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PubMed2026

[Microbiological Characterization of Exacerbations in Severe Asthma and Their Impact on Therapeutic Decision-Making].

INTRODUCTION: Severe asthma (SA) exacerbations impose a substantial healthcare burden. Microbiological characterization using molecular techniques may improve pathogen identification and contribute to a more individualized therapeutic approach. OBJECTIVE: To characterize the microbiological profile of exacerbations in patients with severe asthma and to analyze the prescription patterns for antibiotics (ATB) and systemic corticosteroids (SC). METHODS: This retrospective observational study was conducted in a Severe Asthma Unit. A total of 103 exacerbations were investigated using conventional microbiological methods and multiplex polymerase chain reaction (FilmArray™) performed on respiratory samples. Bacterial findings were classified according to operational criteria compatible with infection or colonization based on genomic load and culture results. Associations between clinical, microbiological, and therapeutic variables were explored using univariate analyses. RESULTS: Microbiological detection was achieved in 78.6% of exacerbations. Viruses were identified in 59.2% of episodes, with rhinovirus representing the predominant pathogen (62.3% of viral detections). Bacteria were identified in 53.4% of exacerbations (H. influenzae 36,6%), frequently in association with viral coinfection. Bronchiectasis was associated with a higher probability of bacterial detection (OR 2.50; p = 0.031). ATB and SC were prescribed in 61.2% and 44.6% of exacerbations, respectively, with frequent use of combination therapy. No significant differences in overall microbiological detection rates were observed according to biologic therapy status. Considerable microbiological variability was observed across recurrent exacerbations in the same patient. CONCLUSIONS: Microbiological findings were common during severe asthma exacerbations, with respiratory viruses, particularly rhinovirus, being the most frequently identified pathogens. Bronchiectasis was associated with higher rates of bacterial detection and ATB use. The marked variability observed between episodes supports the potential value of individualized microbiological assessment during exacerbations and warrants prospective studies aimed at optimizing therapeutic decision-making.

Biologic therapies.↗

PubMed1990

Changes in plasma levels of interleukin-2 receptor in relation to disease exacerbations and levels of anti-dsDNA and complement in systemic lupus erythematosus.

Interleukin-2 receptor (IL-2R) is expressed and released predominantly by activated T cells. In order to investigate whether disease exacerbations of systemic lupus erythematosus (SLE) are preceded by T cell activation, we prospectively measured levels of IL-2R once a month, from 6 months prior to exacerbations until 1 month afterwards. To assess the temporal relation between T cell activation and B cell activation, we measured, in addition, levels of anti-dsDNA, complement C3/C4, and total IgG. During a mean follow-up period of 23 months, 40 exacerbations occurred in 21 out of the 71 participating patients. For the present study one exacerbation per patient was evaluated. During exacerbation levels of IL-2R were increased in 18 out of the 21 cases and correlated with levels of anti-dsDNA (P less than 0.02), C3 (P less than 0.02), and C4 (P less than 0.01), but not with the score of the disease activity index. Levels of IL-2R rose prior to the exacerbation (P less than 0.02) and fell afterwards following treatment (P less than 0.05). Even in the absence of disease activity or during minor disease symptoms IL-2R levels were higher (P less than 0.01) than in healthy controls. Sixteen out of the 21 exacerbations (76%) were preceded by a significant increase in IL-2R. Changes in levels of anti-dsDNA and complement C3/C4 tended to precede changes in levels of IL-2R. We conclude that increased levels of IL-2R, compatible with T cell activation, are present in SLE already during inactive disease. These levels further increased prior to exacerbations of disease. As such, IL-2R is an indicator of disease activity in SLE. Serial measurement of IL-2R is a sensitive test for predicting disease exacerbations of SLE.

Adolescent↗

PubMed1990

C-reactive protein levels during disease exacerbations and infections in systemic lupus erythematosus: a prospective longitudinal study.

