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PubMed2000

Recurrent exacerbations in severe asthma are associated with enhanced airway closure during stable episodes.

Excessive airway narrowing is a cardinal feature of asthma, and results in closure of airways. Therefore, asthmatic patients in whom airway closure occurs relatively early during expiration might be prone to severe asthma attacks. To test this hypothesis, we compared closing volume (CV) and closing capacity (CC) in a group of asthmatic patients with recurrent exacerbations (more than two exacerbations in the previous year; difficult-to-control asthma), consisting of 11 males and two females, aged 20 to 51 yr, with those in a group of equally severely asthmatic controls without recurrent exacerbations (stable asthma) consisting of 13 males and two females aged 18 to 52 yr. Both groups used equivalent doses of inhaled corticosteroids and were matched for sex, age, atopy, postbronchodilator FEV(1), and provocative concentration of methacholine causing a 20% decrease in FEV(1). They were studied during a clinically stable period of their disease. The patients inhaled 400 microg salbutamol via a spacer device, after which TLC and RV were measured by multibreath helium equilibration, together with the slope of Phase 3 (dN(2)), CV, and CC, by single-breath nitrogen washout. CV and CC were expressed as ratios of VC and TLC, respectively, and all data are presented as % predicted (mean +/- SEM). There was no difference in TLC in patients with difficult-to-control asthma and those with stable asthma (106.7 +/- 4.0% predicted versus 101.7 +/- 4.3% predicted, p = 0.40), RV (113.1 +/- 7.8% predicted versus 100.9 +/- 7.1% predicted, p = 0.26), or dN(2) (142.7 +/- 16.3% predicted versus 116.0 +/- 20.2% predicted, p = 0.23). In contrast, CV and CC were increased in the patients with difficult-to-control asthma as compared with the group with stable asthma (CV: 159.5 +/- 26.8% predicted versus 98.8 +/- 12.5% predicted, p = 0.024; CC: 114.0 +/- 6.4% predicted versus 99.9 +/- 3. 6% predicted, p = 0.030). These findings show that asthmatic individuals with recurrent exacerbations have increased CV and CC as compared with equally severely asthmatic but stable controls, even after bronchodilation during well-controlled episodes. The findings imply that airway closure at relatively high lung volumes under clinically stable conditions might be a risk factor for severe exacerbations in asthmatic patients.

Adolescent↗
PubMed2001

Exacerbations of Bronchitis: bronchial eosinophilia and gene expression for interleukin-4, interleukin-5, and eosinophil chemoattractants.

Eosinophilia has been reported during exacerbations of bronchitis, but the mechanisms of tissue recruitment of eosinophils are unclear. We quantified eosinophils and the concurrent expression of cytokines and chemokines probably responsible for the tissue eosinophilia in bronchial biopsies obtained from three groups of nonatopic subjects: (1) healthy nonsmokers (n = 7; FEV1 % predicted = 108 +/- 4 [mean +/- SEM]); (2) nonasthmatic smokers with chronic bronchitis (CB) in a stable phase of their disease (n = 11; FEV1 % predicted: 75 +/- 5); and (3) nonasthmatic subjects with CB who sought medical advice for an exacerbation of their condition (n = 9; FEV(1) % predicted: 61 +/- 8). We applied anti-EG2 antibody and immunostaining to detect and count eosinophils. We performed in situ hybridization to visualize and enumerate cells expressing the genes for interleukin (IL)-4 and IL-5 and the eosinophil chemokines eotaxin, monocyte chemoattractant protein (MCP)-4, or regulated on activation, normal T-cell expressed and secreted (RANTES). We confirmed an increase in EG2-positive eosinophils in patients with CB in exacerbation. We found messenger RNA (mRNA) positivity for IL-4 and IL-5 in CB, but the between-group differences were not statistically significant. However, the numbers of lymphomononuclear cells expressing eotaxin mRNA were significantly greater in the smokers with CB than in the healthy nonsmokers without CB (p < 0.01). Following an exacerbation, RANTES expression was upregulated and this chemokine was strongly expressed in both the surface epithelium and in subepithelial lymphomononuclear cells: only RANTES showed a significant positive correlation with the increasing number of EG2-positive cells (r = 0.51; p < 0.03). In conclusion, an allergic profile of inflammation can also occur in CB: the marked upregulation of RANTES in the epithelium and subepithelium most likely accounts for the increased eosinophilia associated with an exacerbation of bronchitis.

