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PubMed1983

Oral acetylcysteine reduces exacerbation rate in chronic bronchitis: report of a trial organized by the Swedish Society for Pulmonary Diseases.

This multicentre trial was undertaken to confirm previous results indicating that long-term treatment with oral acetylcysteine reduces the exacerbation rate in patients with chronic bronchitis. Two hundred and eighty-five patients, smokers or ex-smokers, with chronic bronchitis started a pre-trial placebo-period of 1 month. After this run-in period 259 patients were included in the trial and randomized into two parallel groups. The patients were treated in a double-blind way either with acetylcysteine 200 mg b.i.d. or placebo b.i.d. for 6 months. The trial was completed by 98 patients in the acetylcysteine group and by 105 patients in the placebo group. Initially, there were no significant differences between the groups. Twice weekly, the patients filled in a diary card concerning symptoms. The number of exacerbations was assessed from these cards and at visits 2, 4 and 6 months after institution of therapy. The exacerbation rate was significantly lower in the acetylcysteine group in which 40% of the patients remained free from exacerbations compared to 19% in the placebo group. Sick-leave due to acute exacerbation was significantly less common in the acetylcysteine group. The drug was well tolerated.

Acetylcysteine↗
PubMed1994

Stress exacerbates neuron loss and cytoskeletal pathology in the hippocampus.

Glucocorticoids (GCs), the adrenal steroids secreted during stress, endanger the hippocampus, compromising its ability to survive neurological insults. GCs probably do so by disrupting energetics in the hippocampus, thus impairing its ability to contain damaging fluxes of excitatory amino acids and calcium. Superficially, these observations suggest that stress itself should also exacerbate the toxicity of neurological insults. However, most studies have involved unphysiologic GC manipulations, limiting speculations about the endangering effects of stress. In this study, rats were infused with the excitotoxin kainic acid (KA) after either having been adrenalectomized and replaced with a range of physiologic concentrations of GCs, or having been stressed intermittently. We observed that within the CA3 region, increasing CORT concentrations exacerbated the KA-induced neuron loss, the extent of tau immunoreactivity, and of spectrin proteolysis. The transitions from low to high basal GC concentrations and from high basal to stress GC values were both associated with significant exacerbation of neuron loss and tau immunoreactivity; the extent of spectrin proteolysis was less sensitive to increments in GCs. As would be expected from these data, exposure to intermittent stress prior to KA infusion also exacerbated neuron loss, tau immunoreactivity, and spectrin proteolysis in CA3. Thus, physiological elevations of GCs, and stress itself, can exacerbate hippocampal neuron loss and the attendant degenerative markers following an excitotoxic insult. Of significance, seizure and hypoxia-ischemia provoke considerable GC stress responses, which may thus worsen the resultant damage. Furthermore, a number of neuropsychiatric disorders, as well as aging, are associated with elevated basal GC concentrations, which may endanger the hippocampus in the event of neurological insult.

Animals↗
PubMed1994

[Two cases of IIP which developed acute exacerbation after bronchoalveolar lavage].

We reported two cases of idiopathic interstitial pneumonia (IIP) who developed acute exacerbation after bronchoalveolar lavage (BAL). One case was a 67-year-old male who presented with dry cough and exertional dyspnea. He was diagnosed as IIP and transbronchial lung biopsy revealed alveolitis. BAL was performed after administration of prednisolone. He complained of severe dyspnea after BAL and was diagnosed as having an acute exacerbation of IIP. In spite of extensive treatment including pulse therapy with methylprednisolone, he died. The other case was a 57-year-old male noted to have a chest X-ray abnormality who presented with dry cough and dyspnea on exertion. He was diagnosed as having IIP and primary lung cancer. BAL was performed to evaluate the activity of IIP, and respiratory distress subsequently became severe. After BAL, he developed an acute exacerbation of IIP and died in spite of treatment. In both cases, peripheral white blood cell counts were increased just before BAL. It was suggested that this condition might participate in acute exacerbation of IIP. It should be kept in mind that some patients with IIP may develop acute exacerbation after BAL.

Aged↗
PubMed1995

Causes of acute exacerbations of chronic hepatitis B.

