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PubMed2002

Pilot safety study of liposomal prostaglandin (PGE1) in respiratory exacerbations in cystic fibrosis.

BACKGROUND: A pilot evaluation to assess the safety and possible benefits of TLC C-53, (prostaglandin E(1) associated with egg phosphatidylcholine liposomes) in acute respiratory exacerbations in children with cystic fibrosis (CF). METHODS: Randomised, double-blind, placebo-controlled study in 20 P. aeruginosa colonised patients. All received intravenous antibiotics. Subjects were given a rising dose of TLC C-53 (0.15-1.8 microg/kg) by 4 x 1-h infusions. Primary outcome measures were sputum IL-6, IL-8 and sputum neutrophil elastase. The rate of decline in lung function was determined at 6 weeks post-therapy as was the interval until the next respiratory exacerbation requiring intravenous antibiotic therapy. RESULTS: Analysis of primary and secondary outcome measures failed to show any significant differences between the two groups, although trends favoured the treated group. Decline in lung function over 6 weeks favoured the TLC C-53 group (FEV(1) mean difference 4.3%, 95% CI=-6.8, 15.4%). Time to next exacerbation also favoured the TLC C-53 group with a mean time to exacerbation for TLC C-53 of 26.0 weeks against 11.9 weeks. CONCLUSIONS: A larger multi-centre trial of TLC C-53 as an adjunct to antibiotic therapy in respiratory exacerbations in CF would appear warranted.

Adolescent↗
PubMed2004

[Risk factors of readmission in acute exacerbation of moderate-to-severe chronic obstructive pulmonary disease].

OBJECTIVES: More effective management of chronic obstructive pulmonary disease (COPD) and improved survival of COPD patients requires a better understanding of the risk factors for exacerbation. The aim of this study was to identify factors related to readmission in patients with moderate-to-severe COPD. PATIENTS AND METHODS: Ninety patients with moderate-to-severe COPD hospitalized consecutively for acute exacerbation were studied prospectively. At discharge, the following potential predictors were assessed: clinical and spirometric variables, arterial blood gases, and respiratory muscle strength determined noninvasively. The patients were followed for a period of 3 months. Readmission for exacerbation and time intervals free of hospitalization were recorded. RESULTS: Univariate analysis showed that the presence of cor pulmonale (P<.05), long-term oxygen therapy (P<.05), hypercapnia (P<.05), and high inspiratory load--mean inspiratory airway pressure measured at the mouth exceeding 0.40 cm H2O and a pressure-time index greater than 0.25 (P<.05 for both variables)--increased the risk of hospitalization for exacerbation. Multivariate analysis showed that only cor pulmonale (P<.05) and a high pressure-time index (>0.25, P<.05) were independently related to risk of readmission. CONCLUSIONS: Cor pulmonale and a high pressure-time index are independent risk factors for hospitalization for exacerbation of moderate-to-severe COPD.

Acute Disease↗
PubMed2001

Acute pancreatitis complicating acute exacerbation of chronic hepatitis B infection carries a poor prognosis.

The clinical outcome of acute pancreatitis complicating acute exacerbation of chronic hepatitis virus B (HBV) infection has never been studied. Ninety patients with acute pancreatitis were recruited. Five patients (5.6%) (Group 1) had acute pancreatitis superimposed on acute exacerbation of chronic HBV infection with no other causes of acute pancreatitis being identified. The clinical outcome of these five patients was compared to the 85 non-HBV infected patients (Group 2) with acute pancreatitis. A third group (Group 3) of patients (n=406) with acute exacerbation of chronic HBV infections without acute pancreatitis was also recruited for comparison. Group 1 had a significantly higher mortality rate (4 out of 5, 80%) compared to those of Group 2 (13 out of 85, 15.3%, P=0.0041) and Group 3 (9 out of 406, 2.2%, P < 0.0001). In Group 1 patients, the acute pancreatitis occurred during the initial rise of HBV DNA with relatively low or normal level of alanine aminotransferase (ALT) in two patients, during the rise of ALT with declining level of HBV DNA in one patient, and during the cholestatic phase of the acute exacerbation in one patient. The acute pancreatitis was clinically silent and only diagnosed by computerized tomography in the remaining patient. Direct viral damage and/or immunological attack to the pancreatic tissue were probably the underlying pathogenesis of the acute pancreatitis in these patients. In conclusion, acute pancreatitis complicating acute exacerbation of chronic HBV infection carried an extremely poor prognosis with high mortality.

