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Objective:To investigate the clinical manifestations and prognosis of severe coronal virus disease 2019(COVID-19)pneumonia combined with coronary artery disease(CAD)in the elderly.Methods:A total of 351 old patients(≥60 years)with severe COVID-19 pneumonia combined with CAD admitted to Tongji Hospital of Wuhan from February 2020 to March 2020 were enrolled in this retrospective study.The patients were divided into CAD group(n=52)and non-CAD group(n=299). The clinical data, the changes of blood tests and cardiovascular complications were observed.Results:Compared with non-CAD group, CAD group showed a longer time of stay in hospital[(12.3±2.6)d and(9.3±2.1)d, t=3.24, P=0.002], and higher incidence of cardiovascular complications, such as myocardial infarction(7.7% and 0.0%, χ2=21.6, P<0.001), heart failure(15.4% and 0.3%, χ2=34.7, P<0.001), arrhythmia(50.0% and 12.4%, χ2=24.45, P<0.001)and all-cause mortality(15.4% and 4.3%, χ2=7.94, P=0.005). The serum levels of interleukin-2 receptor, interleukin 6, CK-MB, cTnI, NT-proBNP, D-dimer and fibrinogen were higher in CAD group than in non-CAD group.The oxygenation index was significantly lower and the blood lactic acid level was higher in CAD group than in non-CAD group. Conclusions:The aged patients with severe COVID-19 pneumonia combined with CAD show obvious inflammatory reaction, high incidence of cardiovascular complications and high mortality.
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Objective:To investigate the relationship of polymorphism of leptin receptor gene Gln223Arg with asthma and metabolic syndrome.Methods: Collected 120 asthma patients,92 metabolic syndrome patients,54 asthma combined metabolic syndrome patients and 81 normal controls.According to the severity,the asthma patients were divided into mild-medium group and severe group.The serum leptin level was measured by ELISA,the genotypes of leptin receptor were analyzed by the method of polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP),and statistcs of each subject′s MBI,blood pressure,lung function and fasting blood glucose were collected.Results: ①There were significant differences in genotype and allele frequency in leptin receptor gene Gln223Arg between the metabolic syndrome group,asthma combined metabolic syndrome group and normal control group(P<0.05).②The allele frequency and genotype in leptin receptor gene Gln223Arg were significant different between the severe asthma group and normal control group(P<0.05).③The serum leptin level,BMI and systolic blood pressure of AA+AG genotype group were significiant higher than GG genotype group(P<0.05),while the value of FEV1% and FEV1/FVC of lung function were lower than GG genotype group(P<0.05).Conclusion: Leptin receptor gene Gln223Arg polymorphism is correlated with asthma and metabolic syndrome,and by causing leptin resistance,the A allele might be the genetic factor that contribute to individual susceptibility for asthma and metabolic syndrome.
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Objective To investigate the clinical characteristics and prognosis in the patients with type 2 diabetes mellitus and invasive pulmonary aspergillosis(IPA) for better management of the disease .Methods Clinical data of 9 cases of type 2 diabetes associated with IPA treated in Qingdao Municipal Hospital from January 2008 to December 2013 were analyzed retrospectively . Results The diagnosis of IPA was proven in 5 and probable in 4 of the 9 patients .The main clinical manifestations were fever , cough and expectoration .The findings of CT scan mainly showed pulmonary nodules along the bronchovascular bundle and cavity signs .Bronchoscopy showed congestion ,edema ,and erosion of bronchial mucosa covered with yellow‐white or brown pus ,partially or completely blocking the lumen .Antifungal treatment was effective for 4 patients .The other five patients died . Conclusions Type 2 diabetes mellitus is a risk factor for developing invasive pulmonary aspergillosis .Early diagnosis and proper treatment are critical for improved prognosis .
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Objective To investite the effect of endotoxin pretreatment on lung injury induced by hepatic ischemia reperfusion in rabbits and its mechanism. Method Forty-eight New Zealand white rabbits were randomly divided into4 groups with 12 rabbits each group:routine control group,pretreatment control group,ischemia reperfusion group (IR group), and preperfusion group( LPS + IR group). Rabbits of routine control group received operative dissector only, and those of pretreatment control group received pretratment of daily intraabdominal injection of lipopo|ysaccharide(O.5,0.5,and 1.0 mg/kg,respectively)in the 3 days before operative dissector.Livers of IR group were rendered and ischeraic for 30 minutes, and repeffused for up to 4 hours. Rabbits of LPS +IR group received the preueaunent before heretic ischemia repeffusion. Four hours after reperfusion, serum endotoxin,tumor necrosis factor-α(TNF-α), wet/dry ratio and broncho-alveolar lavage fluid protein content of lung,malondialdehyde(MDA) and mpenrxide dismutase(SOD) in lung homogenate, lung injury ratio, and activity of Nuclear factor-kB(NF-kB) in alveolar macrophage wene examined. Differences within the groups were analyzed using One way ANOVA. Results Between the two control groups,there were no significant differences in all indexes(P>0.05). The TNF-α[ (48.31±5.31)pg/ml vs.(56.47±5.09)pg/ml, P<0.01],wet/dry ratio [(4.98±0.33)vs. (5.22±0.31), P = 0.03],broncho-alveolar hvage fluid protein content[(0.68±0.11)g/L vs. (0.76±0.10)g/L, P =0.04],MDA[(0.86±0.06)nmol/mg vs. (0.93±0.07)nmol/mg, P =0.02],lung injury ra-tio[(13.4±4.3)% vs. (17.4±4.1)%, P = 0.03],and the activity of NF-gB[(5.82±1.12)OD/mm2 vs.(7.40±1.26)OD/mm2, P<0.01] in alveolar macrophage of the LPS+ IB group were all significantly lower than those of IB group, while the SOD[ (90.30±7.38 )U/rag vs. (84.44±7.90 )U/rag, P = 0.04]of LPS + IR group was significantly higher than that of IR group. Conclusions Endotoxin pretrealment may ameliorate the lung injury induced by hepatic isehernia reperfusion. The mechanism may be that endotoxin pretreatment deoreases production of serum TNF-α and the activity of NF-kB in alveolar maerophage.