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PubMed2006

Does heart failure exacerbation increase response to warfarin? A critical review of the literature.

BACKGROUND: Numerous factors, such as other drugs, diet, and age, are well documented as altering response to warfarin. Less attention has been focused on the effect of disease states on the response to oral anticoagulants. Decompensated heart failure is reported to increase response to warfarin, but documentation is limited. OBJECTIVE: The purpose of this review is to critically examine the evidence of a possible effect of heart failure exacerbations on response to warfarin. RESEARCH DESIGN AND METHODS: A literature search was completed of the last 60 years using several databases, including PubMed, MEDLINE, EMBASE, and SCOPUS. Key terms in our search included 'warfarin' AND 'heart failure' and 'heart failure exacerbation' (or 'decompensated heart failure') AND 'effect on warfarin'. When relevant citations were found, the references cited by those authors were checked. RESULTS: Several reports from 1946-1989 suggested that decompensated heart failure increases response to oral anticoagulants. Unfortunately, these early reports have important limitations. More recent reports, since the widespread use of the international normalized ratio (INR), also suggest that heart failure exacerbations are associated with increased response to warfarin. Patient populations are small in these reports. CONCLUSIONS: Heart failure exacerbations may be associated with an increased response to warfarin and other vitamin K antagonists, but many reports are inadequate, and it appears that not all patients are susceptible to this effect. More frequent monitoring of INR in patients with decompensated heart failure is warranted. It is prudent to initiate warfarin at lower doses in patients with a history of heart failure and to monitor INR every 1-2 weeks during times of instability in ambulatory patients, and daily INRs in hospitalized patients. Given the large number of variables that impact on warfarin dose requirement, it is difficult to clearly establish the effect of decompensated heart failure on response to warfarin. Further studies must take all of these variables into account.

Anticoagulants↗
PubMed2006

Interactions between IL-32 and tumor necrosis factor alpha contribute to the exacerbation of immune-inflammatory diseases.

IL-32 is a newly described cytokine in the human found to be an in vitro inducer of tumor necrosis factor alpha (TNFalpha). We examined the in vivo relationship between IL-32 and TNFalpha, and the pathologic role of IL-32 in the TNFalpha-related diseases - arthritis and colitis. We demonstrated by quantitative PCR assay that IL-32 mRNA was expressed in the lymphoid tissues, and in stimulated peripheral T cells, monocytes, and B cells. Activated T cells were important for IL-32 mRNA expression in monocytes and B cells. Interestingly, TNFalpha reciprocally induced IL-32 mRNA expression in T cells, monocyte-derived dendritic cells, and synovial fibroblasts. Moreover, IL-32 mRNA expression was prominent in the synovial tissues of rheumatoid arthritis patients, especially in synovial-infiltrated lymphocytes by in situ hybridization. To examine the in vivo relationship of IL-32 and TNFalpha, we prepared an overexpression model mouse of human IL-32beta (BM-hIL-32) by bone marrow transplantation. Splenocytes of BM-hIL-32 mice showed increased expression and secretion of TNFalpha, IL-1beta, and IL-6 especially in response to lipopolysaccharide stimulation. Moreover, serum TNFalpha concentration showed a clear increase in BM-hIL-32 mice. Cell-sorting analysis of splenocytes showed that the expression of TNFalpha was increased in resting F4/80+ macrophages, and the expression of TNFalpha, IL-1beta and IL-6 was increased in lipopolysaccharide-stimulated F4/80+ macrophages and CD11c+ dendritic cells. In fact, BM-hIL-32 mice showed exacerbation of collagen-antibody-induced arthritis and trinitrobenzen sulfonic acid-induced colitis. In addition, the transfer of hIL-32beta-producing CD4+ T cells significantly exacerbated collagen-induced arthritis, and a TNFalpha blockade cancelled the exacerbating effects of hIL-32beta. We therefore conclude that IL-32 is closely associated with TNFalpha, and contributes to the exacerbation of TNFalpha-related inflammatory arthritis and colitis.

Adoptive Transfer↗
PubMed1996

The dominant white spotting oncogene allele Kit(W-42J) exacerbates XY(DOM) sex reversal.