Adult↗
PubMed2001

Risk factors for hospitalization for a chronic obstructive pulmonary disease exacerbation. EFRAM study.

Although exacerbation of chronic obstructive pulmonary disease (COPD) is important in terms of health and costs, there is little information about which are the risk factors. We estimated the association between modifiable and nonmodifiable potential risk factors of exacerbation and the admission for a COPD exacerbation, using a case-control approach. Cases were recruited among admissions for COPD exacerbation during 1 yr in four tertiary hospitals of the Barcelona area. Control subjects were recruited from hospital's register of discharges, having coincided with the referent case in a previous COPD admission but being clinically stable when the referent case was hospitalized. All patients completed a questionnaire and performed spirometry, blood gases, and physical examination. Information about potential risk factors was collected, including variables related to clinical status, characteristics of medical care, medical prescriptions, adherence to medication, lifestyle, quality of life, and social support. A total of 86 cases and 86 control subjects were included, mean age 69 yr, mean FEV(1) 39% of predicted. Multivariate logistic regression showed the following risk (or protective) factors of COPD hospitalization: three or more COPD admissions in the previous year (odds ratio [OR] 6.21, p = 0.008); FEV(1) (OR 0.96 per percentual unit, p < 0.0005); underprescription of long-term oxygen therapy (LTOT) (OR 22.64, p = 0.007); and current smoking (OR 0.30, p = 0.022). Among a wide range of potential risk factors we have found that only previous admissions, lower FEV(1), and underprescription of LTOT are independently associated with a higher risk of admission for a COPD exacerbation.

Aged↗
PubMed2004

Bronchiectasis, exacerbation indices, and inflammation in chronic obstructive pulmonary disease.

Relationships between high-resolution computed tomography (HRCT) findings in chronic obstructive pulmonary disease (COPD) and bacterial colonization, airway inflammation, or exacerbation indices are unknown. Fifty-four patients with COPD (mean [SD]: age, 69 [7] years; FEV(1), 0.96 [0.33] L; FEV(1) [percent predicted], 38.1 [13.9]%; FEV(1)/forced vital capacity [percent predicted], 40.9 [11.8]%; arterial partial pressure of oxygen, 8.77 [1.11] kPa; history of smoking, 50.5 [33.5] smoking pack-years) underwent HRCT scans of the chest to quantify the presence and extent of bronchiectasis or emphysema. Exacerbation indices were determined from diary cards over 2 years. Quantitative sputum bacteriology and cytokine measurements were performed. Twenty-seven of 54 patients (50%) had bronchiectasis on HRCT, most frequently in the lower lobes (18 of 54, 33.3%). Patients with bronchiectasis had higher levels of airway inflammatory cytokines (p = 0.001). Lower lobe bronchiectasis was associated with lower airway bacterial colonization (p = 0.004), higher sputum interleukin-8 levels (p = 0.001), and longer symptom recovery time at exacerbation (p = 0.001). No relationship was seen between exacerbation frequency and HRCT changes. Evidence of moderate lower lobe bronchiectasis on HRCT is common in COPD and is associated with more severe COPD exacerbations, lower airway bacterial colonization, and increased sputum inflammatory markers.

Aged↗
PubMed2005

The effect of infective exacerbations on sleep and neurobehavioral function in cystic fibrosis.

RATIONALE: Adults with cystic fibrosis (CF) are susceptible to hypoxemia, hypercapnia, arousal from sleep, and neurobehavioral impairment. OBJECTIVES: We hypothesized that pulmonary exacerbations would adversely affect sleep and neurobehavioral performance. METHODS: Patients with exacerbations (cases) had sleep studies and neurobehavioral testing before and after inpatient intravenous therapy. Adults with stable CF underwent the same testing procedures (control subjects). MEASUREMENTS AND MAIN RESULTS: When clinically stable, cases and control subjects had similar lung function, intelligence, and body mass index. Among cases, treatment of an exacerbation improved lung function, quality of life, mood, sleepiness, and activation. Cases spent more time awake after sleep onset (p = 0.02), less time in REM sleep (p = 0.03), and were more hypoxemic than control subjects when unwell. The severity of hypoxemia correlated with lung function. On admission, cases had slower throughput than control subjects in the serial addition and subtraction task (cases, 16 +/- 4, vs. control subjects, 17 +/- 3; F[1, 36] = 5.15, p = 0.03) and a slower response time on the digit symbol substitution task (F[1, 36] = 11.91, p = 0.001), which persisted after treatment (F[1, 36] = 8.48, p = 0.006). Cases experienced significant improvements in sleep efficiency, amount of REM sleep, and hypoxia with treatment. Their performance in the serial addition and subtraction task, psychomotor vigilance task, and simulated driving task also improved with treatment. Sex modified the effect of an exacerbation on some aspects of performance. CONCLUSIONS: Exacerbations of lung disease in adults with CF adversely affect sleep and tests of neurobehavioral performance regardless of underlying disease severity. The implications for performance in daily life need further evaluation because patients often delay admission to hospital to fulfill study or work commitments.