The authors analyzed acute exacerbations of chronic hepatitis B in 24 chronic HBsAg carriers (20 with positive HBeAg, 4 with anti-HBe), more than half of whom were treated with glucocorticoids, by examining specific antigens and antibodies of the hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis delta virus (HDV), Epstein-Barr virus (EBV) and cytomegalovirus (CMV). Of 38 observed exacerbations of the disease they found in 7 (18%) deterioration after discontinuation of glucocorticoids, in 7 (18%) seroconversion of HBeAg to anti-HBe, in 9 (24%) spontaneous exacerbation of chronic hepatitis B, in 11 (29%) chronic activation, reactivation of EBV superinfection, in 3 (8%) CMV reactivation or superinfection and in one (3%) HDV superinfection. In no instance HAV superinfection was observed. Exacerbations were found five times more frequently in subjects in the stage of active viral replication (in HBeAg+ subjects) than in subjects with anti-HBe. In eight patients EBV reactivation was found after glucocorticoids withdrawal: in five patients after an average period of 5 months (range 3-7) and in three patients after an average period of 33 months (range 22-48). The results provide evidence that in addition to already known causes of acute exacerbations of chronic hepatitis B in our geographical area probably an important cause of deterioration of hepatitis is reactivation or superinfection with EBV and CMV in some patients in conjunction with previous glucocorticoid treatment.

Acute Disease↗
PubMed1996

Airway eosinophilia and expression of interleukin-5 protein in asthma and in exacerbations of chronic bronchitis.

BACKGROUND: An increased number of eosinophils in the bronchial mucosa has been demonstrated both in asthma and in exacerbations of chronic bronchitis. OBJECTIVE: To investigate whether the airway eosinophilia present in asthma and in chronic bronchitis during exacerbations is associated with interleukin (IL)-5 protein expression in the bronchial mucosa. METHODS: We obtained bronchial biopsies in 18 subjects with asthma (four intrinsic, seven extrinsic and seven occupational) and in 11 subjects with chronic bronchitis examined during an exacerbation. The findings were compared with those of bronchial biopsies from 10 subjects with chronic bronchitis examined under baseline conditions and from seven normal subjects, taken as controls. By immunohistochemistry, we assessed the expression of IL-5 protein and the number of eosinophils (EG2), mast cells (tryptase), and T-lymphocytes (CD3) in the submucosa. RESULTS: As compared with controls, the number of eosinophils was increased to a similar degree in both asthma (P < 0.001) and in exacerbations of chronic bronchitis (P < 0.001), whereas the number of IL-5 immunopositive cells was increased significantly only in asthma (P < 0.01). No differences were observed in the number of mast cells and T-lymphocytes between the four groups of subjects examined. CONCLUSIONS: This study shows that the degree of airway eosinophilia is similar in asthma and in exacerbations of chronic bronchitis, but only in asthma is it associated with an increased expression of IL-5 protein in the bronchial mucosa.

Adult↗
PubMed2002

Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial.

CONTEXT: Little randomized evidence is available to guide the in-hospital management of patients with an acute exacerbation of chronic heart failure. Although intravenous inotropic therapy usually produces beneficial hemodynamic effects and is labeled for use in the care of such patients, the effect of such therapy on intermediate-term clinical outcomes is uncertain. OBJECTIVE: To prospectively test whether a strategy that includes short-term use of milrinone in addition to standard therapy can improve clinical outcomes of patients hospitalized with an exacerbation of chronic heart failure. DESIGN: Prospective, randomized, double-blind, placebo-controlled trial conducted from July 1997 through November 1999. SETTING: Seventy-eight community and tertiary care hospitals in the United States. PARTICIPANTS: A total of 951 patients admitted with an exacerbation of systolic heart failure not requiring intravenous inotropic support (mean age, 65 years; 92% with baseline New York Heart Association class III or IV; mean left ventricular ejection fraction, 23%). INTERVENTION: Patients were randomly assigned to receive a 48-hour infusion of either milrinone, 0.5 microg/kg per minute initially (n = 477), or saline placebo (n = 472). MAIN OUTCOME MEASURE: Cumulative days of hospitalization for cardiovascular cause within 60 days following randomization. RESULTS: The median number of days hospitalized for cardiovascular causes within 60 days after randomization did not differ significantly between patients given milrinone (6 days) compared with placebo (7 days; P =.71). Sustained hypotension requiring intervention (10.7% vs 3.2%; P<.001) and new atrial arrhythmias (4.6% vs 1.5%; P =.004) occurred more frequently in patients who received milrinone. The milrinone and placebo groups did not differ significantly in in-hospital mortality (3.8% vs 2.3%; P =.19), 60-day mortality (10.3% vs 8.9%; P =.41), or the composite incidence of death or readmission (35.0% vs 35.3%; P =.92) CONCLUSION: These results do not support the routine use of intravenous milrinone as an adjunct to standard therapy in the treatment of patients hospitalized for an exacerbation of chronic heart failure.