The Y chromosome from certain populations of M. m. domesticus is incapable of normal testis determination in the B6 inbred strain resulting in XY hermaphrodites or XY females (XY(DOM) sex reversal). B6 consomic strains have been developed with either transient (B6-Y(AKR)) or severe (B6-Y(TIR)) XY(DOM) sex reversal. We report that a point mutation, the dominant white spotting oncogene allele, Kit(W-42J), exacerbates XY(DOM) sex reversal. In B6-Y(AKR), penetrance of the trait is low; however, in B6-Y(TIR), Kit(W-42J) exacerbated sex reversal to such an extent that almost all XY progeny developed into females. The exacerbation of sex reversal was not linked to retardation of early fetal growth or reduction of testis size. Furthermore, semiquantitative RT-PCR for the testis-determining gene, Sry, suggests that exacerbation of sex reversal in B6-Y(TIR) is not due to blockade of Sry expression, a substantial delay in initiation of Sry expression, or exceptionally low levels of Sry mRNAs. We propose that Kit(W-42J) enhances sex reversal by adversely affecting a critical step in testis differentiation that is downstream of Sry.

Alleles↗
PubMed2002

Intravenous versus oral corticosteroids for treatment of acute asthma exacerbations.

OBJECTIVE: To compare the duration of hospitalization of patients treated with either oral or intravenous corticosteroids for an acute asthma exacerbation. METHODS: A retrospective chart review was performed on a random sample of inpatients. Patients were included with the following: a discharge diagnosis of an acute asthma exacerbation, a past medical history significant for asthma, age between 16 and 60 years, and treatment with either oral or intravenous corticosteroids at the time of admission. Exclusion criteria included: patients receiving chronic prednisone therapy, a past medical history significant for chronic obstructive pulmonary disease, an admission to the intensive care unit, or a consistent smoking habit of at least 1 pack daily. Length of hospitalization was the primary outcome measured. Secondary outcomes included 24-hour peak expiratory flow rate, 24-hour pulse oximetry (pO(2)), and amount of beta-agonist and ipratropium used. RESULTS: Fifty-three patients were included in the final data analysis. Patients were grouped by route of corticosteroid administration (intravenous or oral). No significant differences were noted between the 2 groups for race, gender, age, height, weight, admission peak expiratory flow rate, admission pO(2), or types of asthma medications used prior to admission. No significant differences were demonstrated in any of the outcome measures. CONCLUSIONS: Both the intravenous and oral corticosteroid groups demonstrated similar clinical outcomes and lengths of hospitalization in the treatment of acute asthma exacerbations. These results support the initial use of oral corticosteroids for the treatment of acute asthma exacerbations in adult patients admitted to a general medical service.

Acute Disease↗
PubMed1993

Resting energy expenditure. Evolution during antibiotic treatment for pulmonary exacerbation in cystic fibrosis.

