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PubMed2005

How much do Pseudomonas biofilms contribute to symptoms of pulmonary exacerbation in cystic fibrosis?

Recent studies suggest that chronic Pseudomonas aeruginosa lung infections in cystic fibrosis (CF) involve anaerobic biofilms, and that these biofilms are the reason chronic infections are rarely eradicated by antibiotic therapy, regardless of the in vitro susceptibility of infecting bacteria. These observations led to the development of an in vitro method for testing antibiotic susceptibility of CF clinical isolates in biofilms (Moskowitz et al., J Clin Microbiol 2004;42:1915-1922) and unearthed an apparent paradox. Antibiotics that remain cornerstones of clinical management of CF pulmonary exacerbations (e.g., beta-lactam antibiotics) appear to have little to no activity at clinically achievable concentrations when tested in vitro against clinical P. aeruginosa isolates growing in biofilms. The proven clinical efficacy of beta-lactam antibiotics in treating exacerbations, and the selection for beta-lactam resistance in vivo, suggest that planktonic bacteria play a significant role in pulmonary exacerbations of CF. A model of infection architecture is proposed in which biofilm and planktonic compartments each play a role in infection persistence and pulmonary exacerbation, respectively. Infection architecture may partially account for the observed lack of correlation between in vitro antibiotic susceptibility testing and clinical response to antibiotic therapy.

Anti-Bacterial Agents↗
PubMed1996

Intravenous immunoglobulin treatment in the prevention of childbirth-associated acute exacerbations in multiple sclerosis: a pilot study.

Acute exacerbations frequently occur after childbirth in patients with relapsing-remitting multiple sclerosis (MS). The present pilot study was initiated in an attempt to reduce the number of childbirth-associated acute exacerbations in the postpartum period. We treated nine MS patients with a history of 12 childbirth-associated acute exacerbations that had occurred 2-9 weeks after previous deliveries. The patients were administered intravenous immunoglobulin (IVIg) at a dose of 0.4 g/kg per day for 5 consecutive days during the 1st week after childbirth and at 6 and 12 weeks thereafter. None of the treated patients relapsed during the 6-month period after delivery. However, three patients had a remote relapse, two at 8 months and one at 10 months after childbirth, but these probably represented the natural course of disease and were not associated with childbirth. We conclude that IVIg treatment may prevent acute childbirth-associated exacerbations in relapsing-remitting MS patients.

Adult↗
PubMed1990

Etiology of acute exacerbation in patients with severe chronic active hepatitis by in situ HBVDNA hybridization technique.

To explore etiology of acute exacerbation in severe chronic active hepatitis, in situ HBVDNA hybridization was carried out combined with detection of HBV markers in the serum and the liver as well as intrahepatic HDAg in 15 cases. Four subgroups were identified based on the etiological evidence: 1) 9 cases were still undergoing HBV active replication or reactivation with cytoplasmic and membraneous HBcAg expression, often associated with the hepatic necrosis foci; 2) 3 cases showed HBsAg or/and HBVDNA positivity despite absence of HBcAg expression, the membranous and homogeneous HBsAg expression being closely related with hepatic necrosis; 3) 2 cases were HDAg positive; 4) the remaining case exhibited no HBV infection evidence. All findings suggested that HBV active replication or reactivation was the major cause of the exacerbation in severe chronic active hepatitis. In addition, HBV superinfection accounted for over 10% of cases with acute exacerbation. Hepatitis A or C may contribute to some episodes of exacerbation.

Acute Disease↗
PubMed2002

The role of systemic corticosteroids in acute exacerbation of chronic obstructive pulmonary disease.

The administration of systemic corticosteroids for patients with exacerbations of chronic obstructive pulmonary disease (COPD) has become common practice over the past 25 years. This practice remained somewhat controversial because corticosteroids can have serious adverse effects and initial clinical trials provided inconclusive evidence concerning their efficacy. Results from recent clinical trials indicate that systemic corticosteroids are modestly effective in shortening the duration of severe exacerbations of COPD. Systemic corticosteroids administered intravenously or orally to hospitalized patients with exacerbations of COPD reduced the absolute treatment failure rate by about 10%, increased the forced expiratory volume in 1 second (FEV1) by about 100 ml, and shortened the hospital stay by 1 to 2 days. Oral corticosteroids probably confer similar benefits when used for treating moderately severe COPD exacerbations in an out-patient setting. The optimal starting dose of corticosteroids is not known, but the duration of treatment should not extend longer than 2 weeks. Hyperglycemia is the most common adverse event, but secondary infections, mental disturbances, and myopathies may also occur.