Adolescent↗
PubMed1992

Acute exacerbations of chronic type B hepatitis are accompanied by increased T cell responses to hepatitis B core and e antigens. Implications for hepatitis B e antigen seroconversion.

T cell proliferative responses to hepatitis B virus-encoded envelope antigen (S + preS2 + preS1), recombinant core antigen (HBcAg), and natural hepatitis B e antigen (HBeAg) were examined in 22 HBeAg-positive patients with chronic type B hepatitis and 17 healthy hepatitis B surface antigen (HBsAg) carriers. The results showed that HBeAg-positive patients had (a) higher levels of T cell responses to HBcAg/HBeAg than those of healthy HBsAg carriers (P less than 0.001 and P less than 0.01, respectively); (b) a further increase in these T cell responses during acute exacerbations (P less than 0.05 and P less than 0.05, respectively); (c) subsidence in the T cell responses to HBcAg/HBeAg after recovery from acute exacerbations and HBeAg seroconversion, whereas the responses would persist at high levels if the patients did not enter a clinical remission; and (d) low levels of T cell responses to S + preS2 + preS1 either before or after HBeAg seroconversion. The appearance of increasing T cell responses to HBcAg/HBeAg usually occurred in the early phase of acute exacerbations. These findings imply that HBcAg/HBeAg-specific T cells play an important role in the exacerbations of chronic hepatitis B and in HBeAg seroconversion. HBcAg/HBeAg-specific precursor T cell frequencies were serially studied in selected cases by limiting dilution assay. Elevation (two- to fourfold) of HBcAg/HBeAg-specific precursor T cell frequencies contributed to the increase of HBcAg/HBeAg-specific T cell proliferation during acute exacerbations.

Adult↗
PubMed2001

Effectiveness of inhaled corticosteroids in controlling acute asthma exacerbations in children at home.

Many clinicians advise their patients to increase the dose of inhaled corticosteroids during acute asthma exacerbations, without strong clinical evidence supporting this treatment. This study investigates the effectiveness of inhaled corticosteroids in controlling acute asthma exacerbations in children at home. The study population consisted of children with mild intermittent, mild and moderate persistent asthma aged 1 to 14 years who were treated in our outpatient clinic with inhaled budesonide for 1 year. After participating in an asthma education session, the parents were instructed to initiate treatment with inhaled budesonide at the first signs of asthma exacerbation, starting with 200 to 400 microg budesonide, in combination with beta-2 agonists 4 times a day and followed by a decrease in the dose in 4 to 8 days. Asthma status and peak expiratory flow rates were measured in the 3 monthly follow-up visits. Only children who complied with the treatment regimen and came for follow-up visits regularly were included in the final analysis. One hundred fifty children used our treatment protocol with inhaled budesonide to control their asthma attacks. Clinical improvement of asthma symptoms was achieved after a mean of 1.8 +/- 0.7 days from the beginning of treatment. The parents were able to control 94% of the 1,061 episodes of asthma exacerbation occurring during a cumulative follow-up period of 239 years. In the 3-month period before enrollment, 101 children (67%) had used oral corticosteroids to control their asthma attacks and 50 (33%) were hospitalized. During the entire follow-up period, only 11 children (7%) used oral corticosteroids, and none of the children were hospitalized. The present study demonstrates that children with asthma can control their exacerbations at home using inhaled corticosteroids (budesonide). Treatment, starting with relatively high doses followed by a rapid reduction in dose over 4-8 days, resulted in a decrease in the use of oral steroids and in hospitalization. To achieve good results, patient compliance is essential.

