Incidence, risk factors, and outcome of bronchial asthma exacerbation in pregnancy: is there a change from prior estimates?
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Aim To explore the changes regarding the incidence, risk factors, and outcome of bronchial asthma (BA) exacerbation in pregnancy in the setting of advancements in the management and pharmacotherapy of asthma compared with that previously reported. Patients and methods A prospective cohort study recruited 308 pregnant asthmatic patients in the period from January 2015 to January 2018. All patients received asthma health education (adherence to medications, proper usage of inhalers, written action plan, trigger avoidance, and smoking cessation counseling) and a monthly revision and adjustment of asthma medications according to its control together with treatment of exacerbation when present until 36 weeks of gestation. BA exacerbation was the primary outcome of the present study. Results Seventy-seven (25%) patients experienced exacerbations, and 25 of them were hospitalized, with ICU admissions in 11 (3.5%) patients. Exacerbation was evident in those with higher;Deg;BM;Deg;I (32.86±3.53 kg/m2, P=0.01), current smoker (28.6%, P<0.001), low education level (42.9%, P=0.01), and severe baseline asthma (57.1%, P<0.001). Multivariate logistic analysis identified certain independent predictors of exacerbation and hospitalization in pregnant asthmatics. Pregnant asthmatic with;Deg;BM;Deg;I more than 32.5 kg/m2 [odds ratio (OR), 1.6; 95% confidence interval (CI), 1.67–3.99; P=0.026) and current smoker (OR, 1.4; 95% CI, 1.39–4.79; P=0.03) were more likely to have exacerbation. Moreover, those with baseline severe asthma (OR, 1.2; 95% CI, 1.12–2.31; P=0.028) were at increased risk of hospitalization owing to exacerbation. There was no association between adverse perinatal outcomes and;Deg;BA;Deg; exacerbation in pregnant asthmatics. Conclusion The incidence of BA exacerbation during pregnancy is observed to be reduced in the present study compared with the previously reported. Being smoker and having higher BMI were predictors of exacerbation, whereas severe baseline asthma was predictor of hospitalization in pregnant asthmatics.Abstract Background: At present, there is little information in Bulgaria regarding the rate and stability of frequent-exacerbation phenotype in COPD patients. Aim: To study the rate and stability of frequent-exacerbation phenotype in COPD patients. Materials and methods: We followed up 465 COPD patients for exacerbations over a 3-year period. Exacerbations were defined as events that resulted in treatment with antibiotics and/or corticosteroids (moderate), or that led to hospitalization (severe). Result: Approximately 10% of the patients had two or more exacerbations per year (frequent-exacerbation phenotype), and this structure stayed stable over the study period. The exacerbation rate in the first year of follow up was 0.33 per stage I COPD patients (according to GOLD stages), 0.49 per stage II COPD patients; 0.69 - for stage III, and 1.06 for stage IV COPD patients. The frequent-exacerbation rate increased from stage I to stage IV by 4.35%, 9.17%, 10.79%, and 20.97%, respectively. A history of previous year exacerbations increased the risk of new exacerbations: with a history of one exacerbation - OR 2.1820 (95% CI: 1.4018 to 3.3965, p = 0.0005), and with a history of two exacerbations - OR 4.6460 (95% CI: 2.3286 to 9.2696; p < 0.0001). The frequent-exacerbation phenotype appeared to be unstable over the study period - up to 33% from those patients stayed in the phenotype for the next year. Conclusions: The exacerbation frequency and the rate of frequent-exacerbation phenotype increases with COPD progression. History of exacerbations in the previous year is a significant risk factor for exacerbations of COPD. The frequent-exacerbation phenotype appeared to be unstable over the study period. The pheno-type of non-exacerbators was more likely to remain stable over time.
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Interferon-β (IFN-β) is an effective drug in multiple sclerosis (MS) but it may cause acute exacerbation of MS following the initiation of treatment. This study evaluated patients with rapid exacerbation of multiple sclerosis (REMS) following the initiation of IFN-β.We retrospectively reviewed the clinical records of 2350 patients with multiple sclerosis who started treatment with IFN-β and were registered with Isfahan MS Society (IMSS). Patients with rapid exacerbation of multiple sclerosis within 24 hours after initiation of IFN-β treatment were selected and their demographic and clinical data were extracted.We identified nine patients with rapid exacerbation of multiple sclerosis following the initiation of IFN-β. Their mean age at the time of treatment with IFN-β was 37.3 ± 6.28 years. Seven patients had rapid exacerbation of multiple sclerosis after initiation of IFN-β 1a and two patients after IFN-β 1b. The course of disease in all of these patients was relapsing-remitting. However, all had converted into secondary progression within the first year after occurrence of rapid exacerbation of multiple sclerosis following the initiation of IFN-β.This study may indicate that the effects of IFN-β are not purely anti-inflammatory and a small percentage of MS patients experience rapid exacerbation of multiple sclerosis following the initiation of IFN-β. Future studies are needed to validate our findings.