Acute Disease↗
PubMed2000

Prehospital management of exacerbations of asthma: relation to patient and disease characteristics.

OBJECTIVE: Admission to hospital due to an exacerbation of asthma may represent a failure of prehospital management to prevent an attack or bring about its remission. We aim to describe the steps taken prior to hospital attendance in patients with asthma and to identify patient or disease characteristics that were associated with failure to take appropriate actions. METHODOLOGY: Patients aged over 15 years who were discharged from hospital or the Emergency Department with a primary diagnosis of asthma completed a questionnaire about the impact of asthma and its management prior to the onset of the recent exacerbation. The impact of asthma on quality of life was measured using our Asthma Quality of Life Questionnaire (AQLQ). RESULTS: Seventy-eight subjects completed the questionnaire including 49 who had been inpatients and 29 who had been discharged from the Emergency Department. They included many subjects with severe asthma: 41% had nocturnal symptoms three or more times per week and 41% had been admitted to hospital with asthma in the 12 months prior to this episode. Their AQLQ scores were high (severe) (mean 4.5+/-2.2). Most subjects described their presenting exacerbation as slow in onset and moderate or severe in intensity. During this exacerbation and prior to hospital attendance, only 27% of subjects had measured their peak expiratory flow rate, 19% had commenced or increased the dose of inhaled steroids, and 22% had commenced oral steroids. These actions were not related to the self-perceived speed of onset of the attack. Patients with lower levels of asthma-related concerns for health and more severe mood disturbance associated with asthma were less likely to take these appropriate self-management steps. CONCLUSIONS: This study shows that the failure of prehospital management to prevent the necessity of hospital attendance in most cases stems from a failure to implement currently recommended actions or treatments for exacerbations. Addressing this problem should result in a reduction in rates of hospitalization for asthma.

Adult↗
PubMed1994

Effect of aerosolized recombinant human DNase on exacerbations of respiratory symptoms and on pulmonary function in patients with cystic fibrosis. The Pulmozyme Study Group.

BACKGROUND: Respiratory disease in patients with cystic fibrosis is characterized by airway obstruction caused by the accumulation of thick, purulent secretions, which results in recurrent, symptomatic exacerbations. The viscoelasticity of the secretions can be reduced in vitro by recombinant human deoxyribonuclease I (rhDNase), a bioengineered copy of the human enzyme. METHODS: We performed a randomized, double-blind, placebo-controlled study to determine the effects of once-daily and twice-daily administration of rhDNase on exacerbations of respiratory symptoms requiring parenteral antibiotics and on pulmonary function. A total of 968 adults and children with cystic fibrosis were treated for 24 weeks as outpatients. RESULTS: One or more exacerbations occurred in 27 percent of the patients given placebo, 22 percent of those treated with rhDNase once daily, and 19 percent of those treated with rhDNase twice daily. As compared with placebo, the administration of rhDNase once daily and twice daily reduced the age-adjusted risk of respiratory exacerbations by 28 percent (P = 0.04) and 37 percent (P < 0.01), respectively. The administration of rhDNase once daily and twice daily improved forced expiratory volume in one second during the study by a mean (+/- SD) of 5.8 +/- 0.7 and 5.6 +/- 0.7 percent, respectively. None of the patients had anaphylaxis. Voice alteration and laryngitis were more frequent in the rhDNase-treated patients than in those receiving placebo but were rarely severe and resolved within 21 days of onset. CONCLUSIONS: In patients with cystic fibrosis, the administration of rhDNase reduced but did not eliminate exacerbations of respiratory symptoms, resulted in slight improvement in pulmonary function, and was well tolerated.