Administration, Inhalation↗
PubMedDate not supplied

Work-related exacerbation of asthma.

Adults with asthma who had been enrolled in an HMO for at least a year were requested to complete a questionnaire about their health status. Approximately 25% of the 1,461 participants responded positively to "Does your current work environment make your asthma worse?" and were classified as having workplace exacerbation of asthma. Those with workplace exacerbation were more likely to have never attended college, be current or former smokers, have a history of other respiratory diseases, have missed work or usual activities at least one day in the past for weeks, and report their asthma was moderate, severe, or very severe. Percentages with workplace exacerbation of asthma were highest for mining and construction (36%), wholesale and retail trade (33%), and public administration (33%), and lowest for educational services (22%), finance, insurance, and real estate (22%), and non-medical and non-educational services (18%). Future studies are needed for objective validation of self-reported workplace exacerbation, and to follow subjects prospectively to clarify the temporal sequence of workplace exacerbation and asthma severity, and how other respiratory conditions and smoking might contribute to work-related worsening of asthma.

Adolescent↗
PubMed2004

Acute Chlamydia pneumoniae and Mycoplasma pneumoniae infections in community-acquired pneumonia and exacerbations of COPD or asthma: therapeutic considerations.

Rates of acute Chlamydia pneumoniae and Mycoplasma pneumoniae infections were determined in 115 adults hospitalized for community-acquired pneumonia (CAP), purulent exacerbations of COPD and acute exacerbations of bronchial asthma, by means of serology and molecular methods. Results were compared with those obtained in a matched control group. Common respiratory pathogens were isolated by cultures in 22.5% and 22.2% of CAP and exacerbated COPD patients, respectively. Cultures from exacerbated asthma patients were always negative. Serological and molecular evidence of current C. pneumoniae infection was obtained in 10.0%, 8.9% and 3.3% of CAP, COPD and asthma cases. The corresponding rates of acute M. pneumoniae infection were 17.5%, 6.7% and 3.3%, respectively. Finally, no difference was found between typical and atypical pathogen rates. These findings highlight the importance of taking into account C. pneumoniae and M. pneumoniae infections in guiding the choice of empirical antibacterial treatment for CAP and purulent exacerbations of COPD.

Acute Disease↗
PubMed2001

Factors associated with relapse after ambulatory treatment of acute exacerbations of chronic bronchitis. DAFNE Study Group.

This study aimed to identify the risk factors for relapse after ambulatory treatment of acute exacerbations of chronic bronchitis (AECB) that can easily be used in a primary care setting. Data were prospectively collected on 2,414 ambulatory patients with AECB from 268 general practices located throughout Spain. A multivariate model to identify risk factors independently associated with failures was developed and validated from the information recorded at the inclusion visit and at 30-days follow-up visit. A total of 507 patients relapsed (21%); of these, 84 required admission (16.5%). The multivariate model for prediction of the risk of relapse included 2,414 cases: 1,689 for the developmental sample and 725 in the validation sample. The model obtained contained three readily-obtainable variables: ischaemic heart disease (odds ratio (OR)=1.63; 95% confidence interval (CI)=1.07-2.47), degree of dyspnoea (OR = 1.31; 1.14-1.50) and number of visits to the general practitioner the previous year (OR = 1.07; 1.04-1.10). The model calibrated well in developmental and validation samples (goodness-of-fit tests: p = 0.295 and p = 0.637, respectively). Severity of the exacerbation was not associated with increased risk of relapse in either univariate or multivariate analysis. The present results suggest that baseline characteristics of the patients such as degree of dyspnoea, coexisting ischaemic heart disease and number of previous visits to the general practitioner for respiratory problems are strongly associated with increased risk of relapse after ambulatory treatment of acute exacerbations of chronic bronchitis. In contrast, exacerbation severity was not associated with clinical failure. Guidelines for management of acute exacerbations of chronic bronchitis should consider such risk factors and advocate intensive broad spectrum treatment and closer follow-up of patients exhibiting them.

Aged↗
PubMed2003

Increased serum concentration of urinary trypsin inhibitor with asthma exacerbation.