Acute Disease↗
PubMed2004

Doubling the dose of budesonide versus maintenance treatment in asthma exacerbations.

BACKGROUND: Previous guidelines recommend doubling the daily dose of maintenance inhaled corticosteroid to treat or prevent progression of exacerbations of asthma. METHODS: Over a 6 month period a cohort of patients were evaluated prospectively and randomised in a double blind controlled trial to treatment with either a continued maintenance dose (MD) of inhaled corticosteroid or doubling the dose (DD) at the time of an exacerbation. RESULTS: A total of 290 patients were randomised (33% male) and 98 (DD, n = 46) experienced evaluable asthma exacerbations during the study period. Mean (SD) baseline characteristics at randomisation (age 33.5 (14.0) years; forced expiratory volume in 1 second (FEV(1)) 2.8 (0.7) l; peak expiratory flow (PEF) 422.9 (110.5) l/min) were similar in both groups. In the DD group 41% of patients were considered treatment failures because they either required systemic steroids (n = 12), had an unscheduled visit to a physician (n = 1), or their asthma did not return to baseline (n = 6). This did not differ from the MD group in which 40% were treatment failures (n = 9, 0, and 12, respectively; p = 0.94). CONCLUSIONS: In patients who regularly take an inhaled corticosteroid, doubling the maintenance dose may not affect the pattern of the exacerbation.

Adolescent↗
PubMed1998

Outcomes of acute exacerbation of severe congestive heart failure: quality of life, resource use, and survival. SUPPORT Investigators. The Study to Understand Prognosis and Preferences for Outcomes and Risks of Treatments.

BACKGROUND: Congestive heart failure (CHF) is a common disease with high health care costs and high mortality rates. Knowledge of the health-related quality of life outcomes of CHF may guide decision making and be useful in assessing new therapies for this population. METHODS: A prospective cohort study was conducted involving 1390 adult patients hospitalized with an acute exacerbation of severe CHF (New York Heart Association class III-IV). Demographic data and health-related quality of life were determined by interview; physiologic status and cost and intensity of care were determined from hospital charts. RESULTS: The median (25th, 75th percentiles) age of patients was 68.0 (58.2, 76.9) years; 61.7% were male. Survival was 93.4% at discharge from the index hospitalization, 72.9% at 180 days, and 61.5% at 1 year. Of patients interviewed at 180 days, the median health rating on a scale of 0 to 100 (0 indicates death; 100, excellent health) was 60 (interquartile range, 50-80), and 59.7% were independent in their activities of daily living. Overall quality of life was reported to be good, very good, or excellent in 58.2% at 180 days. Patients with worse functional capacity were more likely to die. Health perceptions among the patients with available interview data improved at 60 and 180 days after acute exacerbation of severe CHF. CONCLUSIONS: Patients hospitalized for acute exacerbation of severe CHF have a generally poor 6-month survival, but survivors retain relatively good functional status and have good health perceptions. Furthermore, health perceptions improve after the acute exacerbation.

Acute Disease↗
PubMed2001

Acute precipitants of congestive heart failure exacerbations.

