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PubMed2006

[Effectiveness of a specific program for patients with chronic obstructive pulmonary disease and frequent exacerbations].

OBJECTIVE: Patients with chronic obstructive pulmonary disease (COPD) and a history of frequent exacerbations are a target population of particular interest from both a clinical and an economic standpoint. The objective of this study was to evaluate the effectiveness of a program designed specifically to manage patients in this subgroup. PATIENTS AND METHODS: This was a 1-year randomized controlled trial designed to compare the effectiveness of a specific program (SP) with that of conventional management (CM) in a group of patients with a high frequency of exacerbations (3 or more per year). Within-group and between-group comparisons were carried out for a number of variables related to the patients medical care, dyspnea, health-related quality of life (HRQL), inhalation technique, and pulmonary function. RESULTS: A total of 26 patients were enrolled in the study (all men). The mean (SD) age was 73 (8) years, and mean forced expiratory volume in 1 second (FEV1) expressed as a percentage of the reference value was 43% (15%). Exacerbations requiring hospital care (emergency department visits and/or admission) decreased in both groups: by 24.4% (P not significant) in the CM group and 44.1% (P=.061) in the SP group. Hospital admissions decreased 73.3% in the SP group and increased 22% in the CM group (P< .001). While length of hospital stay decreased 77.3% in the SP group, this figure almost doubled in the CM group (P=.014). Dyspnea, HRQL, and inhalation technique improved in both groups. FEV1 fell by 46 mL/year in the CM group and increased 10 mL/year in the SP group (P not significant). CONCLUSIONS: The use of a simple program to manage selected patients with a history of frequent exacerbations produces a significant reduction in the number of hospital admissions, an improvement in HRQL, and may improve prognosis.

Aged↗
PubMed2003

Bacterial infection in exacerbated COPD with changes in sputum characteristics.

We examined the risk factors for bacterial exacerbation, defined as the presence of pathogenic bacteria in sputum, in 90 chronic obstructive pulmonary disease (COPD) patients with an exacerbation and changes in sputum characteristics. Smoking, alcohol, lung function, body mass index, medical visits and treatments were the independent variables assessed using multivariable logistic regression modelling (OR, 95% CI). A bacterial exacerbation was diagnosed in 39 (43.3%) of 90 patients. Bacterial exacerbations were more prevalent among current smokers (OR 3.77, 95% CI 1.17-12.12), in patients with poor compliance with inhalation therapy (OR 3.25, 95% CI 1.18-8.93) and with severe lung function impairment (FEV1 OR 0.96, 95% CI 0.93-1.00). Prior use of antibiotics was a risk factor for Pseudomonas aeruginosa infection (OR 6.06, 95% CI 1.29-28.44) and influenza vaccination appeared to have a protective effect against this infection (OR 0.15, 95% CI 0.03-0.67). We conclude that severe impairment of lung function, smoking and poor compliance with therapy are risk factors for bacterial infection in COPD, and P. aeruginosa should be suspected in patients who have been treated with antibiotics and in those not vaccinated against influenza.

Aged↗
PubMed2001

Hepatitis B virus genomes of chronic hepatitis patients do not contain specific mutations related to acute exacerbation.

To determine the specific viral variants associated with acute exacerbation of chronic hepatitis from hepatitis B virus (HBV) infection, we analyzed the complete nucleotide sequences of the HBV genome in serial serum samples from two chronic active hepatitis patients who seroconverted from HBeAg to anti-HBe. HBV DNA was amplified by polymerase chain reaction (PCR) and sequenced. A 1896 precore stop codon mutant (G to A at nt 1896) coexisting with the wild sequence was found in both patients prior to seroconversion from HBeAg to anti-HBe. Core promoter mutations at nucleotide positions 1762 (A to T) and 1764 (G to A) were found in both patients throughout the observation period. Mutations were observed in the HBV genome of the two patients at different time points, and there was no correlation between the mutations and liver disease or DNA polymerase levels. The nucleotide divergence rate and the composition of quasispecies in the HBV sequence at the time of acute exacerbation were almost the same as were found at other time points. These results suggest that acute exacerbation does not appear to be caused by a characteristic HBV species. The multiple factors that cause generalized HBV replication activation may contribute to acute exacerbation.

Child, Preschool↗
PubMed2004

[Exacerbations of COPD--new aspects in pathogenesis and therapy].