Adolescent↗
PubMed2006

Mortality after an emergency department visit for exacerbation of chronic obstructive pulmonary disease.

OBJECTIVE: To describe the mortality after emergency department (ED) visits for chronic obstructive pulmonary disease (COPD) exacerbation. DESIGN: Retrospective cohort study of ED patients with COPD exacerbation. Setting. Administrative data analysis. PARTICIPANTS: Patients age 55 and over who visited the ED during a 2-year period with primary ICD-9 codes of 491, 492, or 496. MEASUREMENTS: Demographic characteristics, comorbid conditions, hospital utilization for COPD, and vital status. RESULTS: During the study period, there were 482 index visits with a median follow-up of 1,128 days (3.1 years). Demographic characteristics of the cohort were as follows: mean age 72 years, 56% female, 93% White, and 37% currently married. Mortality increased over time: 5% at 30 days, 9% at 60 days, 11% at 90 days, 16% at 180 days, 23% at 1 year, 32% at 2 years, and 39% at 3 years. At the end of follow-up, 220 (46%) patients had died. On multivariate analysis, independent predictors of mortality were increasing age (hazard ratio [HR] 1.3 per 5-year increase, 95% CI 1.2-1.4), having congestive heart failure (HR 1.6, 95% CI 1.2-2.1), having metastatic solid tumor (HR 3.3, 95% CI 2.0-5.5), and hospital utilization for COPD exacerbation during past year (HR 1.9, 95% CI 1.4-2.6). CONCLUSION: The mortality rate after an ED visit for COPD exacerbation is quite high. Mortality is related to older age, specific comorbid conditions, and history of prior COPD exacerbations.

Aged↗
PubMed2004

Factors associated with outcomes of acute exacerbations of chronic obstructive pulmonary disease.

The purpose of this article is to provide a general review of the current literature on the factors associated with the outcomes of hospitalizations, survival and health-related quality of life in acute exacerbations of chronic obstructive pulmonary disease (AECOPD), highlighting the limitations and the complexities in interpretation of the results of current studies. There is no consensus definition for AECOPD; onsets may be difficult to define and the determination of duration elusive. The prevalence of acute exacerbations of COPD (AECOPD) in the community appears to be underestimated as exacerbations are underreported by patients and their doctors. Hospitalization for COPD is due mainly to severe AECOPDs which drive the cost of care. There are few longitudinal epidemiological studies on factors associated with hospitalizations for AECOPD. The results of current studies do not allow clear differentiation between associations that are predictors of event, the consequences of the event, or indicators of severity. Strategies to reduce severe exacerbations of COPD include pharmacological treatment, vaccinations, pulmonary rehabilitation, and home care programs. The optimal strategy for the reduction of hospitalization in COPD remains unclear. Long-term interventional studies are needed to provide clearer information for the prevention of exacerbations and hospitalizations in COPD.

Disease Progression↗
PubMed2005

Increased oxidative stress in acute exacerbations of asthma.

Oxidant-antioxidant imbalance may play an important role in the pathogenesis of asthma, especially during acute exacerbations. To compare the systemic oxidant-antioxidant status in patients with acute exacerbations and stable asthma, we measured a wide range of parameters of oxidant-antioxidant balance in leukocytes, plasma, and red cells of 32 patients with acute exacerbations and 97 patients with stable asthma. These included measurement of superoxide anion generation by leukocytes, lipid peroxidation (measured as TBARS), total nitrates and nitrites, protein carbonyls, and protein sulfhydryls in plasma. Antioxidant status was evaluated by measuring the red cell superoxide dismutase and catalase activity, total blood glutathione, glutathione peroxidase activity in red cell and plasma, and total antioxidant capacity (assessed as ferric reducing antioxidant power) in plasma. Plasma total antioxidant capacity and total protein sulfhydryls were found to be decreased (p < 0.01), whereas plasma lipid peroxides were found to be increased (p < 0.05), in acute exacerbations of asthma. No significant differences were found in plasma glutathione peroxidase, protein carbonyls, and total nitrates and nitrites, red cell antioxidative enzyme activities, superoxide anion release from leukocytes, and total blood glutathione between the two groups (p > 0.05). Our observations suggest that acute exacerbations of asthma are associated with increased oxidative stress that is evident from some of the parameters in the plasma. Failure to observe simultaneous changes in all parameters of oxidative stress may be due to the possibility of their responses being dissociated in time or compensatory changes occurring in some of these.