STUDY OBJECTIVES: To compare the changes in resting energy expenditure (REE) to concomitant changes in clinical status and pulmonary function in cystic fibrosis (CF) patients during treatment for acute pulmonary exacerbation. To determine if weight loss during exacerbation in CF is related to decreased calorie intake or increased energy needs. DESIGN: Measurements of REE, pulmonary function tests, oxygen saturation, respiratory rate, maximal inspiratory pressure (MIP), white blood cell count, chest x-ray films and attribution of clinical score (ACS) on admission, mid-hospitalization, and discharge. Anthropometric measurements on admission, assessment of dietary intake and nitrogen balance upon admission and prior to discharge. SUBJECTS: Thirteen CF patients admitted for treatment of acute pulmonary exacerbation with a mean age of 11.0 +/- 7.9 (SD) years. RESULTS: From admission to discharge, REE decreased from 44.5 +/- 9.0 to 33.8 +/- 8.5 kilocalorie (kcal)/kg/d (p < 0.003). Similarly, the ACS improved from 7.5 +/- 2.0 to 4.0 +/- 2.2 (p < 0.0001); the absolute neutrophil count decreased from 10,685 +/- 6,226/microliters to 6,363 +/- 168/microliters (p < 0.005); respiratory rate decreased from 32.6 +/- 6.2 to 25.0 +/- 3.7 breaths per minute (p < 0.01); and MIP increased from 77.5 +/- 20.0 to 90.0 +/- 20.4 cm H2O (p < 0.01). In parallel, less significant improvements occurred in pulmonary function tests, oxygen saturation and chest x-ray film scores. Calorie intake was 1,893 +/- 635 and 2,054 +/- 707 kcal/d on admission and discharge, respectively (p = NS); during hospitalization, weight increased from 23.6 +/- 10.1 to 25.7 +/- 10.1 kg (p < 0.005). While carbohydrate and fat content of the diet remained essentially unchanged, a significant increase in protein intake (3.15 +/- 0.92 to 3.5 +/- 0.81 g/kg/d [p < 0.05]) and in nitrogen balance (1.8 +/- 2.5 to 5.6 +/- 2.9 g of nitrogen per day [p < 0.05]) were observed. CONCLUSIONS: In acute CF, pulmonary exacerbation, changes in REE parallel those of clinical improvements and are more sensitive than pulmonary function tests and chest x-ray films as an objective clinical correlate. Increased metabolic requirements but not decreased dietary intake are the cause of weight loss in CF patients.

Acute Disease↗
PubMed1995

The contribution of respiratory viruses to severe exacerbations of asthma in adults.

Viral infections are known to be associated with severe exacerbations of asthma in children. In contrast, there is limited data that viral infections evoke acute episodes of asthma that require emergency care in adults. To determine the role of viral infections in exacerbations of asthma in adults, we examined 33 patients who presented to the emergency room with 35 exacerbations of asthma between September 1990 and March 1991 for the presence of a viral infection. A nasal swab was obtained for virus isolation by culture and rapid antigen detection by fluorescent staining. In 16 patients, serum was collected at initial presentation and 3 to 4 weeks later for acute and convalescent viral antibody titers. All patients had acute episodes of asthma ascertained by medical history and physical examination. About 56% of the patients with asthma exacerbations had symptoms suggestive of viral illness. Rapid antigen detection and viral cultures for influenza A and B, parainfluenza-1, 2, 3, respiratory syncytial virus, adenovirus, and rhinovirus were negative on all patients. Likewise, in all 16 patients tested, acute and convalescent serologic studies did not show a significant rise in titer by complement fixation test. Thus, despite symptoms consistent with viral infection, viral pathogens could not be shown by current virologic techniques. This study suggests that viral infection may not be as prevalent a precipitate of asthma in adults requiring emergency room treatment as is generally thought.

Acute Disease↗
PubMed1999

Relationship between bacterial flora in sputum and functional impairment in patients with acute exacerbations of COPD. Study Group of Bacterial Infection in COPD.

STUDY OBJECTIVES: To investigate the possible relationship between functional respiratory impairment measured by FEV1 and isolation of diverse pathogens in the sputum of patients with exacerbations of COPD. DESIGN: Multicenter, cross-sectional, epidemiologic study. SETTING: Pneumology units in six secondary or tertiary hospitals in Spain. PATIENTS: Ninety-one patients with acute exacerbation of COPD were included. INTERVENTIONS: A quantitative sputum culture was performed, and bacterial growth was considered significant only when the germ was isolated at concentrations > 10(6) cfu (> 10(5) for Streptococcus pneumoniae) in samples with < 10 epithelial cells and > 25 leukocytes per low magnification field (x 100). RESULTS: Germs isolated were the following: Haemophilus influenzae (20 cases; 22%), Pseudomonas aeruginosa (14 cases; 15%), S. pneumoniae (9 cases; 10%), Moraxella catarrhalis (8 cases; 9%), other gram-negative bacteria (7 cases; 7%), and non-potentially pathogenic microorganisms (non-PPMs; 33 cases; 36%). P. aeruginosa and H. influenzae were isolated more frequently among the patients with FEV1 < 50% than among those with FEV1 > 50% (p < 0.05). All patients with P. aeruginosa in sputum had FEV1 < 1,700 mL. FEV1 < 50% was associated with a very high risk of P. aeruginosa or H. influenzae isolation: the odds ratios (ORs) are 6.62 (95% confidence interval [CI], 1.2 to 123.6) and 6.85 (95% CI, 1.6 to 52.6), respectively. Furthermore, active tobacco smoking was associated with a high risk of H. influenzae isolation (OR, 8.1; 95% CI, 1.9 to 43.0). CONCLUSIONS: Patients with the greatest degree of functional impairment, as measured by their FEV1, presented a higher probability of having an isolation of P. aeruginosa or H. influenzae in significant concentrations in sputum during an exacerbation. The diagnostic yield of sputum in patients with an FEV1 > 50% was low, with a predominance of non-PPMs. Low FEV1 and active tobacco smoking are data that should be considered when establishing an empiric antibiotic treatment for exacerbated COPD.