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Background: We tested the hypothesis that genetically reduced activity of glutathione S -transferases (GST) T1 and M1 were associated with increased risk for asthma.
Methods: We genotyped participants in the Copenhagen City Heart Study (n=10,335) for the exact number of GSTT1 and GSTM1 gene copies and recorded asthma outcomes. We also performed a meta-analysis of 37 studies comprising 5954 asthma cases and 14513 controls to assess the risk for asthma in GSTT1*0/0 homozygotes.
Results: The odds ratio for asthma was stepwise increased with decreasing number of GSTT1 gene copies (P=0.03): GSTT1*0/0 homozygotes and *1/0 heterozygotes had adjusted odds ratios for asthma of 1.27 (95%CI: 1.03-1.56) and 1.07 (0.92-1.25), respectively, compared with *1/1 homozygotes. When the asthma definition was restricted to participants who only had allergic asthma or took asthma medication, GSTT1*0/0 versus *1/1 homozygotes had adjusted odds ratios of 1.34 (1.01-1.79) for allergic asthma and of 1.20 (0.88-1.64) for asthma medication. When the asthma definition included any of the three different asthma definitions, GSTT1*0/0 homozygotes had an adjusted odds ratio for any asthma of 1.24 (1.02-1.51) compared with *1/1 homozygotes. In meta-analysis, random effects odds ratio for asthma was increased at 1.35 (1.14-1.59) in GSTT1*0/0 homozygotes versus individuals with *1/0 or *1/1 genotypes. None of the risk estimates for GSTM1 genotypes differed from 1.0 for any of the four different definitions of asthma (P=0.17-0.95).
Conclusion: The results suggest that individuals with genetic GSTT1 deficiency have increased risk for asthma, while asthma risk is unaffected by GSTM1 deficiency.
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Background Many human epidemiologic studies demonstrate that maternal asthma confers greater risk of asthma to offspring than does paternal disease. However, a handful have shown the opposite. Given this disparity, a meta-analysis is necessary to determine the veracity and magnitude of the "maternal effect." Methodology/Principal Findings We screened the medical literature from 1966 to 2009 and performed a meta-analysis to compare the effect of maternal asthma vs. paternal asthma on offspring asthma susceptibility. Aggregating data from 33 studies, the odds ratio for asthma in children of asthmatic mothers compared with non-asthmatic mothers was significantly increased at 3.04 (95% confidence interval: 2.59–3.56). The corresponding odds ratio for asthma in children of asthmatic fathers was increased at 2.44 (2.14–2.79). When comparing the odds ratios, maternal asthma conferred greater risk of disease than did paternal asthma (3.04 vs. 2.44, p = 0.037). When analyzing the studies in which asthma was diagnosed by a physician the odds ratios were attenuated and no significant differences were observed (2.85 vs. 2.48, N = 18, p = 0.37). Similarly, no significant differences were observed between maternal and paternal odds ratios when analyzing the studies in which the patient population was 5 years or older (3.15 vs. 2.60, p = 0.14). However, in all cases the trend remained the same, that maternal asthma was a greater risk factor for asthma than paternal. Conclusions/Significance The results show that maternal asthma increases offspring disease risk to a greater extent than paternal disease.
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To determine whether an increase in plasma concentration of S-100 protein can serve as a marker for acute exacerbation of multiple sclerosis.The plasma level of S-100 protein was investigated in 28 patients suffering from multiple sclerosis. Of these, 17 patients were admitted for acute exacerbation and 11 patients had a stable disease with no clinical signs for acute exacerbation. S-100 protein concentrations in plasma were determined with an immunofluorometric sandwich assay.Plasma concentrations were significantly elevated in patients who were examined within 7 days after the onset of acute exacerbation (n = 6). S-100 levels of patients 8 to 28 days after the onset of acute exacerbation (n = 11) did not differ from healthy controls (n = 120). Eleven patients with multiple sclerosis without acute exacerbation had moderately elevated plasma levels.The plasma concentration of S-100 protein is a sensitive although unspecific indicator of neuronal damage and may be of use as a marker of disease activity in multiple sclerosis.
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Background: Bronchiectasis and asthma are different disease, However, some patients have both diseases. There are insufficient data for the effect of bronchiectasis on asthma exacerbations. Methods: We investigated 2270 patients having asthma in our hospital. Fifty patients had bronchiectasis and asthma. These patients were compared with fifty age and gender matched patients having asthma only. We evaluated frequency of asthma exacerbations (steroid use, emergency room (ER) visit and hospitalization) in each group. Results: The prevalence of bronchiectasis among the asthma patients was 2.2%. Follow up duration of each group was 51.9 ± 35.2 months for asthma with bronchiectasis and 53.8 ± 29.8 months for pure asthmatics. The number of asthma exacerbation/year (1.08±1.68 vs 0.35±0.42, p=0.004), steroid use/year (0.9±1.54 vs 0.26±0.36, p=0.006), ER visit/year (0.46±0.84 vs 0.26±0.36, p=0.001) and hospitalization/year (0.7±1.44 vs 0.1±0.17, p=0.4) due to asthma exacerbation was higher in asthma with bronchiectasis. Conclusion: The number of asthma exacerbation, steroid use, and ER visit due to asthma exacerbation was higher in asthma with bronchiectasis than pure asthma.
