An unexpected bronchoscopic finding possibly induced by extracorporeal membrane oxygenation: A case report of bronchial Dieulafoy disease.

RATIONALE: Bronchial Dieulafoy disease (BDD), a rarely reported disease, comes from dilated or abnormal arteries under the bronchial mucosa. Patients with BDD are generally asymptomatic so this disease is frequently misdiagnosed. However, the submucosal arteries may dilate and rupture for various reasons, leading to recurrent respiratory tract bleeding and potentially life-threatening conditions. With the change of reversible factors such as intravascular pressure, the arteries may return to normal, allowing patients to recover to an asymptomatic state. This phenomenon has not been mentioned and concerned in previous studies, but it may have important implications for our correct understanding of this disease. PATIENT CONCERNS: A 44-year-old female was admitted to intensive care unit with recurrent malignant arrhythmias. With the assistance of VA-extracorporeal membrane oxygenation (ECMO), both her vital signs and internal environment were all gradually stabilized. However, she had been experiencing recurrent respiratory tract bleeding. While removing the bloody secretion with a fiber bronchoscopy, a congested protruding granule on the wall of the patient's left principal bronchus was found. DIAGNOSIS: The patient was diagnosed with BDD and the granule was thought to be an abnormal artery of BDD. INTERVENTIONS: For the patient's condition, we did not implement any targeted interventions with the abnormal artery. OUTCOMES: After the weaning of VA-ECMO, the patient's granule could not be found and the bleeding had also disappeared. She gradually weaned off the mechanical ventilation and was transferred to the Department of Cardiology. Then the patient was discharged after her condition stabilized. In more than half a year, the patient is in a normal physical condition. LESSONS: The appearance and disappearance of abnormal artery is an interesting phenomena of BDD. The change of intravascular pressure due to various causes such as VA-ECMO may be the primary factor of it.

Risk of sudden coronary death based on genetic background in Chinese Han population.

Associations between gene variations and sudden cardiac arrest or coronary artery disease have been reported by genome-wide association studies. However, the implication of the genetic status in cases of sudden coronary death (SCD) from the Chinese Han population has remained to be investigated. The present study established a mini-sequencing system to examine putative death-causing single nucleotide polymorphisms (SNPs) using multiplex PCR, single base extension reaction and capillary electrophoresis techniques. A total of 198 samples from the Chinese Han population (age range, 34-71 years; mean age, 53.86 years) were examined using this method. Samples were classified into three groups: Coronary heart disease (CHD, n=70), SCD (n=53) and control (n=75) group. Significant associations were identified for 10, 4 and 6 SNPs in CHD, SCD and sudden death from CHD, respectively, using the χ2 test. The SNPs obtained by binary logistic regression may be used to assess and predict the risk of disease. The predictive accuracy of the SNPs in each prediction model and their area under the receiver operating characteristic curve (AUC) values were determined. The AUC of the four SNPs (rs12429889, rs10829156, rs16942421 and rs12155623) to predict CHD was 0.928, the AUC of the six SNPs (rs2389202, rs2982694, rs10183640, rs597503, rs16942421 and rs12155623) to predict SCD was 0.922 and the AUC of the four SNPs (rs16866933, rs4621553, rs10829156 and rs12155623) to predict sudden death from CHD was 0.912. The multifactor dimensionality reduction values were as follows: 0.8690 (prediction model of CHD), 0.7601 (prediction model of SCD) and 0.7628 (prediction model of sudden death from CHD). Taken together, the results of the present study suggested that these SNPs have considerable potential for application in genetic tests to predict CHD or SCD. However, further studies are required to investigate the putative functions of these SNPs.

Diagnostic efficacy of serum procalcitonin, C-reactive protein concentration and clinical pulmonary infection score in Ventilator-Associated Pneumonia.

