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Biomedical subjects

Edward L Peterson

Publications and source records attributed to Edward L Peterson.

At least 19 recordsLinked to original sources

Identifying students with self-report of asthma and respiratory symptoms in an urban, high school setting.

Strategies for identifying urban youth with asthma have not been described for high school settings. African-American high school students are rarely included in asthma studies, despite a high risk of asthma mortality when compared to other age and race groups. Identification and follow-up of children with uncontrolled respiratory symptoms are necessary to reduce the burden of asthma morbidity and mortality, especially in underserved areas. We describe a process used to identify high school students who could benefit from intervention based on self-report of asthma and/or respiratory symptoms, and the costs associated with symptom-identification. Letters announcing a survey were mailed to parents of 9th-11th graders by an authorized vendor managing student data for the school district. Scan sheets with student identifiers were distributed to English teachers at participating schools who administered the survey during a scheduled class. Forms were completed by 5,967 of the 7,446 students assigned an English class (80% response). Although prevalence of lifetime asthma was 15.8%, about 11% of students met program criteria for enrollment through report of an asthma diagnosis and recent symptoms, medication use, or health care utilization. Another 9.2% met criteria by reported symptoms only. Cost of symptom-identification was $5.23/student or $32.29/program-eligible student. There is a need for school-based asthma programs targeting urban adolescents, and program initiation will likely require identification of students with uncontrolled symptoms. The approach described was successfully implemented with a relatively high response rate. Itemized expenses are presented to facilitate modifications to reduce costs. This information may benefit providers, researchers, or administrators targeting similar populations.

Absenteeism↗

Race-ethnicity, crime, and other factors associated with adherence to inhaled corticosteroids.

BACKGROUND: Previous studies have shown differences in adherence to inhaled corticosteroids (ICSs) by race-ethnicity, yet little is known about factors that contribute to adherence within these groups. Environmental stressors, such as crime exposure, which has been associated with asthma morbidity, might also predict ICS adherence. OBJECTIVE: We sought to identify factors associated with ICS adherence among patients with asthma and among African American patients and white patients separately. METHODS: Study patients with asthma were aged 18 to 50 years and were enrolled in a large southeast Michigan health maintenance organization between January 1, 1999, and December 31, 2001. The primary outcome, ICS adherence, was calculated by linking prescription-fill data with dosage information. Predictor variables included age, sex, race-ethnicity, measures of socioeconomic status (SES), average ICS copay, existing comorbidities, and crime rate in area of residence. RESULTS: Adherence information was available for 176 patients. ICS adherence was lower among African American patients (n = 75) when compared with white patients (n = 94; 40% vs 58%, respectively; P = .002). Among white patients, adherence was significantly lower for women when compared with men. Among African American patients, age and residential crime rates were positively and negatively associated with ICS adherence, respectively. Area crime remained a predictor of adherence in African American patients, even after adjusting for multiple measures of SES. CONCLUSIONS: This study suggests that an environmental stressor, area crime, provides additional predictive insight into ICS-adherent behavior beyond typical SES factors. CLINICAL IMPLICATIONS: Better understanding of environmental factors that influence ICS adherence might aid in efforts to improve it.

Administration, Inhalation↗

Gene-environment interactions with CD14 C-260T and their relationship to total serum IgE levels in adults.

BACKGROUND: Both endotoxin exposure and a single nucleotide polymorphism in one of its receptors, CD14 C-260T, have been separately associated with total serum IgE levels. Furred pets might also influence IgE levels through their effects on endotoxin levels. However, how these factors interact to influence total IgE levels is not well known, especially in adults. OBJECTIVE: We sought to investigate the interactive relationship between endotoxin levels, pet exposure, and CD14 C-260T genotype on total serum IgE levels in adults. METHODS: Mothers enrolled in an ongoing cohort study were genotyped for the CD14 C-260T polymorphism. Exposure to pets was assessed by using questionnaires and dust allergen levels collected in the home. Endotoxin exposure was estimated by using dust collected from mothers' bedroom floors. The primary outcome measure was total serum IgE level. RESULTS: CD14 C-260T genotype was assessed in 517 (85.2%) of the 607 women enrolled in the study. The CD14 C-260T genotype was significantly associated with total IgE levels; however, this relationship appeared to be modified by the level of endotoxin exposure. Similar interactions between CD14 C-260T and pet exposure were not seen, regardless of the measure of pet exposure used. CONCLUSIONS: The CD14 C-260T genotype and endotoxin exposure together appear to influence total serum IgE levels in adults. The absence of a similar gene-environment interaction for pet exposure suggests separate mechanisms of action. CLINICAL IMPLICATIONS: A common polymorphism in the endotoxin receptor, CD14 C-260T, and dust endotoxin levels in the home might interact to influence total serum IgE levels into adulthood.