Exacerbations of COPD are a common cause of morbidity and mortality in this chronic lung disease. Many exacerbations are caused by bacterial or viral infections, but the cause of about 30% of exacerbations cannot be identified. Clinical symptoms (increased dyspnea, cough, and sputum) are due to increased inflammation of the central and peripheral airways, resulting in increased mucus production and bronchoconstriction. Home management consists of an intensive bronchodilator therapy (beta-agonists and anticholinergics), oral glucocorticosteroids and possibly antibiotics, depending on the clinical situation. Hospitalisation has to be considered if initial medical management fails, if there are significant co-morbidities or complications, or if the underlying COPD is severe. Several possibilities to prevent recurrence of COPD exacerbations are discussed.

Anti-Bacterial Agents↗
PubMed2003

Decreased intercellular adhesion molecule-1 (CD54) and L-selectin (CD62L) expression on peripheral blood natural killer cells in asthmatic children with acute exacerbation.

BACKGROUND: The capacity of inflammatory cells to adhere involves an array of adhesion molecules, and is critical to the inflammatory responses seen in childhood asthma. We aimed to determine the changes of intercellular adhesion molecule-1 (ICAM-1) and L-selectin expressed on peripheral blood (PB) T lymphocytes and natural killer (NK) cells in asthmatic children with acute exacerbation and after prednisolone therapy. METHODS: Flow cytometric analysis was performed to determine the expression of ICAM-1 (CD54) and L-selectin (CD62L) on T (CD3+) cells and NK (CD3-/CD56+) cells of PB from children with allergic asthma with acute exacerbation and in a stable condition after prednisolone therapy. Atopic subjects without asthma and age-matched controls were also included for comparison. RESULTS: Percentages of PB non-CD3, CD56+ NK cells, but not CD3+ T cells, increased in asthmatic children with acute exacerbation, compared to those assessed in a stable condition after a course of prednisolone. However, significant decrease of ICAM-1 (P = 0.01) and L-selectin (P = 0.01) expression on PB NK cells, but not on T cells, were found in children with acute asthma compared to those in a stable condition. NK cells in children with acute asthma showed minimal expression of CD69 and CD25. CONCLUSIONS: Results suggests that either NK cells expressing ICAM-1 and L-selectin selectively migrated into inflamed lung tissues, or subsets of NK cells not expressing ICAM-1/L-selectin were expanded during acute exacerbation of childhood asthma.

Acute Disease↗
PubMed1999

Serial measurements of exhaled nitric oxide during exacerbations of chronic obstructive pulmonary disease.

Excessive inflammation seems important in chronic obstructive pulmonary disease (COPD), particularly during exacerbations of the disease. Exhaled nitric oxide concentration ([NOexh]) is a sensitive marker of bronchial inflammation in asthma; it is unclear if this is also the case in COPD. This study: 1) quantifies [NOexh] in patients with COPD (during an exacerbation and while clinically stable); 2) investigates the response of [NOexh] to i.v. steroid therapy, and its potential relationship with other relevant physiological variables; and 3) assesses the relative contributions of the central and peripheral airways to [NOexh] by collecting exhaled air in two different bags connected in series. Seventeen COPD patients (forced expiratory volume in one second (FEV1) 37.6+/-3.4% of the predicted value (+/-SEM)) hospitalized because of an exacerbation of the disease (arterial oxygen tension (Pa,O2) (7.46+/-0.72 kPa 56.1+/-5.4 mmHg), arterial carbon dioxide tension (Pa,CO2) 5.63+/-0.37 kPa 42.3+/-2.8 mmHg), pH 7.41+/-0.02) and 10 healthy subjects that served as controls were studied. On admission, [NOexh] in COPD was higher than normal (41.0+/-5.1 versus 13.3+/-0.8 parts per billion (ppb), respectively, p<0.001). Despite i.v. steroid therapy, [NOexh] remained elevated throughout recovery (37.9+/-4.8 ppb, p<0.001) until discharge (40.9+/-4.3 ppb, p<0.001). In contrast, when the patients were clinically stable (several months later), [NOexh] was significantly reduced (15.8+/-3.8 ppb, p<0.001), and no longer different from control values. [NOexh] was not related to any of the physiological variables measured during recovery (pulmonary gas exchange) or at discharge (forced spirometry, lung volumes, diffusing capacity). Finally, the contribution of the central and peripheral airways to [NOexh] was not different at any point in time. These results indicate that during exacerbations of chronic obstructive pulmonary disease, the exhaled nitric oxide concentration: 1) is higher than normal; 2) is not reduced acutely by i.v. steroids but is normalized several months after discharge; 3) is unrelated to several physiological indices of disease severity; and 4) appears to be produced homogeneously in central and peripheral airways. Overall, these results are different from those reported in asthma, suggesting that different inflammatory mechanisms are operating in both diseases.