We prospectively studied the value of measuring C-reactive protein (CRP) levels in patients with systemic lupus erythematosus (SLE) to distinguish between disease exacerbation and infection. During a 2 year followup of 71 lupus patients, 38 episodes of disease exacerbation and 36 episodes of infection could be analyzed. Plasma samples were obtained at least once a month. CRP levels were increased (greater than 6 mg/l) during 25 of the 38 exacerbations and during 32 of the 36 infections. Median CRP levels during infection (60 mg/l; range 1-400) were higher than during disease exacerbation (16.5 mg/l; range 1-375) (p less than 0.05). Levels of CRP rose prior to the exacerbation (p less than or equal to 0.01) and fell afterwards (p less than or equal to 0.01). During exacerbations accompanied by serositis, median levels of CRP (76 mg/l; range 2-375) were higher than during exacerbations without serositis (16 mg/l; range 1-53) (p less than 0.02). CRP levels exceeding 60 mg/l during exacerbations without serositis indicated infection in all cases. Thus, measurement of CRP in SLE is valuable to distinguish between infection and exacerbation only in the absence of serositis.

Adolescent↗

PubMed1991

Rises in anti-double stranded DNA antibody levels prior to exacerbations of systemic lupus erythematosus are not merely due to polyclonal B cell activation.

We investigated whether rises in anti-double stranded DNA (anti-ds DNA) antibody levels prior to disease exacerbations of systemic lupus erythematosus (SLE) are part of a restricted immune response or merely the consequence of polyclonal B cell activation. As possible inducers of polyclonal B cell activation, we analyzed, in addition, the role of clinically apparent infections in relation to changes in levels of anti-ds DNA and disease exacerbations. We prospectively followed 72 lupus patients who were examined for disease activity and infections at least every 3 months by history and physical examination according to a protocol. Once a month, we measured levels of IgG-class antibodies to an unrelated recall antigen (tetanus toxoid), levels of IgG-class antibodies to a viral antigen (cytomegalovirus late antigens [CMV-LA]), levels of total immunoglobulins G and M, and levels of anti-ds DNA (by ELISA and Farr assay). Thirty-three exacerbations and 31 infections were observed during a follow-up period of an average of 18.5 patient months. Twenty-four out of the 27 exacerbations accompanied by a positive test for anti-ds DNA were preceded by a significant rise in anti-ds DNA: in 17 cases by ELISA and in 22 cases by Farr assay. These 24 rises in levels of anti-ds DNA prior to the exacerbation were paralleled by a significant rise in levels of IgG-class anti-tetanus antibodies in 8 cases, anti-CMV-LA antibodies in 9 cases, total IgG in 7 cases, and total IgM in 15 cases. Median rise in anti-ds DNA, as measured both by ELISA and Farr assay, exceeded the median rise in anti-tetanus antibodies, anti-CMV-LA antibodies, and total IgG and IgM (P less than 0.0001). Only one infection was recorded within a period of 3 months prior to an exacerbation, whereas infections never occurred within a period of 3 months prior to a rise in anti-ds DNA. We conclude that rises in anti-ds DNA prior to exacerbations of SLE are largely due to preferential activation of anti-ds DNA-specific B cells and not merely to polyclonal B cell hyperactivity. Clinically significant infections are not related to rises in levels of anti-ds DNA nor to the induction of exacerbations in SLE.

Adolescent↗

PubMed1991

Changes in levels of antibodies against the 70 kDa and a polypeptides of the U1RNP complex in relation to exacerbations of systemic lupus erythematosus.