Aged↗
PubMed2000

Toward a consensus definition for COPD exacerbations.

In patients with COPD, an acute worsening of respiratory symptoms is often described as an exacerbation. Exacerbations are associated with a significant increase in mortality, hospitalization, and health-care utilization, but there is currently no widely accepted definition of what constitutes an exacerbation of COPD. This paper summarizes the discussions of the workshop, "COPD: Working Towards a Greater Understanding," in which the participants proposed the following working definition of an exacerbation of COPD: a sustained worsening of the patient's condition, from the stable state and beyond normal day-to-day variations, that is acute in onset and necessitates a change in regular medication in a patient with underlying COPD.

Diagnosis, Differential↗
PubMed2001

Systemic glucocorticoids in severe exacerbations of COPD.

OBJECTIVE: This study aimed to compare the efficacies of 3-day and 10-day courses of methylprednisolone (MP) treatment in severe COPD exacerbations necessitating hospitalization for respiratory failure. DESIGN: Prospective, randomized, single-blind study. SETTING: Tertiary-care center. PATIENTS AND METHODS: Thirty-six patients were included in the study and randomized into two groups: group 1 received MP, 0.5 mg/kg q6h for 3 days, and group 2 was administered the same dosage of MP for the first 3 days, after which it was tapered and terminated on the tenth day. There was no difference between the groups for age, baseline FEV(1), PaO(2), PaCO(2), and pH levels. One patient in group 1 who developed pneumothorax and one patient in group 2 who had steroid-related psychosis could not complete the study. RESULTS: Both groups showed significant improvements in PaO(2) and FEV(1) levels, but these were more marked in group 2 (p = 0.012 and p = 0.019, respectively). There was a significant increase in FVC levels in group 2 only (p = 0.003). Group 2 also had a more marked improvement in dyspnea on exertion. There was no difference between the two groups with regards to other parameters, including pH, PaCO(2) levels, and other symptom scores. Six patients in group 1 and five patients in group 2 developed new exacerbations within the following 6 months. Hyperglycemia occurred in two patients in each group. CONCLUSION: In severe COPD exacerbations, a 10-day course of steroid treatment is more effective than a 3-day course in improving the outcome, but has no benefit in reducing exacerbation rates.

Acute Disease↗
PubMed2001

Management of acute exacerbations of COPD: a summary and appraisal of published evidence.

STUDY OBJECTIVES: To critically review the available data on the diagnostic evaluation, risk stratification, and therapeutic management of patients with acute exacerbations of COPD. DESIGN, SETTING, AND PARTICIPANTS: English-language articles were identified from the following databases: MEDLINE (from 1966 to week 5, 2000), EMBASE (from 1974 to week 18, 2000), HealthStar (from 1975 to June 2000), and the Cochrane Controlled Trials Register (2000, issue 1). The best available evidence on each subtopic then was selected for analysis. Randomized trials, sometimes buttressed by cohort studies, were used to evaluate therapeutic interventions. Cohort studies were used to evaluate diagnostic tests and risk stratification. Study design and results were summarized in evidence tables. Individual studies were rated as to their internal validity, external validity, and quality of study design. Statistical analyses of combined data were not performed. MEASUREMENT AND RESULTS: Limited data exist regarding the utility of most diagnostic tests. However, chest radiography and arterial blood gas sampling appear to be useful, while short-term spirometry measurements do not. In terms of the risk of relapse and the risk of death after hospitalization for an acute exacerbation, there are identifiable clinical variables that are associated with these outcomes. Therapies for which there is evidence of efficacy include bronchodilators, corticosteroids, and noninvasive positive-pressure ventilation. There is also support for the use of antibiotics in patients with more severe exacerbations. Based on limited data, mucolytics and chest physiotherapy do not appear to be of benefit, and oxygen supplementation appears to increase the risk of respiratory failure in an identifiable subgroup of patients. CONCLUSIONS: Although suggestions for appropriate management can be made based on available evidence, the supporting literature is spotty. Further high-quality research is needed and will require an improved, generally acceptable, and transportable definition of the syndrome "acute exacerbation of COPD" and improved methods for observing and measuring outcomes.