Asthma Exacerbations
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Introduction and Objectives
Exacerbations in COPD significantly affect quality of life and mortality. Predicting which patients are likely to exacerbate most frequently could provide opportunities to introduce treatment strategies to reduce future exacerbations. To determine whether established exacerbation risk factors can predict future exacerbation frequency and to assess the severity of an exacerbation risk factor on exacerbation outcomes.Methods
From the literature we identified risk factors associated with COPD exacerbations and categorised these into 'moderate' and 'severe'. We identified all patients who presented with a severe exacerbation of COPD to our unit from 01 January 2018 to 31 December 2018 and recorded their number of exacerbations over 18 months. Patients were divided into 8 groups based on exacerbation frequency. Standard statistical methods were applied.Results
A total of 213 patients were studied. Across all 8 patient groups there is a positive association between number of exacerbation risk factors and exacerbation frequency. The highest exacerbation frequency group has on average 5.0 severe risk factors compared to 2.3 severe risk factors for the lowest frequency group (p<0.001), and 2.7 moderate risk factors compared to 1.8 moderate risk factors for the lowest frequency group (p<0.05).Conclusions
The study demonstrates that it is possible to predict future exacerbation frequency amongst patients with COPD. Identifying which patients are at most risk of exacerbations may help clinicians to introduce pre-emptive individualised treatment strategies to reduce future exacerbation frequency.Copd exacerbation
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Abstract COPD exacerbations are commonly quantified as rate per year. However, the total amount of time a patient suffers from exacerbations may be stronger related to his or her disease burden than just counting exacerbation episodes. In this study, we examined the relationship between exacerbation frequency and exacerbation-free time, and their associations with baseline characteristics and health-related quality of life. A total of 166 COPD patients reported symptom changes during 12 months. Symptom-defined exacerbation episodes were correlated to the number of exacerbation-free weeks per year. Analysis of covariance was used to examine the effects of baseline characteristics on annual exacerbation frequency and exacerbation-free weeks, Spearman’s rank correlations to examine associations between the two methods to express exacerbations and the Chronic Respiratory Questionnaire (CRQ). The correlation between exacerbation frequency and exacerbation-free weeks was −0.71 ( p < 0.001). However, among frequent exacerbators (i.e., ≥3 exacerbations/year, n = 113) the correlation was weak ( r = −0.25; p < 0.01). Smokers had less exacerbation-free weeks than non-smokers ( β = −5.709, p < 0.05). More exacerbation-free weeks were related to better CRQ Total ( r = 0.22, p < 0.05), Mastery ( r = 0.22, p < 0.05), and Fatigue ( r = 0.23, p < 0.05) scores, whereas no significant associations were found between exacerbation frequency and CRQ scores. In COPD patients with frequent exacerbations, there is substantial variation in exacerbation-free time. Exacerbation-free time may better reflect the burden of exacerbations in patients with COPD than exacerbation frequency does.
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Higher exacerbation incidence rates in chronic obstructive pulmonary disease (COPD) are associated with more rapid decline in lung function and poorer quality of life, yet the mechanisms determining susceptibility to exacerbation remain ill-defined. The same viruses responsible for common colds are frequently isolated during exacerbations. The current authors hypothesised that exacerbation frequency may be associated with an increased frequency of colds, and investigated whether increased exacerbation frequency was associated with increased acquisition of colds, or a greater likelihood of exacerbation once a cold has been acquired. A total of 150 patients with COPD completed diary cards recording peak expiratory flow, and respiratory and coryzal symptoms for a median 1,047 days. Annual cold and exacerbation incidence rates (cold and exacerbation frequency) were calculated, and the relationships between these variables were investigated. This analysis is based on 1,005 colds and 1,493 exacerbations. Frequent exacerbators ( i.e. those whose exacerbation frequency was greater than the median) experienced significantly more colds than infrequent exacerbators (1.73 versus 0.94·yr −1 ). The likelihood of exacerbation during a cold was unaffected by exacerbation frequency. Patients experiencing frequent colds had a significantly higher exposure to cigarette smoke (46 versus 33 pack-yrs). Exacerbation frequency in chronic obstructive pulmonary disease is associated with an increased frequency of acquiring the common cold, rather than an increased propensity to exacerbation once a cold has been acquired.
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