Objective To analyze the clinical features and etiologic of community-acquired pneumonia (CAP) among the elderly aged 80 and over, and provide evidence for clinical diagnosis and treatment. Methods The clinical characteristics and etiology of the elderly CAP (≥80 years old) were analyzed by collecting and comparing the clinical characteristics and etiology between the very elderly CAP group (≥80 years old, 94 cases) and control group (65 to 79 years old, 100 cases). Results On clinical symptoms, there were statistical differences in dyspnea and gastrointestinal symptoms, systemic symptoms, and mental status (P<0.05) between the two groups. There was no statistically significant difference in upper respiratory tract symptoms, fever, cough, sputum, hemoptysis and chest pain between the two groups (P>0.05). On the complications, the very elderly CAP group was more prone to respiratory failure, sepsis, urinary tract infection and electrolyte metabolism than the control group (P<0.05). On the experimental indicators, anemia and abnormal renal function in the elderly CAP group were high (P<0.05). There was no statistical difference between the two groups of inflammation indicators (white blood count, procalcitonin, C-reactive protein, erythrocyte sedimentation rate, neutrophil alkaline phosphatase score). The pneumonia severity index score and CURB-65 score of the very elderly CAP group were significantly higher than those of the control group (P<0.001). On pathogen analysis, in the very elderly CAP group the number of bacterial infections (23/94), viral infections (21/94) and bacterial mixed virus infections (21/94) were probably equivalent, and the proportion of bacterial infections of two or more types accounted for 17.0% (16/94); The bacteria detection rate was Streptococcus pneumoniae (22.4%), Pseudomonas aeruginosa (19.4%), Stenotrophomonas maltophilia (16.4%), Staphylococcus aureus (14.9%). Viral infection mainly focused on influenza A virus (23/94) and human cytomegalovirus (21/94). Bacterial mixed virus infection was mainly caused by Streptococcus pneumoniae and influenza A virus infection. Comparing the two groups, the most common bacterial pathogen both of them was Streptococcus pneumoniae, but the overall proportion was dominated by gram-negative bacteria, Pseudomonas aeruginosa, Stenotrophomonas maltophilia, Acinetobacter baumannii and Klebsiella pneumoniae were more common; the gram-positive bacteria in the two groups were mainly Streptococcus pneumoniae and Staphylococcus aureus. There was no significant difference in the detection rate of above Gram-positive bacteria between the two groups (P>0.05). The two groups of virus infections were mainly influenza A virus, and the difference was not statistically significant (P>0.05). The two groups of single bacteria rate, single virus infection rate, double virus infection rate and bacterial mixed virus infection rate were similar, the difference had not been found (P>0.05). Conclusions The elderly (aged 80 and over) CAP group is prone to dyspnea, often presents with extrapulmonary atypical symptoms such as digestive tract symptoms, systemic symptoms and psychiatric symptoms, and usually accompanied with many complications. The etiological treatment mainly covers gram-negative bacteria, and we must pay attention to the possibility of combined virus infection.