Adult↗

Relationship between extremely low total serum IgE levels and rhinosinusitis.

BACKGROUND: The few studies examining clinical manifestations in adults with serum IgE levels less than 2.0 IU/mL provide conflicting information. OBJECTIVE: To examine self-reported respiratory disease in women with total serum IgE levels less than 2.0 IU/mL to further elucidate previous reports of an association between IgE deficiency and chronic rhinosinusitis. METHODS: In a geographically based cohort of 626 pregnant women, total serum IgE levels were measured using a standard assay with a lower limit of detection of 2.0 IU/mL. Sera with IgE levels less than 2.0 IU/mL were assayed again using a low IgE protocol with a detection limit of 0.02 IU/mL. RESULTS: Twenty-one individuals (3.4%) were found to have IgE levels less than 2.0 IU/mL. On repeated assay, 20 of these individuals with available clinical data were found to have detectable IgE levels ranging from 0.5 to 2.1 IU/mL (geometric mean, 1.2 IU/mL). None of these individuals with low IgE levels had physician-diagnosed sinusitis compared with 19.3% (113/585) of those with IgE levels of 2.0 IU/mL or greater (P = .03). Physician-diagnosed asthma was also less prevalent (1/19, 5.3%) in the low IgE group compared with 20.6% in those with higher IgE levels, but this was not significant (P = .14). The low IgE group reported a higher prevalence of hay fever symptoms than the remaining cohort (31.6% vs 24.4%; P = .43) but had less physician-diagnosed hay fever (5.3% vs 15.8%; P = .34). CONCLUSIONS: Low serum IgE levels were relatively common in these pregnant women. In contrast to previous studies, a low IgE level was not associated with chronic rhinosinusitis.

Adult↗

Adventitial delivery of dominant-negative p67phox attenuates neointimal hyperplasia of the rat carotid artery.

Several essential components of NADPH oxidase, including p22phox, gp91phox (nox2) and its homologs nox1 and nox4, p47phox, p67phox, and rac1, are present in the vasculature. We previously reported that p67phox is essential for adventitial fibroblast NADPH oxidase O2- production. Thus we postulated that inhibition of adventitial p67phox activity would attenuate angioplasty-induced hyperplasia. To test this hypothesis, we treated the adventitia of carotid arteries with a control adenovirus (Ad-control), a virus expressing dominant-negative p67phox (Ad-p67dn), or a virus expressing a competitive peptide (gp91ds) targeting the p47phox-gp91phox interaction (Ad-gp91ds). Common carotid arteries (CCAs) from male Sprague-Dawley rats were transfected with Ad-control, Ad-p67dn, or Ad-gp91ds in pluronic gel. After 2 days, a 2-F (Fogarty) catheter was used to injure CCAs in vivo. After 14 days, CCAs were perfusion-fixed and analyzed. In 13 experiments, digital morphometry suggested a reduction of neointimal hyperplasia with Ad-p67dn compared with Ad-control; however, the reduction did not reach statistical significance (P = 0.058). In contrast, a significant reduction was achieved with Ad-gp91ds (P = 0.006). No changes in medial area or remodeling were observed with either treatment. Moreover, adventitial fibroblast proliferation in vitro was inhibited by Ad-gp91ds but not by Ad-p67dn, despite confirmation that Ad-p67dn inhibits NADPH oxidase in fibroblasts. These data appear to suggest that a multicomponent vascular NADPH oxidase plays a role in neointimal hyperplasia. However, inhibition of p47phox may be more effective than inhibition of p67phox at attenuating neointimal growth.