Acute Disease↗
PubMed2003

Cardiac troponin I in patients with severe exacerbation of chronic obstructive pulmonary disease.

OBJECTIVES: Co-morbid conditions including risk factors for cardiovascular diseases and left ventricular dysfunction are common in patients with chronic obstructive pulmonary disease (COPD). This study assessed the incidence of cardiac troponin I (cTnI) elevation, a specific marker for cardiac injury, and its prognostic significance during severe exacerbation of COPD. DESIGN: Prospective cohort study. SETTING: Two intensive care units. PARTICIPANTS: Seventy-one consecutive patients admitted for severe exacerbation of COPD. INTERVENTION: None. MEASUREMENTS AND RESULTS: Cardiac troponin I was assayed in blood samples obtained on admission and 24 h later (Stratus II immunoassay analyser, Dade International). Levels above 0.5 ng/ml were considered positive. The following data were recorded prospectively: clinical symptoms, co-morbidities, cause of the exacerbation, diagnostic procedures and treatment, general severity score (SAPS II) and in-hospital outcome. CTnI was positive in 18% of patients (95% confidence interval (CI(95)), 11-29%), with a median value at 1.00 ng/ml; CI(95 )(0.60-1.70). Eighteen patients died in the hospital (25%; CI(95), 17-37%). Only cTnI (adjusted odds ratio (ORa), 6.52; CI(95),1.23-34.47) and SAPS II 24 h after admission (ORa, 1.07; CI(95), 1.01-1.13) were independent predictors of in-hospital mortality. CONCLUSION: Elevated cTnI is a strong and independent predictor of in-hospital death in patients admitted for acutely exacerbated COPD.

Aged↗
PubMed2002

Identifying general practice patients diagnosed with asthma and their exacerbation episodes from prescribing data.

OBJECTIVE: To determine the reliability of identifying patients diagnosed with asthma in general practice and their asthma exacerbation episodes from prescribing data. DATA SOURCE: Automated database from 17 general practitioners (29,805 patients) in the northern Netherlands. STUDY DESIGN: Sensitivity, specificity and predictive values of four criteria for identifying patients diagnosed with asthma and two criteria for identifying asthma exacerbation episodes were calculated using the registered diagnosis as gold standard. RESULTS: Prescription of one or more anti-asthma medications identified 95% of patients with an asthma diagnosis (positive predictive value 0.70), while two or more anti-asthma medications identified 71% (positive predictive value 0.79). A combination of oral corticosteroids or antibiotics identified 55% of exacerbations. CONCLUSIONS: Asthma patients can be identified reliably from prescribing data, but identification of asthma exacerbations was poor. The preference for one criterion over another for identifying patients diagnosed with asthma will depend on the reason for patient selection.

Adolescent↗
PubMed1992

Exacerbation of experimental colitis by nonsteroidal anti-inflammatory drugs is not related to elevated leukotriene B4 synthesis.

The ability of nonsteroidal anti-inflammatory drugs to exacerbate experimental colitis, and the possible contributions of the "shunting" of arachidonate via the 5-lipoxygenase pathway, were investigated using a rat model in which colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid in a vehicle of 50% ethanol. Twice daily treatment with indomethacin (0.1-1 mg/kg SC) during the first week after trinitrobenzene sulfonic acid/ethanol administration resulted in dose-dependent increases in the severity of colitis and in the incidence of mortality. Mortality was not observed in vehicle-treated colitic rats or in normal rats treated with indomethacin. Similar exacerbation of colitis was observed in rats treated with naproxen (5 mg/kg). Whereas treatment with a 5-lipoxygenase inhibitor, PF-5901 (100 mg/kg PO), resulted in a significant reduction of the severity of colitis, concomitant administration of PF-5901 and indomethacin (0.5 mg/kg SC) did not inhibit the exacerbative effects of the indomethacin in this model. In separate studies, administration of indomethacin was found to significantly increase colonic myeloperoxidase activity (a measure of tissue granulocyte numbers) and suppress colonic prostaglandin E2 synthesis, while not significantly affecting colonic leukotriene B4 synthesis. The effect on myeloperoxidase activity was seen during the period 21-24 hours after trinitrobenzene sulfonic acid ethanol administration, but not during the period 45-48 hours after induction of colitis. In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis, inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis. These results suggest that inhibitors of colonic prostaglandin synthesis can markedly exacerbate colitis, and that this effect is unrelated to alterations in colonic leukotriene B4 synthesis. Endogenous prostaglandins may exert anti-inflammatory effects during the acute stages of colitis.