OBJECTIVE: The aim of this study was to evaluate the diagnostic efficacy of serum procalcitonin (PCT), c-reactive protein (CRP) concentration and clinical pulmonary infection score(CPIS) in ventilator-associated pneumonia(VAP). METHODS: Forty-nine patients who were admitted to the intensive care unit (ICU) of Zhejiang Hospital with suspected VAP were recruited in this study. The serum level of PCT and CRP of all patients were measured and CPIS was calculated at the time of VAP suspected diagnosis. Of the included 49 patients, 24 were finally confirmed of VAP by microbiology assay. And the other 25 patients were considered as clinical suspected VAP without microbiology confirmation. The diagnostic sensitivity, specificity and area under the receiver operating characteristic (ROC) curve (AUC) were calculated using the serum PCT, CRP concentration and CPIS. The correlation among serum PCT, CRP concentration and CPIS were also evaluated by Spearson correlation test. RESULTS: A total of 100 bronchoscopic aspiration sputum specimen were examined in bacterial culture. 30 samples were found with suspected pathogenic bacteria. Six samples were found with 2 types of suspected pathogenic bacteria. PCT serum concentration and CPIS score were significantly different (P<0.05) between the patient group [1.4 (0.68 ∼ 2.24), 6.0 (4.25 ∼ 8.00)] and the control group [0.4 (0.17 ∼ 1.39), 3.0 (1.00 ∼ 5.00)] ; However, the serum CRP [102.8(66.75 ∼ 130.90) vs 86.1(66.95 ∼ 110.10)] was not statistically different between the two groups (P>0.05). A significant correlation was found between serum PCT and CRP concentrations (r=0.55, P<0.01), but not between PCT vs CPIS and CRP vs CPIS (p>0.05). The diagnostic sensitivity, specificity and AUC were 72.0%, 75.0%, 0.81 (0.69 ∼ 0.93) for CPIS; 60.0%, 87.5%, 0.76 (0.62 ∼ 0.90) for PCT and 68.0%, 58.3%, 0.59 (0.43 ∼ 0.76) for CRP. CONCLUSION: PCT serum level and CPIS score are elevated in VAP patients and could therefore represent potential biomarkers for VAP early diagnosis.

Antigen-specific immature dendritic cell vaccine ameliorates anti-dsDNA antibody-induced renal damage in a mouse model.

OBJECTIVES: Dendritic cells (DCs) can inhibit immune response by clonal anergy when immature. Recent studies have shown that immature DCs (iDCs) may serve as a live cell vaccine after specific antigen pulse based on its potential of blocking antibody production. In this study, we aimed to investigate the effects of nuclear antigen-pulsed iDCs in the treatment of lupus-like renal damages induced by anti-dsDNA antibodies. METHODS: iDCs were generated from haemopoietic stem cells in bone marrow and then pulsed in vitro with nuclear antigen. The iDC vaccine and corresponding controls were injected into mice with lupus-like renal damages. The evaluation of disease was monitored by biochemical parameters and histological scores. Anti-dsDNA antibody isotypes and T-lymphocyte-produced cytokines were analysed for elucidating therapeutic mechanisms. RESULTS; The mice treated with antigen-pulsed iDCs had a sustained remission of renal damage compared with those injected with non-pulsed iDCs or other controls, including decreased anti-dsDNA antibody level, less proteinuria, lower blood urea nitrogen and serum creatinine values, and improved histological evaluation. Analysis on isotypes of anti-dsDNA antibody showed that iDC vaccine preferentially inhibited the production of IgG3, IgG2b and IgG2a. Furthermore, administration of antigen-treated iDCs to mice resulted in significantly reduced IL-2, IL-4 and IL-12 and IFN-γ produced by T-memory cells. Conversely, the vaccination of antigen-pulsed mature DCs led to increased anti-dsDNA antibody production and an aggravation of lupus-like disease in the model. CONCLUSIONS; These results suggested the high potency of iDC vaccine in preventing lupus-like renal injuries induced by pathogenic autoantibodies.