Acute Disease↗
PubMed2002

Measurement of short-term changes in dyspnea and disease-specific quality of life following an acute COPD exacerbation.

STUDY OBJECTIVE: To determine whether currently available measurement tools can be used to obtain valid measurements of short-term changes in dyspnea and disease-specific quality of life (QOL) in outpatients with an acute COPD exacerbation. DESIGN: Prospective cohort study. METHODS: Sixty-six patients with an acute COPD exacerbation who presented to the emergency department completed the chronic respiratory disease index questionnaire (CRQ) and the baseline dyspnea index (BDI) and were discharged home receiving 10 days of medical therapy. Reassessment with the CRQ and the transitional dyspnea index (TDI) occurred within 48 h of relapse (defined as an urgent hospital revisit within 10 days because of worsening respiratory symptoms), or 10 days later if relapse did not occur. RESULTS: Patients who did not relapse (n = 49) showed moderate-to-large improvements in disease-specific QOL across all four CRQ domains (improvements in each domain of 1.4 to 1.9 U; p < 0.001 for all domains) and large positive changes in the TDI (total TDI score, + 5.02 plus minus 0.55 U; p = 0.0001). In contrast, patients who had a relapse (n = 17) did not have improved CRQ or TDI scores (mean negative change in three of four CRQ domains, total TDI score - 3.06 plus minus 1.14 U; p = 0.02). Changes in the CRQ dyspnea score and TDI correlated with each other (r = 0.78; p = 0.0001) and with changes in FEV(1) (CRQ, r = 0.48 and p = 0.0001; TDI, r = 0.46 and p = 0.0002). Ten control patients with stable COPD showed no changes in the CRQ or TDI over 10 days. CONCLUSION: The CRQ and BDI/TDI can be used to obtain valid, responsive measures of acute changes in QOL and dyspnea associated with a COPD exacerbation. The direction and magnitude of change in these scores was highly correlated with clinical outcome and with other health measures. Most outpatients treated for a COPD exacerbation experience significant short-term improvements in QOL and dyspnea, with the exception of patients who have a clinical relapse of symptoms.

Aged↗
PubMed2002

Pneumonic vs nonpneumonic acute exacerbations of COPD.

STUDY OBJECTIVE: To describe and compare the background, clinical manifestations, disease course, and infectious etiologies of pneumonic acute exacerbations (PNAE) vs nonpneumonic acute exacerbations (NPAE) of COPD. DESIGN: A prospective, observational study. SETTING: A tertiary university medical center in southern Israel. PATIENTS: Twenty-three hospitalizations for PNAE and 217 hospitalizations for NPAE were included in the study. Paired sera were obtained for each of the hospitalizations and were tested serologically for 12 pathogens. Only a significant change in antibody titers or levels was considered diagnostic. RESULTS: No significant differences were found between the two groups for any of the parameters related to COPD or comorbidity. The clinical type of the exacerbation was not significantly different between the groups. Compared to NPAE, patients with PNAE had lower PO(2) values at hospital admission (p = 0.004) but higher rates of abrupt onset (p = 0.005), ICU admissions (p = 0.006), invasive mechanical ventilation (p = 0.01), mortality (p = 0.007), and longer hospital stay (p = 0.001). In 22 PNAE hospitalizations (96%) and in 153 NPAE hospitalizations (71%), at least one infectious etiology was identified (p = 0.001). Mixed infection was found in 13 patients with PNAE (59%) and in 59 patients with NPAE (39%; not significant [NS]). Viral etiology was identified in 18 patients with PNAE (78%) compared with 99 patients with NPAE (46%; p = 0.003). Pneumococcal etiology was found in 10 patients with PNAE (43%) and in 38 patients with NPAE (18%; p = 0.006). An atypical etiology was identified in 8 patients with PNAE (35%) and 64 patients with NPAE (30%; NS). CONCLUSIONS: Community-acquired pneumonia is common among patients hospitalized for an acute exacerbation of COPD and is generally manifested by more severe clinical and laboratory parameters. In PNAE, compared to NPAE, viral and pneumococcal etiologies are more common, but the rate of atypical pathogens is similar. The therapeutic significance of these findings should be investigated further.