ObjectiveTo investigate the relationship between pulmonary ventilation function (obstructive and restrictive ventilation dysfunction) and atherosclerosis, and explore the correlation between brachial-ankle pulse wave velocity (ba-PWV, an effective index for evaluating atherosclerosis) and pulmonary ventilation function.MethodsFrom January to August 2018, a total of 6403 healthy subjects who reported no major chronic diseases such as stroke, myocardial infarction, cor pulmonale or malignant tumor were selected. Past history such as smoking history, hypertension, diabetes, blood biochemistry, and blood hypersensitive C reactive protein (hs-CRP), hemodynamic indexes such as systolic pressure, diastolic pressure and ba-PWV, body measurement indexes such as height, weight, waist circumference and pulmonary ventilation function were collected. The relationship between ba-PWV and pulmonary ventilation function were evaluated.ResultsA total of 2433 subjects were included, including 916 males and 1517 females. Ba-PWV showed significant positive correlations with age, smoking index, waist circumference, systolic blood pressure, diastolic blood pressure, triglyceride, cholesterol, low density lipoprotein, hs-CRP, glycosylated hemoglobin, and significant negative correlations with height, percentage of forced vital capacity (FVC) in the predicted value (FVC%pred), forced expiratory volume in one second (FEV1), percentage of FEV1 in the predicted value (FEV1%pred), FEV1/FVC ratio and percentage of maximun midexpiratory flow (MMEF) in the predicted value (MMEF%pred). The ba-PWV was not correlated with weight, body mass index, FVC, MMEF, γ-glutamyl transpeptidase, high density lipoprotein, creatinine or uric acid. In multiple regression analysis using factors other than ba-PWV and respiratory function as adjustment variables, both FVC%pred and FEV1%pred showed significant negative relationships with ba-PWV (P<0.05).ConclusionsThe results indicate that FEV1/FVC, an indicator of airflow limitation, is not a predictor of ba-PWV. However, since ba-PWV showed significant negative relationship with FVC%pred and FEV1%pred, clinically assessment of arterial stiffness might be considered in individuals with impaired pulmonary ventilation.
ObjectiveBenign familial epilepsies that present themselves in the first year of life include benign familial neonatal epilepsy (BFNE), benign familial neonatal-infantile epilepsy (BFNIE) and benign familial infantile epilepsy (BFIE). We aim to investigate gene mutations and the relationship between genotypes and clinical phenotypes in benign familial epilepsies in the first year of life.MethodsWe recruited families with benign familial epilepsies in the first year of life at Peking University First Hospital from September 2006 to January 2018. Clinical information and blood samples were obtained from probands and their family members. For BFIE families, mutation screening of PRRT2 was performed by using the polymerase chain reaction (PCR) and Sanger sequencing at first. The PRRT2 mutation negative probands of BFIE families were further screened for pathogenic mutations by targeted next-generation sequencing. The probands of BFNE and BFNIE families were screened for pathogenic mutations by targeted next-generation sequencing.ResultsA total of 89 families with benign familial epilepsies in the first year of life were collected. Of the 89 families, 4 were classified as BFNE, 7 as BFNIE, and 78 as BFIE. Genetic testing led to the identification of gene mutations in 68 families (76.4%), including 50 families had PRRT2 mutations (hotspot mutation c.649dupC was detected in 32 families; c.649delC was detected in 6 families), 9 families had KCNQ2 mutations, 8 families had SCN2A mutations, and one family had GABRA6 mutation. In the 4 BFNE families, causative mutations were only found in KCNQ2, which was identified as the causative gene in 3 families. The remaining one BFNE family was not detected with any pathogenic mutation. All 7 BFNIE families had identifiable gene mutations, KCNQ2 was found in 3 families, SCN2A in 3 families, and PRRT2 in one family. In the 78 BFIE families, gene mutations were identified in 58 families (74.4%), with PRRT2 mutations found in 49 families (62.8%), SCN2A mutations found in 5 families, KCNQ2 mutations found in 3 families, and a novol GABRA6 mutation found in one family. Twenty BFIE families were not identified with any gene mutations. In 78 BFIE families, 18 were subclassified as infantile convulsions with paroxysmal choreoathetosis syndrome(ICCA). 17 of 18 ICCA families were detected with PRRT2 mutations (17/18, 94.4%). The remaining ICCA family was not detected with any pathogenic mutation.ConclusionsOur results confirmed that mutations in KCNQ2, SCN2A, and PRRT2 are major genetic causes of benign familial epilepsy in the first year of life in the Chinese population. KCNQ2 is the major gene related to BFNE. PRRT2 is the main gene responsible for BFIE. KCNQ2 and SCN2A mutations are common in BFNIE families. GABRA6 mutation might be a new cause of BFIE. Identification of underlying gene mutation can be helpful for clinical diagnosis and judgement of the prognosis.