The aim of the study was to determine whether the amount of urinary trypsin inhibitor (UTI) in serum, a degenerate induced by neutrophil elastase (NE), reflects the degree of bronchial inflammation in children with acute asthma exacerbation. The involvement of neutrophil-mediated inflammation plays as important a role as eosinophil-mediated inflammation in the pathogenesis of acute asthma exacerbation. However, no measurable marker is sensitive enough to assess neutrophil-mediated inflammation in the airways. The pre-alpha-/inter-alpha-trypsin inhibitors are assumed to be precursors of UTI. NE degrades pre-alpha-/inter-alpha-trypsin inhibitors to liberate UTI. UTI concentrations in 25 childhood patients admitted with asthma exacerbation and 15 control subjects were measured by means of one-step sandwich-type enzyme immunoassay. Serum UTI concentrations in the patients at admission were significantly higher than control values (10.597+/-0.649 and 6.136+/-0.303 U x mL(-1), respectively (mean+/-SEM)). These levels returned to baseline values with improvement in the asthmatic symptoms. However, serum NE and alpha1 antitrypsin concentrations were not significantly different between patients and controls, even during acute exacerbation in the former. The findings suggest that neutrophil-mediated inflammatory events are involved in exacerbation of childhood asthma. The monitoring of urinary trypsin inhibitor concentrations might be useful for evaluating the neutrophil-mediated inflammation in childhood asthma attack.

Acute Disease↗
PubMed2004

Reduced spontaneous apoptosis in peripheral blood neutrophils during exacerbation of COPD.

A major feature of acute exacerbation of chronic obstructive pulmonary disease (COPD) is the accumulation of activated neutrophils in the bronchial tree. This phenomenon can be explained by an increased migration and/or by a prolonged survival due to an inhibition of spontaneous apoptosis. The aim of this study was to assess the apoptotic behaviour of peripheral blood neutrophils in COPD patients during an acute exacerbation. Thirty-six hospitalised COPD patients with an acute exacerbation and 10 healthy volunteers were included. Blood samples were obtained at admission, after 3-5 days and at discharge. Spontaneous apoptosis of isolated neutrophils was measured based on Annexin V-PE binding and nuclear morphology after culturing for 18 h. At admission, significantly lower rates of spontaneous apoptosis were noted in COPD patients compared with healthy volunteers (mean +/- SD 31 +/- 13% versus 44 +/- 18%). The mean percentages of apoptotic neutrophils were 31 +/- 13% at admission, 39 +/- 15% after 3-5 days and 47 +/- 18% at discharge. There was a statistically significant difference between the rates of spontaneous apoptosis on the first day and at discharge. Neither forced expiratory volume in one second < 35% predicted, smoking habit, corticosteroid therapy nor evidence of bacterial infection showed any influence on the spontaneous apoptosis in this study. In conclusion, during acute exacerbations of chronic obstructive pulmonary disease, neutrophil granulocytes show a reduced spontaneous apoptosis that increases progressively after treatment and clinical remission. This raises the question of the importance of neutrophil apoptosis in the development and resolution of exacerbations of chronic obstructive pulmonary disease.

Aged↗
PubMed2006

Novel insights into the aetiology and pathophysiology of increased airway inflammation during COPD exacerbations.

Airway inflammation increases during acute exacerbations of COPD. Extrinsic factors, such as airway infections, increased air pollution, and intrinsic factors, such as increased oxidative stress and altered immunity may contribute to this increase. The evidence for this and the potential mechanisms by which various aetiological agents increase inflammation during COPD exacerbations is reviewed. The pathophysiologic consequences of increased airway inflammation during COPD exacerbations are also discussed. This review aims to establish a cause and effect relationship between etiological factors of increased airway inflammation and COPD exacerbations based on recently published data. Although it can be speculated that reducing inflammation may prevent and/or treat COPD exacerbations, the existing anti-inflammatory treatments are modestly effective.

Air Pollutants↗
PubMed2004

Randomised, controlled trial of N-acetylcysteine for treatment of acute exacerbations of chronic obstructive pulmonary disease [ISRCTN21676344].