In order to investigate whether disease exacerbations of systemic lupus erythematosus (SLE) are accompanied or preceded by changes in antibody levels against the U1RNA associated 70 kDa and A polypeptides, we prospectively collected plasma specimens from 71 patients with SLE. We compared changes in anti-70 kDa/anti-A levels, measured by ELISA using cloned antigens, with changes in levels of anti-dsDNA and total IgG. Measurable levels of anti-70 kDa (n = 10) and/or anti-A antibodies (n = 6) were detected during 10 exacerbations. Four of the 10 exacerbations with a measurable level of anti-70 kDa antibodies were preceded by a significant rise in anti-70 kDa levels, 2 by a significant fall, while levels of anti-70 kDa did not change in the remaining 4 cases. Only one of the 6 exacerbations with detectable anti-A antibody levels was preceded by a significant rise in anti-A antibodies, while levels did not change before exacerbation in the other 5 cases. Six of the 10 exacerbations were preceded by a significant rise in anti-dsDNA; in 4 cases levels of anti-dsDNA did not change before exacerbation. In contrast to anti-dsDNA, no relation was found between changes in levels of anti-70 kDa/anti-A and changes in disease activity. Significant changes in levels of anti-70 kDa/anti-A, occurring in 6 cases, were accompanied by parallel changes in total IgG in 5 of these 6. We conclude that, in contrast to anti-dsDNA, serial measurement of levels of anti-70 kDa/anti-A is not useful for monitoring disease activity or predicting disease exacerbations in SLE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Acute exacerbations in Chinese patients with chronic hepatitis B virus (HBV) infection. Incidence, predisposing factors and etiology.

Three hundred and eighty-six Chinese patients (262 men and 124 women), age 5-74 years, with chronic hepatitis B virus (HBV) infection were prospectively followed for 1-5 years to determine the incidence, predisposing factors and etiology of acute exacerbations that occurred during the course of chronic HBV infection. Group I consisted of 334 patients with serum alanine aminotransferase (ALT) levels below 200 IU/l at presentation. Of these, 29 (8.7%) patients developed 32 episodes of acute exacerbation during follow-up. The cumulative probabilities of developing exacerbations were 6.3% and 15% at the end of 1 and 4 years, respectively. Group II included 52 patients with ALT levels above 200 IU/l at presentation. Of these, 19 (37%) patients developed 26 episodes of exacerbation during follow-up. The cumulative probabilities of developing eacerbations were 24% and 47% at the end of 1 and 4 years, respectively. In both groups, the probability of developing exacerbations was slightly higher in men and significantly higher in those above the age of 20 and those who were HBeAg positive. Logistic regression analysis showed that HBeAg positivity (p less than 0.00001), elevated ALT levels (greater than 200 IU/l) at presentation (p less than 0.0001) and male sex (p = 0.03) were associated with a significantly higher probability of developing exacerbations. Twenty eight (48%) episodes of exacerbation were accompanied by symptoms of acute hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2026

Systemic Platelet Activation and Respiratory Exacerbations, Pulmonary Symptoms, and Mortality among Current and Former Smokers in SPIROMICS.

RATIONALE: Platelet activation is elevated in chronic obstructive pulmonary disease (COPD) and associated with self-reported respiratory symptoms. Observational studies link the antiplatelet drug aspirin to lower exacerbation rates and fewer symptoms. However, it is unknown if platelet activation predicts incident respiratory exacerbations or mortality. OBJECTIVE: Is systemic platelet activation prospectively associated with respiratory exacerbations and mortality among ever-smokers with or at risk for COPD? METHODS: We measured two systemic platelet activation biomarkers, urinary 11-dehydro-thromboxane B2 (11dTxB2) and plasma soluble CD40 ligand (sCD40L), at baseline in self-reported aspirin non-users in the longitudinal SPIROMICS cohort. Adjusted generalized negative binomial and linear mixed-effects models assessed associations between these biomarkers and prospective rates of total and severe exacerbations, plus cross-sectional and longitudinal respiratory health (St. George's Respiratory Questionnaire, COPD Assessment Test, modified Medical Research Council questionnaire, and six minute walk distance). Cox proportional hazard and competing risk models evaluated associations between platelet activation biomarkers and all-cause and cause-specific mortality. RESULTS: Among 2,711 participants, 1,572 (58.0%) reported aspirin non-use; of these, 1,433 and 1,437 had 11dTxB2 and sCD40L measured, respectively. Over a median 6.6 years, a two-fold higher baseline 11dTxB2 was associated with increased rates of total (8.8%; 95%CI: 0.4-17.8%) and severe (18.1%; 95%CI: 5.1-32.6%) exacerbations. Although there were no significant interactions, there was a trend toward higher severe exacerbation rates among current cigarettes smokers and those with COPD. There were no significant results for sCD40L. Among aspirin non-users, higher 11dTxB2, but not sCD40L, was associated with worse cross-sectional respiratory health and modestly increased all-cause mortality over a median 8.2 years (adjusted hazard ratio 1.11; 95%CI: 1.00-1.24). After covariate adjustment, there were no associations with longitudinal respiratory health or cause-specific mortality. CONCLUSIONS: Systemic platelet activation, measured by urinary 11dTxB2, is a statistically significant but modest predictor of respiratory exacerbations and all-cause mortality in individuals with or at risk for COPD, suggesting its potential utility as a prognostic and predictive biomarker for antiplatelet therapy trials. CLINICAL TRIAL REGISTRATION: NCT01969344.