Acute Disease↗
PubMed2005

Moxifloxacin for the treatment of acute exacerbations of chronic obstructive pulmonary disease.

BACKGROUND/PURPOSE: The significant impact of acute exacerbations of chronic obstructive pulmonary disease (AECOPD) is now recognized. This recognition has led to increased efforts to provide evidence-based, appropriate treatment of AECOPD, to minimize its negative impact. This article reviews the bacterial etiology of AECOPD and clinical trials (both placebo-controlled and antibiotic comparison trials) that support the use of antibiotics for AECOPD, with an emphasis on the role of newer fluoroquinolones for the treatment of patients with this condition. A discussion of patient stratification that permits identification of those who require initial aggressive antibiotic therapy is presented. MAIN FINDINGS: Among the treatment modalities for exacerbations, the role and choice of antibiotics is hotly debated. Current evidence supports the use of antibiotics in the treatment of AECOPD, because bacterial pathogens cause approximately half the exacerbations, and because empirical antibiotics have a significant benefit in most exacerbations. Several recent investigations have aided in the development of a rational antibiotic strategy for AECOPD. These include outcome studies that have identified patients who are likely to have a poor outcome of their exacerbation and, therefore, are candidates for aggressive initial antibiotic therapy. Studies of the new fluoroquinolone agents have shown superior short- and long-term clinical results among patients with AECOPD who are at risk of a poor outcome. CONCLUSIONS: Theoretical concerns about the emergence of resistance to the fluoroquinolones dictate not only the appropriate use of these drugs but, also, the use of the most-potent agents available in this class, to sustain their usefulness over time. Such selected use of the new fluoroquinolones balances individual benefit with societal concerns regarding the use of these agents for the treatment of AECOPD.

Adult↗
PubMed2004

New developments in the pathogenesis of acute exacerbations of chronic obstructive pulmonary disease.

PURPOSE OF REVIEW: Acute exacerbations of chronic obstructive pulmonary disease were a poorly defined and understood entity. The application of better study designs and new research methodologies has shed considerable light on the pathogenesis of this common clinical syndrome. RECENT FINDINGS: Inflammation is an important component of the pathogenesis of chronic obstructive pulmonary disease, and exacerbations probably represent acute increases in airway inflammation brought about by one or more etiological agents. Environmental particulate and gaseous pollutants have been linked in epidemiological studies with increased respiratory symptoms and mortality in chronic obstructive pulmonary disease. Bacterial, viral and atypical pathogens, either alone or in concert, induce the majority of acute exacerbations. SUMMARY: A bacterial cause of a substantial proportion of exacerbations is now firmly established by the results of bronchoscopy, molecular epidemiology, immunology and airway inflammation studies. Future research should focus on pathogenic mechanisms and host defence against the microbial pathogens associated with acute exacerbations of chronic obstructive pulmonary disease, in order to develop better treatment and prevention strategies.

Acute Disease↗
PubMed2000

Management of acute exacerbations in chronic obstructive pulmonary disease.