BACKGROUND: Prophylactic treatment with N-acetylcysteine (NAC) for 3 months or more is associated with a reduction in the frequency of exacerbations of chronic obstructive pulmonary disease (COPD). This raises the question of whether treatment with NAC during an acute exacerbation will hasten recovery from the exacerbation. METHODS: We have examined this in a randomised, double-blind, placebo controlled trial. Subjects, admitted to hospital with an acute exacerbation of COPD, were randomised within 24 h of admission to treatment with NAC 600 mg b.d. (n = 25) or matching placebo (n = 25). Treatment continued for 7 days or until discharge (whichever occurred first). To be eligible subjects had to be > or = 50 years, have an FEV1 < or = 60% predicted, FEV1/VC < or = 70% and > or = 10 pack year smoking history. Subjects with asthma, heart failure, pneumonia and other respiratory diseases were excluded. All subjects received concurrent treatment with prednisone 40 mg/day, nebulised salbutamol 5 mg q.i.d and where appropriate antibiotics. FEV1, VC, SaO2 and breathlessness were measured 2 hours after a dose of nebulised salbutamol, at the same time each day. Breathlessness was measured on a seven point Likert scale. RESULTS: At baseline FEV1 (% predicted) was 22% in the NAC group and 24% in the control group. There was no difference between the groups in the rate of change of FEV1, VC, SaO2 or breathlessness. Nor did the groups differ in the median length of stay in hospital (6 days for both groups). CONCLUSIONS: Addition of NAC to treatment with corticosteroids and bronchodilators does not modify the outcome in acute exacerbations of COPD.

Clinical Trial↗
PubMed2005

Intrapulmonary percussive ventilation in acute exacerbations of COPD patients with mild respiratory acidosis: a randomized controlled trial [ISRCTN17802078].

INTRODUCTION: We hypothesized that the use of intrapulmonary percussive ventilation (IPV), a technique designed to improve mucus clearance, could prove effective in avoiding further deterioration in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) with mild respiratory acidosis. METHODS: The study was performed in a medical intensive care unit of a university hospital. Thirty-three patients with exacerbations of COPD with a respiratory frequency >or= 25/min, a PaCO2 > 45 Torr and 7.35 <or= pH <or= 7.38 were included in the study. Patients were randomly assigned to receive either standard treatment (control group) or standard treatment plus IPV (IPV group). The IPV group underwent two daily sessions of 30 minutes performed by a chest physiotherapist through a full face mask. The therapy was considered successful when both worsening of the exacerbation and a decrease in pH to under 7.35, which would have required non-invasive ventilation, were avoided. RESULTS: Thirty minutes of IPV led to a significant decrease in respiratory rate, an increase in PaO2 and a decrease in PaCO2 (p < 0.05). Exacerbation worsened in 6 out of 17 patients in the control group versus 0 out of 16 in the IPV group (p < 0.05). The hospital stay was significantly shorter in the IPV group than in the control group (6.8 +/- 1.0 vs. 7.9 +/- 1.3 days, p < 0.05). CONCLUSION: IPV is a safe technique and may prevent further deterioration in patients with acute exacerbations of COPD with mild respiratory acidosis.

Acidosis, Respiratory↗
PubMed2003

Modulation of dietary vitamins E and C fails to ameliorate b-carotene exacerbation of UV carcinogenesis in mice.

b-Carotene is a strong singlet oxygen quencher and, under most conditions, exhibits strong antioxidant properties. Based on these properties, and a number of epidemiological studies, it was suggested that an above average intake of the carotenoid might reduce cancer risks. Earlier studies had found that b-carotene, when added to commercial closed-formula rodent diets, provided significant photoprotection to ultraviolet light (UV) carcinogenesis. However, clinical trials found that b-carotene supplementation evoked no change in incidence of nonmelanoma skin cancer and that smokers suffered a significant increase in lung cancer incidence. Further, recent studies, employing b-carotene-supplemented semidefined diets, not only failed to find a photoprotective effect, but significant exacerbation of UV carcinogenic expression resulted. Based on the relative electron transfer rate constants for interactions between b-carotene, a-tocopherol (vitamin E), and vitamin C, a mechanism was proposed for the repair of b-carotene radical cation, a strongly oxidizing radical resulting from b-carotene interactions with many oxidizing species. It was theorized that vitamin C repaired the carotenoid radical cation. As mice have no nutritional requirement for vitamin C and smokers are known to exhibit low levels of the vitamin, it was suggested that differences in the relative levels of vitamin C in closed-formula rations (no vitamin C) in which photoprotection occurred, and semidefined diets (containing vitamin C) in which exacerbation resulted, might account for the differences in response. Hairless mice were fed b-carotene-supplemented semidefined diets containing varying levels of vitamins E and C (either increasing their concentrations or reducing them to reflect levels found in closed-formula rations) and subjected to a UV carcinogenesis protocol. Increasing levels of vitamins E and C did not ameliorate b-carotene exacerbation of UV carcinogenesis. Nor did elimination of vitamin C from the diet. Reduced levels of dietary vitamin E augmented b-carotene exacerbation of UV carcinogenic expression, suggesting vitamin E and b-carotene interaction. It is concluded that the photoprotective effect of b-carotene reported earlier by others, or the noninjurious effect of b-carotene found in our studies with closed-formula rations, might depend on interaction with other dietary factors that are either absent, or present in ineffectual concentrations, in the semidefined diet in which exacerbation of UV carcinogenesis occurs. Those factors could be other carotenoids, their isomers, or some yet unidentified phytochemical(s).