BACKGROUND: Few studies have prospectively and systematically explored the factors that acutely precipitate exacerbation of congestive heart failure (CHF) in patients with left ventricular dysfunction. Knowledge of such factors is important in designing measures to prevent deterioration of clinical status. The objective of this study was to prospectively describe the precipitants associated with exacerbation of CHF status in patients enrolled in the Randomized Evaluation of Strategies for Left Ventricular Dysfunction Pilot Study. METHODS: We conducted a 2-stage, multicenter, randomized trial in 768 patients with CHF who had an ejection fraction of less than 40%. Patients were randomly assigned to receive enalapril maleate, candesartan cilexetil, or both for 17 weeks, followed by randomization to receive metoprolol succinate or placebo for 26 weeks. Investigators systematically documented information on clinical presentation, management, and factors associated with the exacerbation for any episode of acute CHF during follow-up. RESULTS: A total of 323 episodes of worsening of CHF occurred in 180 patients during 43 weeks of follow-up; 143 patients required hospitalization, and 5 died. Factors implicated in worsening of CHF status included noncompliance with salt restriction (22%); other noncardiac causes (20%), notably pulmonary infectious processes; study medications (15%); use of antiarrhythmic agents in the past 48 hours (15%); arrhythmias (13%); calcium channel blockers (13%); and inappropriate reductions in CHF therapy (10%). CONCLUSIONS: A variety of factors, many of which are avoidable, are associated with exacerbation of CHF. Attention to these factors and patient education are important in the prevention of CHF deterioration.

Adrenergic beta-Antagonists↗
PubMed2005

Treatment of myasthenia gravis exacerbation with intravenous immunoglobulin: a randomized double-blind clinical trial.

BACKGROUND: The optimal dose of intravenous immunoglobulin (IVIG) in acute exacerbation of myasthenia gravis remains unknown. Increasing the treatment duration might provide added efficacy. OBJECTIVE: To determine the optimal dose of IVIG for treating myasthenia gravis exacerbation. DESIGN: Randomized double-blind placebo-controlled multicenter trial designed to demonstrate superiority of the 2 g/kg dose over the 1 g/kg dose of IVIG, conducted between November 13, 1996, and October 26, 2002. PARTICIPANTS: One hundred seventy-three patients aged 15 to 85 years with acute exacerbation of myasthenia gravis. INTERVENTION: Participants were randomly assigned to receive 1 g/kg of IVIG on day 1 and placebo on day 2 (group 1) vs 1 g/kg of IVIG on 2 consecutive days (group 2). MAIN OUTCOME MEASURE: Improvement in the myasthenic muscular score after 2 weeks. RESULTS: The mean improvements in the myasthenic muscular scores after 2 weeks were 15.49 points (95% confidence interval, 12.09-18.90 points) in group 1 and 19.33 points (95% confidence interval, 15.82-22.85 points) in group 2. However, the difference between the 2 groups was not significant (effect size, 3.84 [95% confidence interval, -1.03 to 8.71]; P = .12). CONCLUSION: This trial found no significant superiority of 2 g/kg over 1 g/kg of IVIG in the treatment of myasthenia gravis exacerbation.

Adolescent↗
PubMed2003

Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: Non-invasive positive pressure ventilation (NPPV) is being used increasingly in the management of patients admitted to hospital with acute respiratory failure secondary to an exacerbation of chronic obstructive pulmonary disease (COPD). OBJECTIVES: To determine the effectiveness of NPPV in the management of patients with respiratory failure due to an acute exacerbation of COPD. SEARCH STRATEGY: An initial search was performed using the Cochrane Airways Group trials register and other relevant electronic databases. SELECTION CRITERIA: Randomised controlled trials comparing NPPV plus usual medical care versus usual medical care alone were selected. Trials needed to recruit adult patients admitted to hospital with respiratory failure due to an exacerbation of COPD and with PaCO2 > 6 kPa (45 mmHg). DATA COLLECTION AND ANALYSIS: Two reviewers independently selected articles for inclusion, evaluated methodological quality of the studies and abstracted the data. MAIN RESULTS: Eight studies were included in the review. NPPV resulted in decreased mortality (Relative Risk [RR] 0.41; 95% Confidence Intervals [CI] 0.26, 0.64), decreased need for intubation (RR 0.42; 95%CI 0.31, 0.59), reduction in treatment failure (RR 0.51; 95%CI 0.39, 0.67), rapid improvement within the first hour in pH (Weight Mean Difference [WMD] 0.03; 95%CI 0.02, 0.04), PaCO2 (WMD -0.40 kPa; 95%CI -0.78, -0.03) and respiratory rate (WMD -3.08 bpm; 95%CI -4.26, -1.89). In addition, complications associated with treatment (RR 0.32; 95%CI 0.18, 0.56) and length of hospital stay (WMD -3.24 days; 95%CI -4.42, -2.06) were also reduced in the NPPV group. REVIEWER'S CONCLUSIONS: Data from good quality randomised controlled trials permit NPPV to be recommended as the first line intervention, coupled with usual medical care, in all suitable patients with respiratory failure secondary to an acute exacerbation of COPD. A trial of NPPV should be considered early in the course of respiratory failure, and before severe acidosis ensures, as a means of avoiding endotracheal intubation, reducing mortality and treatment failure.