aspirin↗

PubMed1990

Lipopolysaccharide from gram-negative bacteria enhances polyclonal B cell activation and exacerbates nephritis in MRL/lpr mice.

Depletion of B cells in mice bearing the lymphoproliferation (lpr) gene reduces lymphoproliferation and polyclonal B cell activation (PBA) and attenuates mononuclear cell vasculitis. We sought to verify whether the obverse was true, i.e. whether enhancement of B cell activity might exacerbate the nephritis of MRL/lpr (MRL) mice, a lupus-prone strain. The experimental approach was designed to address three questions: whether naturally occurring PBA in MRL mice could be further enhanced; whether enhanced PBA would exacerbate nephritis; and whether the mechanism of nephritis exacerbation involved interference with mononuclear phagocyte system (MPS) function. To enhance B cell activity, we injected MRL mice with lipopolysaccharide (LPS) from Gram-negative bacteria, a potent B cell activator. To determine whether nephritis was exacerbated, we performed immunopathologic studies and tests of renal function. To verify whether nephritis exacerbation involved impairment of MPS function, we probed the kinetics of immune complex removal from the circulation, their uptake by the liver and spleen, and their localization in kidney tissue. The results indicate that in MRL mice: (i) spontaneous PBA can be enhanced by LPS; (ii) enhancement of PBA by LPS exacerbates nephritis; and (iii) the MPS is already saturated, presumably due to excessive production of endogenous immune complexes. Thus, further increase in immune complex formation due to enhanced PBA by LPS results in increased localization of immune complexes in kidneys and exacerbated nephritis.

Animals↗

PubMed1991

Bacterial lipopolysaccharide enhances deposition of immune complexes and exacerbates nephritis in BXSB lupus-prone mice.

Systemic autoimmune disease is influenced by genetic, immunological, hormonal, and environmental factors. Although environmental factors are major agents that induce or exacerbate autoimmune diseases, the mechanism(s) and the molecular events by which they operate remain poorly understood. Here we used the lupus-prone BXSB mouse as an animal model of systemic autoimmune disease, and we used a bacterial lipopolysaccharide (LPS) as a surrogate infectious agent to gain some insight into the mechanism(s) by which infectious agents exacerbate autoimmune diseases. Our experimental protocol was designed to address three questions: (i) whether spontaneous polyclonal B cell activation (PBA) that occurs in BXSB mice could be further enhanced by bacterial LPS; (ii) whether repeated exposure to LPS would exacerbate autoimmune disease, as reflected by enhanced deposits of immune complexes (ICs) in kidneys and exacerbated nephritis; and (iii) whether the mechanism by which LPS exacerbates nephritis might involve interference with blood cell carrier function, mononuclear phagocyte function, or both. BXSB mice were injected with LPS (25 micrograms) twice a week for 5 weeks; control autoimmune BXSB mice and immunologically normal (C57BL/6) mice were injected with vehicle only. The three groups of mice were then challenged with soluble ICs to assess the kinetics of their disappearance from the circulation, their uptake by the mononuclear phagocyte system (liver, spleen), their distribution in target organ (kidney), and blood cell carrier function. The results indicate that: (i) spontaneous PBA can be enhanced further by LPS; (ii) exposure to LPS results in increased deposits of endogenous ICs in kidneys and exacerbated nephritis; and (iii) defective handling of ICs by the mononuclear phagocyte system and impaired blood cell carrier function are contributory factors to exacerbated nephritis, but that mechanisms in addition to passive localization of ICs may also be operative.