An acute exacerbation of chronic obstructive pulmonary disease (COPD) is characterized by an acute worsening of symptoms accompanied by lung infection. In severe cases, an acute exacerbation may cause respiratory failure and death. Successful management of acute exacerbation of COPD in either the inpatient or outpatient setting requires attention to a number of key issues. In this review, issues regarding the management of acute exacerbations of COPD are discussed. An inhaled beta-2 agonist along with the inhaled anticholinergic bronchodilator are recommended. Antibiotic therapy has been demonstrated to improve clinical recovery and physical outcomes. It should be directed against the most commonly occurring pathogens and, in more severe cases, coverage against Gram-negative bacteria is considered. Short course of systemic steroids does provide benefit in hospitalized patients. Supplemental oxygen is appropriate for all patients with hypoxemia. Ventilatory support treatment may be necessary, noninvasive ventilatory assistance being preferable early in the course of the acute episode. In a high number of cases, endotracheal intubation may be avoided. Promoting smoking cessation and the use of influenzae and pneumococcal vaccination may help decrease frequency of episodes of these exacerbations.

Administration, Inhalation↗
PubMed2004

Low apolipoprotein A-I level at intensive care unit admission and systemic inflammatory response syndrome exacerbation.

OBJECTIVE: Examine whether a low serum level of apolipoprotein A-I at intensive care unit (ICU) admission is associated with a further increase of the number of systemic inflammatory response syndrome (SIRS) criteria. DESIGN: Prospective observational study. SETTING: A 20-bed, university-affiliated, surgical ICU. PATIENTS: Patients admitted after major surgery, multiple trauma, or acute pancreatitis without septic shock. INTERVENTIONS: We defined as the SIRS Exacerb group patients who presented a further increase of the number of SIRS criteria during their ICU stay or, in the presence of four SIRS criteria at ICU admission, those who presented a further aggravation of organ failure. Other patients were attributed to the SIRS No Exacerb group. From day 1 to 6, we measured apolipoprotein A-I, high-density lipoprotein and total cholesterol, triglycerides, C-reactive protein, procalcitonin, serum amyloid A, interleukin 6, interleukin-1 receptor antagonist, albumin, and other nutrition-linked variables. We looked at laboratory values or factors present at ICU admission according to the two groups. MEASUREMENTS AND MAIN RESULTS: From 63 patients analyzed, 29 (46%) were assigned to the SIRS Exacerb group. Age, sex, and SAPS II and SIRS scores at ICU admission did not differ between the groups. Patients in the SIRS Exacerb group presented more often a septic event (5/29 vs. 0/34, p =.02), had a higher hospital mortality (6/29 vs. 0/34, p =.007), and had a longer ICU stay (p =.0023). At admission, inflammatory variables such as the C-reactive protein, serum amyloid A, interleukin 6, interleukin-1 receptor antagonist plasma levels, and other lipid or nutrition-linked variables were similar between the two groups. Apolipoprotein A-I levels were lower in the SIRS Exacerb group (median [interquartile range]: 68 [56-81] vs. 84 [69-94] mg/dL, p =.028). CONCLUSION: A low serum level of apolipoprotein A-I at ICU admission is associated with an increase of the number of SIRS criteria during the ICU stay.

Adult↗
PubMed2005

Viruses in asthma exacerbations.

PURPOSE OF REVIEW: Respiratory viruses are well recognized as major triggers of acute exacerbations of asthma in children and adults, resulting in frequent outpatients visits and hospitalizations. Clinical and epidemiologic evidence supports this association. The application of molecular diagnostic methods has improved understanding of viral epidemiology and the pathophysiological mechanisms involved in viral induced acute asthma. This article reviews publications since October 2002 for an update of the role of viruses in exacerbations of asthma. RECENT FINDINGS: Respiratory viruses are present in most patients hospitalized for life-threatening asthma and acute non life-threatening asthma. Rhinovirus is the most common, but coinfection with other viruses may be important. Patients with asthma are not more susceptible to upper respiratory tract rhinovirus infections than healthy people but suffer from more severe consequences of the lower respiratory tract infection. Recent epidemiologic studies suggest that viruses provoke asthma attacks by additive or synergistic interactions with allergen exposure or with air pollution. An impaired antiviral immunity to rhinovirus may lead to impaired viral clearance and hence prolonged symptoms. Respiratory viral infections cause asthmatic exacerbations by triggering recruitment of Th2-type cells into the lungs. There is no specific antiviral strategy for prevention of respiratory-triggered asthma exacerbations, although clinical trials of potential antiviral agents are ongoing. Indirect prevention strategies focus on the reduction of overall airway inflammation to reduce the severity of the host response to respiratory viral infections. SUMMARY: Respiratory viral infections are a major cause of morbidity and mortality in asthma. There is a lack of specific antiviral strategies in the prevention or reduction of viral-triggered asthma exacerbations. Recent advances in understanding of the epidemiology and immunopathogenesis of respiratory viral infection in asthma provide opportunities or identification of specific targets for antiviral agents and strategies for management and prevention.