Adult↗
PubMed2004

Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: Non-invasive positive pressure ventilation (NPPV) is being used increasingly in the management of patients admitted to hospital with acute respiratory failure secondary to an exacerbation of chronic obstructive pulmonary disease (COPD). OBJECTIVES: To determine the efficacy of NPPV in the management of patients with respiratory failure due to an acute exacerbation of COPD. SEARCH STRATEGY: An initial search was performed using the Cochrane Airways Group trials register and other relevant electronic databases. An updated search was conducted in September 2003. SELECTION CRITERIA: Randomised controlled trials comparing NPPV plus usual medical care (UMC) versus UMC alone were selected. Trials needed to recruit adult patients admitted to hospital with respiratory failure due to an exacerbation of COPD and with PaCO(2) > 6 kPa (45 mmHg). DATA COLLECTION AND ANALYSIS: Two reviewers independently selected articles for inclusion, evaluated methodological quality of the studies and abstracted the data. MAIN RESULTS: Fourteen studies were included in the review. NPPV resulted in decreased mortality (Relative Risk 0.52; 95%CI 0.35, 0.76), decreased need for intubation (RR 0.41; 95%CI 0.33, 0.53), reduction in treatment failure (RR 0.48; 95%CI 0.37, 0.63), rapid improvement within the first hour in pH (Weight Mean Difference 0.03; 95%CI 0.02, 0.04), PaCO(2) (WMD -0.40 kPa; 95%CI -0.78, -0.03) and respiratory rate (WMD -3.08 bpm; 95%CI -4.26, -1.89). In addition, complications associated with treatment (RR 0.38; 95%CI 0.24, 0.60) and length of hospital stay (WMD -3.24 days; 95%CI -4.42, -2.06) was also reduced in the NPPV group. REVIEWER'S CONCLUSIONS: Data from good quality randomised controlled trials show benefit of NPPV as first line intervention as an adjunct therapy to usual medical care in all suitable patients for the management of respiratory failure secondary to an acute exacerbation of COPD. NPPV should be considered early in the course of respiratory failure and before severe acidosis ensues, as a means of reducing the likelihood of endotracheal intubation, treatment failure and mortality.