Acute Disease↗
PubMed2004

Allergens, viruses, and asthma exacerbations.

In adults and children with asthma, viral infections (rhinovirus [RV] infection being the most prevalent) will often trigger an increase in symptomatology. The mechanisms responsible for viral-induced exacerbations remain uncertain. Proposed mechanisms include direct infection of the lower respiratory tract, the inflammatory response to viruses, increases in bronchial responsiveness and up-regulation of intercellular adhesion molecule-1 expression in bronchial epithelium. In addition, exposure to allergens, especially seasonal allergens, in sensitized asthmatic individuals have been implicated in asthma attacks. Increased levels of exposure in sensitized asthmatics have been related to increases in hospital admissions and emergency room visits, increased bronchial hyperresponsiveness, increased levels of exhaled nitric oxide, lower levels of lung function, increased treatment requirements, and even increased mortality. In recent years studies have suggested that viruses and allergens may have a synergistic effect on individuals with asthma, thus having a greater influence on exacerbation rate together than either factor alone. Models of experimentally induced RV infection in both allergic and nonallergic individuals using bronchoalveolar lavage and segmental allergen challenge have helped researchers to investigate the possibility of an interaction between allergen sensitization, exposure, and virus infection and their role in the induction of an asthma exacerbation. This review aims to summarize the evidence supporting the role of viruses (in particular RV) as well as the role of, and interaction with, allergen sensitization and exposure on exacerbations of asthma.

Adult↗
PubMed2004

Current and future pharmacologic therapy of exacerbations in chronic obstructive pulmonary disease and asthma.

Exacerbations are an important cause of the morbidity and mortality associated with asthma and chronic obstructive pulmonary disease. Newer therapies include long-acting beta(2)-agonists, which are more effective than short-acting bronchodilators. Inhaled corticosteroids and, in asthma, leukotriene receptor antagonists may have roles in the early phase of exacerbation as an alternative to or added to oral prednisolone. In the future, combinations of long-acting beta(2)-agonists and anticholinergic bronchodilators may offer additive clinical benefits. However, although the treatment and prevention of exacerbations of chronic obstructive pulmonary disease and asthma have been improved by using combinations of known therapies, further research addressing the underlying etiology as well as molecular and pathophysiologic mechanisms of exacerbation is needed to better target novel therapies to the appropriate patient populations and to develop new therapeutic strategies.

Adrenal Cortex Hormones↗
PubMed2026

Asthma Exacerbation Risk and School Asthma Readiness.

