Fístulas posquirúrgicas de líquido cefalorraquídeo tras cirugía transesfenoidal de adenomas hipofisarios: análisis de una serie de 302 intervenciones

IntroductionTranssphenoidal surgical removal is the preferred treatment of most pituitary adenomas. Postoperative cerebrospinal fluid (CSF) leakage is the leading cause of morbidity after this procedure, with an incidence rate that varies from 0,5-15% in the main published series.ObjectivesThe primary objective of this study was to establish the incidence of postoperative CSF leakage in a sample of surgeries performed at the University Hospital of La Ribera by the same surgical team. The secondary objectives were to: ascertain the distinctive features between patients with and without postoperative CSF leakage, identify risk factors for their development, evaluate the relationship between the surgical technique for closing the sella turcica and the onset of postoperative CSF leakage and evaluate different treatment regimens for this complication.MethodsThe data of 302 consecutive transsphenoidal surgical procedures for pituitary adenoma removal which were performed between 1999 and 2017 were retrospectively reviewed.Results and conclusionsThe incidence of postoperative CSF leakage in our series was 2,3% (in accordance with similar published studies). It was possible to correlate intraoperative CSF leakage with two variables: pituitary macroadenoma and tumors with suprasellar extension (P < .005). This correlation did not exist for postoperative CSF leakage. We found a statistically significant correlation between intraoperative and postoperative CSF leakage (P < .005). Due to the low incidence of postoperative CSF leakage in our series, it was not possible to identify risk factors for its development.     

Pharmacokinetics and brain penetration study of chlorogenic acid in rats

1. The present study is designed to investigate the brain distribution and plasma pharmacokinetics profiles of chlorogenic acid (CGA) after intranasal administration in Charles–Foster rats to evaluate whether the CGA molecules are transported directly via the nose-to-brain path.

2. The CGA is administered intravenously (IV) and intranasally (IN) at the dose of 10?mg/kg. Further, its concentration in the plasma, cerebrospinal fluid (CSF) and the whole brain is analyzed by HPLC-UV method.

3. The study observes that CGA is rapidly absorbed in plasma with t_max of 1?min similar to IV route after IN administration. The peak plasma concentration and AUC_0–24 are higher by 3.5 and 4.0 times respectively in IV administration, compared to IN delivery that represents the significant less systemic exposure of CGA in IN route.

4. However, the concentration of CGA in the brain is 4, 6.5, 5.3, 5.2 and 4.5 times higher at 30, 60, 120, 240 and 360?min, respectively in IN administration compared to IV administration. The exposure of CGA in the brain after IN administration (AUC_{brain, IN}) was significantly greater (4 times) as compared to the exposure of CGA in the brain (AUC_{brain, IV}) after IV administration reflecting significant brain uptake of CGA through nasal route. Therefore, IN delivery of CGA can be a promising approach for the treatment of stroke and neurodegenerative disorders.     

制作角膜缘干细胞完全缺乏动物模型的新方法

目的提出一种新的角膜缘干细胞完全缺乏模型制作方法,为干细胞缺乏疾病的治疗性研究提供可靠的模型。方法利用9mm环钻划界,板层切除角膜组织,通过临床评分、印迹细胞学、组织病理及免疫组织化学验证模型的成功。结果板层切除术后30~45d,模型眼角膜混浊、上皮缺损、大量新生血管长入,印迹细胞学可见PAS( )的杯状细胞,组织病理学检查上皮符合结膜细胞表型,免疫荧光染色可见结膜杯状细胞特异性标志MUC5AC阳性表达。结论环钻划界加板层切除法为一种可靠、有效的角膜缘干细胞完全缺乏模型制作方法。     

Clinical experience with the use of rhG‐CSF in secondary autoimmune neutropenia

This paper outlines the impact of granulocyte‐colony stimulating factor (G‐CSF) used as a single modality therapy in 17 patients with secondary autoimmune neutropenia (S‐AIN) who had been treated a multiple number of times previously. Fifteen of these patients had demonstrable antineutrophil antibodies and two had cellular S‐AIN with haemopoietic inhibitory T‐cells present in the marrow. Prior to treatment, all had had problems with infection. All patients responded within 7 days of commencement of treatment. Provided G‐CSF neutrophil counts were maintained above 1 × 10⁹/l, no further infections occurred. This was achievable by using G‐CSF administered as infrequently as once every 8 days. Eight of the 17 patients remained on G‐CSF, although five switched to the glycosylated form because of side‐effects. None have developed osteoporosis despite 47.29 patient years of total experience with G‐CSF. In conclusion both glycosylated and nonglycosylated G‐CSF can be used effectively in treating AIN on a long‐term basis.     