Animals↗

Angiotensin-converting enzyme inhibitors: a new mechanism of action.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors are valuable agents for the treatment of hypertension, heart failure, and other cardiovascular and renal diseases. The cardioprotective effects of ACE inhibitors are mediated by blockade of both conversion of angiotensin (Ang) I to Ang II and kinin hydrolysis. Here, we report a novel mechanism that may explain the cardiac antifibrotic effect of ACE inhibition, involving blockade of the hydrolysis of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP). METHODS AND RESULTS: To study the role of Ac-SDKP in the therapeutic effects of the ACE inhibitor captopril, we used a model of Ang II-induced hypertension in rats treated with the ACE inhibitor either alone or combined with a blocking monoclonal antibody (mAb) to Ac-SDKP. These hypertensive rats had left ventricular hypertrophy (LVH) as well as increases in cardiac fibrosis, cell proliferation, transforming growth factor-beta (TGF-beta) expression, and phosphorylation of Smad2 (P-Smad2), a signaling mediator of the effects of TGF-beta. The ACE inhibitor did not decrease either blood pressure or LVH; however, it significantly decreased LV collagen from 13.3+/-0.9 to 9.6+/-0.6 microg/mg dry wt (P<0.006), and this effect was blocked by the mAb (12.1+/-0.6; P<0.034, ACE inhibitor versus ACE inhibitor+mAb). In addition, analysis of interstitial collagen volume fraction and perivascular collagen (picrosirius red staining) showed a very similar tendency. Likewise, the ACE inhibitor significantly decreased LV monocyte/macrophage infiltration, cell proliferation, and TGF-beta expression, and these effects were blocked by the mAb. Ang II increased Smad2 phosphorylation 3.2+/-0.9-fold; the ACE inhibitor lowered this to 0.6+/-0.1-fold (P<0.001), and the mAb blocked this decrease to 2.1+/-0.3 (P<0.001, ACE inhibitor versus ACE inhibitor+mAb). Similar findings were seen when the ACE inhibitor was replaced by Ac-SDKP. CONCLUSIONS: We concluded that in Ang II-induced hypertension, the cardiac antifibrotic effect of ACE inhibitors is a result of the inhibition of Ac-SDKP hydrolysis, resulting in a decrease in cardiac cell proliferation (probably fibroblasts), inflammatory cell infiltration, TGF-beta expression, Smad2 activation, and collagen deposition.

Angiotensin II↗

Smoking and the risk of suicidal behavior: a prospective study of a community sample.

BACKGROUND: A link between cigarette smoking and suicidal behavior has been reported in clinical and epidemiological studies. OBJECTIVE: To examine the association between smoking and suicidal thoughts or attempt in a longitudinal study, in which proximate status of smoking and psychiatric disorders in relation to timing of suicidal behaviors is taken into account. DESIGN: A longitudinal study of young adults interviewed initially in 1989, with repeated assessments over a 10-year follow-up. SETTING AND PARTICIPANTS: The sample was selected from a large health maintenance organization representing the geographic area, except for the extremes of the socioeconomic range. The response rate at each follow-up (3, 5, and 10 years after baseline) exceeded 91%. MAIN OUTCOME MEASURES: Relative risk of occurrence of suicidal behaviors during follow-up intervals by status of smoking and psychiatric disorders at the start of the interval, estimated by generalized estimating equations with repeated measures. The National Institute of Mental Health Diagnostic Interview Schedule was used at baseline and at each reassessment. RESULTS: Current daily smoking, but not past smoking, predicted the subsequent occurrence of suicidal thoughts or attempt, independent of prior depression and substance use disorders (adjusted odds ratio, 1.82; 95% confidence interval, 1.22-2.69). Additionally, current daily smoking, but not past smoking, predicted the subsequent occurrence of suicidal thoughts or attempt, adjusting for suicidal predisposition, indicated by prior suicidality, and controlling for prior psychiatric disorders (adjusted odds ratio, 1.74; 95% confidence interval, 1.17-2.54). CONCLUSIONS: The biological explanation of the finding that current smoking is associated with subsequent suicidal behavior is unclear. Recent observations of lower monoamine oxidase activity (which may play a role in central nervous system serotonin metabolism) in current smokers but not ex-smokers might provide clues, but interpretations should proceed cautiously.

Adult↗

Antibiotic exposure in early infancy and risk for childhood atopy.

BACKGROUND: The increase in pediatric allergy and asthma parallels the increase in use of antibiotics. Antibiotics disturb the flora of the gastrointestinal tract, possibly perturbing the developing immune system. OBJECTIVE: We evaluated whether antibiotic use during early infancy increased the risk for atopy. METHODS: Antibiotic prescriptions documented in medical records were collected from a birth cohort born from 1987 through 1989 (n = 725). At 6 to 7 years of age, 448 were followed by means of examination, including skin prick tests and serum IgE measurements to common allergens. RESULTS: Adjusted odds ratios (aORs) and 95% CIs were calculated comparing children with any versus those with no antibiotic use in the first 6 months and the outcomes of atopy (any positive skin test response), seroatopy (any positive specific IgE test result), either atopy or seroatopy, and both atopy and seroatopy. Atopy increased with antibiotic use approaching statistical significance (aOR, 1.48; 95% CI, 0.94-2.34; P = .09); however, the risk was concentrated among children with less than 2 pets in the home (aOR, 1.73; 95% CI, 1.07-2.80; P = .024) and children breast-fed for 4 or more months (aOR, 3.02; 95% CI, 1.27-7.17; P = .013). The aORs were generally in the same direction for seroatopy and the combined categories. CONCLUSION: Antibiotic use in early life appears to contribute to increased risk for atopy in certain subgroups of children.