Adult↗
PubMed2004

Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: Non-invasive positive pressure ventilation (NPPV) is being used increasingly in the management of patients admitted to hospital with acute respiratory failure secondary to an exacerbation of chronic obstructive pulmonary disease (COPD). OBJECTIVES: To determine the efficacy of NPPV in the management of patients with respiratory failure due to an acute exacerbation of COPD. SEARCH STRATEGY: An initial search was performed using the Cochrane Airways Group trials register and other relevant electronic databases. An updated search was conducted in September 2003 and another in April 2004. SELECTION CRITERIA: Randomised controlled trials comparing NPPV plus usual medical care (UMC) versus UMC alone were selected. Trials needed to recruit adult patients admitted to hospital with respiratory failure due to an exacerbation of COPD and with PaCO2 > 6 kPa (45 mmHg). DATA COLLECTION AND ANALYSIS: Two reviewers independently selected articles for inclusion, evaluated methodological quality of the studies and abstracted the data. MAIN RESULTS: Fourteen studies were included in the review. NPPV resulted in decreased mortality (Relative Risk 0.52; 95%CI 0.35 to 0.76), decreased need for intubation (RR 0.41; 95%CI 0.33 to 0.53), reduction in treatment failure (RR 0.48; 95%CI 0.37 to 0.63), rapid improvement within the first hour in pH (Weight Mean Difference 0.03; 95%CI 0.02 to 0.04), PaCO2 (WMD -0.40 kPa; 95%CI -0.78 to -0.03) and respiratory rate (WMD -3.08 bpm; 95%CI -4.26 to -1.89). In addition, complications associated with treatment (RR 0.38; 95%CI 0.24 to 0.60) and length of hospital stay (WMD -3.24 days; 95%CI -4.42 to -2.06) was also reduced in the NPPV group. REVIEWERS' CONCLUSIONS: Data from good quality randomised controlled trials show benefit of NPPV as first line intervention as an adjunct therapy to usual medical care in all suitable patients for the management of respiratory failure secondary to an acute exacerbation of COPD. NPPV should be considered early in the course of respiratory failure and before severe acidosis ensues, as a means of reducing the likelihood of endotracheal intubation, treatment failure and mortality.

Adult↗
PubMed1994

Seizure exacerbation and status epilepticus related to carbamazepine-10,11-epoxide.

Over a 3-year period, we encountered 6 adults whose seizure control unexpectedly deteriorated with the occurrence of partial status epilepticus and daily multiple seizures. Analysis of the case histories and subsequent clinical follow-up for 1 1/2 to 3 years disclosed the following evidence that demonstrates the role of carbamazepine-epoxide in the development of the seizure exacerbation: (1) There were high serum carbamazepine-epoxide concentrations while serum carbamazepine concentrations were lower than or the same as baseline levels; (2) all patients were taking drugs that are known to increase serum carbamazepine-epoxide concentrations; (3) status epilepticus failed to respond to intravenous phenytoin loading; (4) seizure exacerbation in all patients was corrected by withholding carbamazepine dose; (5) seizure exacerbation recurred in 1 patient who resumed the same dose of carbamazepine; and (6) there were no prior status epilepticus or daily multiple seizures despite previous toxicities with other antiepileptic drugs in 3 patients. Our experience shows that inconspicuous elevation of carbamazepine-epoxide levels during polytherapy may precipitate a distinct state of drug toxicity characterized by severe exacerbation of seizures. Mental retardation may be a predisposition to this condition.

Adult↗
PubMed1991

Exacerbation of experimental murine cutaneous leishmaniasis with CD4+ Leishmania major-specific T cell lines or clones which secrete interferon-gamma and mediate parasite-specific delayed-type hypersensitivity.

Leishmania major-specific T cell lines were derived from mice sensitized to the parasite. The cells were of the CD4+ T cell lineage and, upon adoptive transfer, were found to be capable of inducing parasite-specific delayed-type hypersensitivity. Adoptive transfer of these L. major-specific T cells to syngeneic recipients which were either normal, T cell deficient or B cell and antibody deficient led to exacerbation of infection upon subsequent challenge with L. major. This suggested that host T cells, B cells and antibody were not required for the L. major-specific T cells to exert their exacerbative effect on the course of cutaneous leishmaniasis. Additional studies revealed that the adoptive transfer of graded doses of these L. major-specific T cells always resulted in exacerbation of infection. Study of the localization pattern of the cells following transfer showed that they migrate preferentially to the site of the lesions. Furthermore, although the induction phase of this phenomenon was immunologically specific, its effector phase was not. Finally, T cell clones were derived from the L. major-specific T cell lines. The T cell clones were phenotypically and functionally identical to the T cell lines from which they were derived. Adoptive transfer of these parasite-specific T cell clones to normal syngeneic recipients induced an exacerbated course of infection with L. major. Interestingly, when these cloned T cells were specifically activated in vitro, the cells produced interleukin 2 and interferon-gamma, but no interleukin 4, indicating that they belong to the murine Th1 subset of CD4+ T cells.

Animals↗
PubMed1996

Increase of chemokine levels in sputum precedes exacerbation of acute asthma attacks.