Animals↗
PubMed2004

Interventions to prevent chronic obstructive pulmonary disease exacerbations.

Exacerbations of chronic obstructive pulmonary disease (COPD) have a profound effect on the patient's health status and decline in lung function; they also impose a significant burden on healthcare resource utilization. Prevention and treatment of exacerbations is listed by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as among the major objectives of COPD management, and it is therefore an important outcome measure when studying any new agent. This article discusses pharmacologic therapy and other measures for preventing exacerbations and hospitalizations due to exacerbations of COPD.

Clinical Trials as Topic↗
PubMedDate not supplied

Treatment of chronic rhinosinusitis exacerbations due to methicillin-resistant Staphylococcus aureus with mupirocin irrigations.

INTRODUCTION: Chronic rhinosinusitis (CRS) exacerbations due to methicillin-resistant Staphylococcus aureus (MRSA) are routinely encountered. Treatment often involves intravenous antibiotics that provide only transient benefits. Mupirocin has well-recognized antistaphylococcal activity, and its nasal formulation is approved by the Food and Drug Administration for the eradication of nasal colonization with MRSA. OBJECTIVE: The aim of this study was to describe the use of mupirocin nasal irrigations for the treatment of CRS exacerbations due to MRSA. MATERIALS AND METHODS: Charts of patients who received mupirocin nasal irrigations for MRSA exacerbations of CRS between January 2000 and October 2003 were reviewed. RESULTS: Forty-two MRSA-positive cultures were obtained from 24 patients (mean age, 61 years; range, 38-82 years; 15 women and 6 men). Twenty-eight episodes were treated with mupirocin nasal irrigations and doxycycline; 4 were treated with mupirocin nasal irrigations and trimethoprim-sulfamethoxazole, and 7 episodes were treated with mupirocin nasal irrigations alone. Patients were reevaluated at approximately 4 to 6 weeks. Repeat cultures were not obtained in 12 patients (because of clinical and endoscopic resolution). Adequate follow-up was unavailable for 3 patients, and of the 27 repeat cultures, only 1 grew MRSA. Twelve patients had at least one recurrence, with a mean number of episodes of 1.75 (range, 1-8 episodes). The mean follow-up was 11.8 months (range, 3-27 months). CONCLUSIONS: Mupirocin nasal irrigations may avoid the need for intravenous antibiotics, which often provide temporary benefits and entail greater cost and morbidity. Thus, mupirocin nasal irrigations may provide a relatively simple means for the management of MRSA exacerbations of CRS.

Administration, Intranasal↗
PubMed2005

[Treatment of exacerbation of asthma: what are today's issues?].

During past decades, major progress has been accomplished in the management of acute asthma. Most recent recommendations include evidence-based rationale. The improved quality of clinical guidelines makes them efficient models for medical education. The pediatric pharmacopoeia provides a great variety of choices of drugs as well as for asthma medical devices. These innovations dramatically facilitated the medical management of asthmatic children, but they did not solve all problems. Physicians now use higher doses of salbutamol, but the early prescription of systemic glucocorticoids for moderate exacerbation of asthma is still underused, given the most recent clinical guidelines and meta-analysis. Furthermore, repeated emergency department visits to the wards and lack of primary care physician should systematically be appraised when evaluating severity, as they are both major risk factors for severe exacerbations, even though they are not considered in acute asthma severity scores. Finally, initiating (or reinforcing) patient education at the time of exacerbation also presents important challenges, as emergency visits are a favorable moment to commence the therapeutic education of the child and his family. Indeed, framing the controller medications and educating families about how to manage the disease and to improve their domestic environment are the genuine tools available for the prevention of asthma exacerbations, and particularly those most severe.

Acute Disease↗
PubMed2006

C-reactive protein--can it be used as a marker of infection in patients with exacerbation of chronic obstructive pulmonary disease?