OBJECTIVES: School-based asthma management is a key facet of child asthma care. We aimed to describe the proportion of students whose schools have child-specific components of asthma care, derive a composite metric of these components ("school asthma readiness"), and assess its association with asthma exacerbations (asthma risk) in the preceding year. METHODS: Within a nested cohort of children enrolled in a larger randomized clinical trial, we assessed the baseline proportion of children whose school had elements of necessary asthma care. We then derived a "school asthma readiness" composite and used ordinal logistic regression to model the association between number of asthma exacerbations in the preceding year and the composite, accounting for demographic, clinical, and school characteristics. RESULTS: Of 202 participants aged 5 to 13&#xa0;years, most identified as Black (95%) and non-Hispanic (98%), and most participants (73%) had an emergency department visit for asthma in the year before enrollment. Most students' schools (79%) had awareness of the child's asthma diagnosis, whereas fewer had reliever medications and valved holding chambers (both 31%) and asthma care plans (7%). Asthma exacerbations in the prior year were associated with a significantly higher school asthma readiness in bivariate (odds ratio [OR], 1.44 [95% CI, 1.14-1.82]; P&#x2009;=&#x2009;.002) and multivariable analysis (OR, 1.31 [95% CI, 1.02-1.7]; P&#x2009;=&#x2009;.037). CONCLUSIONS: A minority of children attended schools that were equipped to manage asthma symptoms. More past exacerbations were associated with higher school readiness, suggesting that more work is needed to support proactive asthma care in schools.

Humans↗
PubMed2001

Management of acute exacerbations of chronic obstructive pulmonary disease.

Patients with chronic obstructive pulmonary disease are at high risk for acute exacerbations. Strategies that may prevent exacerbations are smoking cessation, pulmonary rehabilitation, and influenza vaccination. Therapy includes bronchodilators, corticosteroids, and antibiotics. Rapid-acting beta2-agonists are bronchodilating agents of choice. Ipratropium should be considered in patients who fail or cannot tolerate beta2-agonists. Data do not support combining anticholinergics and beta2-agonists in acute exacerbations; however, new data do support systemic corticosteroids for their role in reducing airway inflammation. Antibiotics should be included in the regimen if two of the three following are present: increased dyspnea, increased sputum volume, and increased sputum purulence. Many exacerbations may be caused by viruses or noninfective sources, in which case antibiotics are not indicated. Oxygen administration with or without assisted ventilation may be required for short-term management.

Acute Disease↗
PubMed1988

Severe acute exacerbation in chronic hepatitis B virus infection in Sendai, Japan.

In order to examine the clinical features of severe acute exacerbation in chronic hepatitis B virus (HBV) infection, 297 hepatitis B surface antigen (HBsAg) carriers were followed for 35 +/- 22 months (mean +/- S.D.) in Tohoku University Hospital from 1976 to 1987. Of these, 10 experienced severe acute exacerbation with hepatic decompensation. All of these patients had intense subjective symptoms related to the hepatitis. They were all icteric and 8 had ascites. Three developed to fulminant hepatic failure, eventually died. Histology after the exacerbation showed severe hepatic damage such as massive hepatic necrosis and bridging hepatic necrosis in a half of them. Six cases were suspected to result from spontaneous reactivation and 2 from drug-induced reactivation of chronic HBV infection, and the other 2 from superinfection with non-A, non-B hepatitis agent (s). These results suggest that the reactivation of chronic HBV infection is an important factor of severe acute exacerbations in chronic HBV infection in Japan.

Adult↗
PubMed2006

Asthma pathophysiology and evidence-based treatment of severe exacerbations.

PURPOSE: The pathogenesis of asthma and the treatment approach for acute exacerbations are described. The pharmacology, efficacy, safety, and cost of the beta2 agonist, albuterol, a racemic mixture of equal amounts of R- and S-enantiomers, and levalbuterol, the R-enantiomer, are compared. SUMMARY: Asthma symptoms are the result of bronchial hyperresponsiveness, bronchospasm, and chronic airway inflammation. Short-acting, inhaled beta2 agonists; oxygen; intravenous fluids; and corticosteroids are the mainstays of treatment for acute exacerbations. The R-enantiomer of albuterol is responsible for bronchodilation. The S-enantiomer exhibits broncho-constricting activity in vitro, which may be mediated by muscarinic receptors and may be opposed by adding the anticholinergic agent ipratropium bromide. Levalbuterol improves pulmonary function to a greater extent than racemic albuterol and reduces the need for costly hospitalizations in patients with acute asthma exacerbations. CONCLUSION: Levalbuterol is an alternative to racemic albuterol with the potential to improve patient outcomes and reduce costs in the treatment of acute asthma exacerbations.

Adrenergic beta-Agonists↗