Basophils and eosinophils can be activated in vitro by several chemokines such as RANTES, monocyte chemotactic and activating factor (MCAF/MCP-1), macrophage inflammatory peptide-1 alpha (MIP-1 alpha), and interleukin-8 (IL-8). To explore the clinical relevance of the in vitro observations, we measured here the concentrations of these chemokines in sputa from asthmatic patients during acute attacks. Before the onset of a late-phase exacerbation, sputum MCAF/MCP-1, MIP-1 alpha, and IL-8 levels transiently but markedly increased from the basal levels in all of the patients with exacerbation, whereas the sputum levels of these chemokines remained unchanged during the course in the patients without a late-phase exacerbation. These results suggest the involvement of these chemokines in the late-phase exacerbation of asthma.

Acute Disease↗
PubMed2003

Role of viruses and atypical bacteria in exacerbations of asthma in hospitalized children: a prospective study in the Nord-Pas de Calais region (France).

We studied the role of viruses and atypical bacteria in children hospitalized with exacerbated asthma by a prospective study of children with acute asthma admitted to the Department of Pediatrics in Lille, and to 15 hospitals in the Nord-Pas de Calais region, from October 1, 1998-June 30, 1999. We included children aged 2-16 years with active asthma, defined as three or more recurrent episodes of reversible wheezing. The severity of asthma and of asthmatic exacerbations was recorded. Immunofluorescence assays (IFA) on nasopharyngeal secretions (NPS), serological tests, or both, were used for detection of influenza virus, respiratory syncytial virus (RSV), adenovirus, parainfluenza virus, and coronavirus. Polymerase chain reaction (PCR) assays on NPS were used for rhinovirus and enterovirus. Serological tests for Chlamydia pneumoniae and Mycoplasma pneumoniae were performed. A control group of asymptomatic asthmatic outpatients was examined for respiratory viruses (using IFA and PCR). Eighty-two symptomatic children (mean age, 7.9 years) were examined. Viruses were detected in 38% (enterovirus, 15.8%; rhinovirus, 12%; RSV, 7.3%). Serological tests for atypical bacteria were positive in 10% of patients (C. pneumoniae, 5%; M. pneumoniae, 5%). Among the 27 control subjects (mean age, 7.9 years), one PCR was positive for enterovirus. There was no correlation between severity of chronic asthma or asthmatic exacerbations and the diagnosis of infection. Atypical bacterial pathogen infections were linked with prolonged asthmatic symptoms. In conclusion, we confirmed the high incidence of viral infection in acute exacerbations of asthma, especially enteroviruses or rhinoviruses. Persistent clinical features were more frequently associated with atypical bacterial infections, suggesting that these infections should be investigated and treated in cases of persistent asthmatic symptoms.

Adolescent↗
PubMed2004

Pulmonary exacerbations in cystic fibrosis.

The clinical characteristics most relevant to the decision to treat for a pulmonary exacerbation with antibiotics in cystic fibrosis patients were determined. Variables including age, increased cough frequency and sputum production, new crackles and wheezing, asthma, symptomatic sinusitis, hemoptysis, decreased lung function, weight loss, and new acquisition of Pseudomonas aeruginosa were collected in a large prospective multicenter database (Epidemiologic Study of Cystic Fibrosis). During a 12-month baseline period, data from 11692 patients were compared with data collected during the subsequent 6-month study period. Because pulmonary function assessments were unavailable for patients <6 years of age, separate analyses were done for those <6 and >or=6 years of age. The outcome of interest was any antibiotic treatment in the 6-month study period reported as indicated for an exacerbation. Characteristics with the most discriminatory power were determined using stepwise multiple logistic regression. For patients <6 years of age, the strongest independent associations with treatment for a pulmonary exacerbation were new crackles, increased cough frequency, decline in weight, and increased sputum production. For those patients >or=6 years of age, the strongest independent associations were a relative decrease in percent predicted forced expired volume in 1 sec, increased cough frequency, new crackles, and hemoptysis. The presence of three or more of these key characteristics was strongly associated with the occurrence of a treated exacerbation. The reproducibility of the model over time was confirmed by application to a subsequent set of data. This model has potential for use as an outcome measure in clinical trials, and to assist in treatment decisions for individual patients.

Adolescent↗