BACKGROUND: Far from all patients with exacerbation of chronic obstructive pulmonary disease (COPD) benefit from antibiotic treatment. However, as these patients are often colonized with bacteria, even in a stable phase, there is no reliable method for establishing whether the patients have a significant bacterial infection and would benefit from antibiotic treatment. C-reactive protein (CRP) has proven to be useful as a marker of bacterial infection. The aim of this study was to assess to what degree CRP is elevated in patients with exacerbation of COPD. METHODS: A total of 166 consecutive patients admitted to a department of internal medicine at a university hospital in Copenhagen due to exacerbation of COPD were prospectively included in the study. Patients were asked whether they had experienced increased sputum purulence and whether they were on steroid treatment or not. Blood was drawn for determination of white blood cell count and CRP, and a chest X-ray was taken. Patients whose X-rays of the thorax showed changes compatible with pneumonia were considered to have pneumonia of bacterial origin. RESULTS: Pneumonia was diagnosed in 51 patients. Their median CRP was 97 mg/l (49-145 interquartile range). Among patients without pneumonia, 46% (51/115) had normal CRP values (0-10 mg/l); 64 had no increased sputum purulence and a median CRP of 8 mg/l (2.9-16 mg/l), which is significantly lower than in the 51 patients who reported increased sputum purulence and had a CRP of 45 mg/l (8.5-86 mg/l; p<0.001). CONCLUSION: CRP values are normal in nearly 50% of patients admitted due to exacerbation of COPD. In patients who have increased sputum purulence, the pattern of increase in CRP is similar to that seen in patients with pneumonia. This suggests that CRP may be used as a marker of significant bacterial infection. Thus, it may be used when deciding whether or not to start antibiotic treatment. This should be tested in a controlled trial.

Journal Article↗
PubMed2005

Inhaled fluticasone propionate is effective as well as oral prednisone in reducing sputum eosinophilia during exacerbations of asthma which do not require hospitalization.

The aim of this study was to evaluate whether fluticasone propionate (FP) is effective as well as prednisone (P) in reducing sputum eosinophilia and in improving airway obstruction due to asthma exacerbations not requiring hospitalization. We measured, in a parallel-group, double-blind double-dummy, randomized study, sputum and blood inflammatory cell counts and soluble mediators in 37 asthmatic subjects during a spontaneous exacerbation of asthma (Visit 1) and after a 2 week (Visit 2) treatment with inhaled FP (1000microg bid) (Group A, n=18) or a reducing course of oral P (Group B, n=19). Asthma exacerbation was accompanied by sputum eosinophilia (eosinophils >2%) in almost all patients (95%). FP improved FEV(1) (from 53.9%+/-16.8 at Visit 1 to 76.4%+/-21.2 at Visit 2, p=0.0001) and reduced the percentage of sputum eosinophils (from 38%[0-78] to 3%[1-31, p=0.0008) as well as oral P (FEV(1): from 51.5%+/-14.4 to 83.6%+/-21.1, p=0.0001; sputum eosinophils: from 52%[1-96] to 11%[0-64], p=0.0003). At Visit 2, sputum eosinophils were significantly lower in Group A than in Group B. P but not FP induced significant decrease in blood and sputum ECP. Oxygen saturation, PEF variability, symptom score and use of rescue medication similarly improved in both groups. We conclude that FP is effective at least as well as P in reducing sputum eosinophilia and in improving airway obstruction due to asthma exacerbation. However, the cost/effectiveness ratio of this option should be further evaluated.

Acute Disease↗
PubMed2004

Sputum color as a marker of acute bacterial exacerbations of chronic obstructive pulmonary disease.

We analyzed 795 sputa from 315 patients (233 males, mean age 69.3+/-8.8 years, mean number of exacerbations 2.52/patient) with acute exacerbations of moderate-to-severe chronic obstructive pulmonary disease (COPD) (mean steady-state FEV1 42.5+/-7.8% of predicted). 581/795 sputa were considered adequate. Sputum was analyzed by a quali-quantitative colorimetric scale allowing both color distinction and color degree of intensity. Quantitative culture was then performed (threshold: >10(6)CFU/mL). Samples were distinguished in mucoid (145) and purulent (436) sputa. Absence of bacterial growth was observed in 22% and 5% of mucoid and purulent sputa, respectively. Among mucoid sputa, Gram positive bacterial growth occurred more commonly compared to Gram negative and Pseudomonas aeruginosa/Enterobacteriaceae (56%, 24%, 20%, respectively). In purulent sputa, Gram positives were found in 38% of cases, Gram negatives in 38%, and P. aeruginosa/Enterobacteriaceae in 24%. We evaluated whether functional impairment (FEV1) orientates as to the infectious etiology of exacerbations. Significant differences were observed in the distribution of pathogens. Gram negative and P. aeruginosa/Enterobacteriaceae were isolated more frequently in the sputum when FEV1 was <35%. Our study indicates that purulent sputum is strongly associated with bacterial growth in COPD exacerbations. Deepening sputum color (from yellowish to brownish) was associated with increased yield of Gram negative and P. aeruginosa/Enterobacteriaceae.