Animals↗

PubMed1976

The corticosteroid dose graph. Use in determination of corticosteroid requirements, characterization of patients, and prevention of seasonal exacerbation in corticosteroid-dependent patients.

Sixty-three corticosteroid(CS)-dependent asthmatics were evaluated by a method which records asthmatic exacerbations as a function of change in CS dosage. This method, the Corticosteroid Dose Graph (CSDG), is a graphic representation of the patients' narrative charts. It is useful in assessing and directing the care of these patients and in evaluating the efficacy of altered therapeutic regimens in asthmatics. The CSDG categorizes cooperative patients (CP) and distinguishes these patients from those who are less cooperative (LCP). Evaluation of the progress of CP by the graphic analysis system showed that CP have fewer severe exacerbations of asthma than LCPs. Evaluation of the 63 patients by this graphic method shows a significantly increased incidence of asthmatic exacerbations in the Chicago area in October as compared to other months. The CSDG also demonstrates that some individuals experienced significantly increased numbers of asthma exacerbations at certain times of the year unique to themselves. Because the CSDG predicts exacerbations, it was shown to be applicable to prevent such exacerbations by prophylactic increase in CS dose during a high-risk season for selected CS-dependent asthmatics.

Adolescent↗

PubMed1991

Coughing can relieve or exacerbate symptoms in asthmatic patients.

From about 1190 to the present day opposing views have been expressed about the effects of coughing in patients with asthma. Some accounts have stated that it brought relief and others that it exacerbated asthma, whereas others thought that it could have both effects. In the present investigation, 187 patients with a clinical diagnosis of asthma were asked whether coughing relieved or exacerbated their asthma. In 41.7% coughing caused exacerbation, in 29.9% it brought relief, in 9.9% it had no effect, and in the remaining 18.7% it sometimes exacerbated their symptoms and sometimes brought relief. When asthma was exacerbated, the most common symptom induced was breathlessness, and then wheezing; chest tightness was the least frequent. When coughing brought relief it was mainly through the expectoration of sputum. However, a small proportion of patients found relief even if there was no expectoration. If coughing exacerbates asthma and persists in the face of treatment with standard medication, then treatment specifically directed at its diminution could reduce morbity considerably.

Asthma↗

PubMed1990

Acute exacerbation in patients with liver cirrhosis: a clinicopathological study.

The incidence, clinicopathologic features and etiology of acute exacerbation occurring in patients with liver cirrhosis were assessed prospectively among 332 hepatitis B surface antigen (HBsAg) positive and 71 HBsAg negative patients. During an 11-year period and a mean follow-up duration of 26.8 months, 148 acute exacerbation occurred in 107 HBsAg positive patients and 32 episodes occurred in 18 HBsAg negative patients. The calculated annual incidence was 11.5%. The clinical, laboratory and histologic features were similar to those in patients with chronic hepatitis. Confluent hepatic necrosis and alphafetoprotein elevation over 100 ng/ml occurred frequently, particularly in HBeAg positive patients. In general, acute exacerbations in HBsAg negative patients were less severe than their HBsAg positive counterparts. Of the exacerbations in HBsAg positive patients, 54.8% of the HBeAg positive ones and 38.6% of the HBeAg negative ones were attributable to hepatitis B virus reactivation, while 4.8% and 7.9%, respectively, were due to hepatitis delta virus superinfection. The others might be the results of hepatitis non-A, non-B virus superinfection or increased piecemeal necrosis. The immediate outcome of acute exacerbations in cirrhotic patients was usually good, although 13.8% developed hepatic decompensation and 4.4% died. Further follow-up study is required to evaluate the long-term effect of the frequent occurrence of bridging hepatic necrosis, high elevation of alphafetoprotein and hepatic decompensation during acute exacerbation in cirrhotic patients.