Animals↗

Timing and intensity of early fevers and the development of allergies and asthma.

BACKGROUND: Early childhood fevers appear to protect against later allergies and asthma. What is not known is the time in which fevers exert this effect and whether the degree of temperature increase is important. OBJECTIVE: We sought to examine the relationship between the time and degree of early fevers and later allergies and asthma. METHODS: Eight hundred thirty-five children from southeast Michigan were enrolled at birth. Clinic records from their first 2 years were abstracted for episodes of fever. At age 6 to 7 years, children underwent allergy testing. We examined fevers occurring within 6-month intervals in the first 2 years of life and outcomes at age 6 to 7 years. The primary outcome measures were allergic sensitization, asthma, asthma with allergic sensitization, and asthma without allergic sensitization. RESULTS: In the unadjusted analysis each episode of fever between 7 and 12 months of age was associated with a lower odds of allergic sensitization (odds ratio [OR], 0.71; 95% CI, 0.54-0.93) and asthma with allergic sensitization (OR, 0.43; 95% CI, 0.21-0.90) at age 6 to 7 years. Likewise, every 1 degrees C increase in the maximum temperature between 7 and 12 months was associated with a lower odds of allergic sensitization (OR, 0.77; 95% CI, 0.61-0.96) and asthma with allergic sensitization (OR, 0.62; 95% CI, 0.40-0.94). After adjusting for potential confounders, each episode of fever between 7 and 12 months was associated with a lower likelihood of asthma with allergic sensitization (adjusted OR, 0.33; 95% CI, 0.11-0.94) at age 6 to 7 years. CONCLUSIONS: Both the timing and intensity of childhood fevers appear to be important factors in the development of allergies and asthma.

Asthma↗

Blood lead level and risk of asthma.

Asthma and lead poisoning are prevalent among urban children in the United States. Lead exposure may be associated with excessive production of immunoglobulin E, possibly increasing asthma risk and contributing to racial disparities. The objective of this study was to examine racial differences in the association of blood lead level (BLL) to risk of developing asthma. We established and followed a cohort prospectively to determine asthma onset, using patient encounters and drug claims obtained from hospital databases. Participants were managed care enrollees with BLL measured and documented at 1-3 years of age. We used multiple variable analysis techniques to determine the relationship of BLL to period prevalent and incident asthma. Of the 4,634 children screened for lead from 1995 through 1998, 69.5% were African American, 50.5% were male, and mean age was 1.2 years. Among African Americans, BLL > or = 5 and BLL > or = 10 microg/dL were not associated with asthma. The association of BLL > or = 5 microg/dL with asthma among Caucasians was slightly elevated, but not significant [adjusted hazard ratio (adjHR) = 1.4; 95% confidence interval (CI), 0.7-2.9; p = 0.40]. Despite the small number of Caucasians with high BLL, the adjHR increased to 2.7 (95% CI, 0.9-8.1; p = 0.09) when more stringent criteria for asthma were used. When compared with Caucasians with BLL < 5 microg/dL, African Americans were at a significantly increased risk of asthma regardless of BLL (adjHR = 1.4-3.0). We conclude that an effect of BLL on risk of asthma for African Americans was not observed. These results demonstrate the need for further exploration of the complex interrelationships between race, asthma phenotype, genetic susceptibilities, and socioenvironmental exposures, including lead.

Black or African American↗

Airway hyperresponsiveness to methacholine at age 6 to 8 years in nonasthmatic patients is not related to increased health-care utilization for asthma in the ensuing 5 years: a longitudinal study of a birth cohort.