Acute Disease↗
PubMed2005

Variables associated with recovery from acute exacerbations of chronic bronchitis and chronic obstructive pulmonary disease.

OBJECTIVE: To identify risk factors for late recovery and failure after ambulatory treatment of exacerbations of chronic bronchitis (CB) and chronic obstructive pulmonary disease (COPD). METHODS: Observational, non-randomised study of risk factors carried out in 2001 and 2002 in Primary Care practices. Patients aged 40 or older diagnosed with an exacerbation of CB or COPD of probable bacterial etiology were included in the study and followed up for 10 days. Patients were treated with amoxicillin plus clavulanic acid (co-amoxiclav) 500-125 mg tds for 10 days, clarithromycin 500 mg bd for 10 days or moxifloxacin 400 mg od for 5 days. RESULTS: Two hundred and fifty-two general practitioners participated, registering 1147 valid patients. The rate of failure at day 10 was 15.1% without significant differences among the antibiotic treatments. Median time to recovery was 5 days. Factors significantly associated with late recovery (>5 days) on multivariate analysis were: use of long-term oxygen (OR=1.96; 95%CI=1.35-2.85); use of short-acting beta-2 agonists (OR=1.51; 1.17-1.92). The use of moxifloxacin had a "protective" effect against late recovery compared to co-amoxiclav (OR=0.34; 0.26-0.45) and clarithromycin (OR=0.41; 0.31-2.85). Factors associated with therapeutic failure were: previous hospitalisation (OR=1.61; 1.08-2.42); and 2 or more exacerbations the previous year (OR=1.51; 1.04-2.17); criteria of CB had a protective effect against failure (OR=0.53; 0.35-0.79). CONCLUSIONS: There are readily identifiable risk factors for ambulatory treatment failure of exacerbations of CB and COPD. In addition, long-term oxygen therapy and short-acting beta-2 agonists are associated with late recovery, and the use of moxifloxacin compared with co-amoxiclav and clarithromycin is associated with faster recovery of symptoms.

Acute Disease↗
PubMed2005

Exacerbations as a starting point of pro-active chronic obstructive pulmonary disease management.

Chronic obstructive pulmonary disease (COPD) exacerbations could represent an opportunity for pro-active COPD management rather than mere treatment if previously unknown disease is discovered; the extent of underdiagnosis and undertreatment of COPD in patients attending an emergency department (ED) with an exacerbation is not known. During 2002, we recalled 131 COPD patients in stable conditions, 4-8 weeks after they had attended the ED or been discharged from our University Hospital (North-West of Italy). Information on diagnosis and management prior to the ED attendance were collected; spirometry and arterial blood gas analyses were performed. One-third of patients had never been diagnosed and treated even though 83% of them had moderate-to-very-severe COPD and about 30% already had respiratory failure. Only 20% had received information on the nature of the disease and none had received a written action plan. Only 60% were receiving long-acting bronchodilators and 41% of patients with respiratory failure were receiving long-term oxygen. A substantial number of undiagnosed and untreated patients with moderate-to-very-severe COPD came to our attention through an exacerbation. This enforces the importance of exacerbations as the starting point of pro-active COPD management and of the ED as a valuable sentinel to identify this subset of patients.

Acute Disease↗
PubMed2005

Effect of formoterol/budesonide combination on arterial blood gases in patients with acute exacerbation of COPD.