Acute Disease↗
PubMedDate not supplied

Stressful life events precede exacerbations of multiple sclerosis.

OBJECTIVE: We longitudinally monitored life events and health changes in patients with multiple sclerosis (MS) to determine whether stressful events may trigger exacerbation of MS. METHODS: Twenty-three women with MS were followed for 1 year. Each subject completed the Psychiatric Epidemiologic Research Interview on a weekly basis. Further information on potentially stressful events was acquired using the Life Events and Difficulties Schedule. Neurologic symptoms were also monitored on a weekly basis throughout the year. Potential MS exacerbations were confirmed by a neurologist who was blind to the presence and timing of stressors. RESULTS: Eighty-five percent of MS exacerbations were associated with stressful life events in the preceding 6 weeks. Stressful life events occurred an average of 14 days before MS exacerbations, compared with 33 days before a randomly selected control date (p < .0001). Survival analysis confirmed that an increase in frequency of life events was associated with greater likelihood of MS exacerbations (hazard ratio = 13.18, p < .05). CONCLUSIONS: These results are consistent with the hypothesis that stress is a potential trigger of disease activity in patients with relapsing-remitting MS.

Adult↗
PubMedDate not supplied

Premenstrual exacerbation of depressive disorders in a community-based sample in the United States.

OBJECTIVE: No published epidemiologic study has examined premenstrual exacerbation of depressive disorders (PME-DD) in a representative sample. Knowledge gained should indicate the burden of illness, suggest whom to monitor, and facilitate diagnosis. The objectives were to 1) ascertain the prevalence and predictors of PME-DD; and 2) test competing hypotheses that PME-DD is related to a) severity or history of depression, b) menstrual cyclicity in females in general, or c) a methodological artifact. METHODS: Menstruating females (N = 900) from ages 13 to 53 living in urban or rural Illinois completed semi-structured psychiatric diagnostic interviews and rated symptoms of depression daily for two menstrual cycles; 58 had major depressive, dysthymic, or subclinical depressive disorders, and the remaining 842 were the non-depressed portion of the representative sample. RESULTS: Depressed females had 1.34 (95% confidence interval, 1.02-1.66) symptoms exacerbated premenstrually. The best model for predicting exacerbation contained only age. Older women more often had symptoms worsen. Symptoms during the follicular phase were most severe for clinically depressed, intermediate for subclinically depressed, and least severe for non-depressed participants, ps < 0.001. Consistent with the hypothesis that exacerbation is related to cyclicity in all females, the number of symptoms that became worse did not differ between groups, ps < 0.46. Given no symptoms in one cycle, the odds of having symptoms in the next cycle were 0.91. Only 56% of non-depressed females taking antidepressants were asymptomatic all month long; the remaining 44% still had symptoms premenstrually. CONCLUSIONS: Premenstrual exacerbation of depressive disorders is associated with deteriorated functioning over and above that already experienced by depressed females. Patients may be susceptible regardless of severity of depression, number of episodes, or remission status.

Acute Disease↗
PubMed2006

The role of bacteria in airway inflammation in exacerbations of chronic obstructive pulmonary disease.