Animals↗
PubMed1988

Exacerbation of indomethacin-induced gastric ulceration by systemically administered GABA in rats: possible involvement of peripheral GABA receptors.

Effects of systemically administered gamma-aminobutyric acid (GABA) on indomethacin-induced gastric ulceration were studied in rats. Orally administered GABA significantly exacerbated the ulceration in a dose-dependent manner, although GABA per se had no ulcerogenic activity. The exacerbation was restored by GABA receptor antagonists, bicuculline methiodide, picrotoxin and pentylenetetrazol. Pretreatment with atropine sulfate antagonized the exacerbating effect of GABA on indomethacin-induced ulceration. 3-Amino-1-propanesulfonic acid, but not glycine, taurine or beta-alanine, mimicked the effect of GABA on the ulceration, which was inhibited by picrotoxin. Muscimol and (-)-baclofen could not potentiate the ulceration. However, sodium pentobarbital and diazepam caused synergistic exacerbation of the ulcer when combined with GABA. Since it is known that systemically administered GABA can not penetrate into the brain, these results suggest that systemically administered GABA may stimulate the cholinergic transmission mediating the activation of peripheral GABA receptors, resulting in the exacerbation of indomethacin-induced ulceration.

Animals↗
PubMed1998

Infective exacerbations of chronic bronchitis: relation between bacteriologic etiology and lung function.

STUDY OBJECTIVE: In patients with severe COPD, acute infective exacerbations are frequent. Streptococcus pneumoniae and Haemophilus influenzae are the most commonly isolated bacteria in sputum cultures from these patients. We hypothesized that in patients with advanced disease, Gram-negative bacteria other than H influenzae play at least an equally important role. METHODS: We evaluated clinical data and sputum culture results from 211 unselected COPD patients admitted to our hospital with an acute infective exacerbation of COPD. One hundred twelve patients fulfilled our protocol criteria of reliable microbiologic results and reproducible lung function tests; the patients were categorized according to the recently published three stages of severity. RESULTS: Lung function tests revealed an FEV1 of > or =50% of the predicted value in 30 patients (stage I), an FEV1 of 35% to <50% of the predicted value in 30 patients (stage II), and an FEV1 of < or =35% of the predicted value in 34 patients (stage III). Bacteria were classified into three groups: group 1 contained S pneumoniae and other Gram-positive cocci; group 2, H influenzae and Moraxella catarrhalis; and group 3, Enterobacteriaceae and Pseudomonas spp. For all patients together, the most frequently isolated bacteria were group 3 organisms (Enterobacteriaceae and Pseudomonas spp, 48.2%), followed by group 1 organisms (S pneumoniae and other Gram-positive cocci, 30.4%), and group 2 organisms (H influenzae and M catarrhalis, 21.4%). In stage I patients, 14 of 30 had bacteria from group 1, seven of 30 had group 2, and nine of 30 had group 3. In stage II patients, eight of 30 had group 1 bacteria, 10 of 30 had group 2, and 12 of 30 had group 3. In stage III patients, 12 of 52 had group 1 bacteria, seven of 52 had group 2, and 22 of 52 had group 3. The three groups of bacteria causing infective exacerbations were unevenly distributed among the three severity stages of lung function (p=0.016). CONCLUSION: There is a correlation between deterioration of lung function and the bacteria isolated from patients with infective exacerbations of COPD. In acute infective exacerbations, Enterobacteriaceae and Pseudomonas spp are the predominant bacteria in patients with an FEV1 < or =35% of the predicted value.

Acute Disease↗