Progressive myoclonic ataxia with intrathecal immune activation in six patients

In six patients with slowly progressive sporadic cerebellar ataxia and cortical multifocal action myoclonus, cerebrospinal fluid (CSF) IgG index was persistently very high (1.2–6.7) and numerous oligoclonal bands were detected. Progressive cognitive impairment and MRI cerebellar and cerebral atrophy were observed. No serum antibodies were found. Various degenerative, metabolic, inflammatory and systemic diseases were excluded. The cerebellum may be the main target of a degenerative or immune process and releases antigens that, enhancing a compartmentalised (auto)immune response, as suggested by the persistent intrathecal activation, could lead to further cerebellar damage. As the frequency of CSF oligoclonal banding in myoclonic ataxia is unknown, our patients’ disease might represent a hitherto unreported entity or a subset of progressive myoclonic ataxia.

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Sommario Descriviamo sei pazienti con atassia cerebellare sporadica e mioclono corticale d’azione multifocale, nel cui liquor i valori dell’indice IgG si mantenevano persistentemente elevati ed erano presenti numerose bande oligoclonali. I pazienti manifestavano un progressivo declino cognitivo e la RM mostrava atrofia cerebellare e cerebrale. In assenza di anticorpi identificabili non era possibile formulare una diagnosi di malattia nota. Suggeriamo che il cervelletto possa essere il principale bersaglio di un processo degenerativo o immuno-mediato e che gli antigeni liberati inducano la produzione di anticorpi che ulteriormente provocano danno cerebrale. Poiché non è nota la frequenza delle bande oligoclonali nel liquor di pazienti con atassia mioclonica, non sappiamo se la malattia qui descritta sia una entità nuova o un sottogruppo delle atassie miocloniche.

     

双光气致急性损伤对兔肺泡Ⅱ型细胞形态学的影响

目的：通过对日本大耳兔双光气肺损伤后肺泡Ⅱ型细胞内磷脂和形态学变化的观察，探讨双光气对肺Ⅱ型细胞的损伤及其机制．方法：将纯种日本大耳白兔35只随机分为对照组(n＝10)、染毒即刻组(n＝5)、染毒2h组(n＝5)染毒4h组(n＝5)、染毒8h组(n＝5)、染毒12h组(n＝5)；采用浓度一时间法动态式染毒，染毒后按不同时间点对实验动物进行颈总动脉插管放血处死，取肺并用肺灌洗液对支气管肺泡进行灌洗，然后取肺组织作冰冻切片，进行电镜观察，并测定细胞内磷脂含量．结果：肺Ⅱ型细胞内磷脂含量在染毒即刻开始时较正常组含量下降(P＜0．01)；在染毒2h时降到最低，之后上升(P＜0．05)，而在4h后又下降(P＜0．05)．染毒终止后，损伤逐渐加重，染毒后2h磷脂因消耗而降低．染毒后4h，由于代偿功能启动，磷脂短暂升高，出现致伤性代偿期．从染毒2h后开始，细胞损伤加重，磷脂合成进入失代偿期，合成逐渐减少．到染毒后8h，肺泡Ⅱ型细胞内细胞处于致伤性和致死性细胞改变的临界点，细胞出现致死性改变，磷脂合成、分泌停止，细胞出现死亡．结论：兔在双光气染毒12h内，肺泡表面活性物质磷脂的改变有差异，随细胞损伤程度发生改变，出现明显中毒分期：即致伤性改变期、致伤性代偿期、致伤性失代偿期、致死性改变期．     

延迟性脑脊液鼻漏病理机制及诊治探讨

目的总结15例经手术治疗的延迟性脑脊液鼻漏的临床资料,探讨脑脊液鼻漏的病理机制及其与诊断治疗的关系。方法本组共15例脑脊液鼻漏患者,其中颅底骨折13例,自发性1例和垂体瘤术后1例。重点分析术前CTMRI扫描,术中所见,以及疗效三者之间的关系。结果术中见14例患者神经组织疝入鼻窦,垂体瘤术后鼻漏为鞍上池下疝,其中后7例的CT扫描显示骨缺损,MRI显示神经组织下疝与术中所见完全一致。15例术后14例治愈,1例无效,无手术并发症。结论神经组织或鞍上池经颅底缺损疝入鼻窦为外伤后或自发性脑脊液鼻漏不能自愈的病理机制的重要环节,由于上述组织的疝入,导致粘膜、硬膜、蛛网膜难以修复。冠状CT扫描和MRI可确定瘘口部位,如果冠状CT有骨缺损,MRI检查相应部位有脑组织下疝,应积极早期手术治疗。