Aged↗
PubMed2000

Patients hospitalized for COPD have a high prevalence of modifiable risk factors for exacerbation (EFRAM study).

There is little information available concerning the extent to which chronic obstructive pulmonarv disease (COPD) patients are satisfactorily managed, especially, regards factors supposedly related to COPD exacerbation. The present study assessed the prevalence rates of potentially modifiable risk factors of COPD exacerbation in patients hospitalized for this reason. A systematic sample of one out of two patients admitted for COPD exacerbation, during 1 yr, in four tertiary hospitals in the Barcelona area, Spain, was performed. Patients answered a questionnaire and underwent anthropometric measurements, spirometric tests and arterial blood gas sampling. Prevalence rates and 95% confidence intervals (95% CI) for risk factors were obtained, and the generalized estimating equation (GEE) method was used to allow for patients to provide information on different admissions. The study recruited 353 patients (29 female) with a total of 404 admissions age (mean+/-SD) 69+/-9, median forced expiratory volume in one second (FEV1) 31% of predicted and mean partial pressure of oxygen (PO2) 63+/-13 mmHg. Of these, 28% had not received an influenza vaccination; a high number (86%) did not attend rehabilitation programmes; 28% of patients with PO2 < or =55 mmHg were not using long-term oxygen therapy (LTOT); among LTOT users, 18% used it <15 h a day; 43% of the total failed in some of the essential inhaler manoeuvres; 26% were current smokers; 21% of noncurrent smokers were exposed to passive smoking at home; current occupational exposure was low (5%). In summary, the authors found a moderate to high prevalence of potentially modifiable risk factors in a large representative sample of patients hospitalized for a chronic obstructive pulmonary disease exacerbation, suggesting unsatisfactory features in their management.

Aged↗
PubMed2002

Altered eosinophil levels as a result of viral infection in asthma exacerbation in childhood.

Respiratory viral infection is known to be a significant cause of asthma exacerbation. Eosinophils have been considered to play an important role in the pathogenesis of virus-induced asthma exacerbations. To determine how often asthma exacerbation is caused by virus infections and to examine the relationship between eosinophilia and asthma episode, we investigated 64 children who experienced asthma attacks between October 1999 and March 2000. We used rapid enzyme immunoassays to detect antigens of respiratory syncytial virus (RSV), influenza A virus, and adenovirus in nasopharyngeal secretions (NPS) of these children, and enumerated eosinophils in the blood and NPS. We detected RSV in 27% and influenza A virus in 17% of the patients. No adenovirus infection or RSV/influenza A co-infection was detected. RSV-infected children were younger (3.85 +/- 0.83 years old) than influenza A virus-infected patients (5.23 +/- 1.34 years old). Eighty-two per cent of patients in the RSV group and 36% of patients in the influenza A virus group had moderate-to-severe asthma episodes (p < 0.05). In RSV-infected children, the eosinophil counts in NPS were higher in the 'severe' group, and younger patients had a greater number of eosinophils in their NPS than older patients (p < 0.05). These trends were not found in influenza A virus patients. In conclusion, our results indicate that, compared with influenza A virus-induced asthma attacks, RSV infection had a higher probability of being associated with asthma exacerbation in infants and younger children and induced attacks of greater severity. The increase in the number of eosinophils in the NPS of RSV-infected children may be responsible, in part, for these differences.

Antigens, Viral↗
PubMed2006

Role of deficient type III interferon-lambda production in asthma exacerbations.

Rhinoviruses are the major cause of asthma exacerbations, and asthmatics have increased susceptibility to rhinovirus and risk of invasive bacterial infections. Here we show deficient induction of interferon-lambdas by rhinovirus in asthmatic primary bronchial epithelial cells and alveolar macrophages, which was highly correlated with severity of rhinovirus-induced asthma exacerbation and virus load in experimentally infected human volunteers. Induction by lipopolysaccharide in asthmatic macrophages was also deficient and correlated with exacerbation severity. These results identify previously unknown mechanisms of susceptibility to infection in asthma and suggest new approaches to prevention and/or treatment of asthma exacerbations.

Asthma↗
PubMed1978

Tryptophan pyrrolase, the regulatory free haem and hepatic porphyrias. Early depletion of haem by clinical and experimental exacerbators of porphyria.

