Buried Bumper Syndrome: A common complication of levodopa intestinal infusion for Parkinson disease

BackgroundPercutaneous endoscopic gastrostomy (PEG) is required for Levodopa/Carbidopa Intestinal Gel (LCIG) delivery in patients with advanced Parkinson's disease (PD) as well as for enteral feeding in a variety of neurological disorders. Buried Bumper Syndrome (BBS) is a serious complication of PEG. The frequency of BBS in patients receiving LCIG treatment has never been reported.ObjectivesTo compare the frequency of BBS in patients on LCIG treatment or on enteral feeding over the past 12 years and identify possible risk factors.MethodsWe reviewed prospectively recorded data from 2009 to 2020 on two case-series: LCIG-treated PD patients and non-PD patients on enteral nutrition. We identified all BBS incidences. Patients’ characteristics, clinical manifestations, BBS management, possible risk factors and outcomes were analyzed.ResultsDuring the 12 years, 35 PD patients underwent PEG insertion for LCIG infusion, and 123 non-PD patients for nutritional support. There were eight cases of BBS in six PD patients (17.1%). Six of them were effectively managed without treatment discontinuation. Of the enteral feeding patients, only one developed BBS (0.8%) (p < 0.001). We identified inappropriate PEG site aftercare, weight gain, early onset PD, longer survival, treatment duration, dementia and PEG system design as potential risk factors for BBS development.ConclusionsBBS occurs more frequently in LCIG patients than in patients receiving enteral feeding. If detected early, it can be successfully managed, and serious sequalae or treatment discontinuation can be avoided. Regular endoscopic follow-up visits of LCIG-treated patients and increased awareness in patients and clinicians are recommended.     

Short-Duration Prednisolone in Children with Nephrotic Syndrome Relapse: A Noninferiority Randomized Controlled Trial

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Outcomes and risk management in type B aortic dissection patients with acute kidney injury: a concise review

PurposeType B aortic dissection is a rare but life-threatening disease. Thoracic endovascular aortic repair (TEVAR) was widely used for Type B aortic dissection patients in the last decade due to the lower mortality and morbidity compared with open chest surgical repair (OCSR). AKI in type B aortic dissection is a well-recognized complication and indicates poor short-term and long-term outcome. The objective of this concise review was to identify the risk factors and the impact of AKI on type B aortic dissection patients.Methods and resultsA literature search was performed using PubMed, Embase, MEDLINE, and Cochrane Library with the search terms ‘type B aortic dissection’ and ‘acute kidney injury’ (AKI), and all English-language literatures published in print or available online from inception through August 2020 were thoroughly reviewed. Studies that reported relative AKI risks and outcomes in type B aortic dissection patient were included. Major mechanisms of AKI in type B aortic dissection included renal hypoperfusion, inflammation response, and the use of contrast medium. Type B aortic dissection patients with AKI significantly had increased hospital stay duration, need of renal replacement therapy, and 30-d and 1-year mortality.ConclusionsAKI in type B aortic dissection is a well-recognized complication and associated with poor short-term and long-term outcome. Early identification of high-risk patients, early diagnosis of AKI, stabilization of the hemodynamic parameters, avoidance of nephrotoxic drugs, and optimization of the use of contrast agents are the major strategies for the reduction of AKI in type B aortic dissection patients.     

CYP2C19*2、CYP2C19*3基因分型与急性缺血性脑卒中再发脑卒中的关系

目的探讨细胞色素P450药物代谢酶(CYP)2C19基因分型与氯吡格雷治疗的急性缺血性脑卒中患者再发脑卒中的关系。方法选取2018年5月—2018年12月常州市第一人民医院收治接受氯吡格雷治疗的159例急性缺血性脑卒中患者,检测患者入院后空腹外周血中CYP2C19*2,CYP2C19*3基因分型。对患者进行随访,随访截至2020年2月,观察再发脑卒中的情况,并分析CYP2C19*2,CYP2C19*3基因分型与再发脑卒中关系。结果随访时间14~22个月,平均随访时间为(18.2±1.5)个月,共7例患者失访,共20例(13.2%)患者复发缺血性脑卒中。再发脑卒中患者中CYP2C19*2 GG型及CYP2C19*3 GG型均低于无复发患者(P<0.05),CYP2C19*2 GA型,CYP2C19*2 AA型CYP2C19*3 GA型,CYP2C19*3AA型均高于无复发患者(P<0.05)。Kaplan-Meier法并Log-rank检验结果显示,CYP2C19*2 GG型无复发时间长于AA型,差异有统计学意义(Log-rank=6.759,P=0.034)。CYP2C19*3GG型无复发时间长于AA型,差异有统计学意义(Log-rank x2=8.660,P=0.013)。多因素Cox分析结果显示,糖尿病、氯吡格雷抵抗,CYP2C19*2及CYP2C19*3基因型是再发脑卒中影响因素(P<0.05)。结论在接受氯吡格雷治疗急性缺血性脑卒中患者中,CYP2C19*2及CYP2C19*3突变型再发脑卒中的风险明显增高。     

NUDT15 is a key genetic factor for prediction of hematotoxicity in pediatric patients who received a standard low dosage regimen of 6-mercaptopurine

6-Mercaptopurine (6-MP) is commonly used for treatment of acute lymphoblastic leukemia (ALL). The incidence of hematotoxicity caused by this drug is quite high in Asians even using a standard low dosage regimen. The present study was aimed to elucidate the impact of thiopurine S-methyltransferase (TPMT), a nucleoside diphosphate-linked moiety X-type motif 15 (NUDT15), inosine triphosphatase (ITPA) and ATP Binding Cassette Subfamily C Member 4 (ABCC4) polymorphisms on hematotoxicity in pediatric patients who received a standard low starting dose of 6-MP. One hundred and sixty-nine pediatric patients were enrolled and their genotypes were determined. Patients who carried NUDT15¹3 and NUDT15¹2 genotypes were at a 10–15 fold higher risk of severe neutropenia than those of the wild-type during the early months of the maintenance phase. Risk of neutropenia was not significantly increased in patients with other NUDT15 variants as well as in patients with TPMT, ITPA or ABCC4 variants. These results suggest that NUDT15 polymorphisms particularly, NUDT15¹3 and NUDT15¹2, play major roles in 6-MP-induced severe hematotoxicity even when using a standard low dosage of 6-MP and genotyping of these variants is necessary in order to obtain precise tolerance doses and avoid severe hematotoxicity in pediatric patients.     

原发性干燥综合征生物标志物的研究进展

目前原发性干燥综合征(pSS)诊断仍然依赖于侵入性小涎腺活检手术,常导致其早期诊断异常艰难,因此筛选特定生物标志物可能对pSS诊断和个体化治疗极为有益。本文回顾传统标志物及与B细胞活化和表观遗传相关的新标志物,并综述组学标志物研究进展。尽管生物标志物前景较好,但其可靠性仍需扩大样本量进行验证。