BACKGROUND: Patients with severe chronic airway obstruction might suffer dangerous hypoxemia after administration of a beta-agonist despite bronchodilation. METHODS: We first compared the acute effects on gas exchange of two doses of formoterol Turbuhaler (9 and 18 microg) in 10 patients with acute exacerbation of COPD. Afterwards, we compared the acute effects of formoterol Turbuhaler 9 microug with those of formoterol/budesonide combination in a single inhaler (Turbuhaler) 9/320 microg in 10 other patients with acute exacerbation of COPD. Finally, we compared the changes in PaO(2) induced by formoterol Turbuhaler 9 microg or formoterol/budesonide combination in a single inhaler (Turbuhaler) 9/320 microg with those in FEV(1) in 10 other patients with acute exacerbation of COPD. Each agent was given on separate days, and the patients' arterial blood gases were measured at baseline and at intervals of 120 min. RESULTS: Small but statistically significant declines in PaO(2) were found after administration of both formoterol 9 and 18 microg. In the second group of patients, formoterol 9 microg alone again induced a significant decrease in PaO(2). However, the simultaneous administration of budesonide 320 microg significantly reduced the acute effect of formoterol on PaO(2). In a third group of 10 patients we confirmed a small but significant decrease in PaO(2) after formoterol alone and the reduction of this effect when budesonide was administered simultaneously. Moreover, we also documented that addition of budesonide amplified the fast onset of action of formoterol. CONCLUSIONS: These results suggest that when treating patients suffering from acute exacerbation of COPD with formoterol, it is prudent to check their arterial blood gases. In any case, combined administration of formoterol and budesonide reduces the potential for acute effects of formoterol on blood-gas tensions.

Acute Disease↗
PubMed2006

Expression of priming-associated cellular markers on neutrophils during an exacerbation of COPD.

Chronic inflammation of the airways is a hallmark of chronic obstructive pulmonary disease (COPD). We investigated the kinetics of priming of inflammatory cells in peripheral blood during exacerbations of COPD and during the resolution phase. Modulation of the leukocyte compartment as a consequence of systemic activation by cytokines/chemokines was determined by measuring the expression of priming-associated epitopes by novel antibodies designated A17 and A27. Furthermore, H2O2 was determined in breath condensate as a read out for local inflammation. Leukocytes were obtained from COPD patients (GOLD II-IV) during and after an exacerbation of their disease. During an exacerbation the expression of priming epitopes on leukocytes was increased. This priming phenotype disappeared upon treatment with intravenous corticosteroids. Similarly, H2O2 levels in breath condensate were also increased during an exacerbation and decreased upon treatment. We conclude that the activation status of neutrophils in the systemic compartment can be used as a read-out for systemic innate immune signals involved in the pathogenesis of COPD. The correlation between H2O2 in exhaled air with A27 priming on neutrophils showed that local inflammation has systemic effects on cells of the innate immune system.

Female↗
PubMed1999

A pilot study of penicillin prophylaxis for neuropsychiatric exacerbations triggered by streptococcal infections.

BACKGROUND: Some children with obsessive-compulsive disorder (OCD) and tic disorders appear to have symptom exacerbations triggered by group A beta-hemolytic streptococcal infections in a manner that is similar to rheumatic fever and its neurologic variant, Sydenham's chorea. Because penicillin prophylaxis has proven to be effective in preventing recurrences of rheumatic fever, it was postulated that it might also prevent streptococcal-triggered neuropsychiatric symptom exacerbations in children with Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS). These children are identified by five clinical characteristics: presence of OCD or tic disorder, prepubertal onset, episodic symptom course, neurologic abnormalities (i.e., choreiform movements) and streptococcal-triggered symptom exacerbations. METHODS: Thirty-seven children with PANDAS were enrolled in an 8 month, double-blind, balanced cross-over study. Patients were randomized to receive either 4 months of the active compound (twice daily oral 250 mg penicillin V) followed by 4 months of placebo, or placebo followed by penicillin V. Tic, OCD, and other psychiatric symptoms were monitored monthly. Throat cultures and streptococcal antibody titers were also obtained. RESULTS: There were an equal number of infections in both the active and placebo phases of the study. There was no significant change seen in either the obsessive-compulsive or tic symptom severity between the two phases. CONCLUSIONS: Because of the failure to achieve an acceptable level of streptococcal prophylaxis, no conclusions can be drawn from this study regarding the efficacy of penicillin prophylaxis in preventing tic or OCD symptom exacerbations. Future studies should employ a more effective prophylactic agent, and include a larger sample size.

Adolescent↗