Adult↗

PubMed1992

[Uneven ventilation-perfusion ratio distribution during acute exacerbation of chronic pulmonary diseases].

We studied ventilation-perfusion ratio (VA/Q) unevenness in terms of alveolar-arterial gas tension difference (AaDO2 and aADN2) and of multiple inert gas elimination technique during the chronic stable periods and the acute exacerbation periods of seven cases with chronic pulmonary diseases. Three had idiopathic pulmonary fibrosis, 2 had pulmonary emphysema, 1 had bronchiolitis and the other had a sequelae of pulmonary tuberculosis. Sulfur hexafluoride and cyclopropane dissolved in saline were infused into a peripheral vein at a constant rate and these 2 gases were used as the indicator gases to make analysis of two compartmental VA/Q. During exacerbation all cases showed lower PaO2 than in the stable period. All cases except idiopathic pulmonary fibrosis showed higher PaCO2. Five cases also had higher AaDO2 and aADN2. One case with pulmonary emphysema and one with bronchiolitis actually had lower AaDO2 and aADN2 values during acute exacerbation than during the chronic stable period. We introduced the difference between the logarithm of higher VA/Q and lower VA/Q values (log [(VA/Q)H/(VA/Q)L)] as an index of VA/Q unevenness. Two compartmental VA/Q analysis revealed greater VA/Q differences in all cases during acute exacerbation. This included cases who showed lower AaDO2 and aADN2 values in the acute exacerbation period. In conclusion, worsened VA/Q distribution, during the acute exacerbation period, was elucidated quantitatively using the multiple inert gas elimination technique.

Adult↗

PubMed1992

Antiarrhythmic drug exacerbation of ventricular tachycardia inducibility during electrophysiologic study.

Most studies examining antiarrhythmic drug exacerbation of ventricular arrhythmias have been performed in patients in whom clinical proarrhythmia developed. The clinical significance and predictors of antiarrhythmic drug exacerbation of inducible ventricular arrhythmias during electrophysiologic study have received less attention. Accordingly, a consecutive number of patients undergoing electrophysiologic study for evaluation of ventricular arrhythmias (but who had no history of clinical proarrhythmia) were prospectively examined. Drug-induced exacerbation was defined as no inducible ventricular tachycardia in the baseline drug-free state that increased to inducible nonsustained or sustained ventricular tachycardia, or inducible nonsustained ventricular tachycardia at baseline that increased to inducible sustained ventricular tachycardia. After administration of primarily type IA antiarrhythmic agents (procainamide and quinidine in 97% of the patients), patients were considered drug test negative (n = 80) when they had no increase in inducible ventricular tachycardia, and patients were considered drug test positive (n = 16) when they had exacerbation of inducible arrhythmias. The drug test-positive group's clinical characteristics differed markedly from those of the drug test-negative group. Compared with the drug test-negative group, the drug test-positive group had reduced (less than 40%) left ventricular ejection fractions (80% vs 39%, p = 0.005) and higher prevalences of myocardial infarctions (81% vs 35%, p = 0.027), left ventricular aneurysms (27% vs 5%, p = 0.026), and bundle branch blocks (53% vs 16%, p = 0.005). Thus exacerbation of ventricular tachycardia induction after antiarrhythmic agent administration was most common in patients with significant organic heart disease. The drug test-positive group was more frequently treated with antiarrhythmic therapy than was the drug test-negative group.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗

PubMed1978

Exacerbations of chronic bronchitis: exogenous or endogenous infection?