1. The importance of the early depletion of liver haem in the production of porphyria is discussed and further supporting evidence is presented from experiments with tryptophan pyrrolase, under conditions of exacerbation of experimental porphyria by therapeutic and other agents. 2. In addition to the early depletion of pyrrolase haem by porphyrogens, a further depletion is produced when rats are given a porphyrogen plus an analogue or one of 19 drugs known to exacerbate the human disease. 3. Non-exacerbators of human porphyrias do not cause a further early depletion of pyrrolase haem and it is suggested that this system may be used as a screening test for possible exacerbation of the disease by new and existing drugs. 4. A similar further early depletion of haem is produced by combined administration of lead acetate plus phenobarbitone, thus suggesting that the depletion is a more general phenomenon in experimental porphyria. 5. The relationship between tryptophan pyrrolase and the regulatory free haem is discussed. It is suggested that pyrrolase may play an important role in the regulation of haem biosynthesis.

Animals↗
PubMed2003

Streptococcal throat infections and exacerbation of chronic plaque psoriasis: a prospective study.

BACKGROUND: Guttate psoriasis has a well-known association with streptococcal throat infections but the effects of these infections in patients with chronic psoriasis remains to be evaluated in a prospective study. OBJECTIVES: To determine whether streptococcal throat infections are more common in and can cause exacerbation in patients with chronic psoriasis. METHODS: Two hundred and eight patients with chronic plaque psoriasis and 116 unrelated age-matched household controls were followed for 1 year. At recruitment all patients were examined, their disease severity scored and throat swabs taken. Patients and corresponding controls were then re-examined and tested for streptococcal colonization whenever they reported sore throat or exacerbation of their psoriasis during the study period. RESULTS: The psoriasis patients reported sore throat significantly more often than controls (61 of 208 vs. three of 116, P < 0.0001), and beta-haemolytic streptococci of Lancefield groups A, C and G (M protein-positive streptococci) were more often cultured from the patients than the controls (19 of 208 vs. one of 116, P = 0.003). A significant exacerbation of psoriasis (P = 0.004) was observed only if streptococci were isolated and the patients were assessed 4 days or later after the onset of sore throat. No difference was observed between groups A, C or G streptococci in this respect. CONCLUSIONS: This study confirms anecdotal and retrospective reports that streptococcal throat infections can cause exacerbation of chronic plaque psoriasis. It is concluded that psoriasis patients should be encouraged to report sore throat to their physician and that early treatment of streptococcal throat infections might be beneficial in psoriasis. A controlled trial for assessing potential benefits of tonsillectomy in patients with severe psoriasis should also be considered.

Adolescent↗
PubMed2001

Serum eosinophil cationic protein levels measured during exacerbation of asthma: characteristics of patients with low titres.

BACKGROUND: Serum eosinophil cationic protein (ECP) levels reflect ongoing eosinophilic airway inflammation and are used as a marker for asthma activity. ECP levels, however, may not be elevated in some asthmatic patients, even when they are symptomatic. OBJECTIVE: To clarify the characteristics of patients with 'low' ECP titres despite asthma exacerbation. METHODS: Serum ECP levels were measured in 113 asthmatic patients during exacerbation. Patients were divided into two groups according to ECP titre: a high ECP group (H; ECP > or = 16.0 microg/L) and a low ECP group (L; ECP <16.0 microg/L). Twenty-two patients who had recently received systemic steroids were excluded and the clinical features of the remaining patients in H (n = 54) and L (n = 37 were compared. RESULTS: Gender, atopic or smoking status, disease severity, inhaled steroid or theophylline usage, peak expiratory flow (% personal best) and forced expiratory volume in 1 s (FEV1) (% predicted) did not significantly differ between the two groups. Patients in L were significantly older and had longer disease duration and lower serum IgE levels than those in H. Multivariate analysis combining age, disease duration and IgE levels showed that age and disease duration were independently associated with ECP level. Airway wall thickness, assessed in a subset of patients using computed tomography, was significantly larger in L. CONCLUSION: Serum ECP levels in asthmatic patients may not be elevated during exacerbation and thus may not be a useful marker in patients who are older, have longer disease duration or possibly have thicker airway walls. Mechanisms other than eosinophilic inflammation, such as airway remodelling, may be involved in asthma exacerbation in these patients.

Adolescent↗
PubMed2003

A comparison of pulmonary exacerbations with single and multiple organisms in patients with cystic fibrosis and chronic Burkholderia cepacia infection.