PURPOSE OF REVIEW: Bacteria cause approximately half of all chronic obstructive pulmonary disease exacerbations. The purpose of this review is to evaluate the status of research on the role of bacteria in airway inflammation during exacerbations and the mechanisms by which bacterial antigens induce inflammation. RECENT FINDINGS: Bacteria in the airways of adults with chronic obstructive pulmonary disease release antigens including endotoxin, peptidoglycan fragments, lipoproteins, and other molecules into the airways. These bacterial antigens induce potent inflammatory effects in the airways. Bacterial exacerbations are associated with systemic inflammation. Studies of Haemophilus influenzae, the most common bacterial cause of exacerbations, reveal that strains associated with exacerbations induce more inflammation compared to colonizing strains. H. influenzae antigens induce production of interleukin-8 and tumor necrosis factor-alpha, activate Toll-like 2 receptors, activate NFkappaB and p38 mitogen-activated protein signaling pathways, and have other inflammatory effects. SUMMARY: Research on the role of bacteria in causing inflammation in chronic obstructive pulmonary disease has been neglected for decades. Research should be directed at further evaluating the role of bacterial antigens in airway inflammation. Reducing or modulating bacterial infection of the airways in chronic obstructive pulmonary disease has the potential to reduce airway inflammation by eliminating an important inciting cause.

Adult↗
PubMed2006

Poor response to 18-month lamivudine monotherapy in chronic hepatitis B patients with IgM anti-HBc and acute exacerbation.

BACKGROUND: Appearance of immunoglobulin class M antibody against hepatitis B core antigen is a predictor of beneficial response to interferon-alpha therapy in chronic hepatitis B patients, but its relationship with the efficacy of lamivudine therapy remains unclear. AIM: To investigate the outcome of lamivudine therapy in chronic hepatitis B patients with immunoglobulin class M antibody against hepatitis B core antigen and acute exacerbation. METHODS: Chronic hepatitis B patients with acute exacerbation receiving a national-wide therapeutic trial of 18-month lamivudine monotherapy were enrolled for the analysis. Four consecutive seronegative patients were recruited as individual matching controls of one positive subject. Immunoglobulin class M antibody against hepatitis B core antigen in serum was assayed monthly by an automated microparticle enzyme immunoassay. RESULTS: Fifteen (8.9%) of 167 chronic hepatitis B patients with acute exacerbation were seropositive for IgM anti-HBc. Thus 60 seronegative patients were consecutively recruited as control group. At the end of therapy, two (13.3%) of the 15 seropositive patients achieved a sustained response, significantly lower than 26 (43.3%) of the control group. CONCLUSIONS: Appearance of immunoglobulin class M antibody against hepatitis B core antigen in chronic hepatitis B patients with acute exacerbation is a predictor of poor response to lamivudine monotherapy. This is clinically relevant to the decision-making in treating chronic hepatitis B patients with acute exacerbation.

Adult↗
PubMed2005

Antiphospholipid antibodies in immune thrombocytopenic purpura tend to emerge in exacerbation and decline in remission.

Although the presence of antiphospholipid antibodies (APLA) in immune thrombocytopenic purpura (ITP) has been reported, their clinical significance is not clear. The present study investigated APLA profiles in relation to the clinical stages of ITP. We studied APLA in 40 patients in three stages of ITP: exacerbation/relapse (n=7), stable (n=14) and remission (n=19). Both IgG and IgM APLA to six target antigens were measured by enzyme-linked immunosorbent assay: beta2-glycoprotein 1 (beta2GP1), cardiolipin, phosphatidylcholine, phosphatidylserine, phosphatidylethanolamine and factor VII/VIIa. The central finding was that APLA were common in ITP but differed significantly in disease stages, being highest in exacerbation (86% positive), intermediate in stable disease (57%) and lowest in remission (42%). In exacerbations, APLA were predominantly of IgG class, while in stable disease, IgM predominated. During remission, APLA often became undetectable. Both the frequency and titres of APLA were significantly higher during exacerbation than remission. An inverse correlation was found between platelet count and nearly all APLA (except beta2GP1). Sequential study of six patients revealed that APLA tended to emerge and rise with exacerbation, concurrently with new episodes of bleeding and became undetectable during remission. These findings raise the possibility that APLA may play a role in the exacerbation and remission of ITP or they may be a consequence of platelet destruction.

Adult↗