.78±11.98,两组比较差异有统计学意义（P<0.05）。脑功能指标内专注与PHQ-9的spearman相关系数为0.5310（P<0.01）,与GAD-7的相关系数是0.5378（P<0.01）,故采用内专注筛查入选者焦虑抑郁（内专注>30为有焦虑抑郁组,内专注≤30为无焦虑抑郁组）,结果显示有焦虑抑郁的17例（54.84%）,无焦虑抑郁的14例（45.16%）,总符合率是75.65%。两种方法的诊断结果进行spearman相关分析,相关系数为0.5085,差异有统计学意义（P<0.01）,一致性很好。同时,采取内专注筛选焦虑抑郁患者,焦虑抑郁组的躯体化症状量表得分为36.3±2.7,无焦虑抑郁组的躯体化症状得分为30.3±2.2,两组间无显著性差异。 结论 脑功能指标与常规量表作为评测焦虑抑郁的两种方法,二者具有一致性,利用脑功能指标内专注评测焦虑抑郁,脑功能客观定量指标将有助于对焦虑、抑郁患者的临床评估。     

新版指南解读：急性ST段抬高型心肌梗死的抗栓治疗

急性ST段抬高型心肌梗死（STEMI）是冠状动脉内血栓形成的急性心血管事件,无论是行急诊经皮冠状动脉介入还是药物溶栓,抗栓始终贯穿于治疗的全过程。由于近年来一些大规模随机临床试验结果的公布,欧洲心脏病学会（ESC）、美国心脏病学会基金会（ACCF）及美国心脏协会（AHA）相继公布了ST段抬高型心肌梗死的新版指南。指南指出：急性STEMI一旦确诊,应立即行抗血小板及抗凝治疗,抗血小板治疗为负荷量的阿司匹林（300 mg）及二磷酸腺苷（ADP）受体拮抗剂（氯吡格雷300～600 mg、普拉格雷60 mg、替格瑞洛180 mg）;ESC指南更倾向于使用替格瑞洛或普拉格雷;2个指南维持量的阿司匹林均倾向于小剂量（75～100 mg/d）。新指南对于低分子量肝素应用于急诊PCI的推荐力度有所下降,建议维持时间≤8 d。基于有效性和安全性的考虑,2个指南均建议在STEMI行急诊PCI时使用比伐芦定,尤其是对于伴有高出血风险的患者。     

How to diagnose heart failure with preserved ejection fraction: the HFA–PEFF diagnostic algorithm: a consensus recommendation from the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)

Making a firm diagnosis of chronic heart failure with preserved ejection fraction (HFpEF) remains a challenge. We recommend a new stepwise diagnostic process, the ‘HFA–PEFF diagnostic algorithm’. Step 1 (P=Pre‐test assessment) is typically performed in the ambulatory setting and includes assessment for heart failure symptoms and signs, typical clinical demographics (obesity, hypertension, diabetes mellitus, elderly, atrial fibrillation), and diagnostic laboratory tests, electrocardiogram, and echocardiography. In the absence of overt non‐cardiac causes of breathlessness, HFpEF can be suspected if there is a normal left ventricular (LV) ejection fraction, no significant heart valve disease or cardiac ischaemia, and at least one typical risk factor. Elevated natriuretic peptides support, but normal levels do not exclude a diagnosis of HFpEF. The second step (E: Echocardiography and Natriuretic Peptide Score) requires comprehensive echocardiography and is typically performed by a cardiologist. Measures include mitral annular early diastolic velocity (e′), LV filling pressure estimated using E/e′, left atrial volume index, LV mass index, LV relative wall thickness, tricuspid regurgitation velocity, LV global longitudinal systolic strain, and serum natriuretic peptide levels. Major (2 points) and Minor (1 point) criteria were defined from these measures. A score ≥5 points implies definite HFpEF; ≤1 point makes HFpEF unlikely. An intermediate score (2–4 points) implies diagnostic uncertainty, in which case Step 3 (F₁: Functional testing) is recommended with echocardiographic or invasive haemodynamic exercise stress tests. Step 4 (F₂: Final aetiology) is recommended to establish a possible specific cause of HFpEF or alternative explanations. Further research is needed for a better classification of HFpEF.     

C-JNK信号通路对糖尿病大鼠心肌Ito钾通道重构的影响

目的研究c-JNK信号通路在糖尿病(DM)大鼠左室心肌细胞电压门控钾通道(Kv)重构中的作用和内在调控机制。方法将50只健康SD大鼠随机分为DM组[n=25,采用链尿佐菌素(STZ)诱导成模]和对照组(sham)(n=25)。应用全细胞膜片钳方法记录DM组与sham组大鼠心室肌瞬时外向钾电流(Ito);使用非放射性JNK激酶分析kit进行c-Jun活性测定。应用JNK抑制剂SP600125(10M)对DM大鼠心肌细胞进行体外孵育,观察孵育前后心肌细胞Ito的变化。用硫氧还蛋白还原酶(TrxR)抑制剂金诺芬(AF)对经JNK抑制剂SP600125孵育的大鼠心肌细胞进行处理,观察处理前后心肌细胞Ito的变化。应用抗Kv4.2抗体对Kv4.2的含量进行检测,检测结果使用UVP生物成像系统进行分析。结果DM组心肌JNK活性显著升高超过1倍,而Ito显著降低[Sham组:(31.2±3.4)pA/pF,n=16;DM组:(15.4±3.1)pA/pF,n=17;P<0.05]。DM大鼠心室肌细胞经JNK抑制剂SP600125(10 M)处理4 h后,Ito电流密度可恢复至Sham组水平[DM+SP600125组:(31.9±3.8)pA/pF,n=18;Sham组:(31.2±3.4)pA/pF,n=16;P<0.05];且sham组经SP600125处理后的最大Ito电流强度[(29.8±3.4)pA/pF,n=9]和未经处理的sham组无统计学差异。DM心肌经膜渗透性蛋白抑制剂JNKI-1(10 M)处理后,Ito密度也有显著增加,而sham组经相同处理后无改变。TrxR抑制剂AF显著抑制了SP600125对DM大鼠心肌Ito电流的增大作用[DM+AF+SP600125:(15.5±3.2)pA/pF,n=17],而AF对sham组Ito无明显影响。JNK抑制剂SP600125治疗后DM大鼠心肌的Kv4.2蛋白表达量显著增大,尽管未完全恢复到sham组心肌水平,但与先前在DM大鼠心肌所观察到的Ito电流改变一致。而JNK抑制并没有明显改变sham组心肌的Kv4.2蛋白表达量。结论DM大鼠心肌钾通道重构是氧化还原敏感的,可能通过持续性激活c-JNK信号通路促进Ito重构。在DM心肌中,JNK活性显著增高,Kv通道的电流密度降低;抑制JNK信号通路后可显著改善Kv通道重构,这一过程可能被硫氧还原蛋白系统所调控。