Objective To evaluate the clinical effect of itraconazole oral solutions on pulmonary candidiasis albicans in ICU patients.Methods A total of 71 patients with candida ablicans in their sputum clutures were randomized into two groups.The itraconazole group(n= 36)received itraconazole 200 mg,p.o.(including nasal feeding),q12h for 14 days.The fluconazole group(n=35)received fluconazole 400 mg for the first dose,then 200 mg,i.v.drip,qd for 14 days.Results There were 31 patients in the itraconazole group and 29 paitents in the fluconazole group who completed their treatment.In the itraconazole and fluconazole group,the clearance of candida ablicans was 64.52%(20/31)vs.65.55%(19/29),cleaning time(10.12?2.57)vs(8.87?1.95)days,effective rate 58.06%(18/31)vs 62.07%(18/29),recovery rate is 19.35%(6/31)vs 17.24%(5/29),occurrence of hepatic dysfunction is 25.81%(8/31)vs 24.14%(7/29),and withdrawal for inefficacy was 3.23%(1/31)vs 6.90%(2/29),respectively.These parameters did not have statistical significance.Conclusion Itraconazole oral solutions can be used effectively and safely in the treatment of pulmonary candidiasis albicans in ICU.Patients with renal dysfunction do not need to adjust the dosage.

Objective To evaluate the value of central venous pressure (CVP),central venous oxygen saturation (ScvO2) and venous-arterial carbon dioxide partial pressure gradient (Pv-aCO2) in the diagnosis of septic shock-induced left ventricular dysfunction.Methods Consecutive patients with septic shock were enrolled from September 2013 to September 2014 in ICU at Peking Union Medical College Hospital.The data of CVP,Pv-aCO2 and ScvO2 were recorded and analyzed.According to the left ventricular ejection fraction (LVEF) tested by bedside echocardiography,the patients were divided into two groups:new onset of left ventricular dysfunction (LVEF ＜ 50％) group and non-left ventricular dysfunction (LVEF ≥ 50％) group.A diagnostic model was created by logistic regression.The diagnostic performance and cut-off values of CVP,Pv-aCO2,ScvO2 were determined using receiver operating characteristic (ROC) curve analysis.Results Among 93 patients enrolled,39 were diagnosed with left ventricular dysfunction.In the new onset group,CVP [(12.5±3.9) mmHg(1 mmHg=0.133 kPa) vs (10.4±2.5)mmHg;P=0.005] and Pv-aCO2 [(7.5 ± 3.9) mmHg vs (4.5 ± 2.6) mmHg;P ＜ 0.001] were significantly higher than those in the non-left ventricular dysfunction group,while ScvO2 [(62.4 ± 10.5) ％ vs (72.6 ± 9.0) ％;P ＜ 0.001] was significantly lower.As far as the diagnostic value of these three parameters were concerned for left ventricular dysfunction,the sensitivity of CVP ≥ 12.5 mmHg was 46.2％,specificity 81.5％ with an area under ROC curve (AUCROC) 0.674;the sensitivity of Pv-aCO2 ≥ 5.0 mmHg 76.9％,specificity 37.0％,AUCROC 0.738;the sensitivity of ScvO2 ≤65.8％ 64.1％,specificity 78.6％,AUCROC 0.775.When the cut-off values were determined by ROC,the diagnostic performance of the model was ≥0.377 with the sensitivity,specificity and AUCROC 82.1％,79.6％ and 0.835,respectively.Conclusion In patients with septic shock,the logistic regression model established by CVP,Pv-aCO2 and ScvO2 contributes to the diagnosis of septic shock-induced left ventricular dysfunction.

Spinocerebellar ataxia (SCA) is a group of highly heterogeneous autosomal dominant genetic disease, including many subtypes. SCA11 is a rare subtype of SCA, and is caused by mutant TTBK2 gene. A case of SCA11 was reported in this article. Whole exome sequencing showed that there was a c.1284dupA frameshift mutation in TTBK2 gene. Literature review found that only 6 pedigrees of SCA11 have been reported, but the mutation site of this case is a novel identified mutation that has not been reported in the Human Gene Mutation Database.

Objective:To investigate the clinical, neuropsychological, and neuroimage characteristics in patients with corticobasal syndrome (CBS), and to elucidate the exact diagnosis of CBS patients.Methods:Twelve CBS cases admitted to the Department of Neurology, Huashan Hosiptal,Fudan University from April 2019 to July 2021 were retrospectively enrolled in this study. Those data, including clinical features (demographic data and clinical characteristics of cortical dysfunction and movement disorder), neuropsychological assessment [Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scales score], brain magnetic resonance imaging (MRI) and multi-mode positron emission tomography (PET)/CT, were collected and carefully reviewed. Exact diagnosis of these patients was given according to the disease diagnosis criteria.Results:Cortical dysfunction and asymmetrical movement disorders were found in all cases, with poor response to levodopa. Patients suffered from cognitive impairment (MMSE score 16.16±9.82, MoCA score 13.44±7.35). The cranial MRI demonstrated significant asymmetric atrophy of frontal and parietal lobes, especially in the pre- and post-central gyrus. Fluorodeoxyglucose PET of 12 patients showed asymmetric frontal lobe and basal ganglia (especially caudate and putamen) hypometabolism (obviously on the contralateral side of the affected limb). Tau PET was implemented in 11 patients and displayed that abnormal tau protein deposition was positive in the cortex and/or subcortex in all patients. Of the 4 cases, who completed amyloid PET, amyloid protein deposition was positive in the cortex of 2 patients. As a result, 6 patients were diagnosed as progressive supranuclear palsy, 1 patient was diagnosed as corticobasal degeneration, and 5 patients were diagnosed as Alzheimer′s disease.Conclusions:The etiology of CBS is heterogeneous. The combination of clinical manifestation, cranial MRI and multi-mode PET/CT helps the differential diagnosis of CBS.

Functional cognitive disorder (FCD) refers to complaints of persistent problematic cognitive decline, which is inconsistent between self-reported symptoms and daily function and/or neuropsychological test results, and the symptoms lasted for at least six months without obvious progress. Poor ability to reflect on and monitor cognitive processes has been suggested as a key mechanism underlying the disorder. In this review, the concept, research status, clinical manifestations and diagnosis of FCD were systematically examined, which is helpful to identify the subjective cognitive decline caused by non-degenerative diseases and conduct individualized intervention treatment.