STUDY OBJECTIVES: To compare pulmonary exacerbations with single and multiple organisms in patients with chronic Burkholderia cepacia infection. DESIGN: Data was collected over a 23-month period and for each of the patients two episodes of pulmonary exacerbation were identified, one with B. cepacia isolated as the sole respiratory pathogen and the other with one or more coinfecting organisms grown from the sputum culture. SETTING: Regional tertiary referral center for Respiratory Medicine and Adult Cystic Fibrosis Center for Northern Ireland, Belfast City Hospital. PATIENTS: Adult (over 16 years) CF patients with chronic (more than 4 years) B. cepacia complex infection who attended the Belfast City Hospital between January 1997 and November 1998. MEASUREMENTS: Forced expiratory volume in 1s, forced vital capacity, forced expiratory flow rate 25-75, C-reactive protein, leucocyte count and body mass index were measured before and after two weeks of treatment and analysed for any differences in change between the two episodes. RESULTS: All variables in both groups improved following treatment except for body mass index, which remained unchanged. No significant differences between the measurements were identified on comparison of single (monomicrobial) and multiple (polymicrobial) isolate episodes. CONCLUSION: Patients with chronic B. cepacia infection who develop a pulmonary exacerbation improve, as reflected by clinical and biochemical markers, following IV antibiotic treatment. Pulmonary exacerbations with multiple organisms are no more severe than those where only B. cepacia is isolated.

Adolescent↗
PubMed2001

Formoterol Turbuhaler for as-needed therapy in patients with mild acute exacerbations of COPD.

Worsening of underlying bronchospasm may be associated with acute exacerbations of chronic obstructive pulmonary disease (COPD). As airway obstruction becomes more severe, the therapeutic option is to add a short-acting inhaled beta2-agonist as needed to cause rapid relief of bronchospasm. Unfortunately however, the most effective dosage may increase above that recommended during acute exacerbations. Formoterol (Oxis) Turbuhaler has a rapid onset of action (within minutes) and demonstrates a maintained effect on a rway function. In this study, we examined the effects of formoterol used as needed in 20 patients with acute exacerbations of COPD. A dose response curve to inhaled formoterol (9 microg per inhalation) or placebo was constructed using three separate inhalations, i.e. a total cumulative dose of 27 microg. Dose increments were given at 20-min intervals, with measurements being made 15 min after each dose. Formoterol, but not placebo, induced a large and significant (P<0.001) dose-dependent increase in forced expiratory volume in 1 sec (FEV1) [mean differences from baseline = 0.1311 after 9 microg formoterol (95% CI: 0.096-0.167)] 0.1811 after 18 microg formoterol (95% CI: 0.140-0.2221) and 0.2081 after 27 microg formoterol (95% CI: 0.153-0.2631). However, 27 microg formoterol did not induce further benefit [0.0271 (95% CI: -0.008-0.0621); P=0.121] when compared wth 18 microg formoterol. Results of this study suggest the use of higher than customary dose of formoterol for as-needed therapy to provide rapid relief of bronchospasm in patients suffering from acute exacerbations of partially reversible COPD.

Acute Disease↗
PubMed2002

Acute effects of higher than customary doses of salmeterol and salbutamol in patients with acute exacerbation of COPD.

Worsening of underlying bronchospasm may be associated with acute exacerbations of chronic obstructive pulmonary disease (COPD). As airway obstruction becomes more severe, the therapeutic option is to add salbutamol, but not salmeterol, as needed to cause rapid relief of bronchospasm. Unfortunately the most effective dosage of beta2-agonists may increase above that recommended during acute exacerbations. In this study, we compared the acute effects of higher than customary doses of salmeterol and salbutamol in 20 patients with acute exacerbation of COPD. A dose-response curve to salmeterol pMDI, 25 microg/puff or salbutamol pMDI, 100 microg/puff, was constructed using 1, 1, and 2 puff' i.e., a total cumulative dose of 100 microg salmeterol or 400 microg salbutamol on 2 consecutive days. After baseline measurements, dose increments were given at 30-min intervals with measurements being made 25 min after each dose. Hear rate (HR) and pulse-oximetry (SpO2) measurements were then taken. Both salmeterol and salbutamol induced a larg and significant (P < 0.05) dose-dependent increase in FEV1 [mean differences from baseline (L) = after 100 microg salmeterol 0.174 (95% CI: 0.112 to 0.237); after 400 microg salbutamol: 0.165 (95% CI: 0.080 to 0.249)], in IC [mean differences from baseline (L) = after 100 microg salmeterol: 0.332 (95% CI: 0.165 to 0.499); after 400 microg salbutamol: 0.281 (95% CI: 0.107 to 0.456)] (Fig. 2), and in FVC mean differences from baseline (L) = after 100 microg salmeterol: 0.224 (95% CI: 0.117 to 0.331); after 400 microg salbutamol: 0.242 (95% CI: 0.090 to 0.395)]. There was no significant difference between the FEV1 values (P=0.418), the ICvalues (P=0.585), and the FVCvalue (P=0.610) after 100 microg salmeterol and 400 microg salbutamol. HR [mean differences from baseline (beats/min) = after 100 microg salmeterol: 3.15 (95% CI: -0.65 to 6.96); after 400 microg salbutamol: 2.30 (95% CI: -0.91 to 5.51)] and SpO2 [mean differences from baseline (%) = after 100 microg salmeterol: -0.20 (95% CI: -1.00 to 0.60); after 400 microg salbutamol: -0.11 (95% CI: -1.00 to 0.79)] did not change significantly from baseline (P > 0.05). These data indicate that salmeterol is effective and safe in the treatment of acute exacerbation of COPD and support its use in this clinical condition.