Six male patients with chronic bronchitis, who were known previously to have excreted Streptococcus pneumoniae and/or Haemophilus influenzae, both at the times of exacerbations and during remission, were studied for 43 to 52 months. Sputum was examined fortnightly and at the time of exacerbations. Strains of Strep. pneumoniae were serotyped and those of Haemophilus species were typed by antibiograms along with other supporting methods. Sera collected before or at the time of an exacerbation and seven and 30 days afterwards were examined by complement fixation tests against respiratory viruses and Mycoplasma pneumoniae. In 18 out of 25 exacerbations there was evidence of a new type of Strep. pneumoniae and/or Haemophilus spp. or of a current virus infection, suggesting exogenous infection in the majority of these cases. There was a possible reason for failure to detect a new pathogen in three of the seven cases in which none was found. In five further exacerbations adequate investigation was not possible.

Aged↗

PubMed1991

Emotional stress and coping in multiple sclerosis (MS) exacerbations.

Ninety-five pairs of MS patients in exacerbation and remission were compared on emotional stress in the previous three months. Patients in exacerbation scored higher on emotional disturbance and intensity of stressful events than patients in remission, but lower on frequency of compensating uplifts. There was also a tendency for more patients in exacerbation than remission to favour emotion-focused coping techniques over problem-solving or social support. Whether patients building to an exacerbation over-react to various events or unresolved emotional stress precipitates exacerbations, MS patients might benefit from counselling in stress reduction techniques.

Adaptation, Psychological↗

PubMed1992

Effectiveness of steroid therapy in acute exacerbations of asthma: a meta-analysis.

The objective of this study was to determine the effect of steroid therapy on pulmonary function, admission rates, and relapse rates in patients presenting with acute exacerbations of asthma. Computerized MEDLINE and SCIENCE CITATION searches were combined with review of reference lists from book chapters and articles to identify published randomized trials on steroid interventions. Over 700 articles were reviewed by two independent reviewers who identified 30 relevant randomized controlled trials for analysis. Study validity was independently assessed by two reviewers and information regarding populations, interventions, and outcomes was abstracted. Binary outcomes were combined and reported as odds ratios (OR), using the Mantel-Haenszel method. Individual and pooled effect sizes (ES) were determined for pulmonary function data. The authors found that the use of steroids early in the treatment of asthmatic exacerbations reduces admissions in adults (common OR 0.47; 95% confidence interval (CI) 0.27, 0.79) and children (OR 0.06-0.42). They found steroids effective in preventing relapse in the outpatient treatment of asthmatic exacerbations (OR 0.15; CI 0.05, 0.44). Oral and intravenous steroids appear to have equivalent effects on pulmonary function in acute exacerbations (ES -0.07; CI -0.39, 0.25). The authors conclude that overall, steroid therapy provides important benefits to patients presenting to emergency departments with acute exacerbations of asthma. Further research into dosage, alternative routes of administration, and alternative outcome measures is needed.

Asthma↗

PubMed1979

Relationship of bacterial and viral infections to exacerbations of asthma.

Fifty-one asthmatic patients were followed for up to 18 months. During this time 111 exacerbations of wheeze were recorded. Involvement by pathogenic respiratory bacteria and viruses was looked for directly by culture and indirectly by antibody studies. Proof of infection was found in only 12 (10.8%) of the 111 exacerbations. Only eight patients provided sputum samples. Potential bacterial pathogens were found in four. Viruses were isolated in four of 27 exacerbation specimens; significant rises in specific viral antibody titres occurred in three. Six patients developed precipitating antibody to respiratory bacteria over the study but only one in relation to an exacerbation. The study therefore indicated that the great majority of exacerbations of asthma in these patients were not due to respiratory tract infection.

Adult↗