Acute Disease↗
PubMed2000

Evidence of bacterial infection in acute exacerbations of chronic bronchitis.

The frequency with which bacterial infection causes exacerbations of chronic obstructive pulmonary disease (COPD) may depend on the dominant pathology present; patients with chronic bronchitis are more susceptible to bacterial bronchial infections than those at the emphysema or asthma ends of the spectrum. However, impairment in respiratory function may be very important in governing the outcome of an exacerbation. Placebo-controlled trials have provided conflicting evidence of the efficacy of antibiotics in acute exacerbations. Overall, there is a significant benefit, particularly in certain patient groups, defined by symptoms and past history. Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis are the species most commonly isolated during exacerbations, and the same species may colonize the bronchial mucosa when the patient is in a stable state. Evidence is accumulating that bacteria are an independent stimulus of mucus hypersecretion and bronchial inflammation, and that they interact with other stimuli such as viral infection, atmospheric pollution, and tobacco smoke. New approaches are being used to investigate the importance of bacterial infection in patients with COPD. There are several good reasons why new more potent antibiotics might be expected to be superior to older standard compounds in the management of patients with problematic COPD. However, future studies should aim to confirm that bacteriologic superiority translates into improved clinical outcomes, and seek to measure the level of benefit.

Acute Disease↗
PubMed2003

Inflammation and infection in exacerbations of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a common disorder with symptoms of chronic cough and progressive dyspnea caused by chronic bronchitis or emphysema. Acute exacerbations of COPD contribute to the accelerated decline in lung function characteristic of this disease and are associated with significant cost, morbidity, and mortality for patients. Controversy exists as to whether exacerbations are caused primarily by inflammation, infection, or perhaps a combination of both conditions. Advances in the pathogenesis of COPD have shed light on the role of inflammation in this condition and highlighted the differences in the inflammatory response present in COPD compared with asthma. Infectious agents often are suspected as causing acute exacerbations of COPD, and antibiotics are frequently prescribed empirically to patients. We review the evidence for an inflammatory and infectious etiology for exacerbations of COPD and compare and contrast how each impacts on this disease.

Humans↗
PubMed2002

Resting energy expenditure in young patients with cystic fibrosis receiving antibiotic therapy for acute respiratory exacerbations.

BACKGROUND: patients with cystic fibrosis commonly have severe malnutrition and growth retardation. Among possible causes of these manifestations are low caloric intake, loss of nutrients and increased resting energy expenditure. This study was designed to assess the influence of antibiotic therapy for infectious exacerbations on resting energy expenditure in young patients with cystic fibrosis. METHODS: We studied 17 patients with cystic fibrosis (mean age, 13.6 years). All were hospitalized to receive intravenous antibiotic therapy (mean duration, 2 weeks) for acute respiratory exacerbations. At the beginning of therapy and after it ended, all patients underwent blood chemical tests, anthropometrical measures, determination of body composition by bioelectrical impedance, spirometry, and indirect calorimetry. RESULTS: Antibiotic therapy led to a significant improvement in biochemical, spirometric variables and in estimated calorimetry measurements expressed in relation to fat-free mass. These findings suggest that infective exacerbations are among the causes of increased resting energy expenditure in young patients with cystic fibrosis. CONCLUSIONS: Indirect calorimetry may prove useful in the diagnosis of infective exacerbations and in monitoring the effect of antibiotic therapy in patients with cystic fibrosis.

Adolescent↗