BACKGROUND: Children with heightened airway responsiveness have a greater tendency to develop asthma symptoms. Many existing studies describing this relationship have relied on self-reported symptoms that may be prone to recall bias. In addition, few studies have examined the relationship of airway hyperresponsiveness (AHR) to indicators of asthma severity such as health-care utilization. OBJECTIVE: To determine whether a positive response to methacholine challenge in children without current or physician-diagnosed asthma at age 6 to 8 years is predictive of the subsequent onset of asthma requiring medical evaluation or treatment in the ensuing 5 years. METHODS: Data were obtained from subjects in a population-based birth cohort (n = 835) enrolled from 1987 to 1989, who were members of a large medical group practice component of a health maintenance organization (HMO). We analyzed a subset of subjects (n = 245) who had completed a methacholine challenge at age 6 to 8 years, had no current or physician-diagnosed asthma, and were still served by the same medical group. These children were followed up from the time of methacholine challenge until HMO disenrollment or through June 2001 (ages 11 to 13 years), whichever came first. Pharmacy claims data and diagnostic codes from physician-patient encounters were evaluated for incident asthma. Incident cases of clinical asthma were defined as any child with two outpatient visits or one hospitalization, one emergency department encounter associated with an asthma diagnostic code (ie, 493.XX), or any child filling prescriptions for two bronchodilators or one antiinflammatory asthma medicine. Methacholine responsiveness was interpreted using American Thoracic Society criteria. RESULTS: Asthma incidence did not differ based on methacholine challenge results for children with normal, borderline, and mild AHR. No child in the study demonstrated moderate-to-severe AHR. CONCLUSION: Our data suggest that AHR with a borderline or weakly positive result in a methacholine challenge in children 6 to 8 years old without current or physician-diagnosed asthma is not related to increased health-care utilization for asthma in the ensuing 5 years.

Bronchial Hyperreactivity↗

Reduction of high-risk polypharmacy drug combinations in patients in a managed care setting.

STUDY OBJECTIVES: To enhance physician and patient awareness of polypharmacy; to decrease the risks, drug costs, and waste resulting from polypharmacy; and to make the business case for reducing misuse, overuse, and underuse of drugs by reducing polypharmacy. DESIGN: Longitudinal, time series cohort. SETTING: Outpatient, managed care, integrated delivery system. PATIENTS: A total of 195,971 patients who received health care from the Henry Ford Medical Group and had health insurance coverage from the Health Alliance Plan. MEASUREMENTS AND MAIN RESULTS: Two identical interventions separated by 1 year were conducted in patients at high risk of harm from polypharmacy based on five categories of high-risk drug combinations (referred to as polypharmacy events). Six months of pharmacy claims data were reviewed before and after each intervention to identify these patients. The intervention program consisted of clinical pharmacists performing drug therapy reviews, educating physicians and patients about drug safety and polypharmacy, and working with physicians and patients to correct polypharmacy problems. Prescription cost/member/month, number of prescriptions/member/month, and rates of polypharmacy events/1000 members were measured before and after each of the two interventions. After the first intervention, the overall rate of polypharmacy events decreased from 29.01 to 9.43/1000 patients (67.5% reduction). The number of prescriptions/member/month decreased from 4.6 to 2.2 (52.2% reduction), prescription cost/member/month decreased from $222 to $113 (49.1% reduction), and overall institution drug cost was reduced by $4.8 million. Six months after the second intervention, the overall rate of polypharmacy events was reduced from 27.99 to 17.07/1000 (39% reduction), the number of prescriptions/member/month decreased from 4.5 to 4.0 (11.1% reduction), and prescription cost/member/month decreased from $264 to $239 (9.5% reduction). Overall institution drug costs were reduced by $1.3 million. Sustained effects were seen for all measures of polypharmacy (p=0.001). CONCLUSIONS: These interventions reduced drug costs and numbers of prescriptions in a managed care cohort of patients at high risk for adverse drug events due to polypharmacy. By providing clinical information, decision support, patient self-management support, and care delivery redesign some of the problems resulting from polypharmacy can be solved.

Aged, 80 and over↗

Multiple risk factors for Parkinson's disease.

OBJECTIVE: To determine the relative contribution of various risk factors to the development of Parkinson's disease (PD). METHODS: Ten variables that were independently associated with PD in a health system population-based case-control study of epidemiological risk factors for the disease were jointly assessed. Stepwise logistic regression, adjusted for sex, race and age was used to develop a multiple variate model that best predicted the presence of PD. The population attributable risk was estimated for each variable in the final model, as well as for all factors together. RESULTS: The 10 initial variables included >20 years occupational exposure to manganese or to copper, individually; >20 years joint occupational exposure to either lead and copper, copper and iron, or lead and iron; a positive family history of PD in first- or second-degree relatives; occupational exposure to insecticides or herbicides; occupational exposure to farming; and smoking. Logistic regression resulted in a final model that included >20 years joint occupational exposure to lead and copper (p=0.009; population attributable risk [PAR]=3.9%), occupational exposure to insecticides (p=0.002; PAR=8.1%), a positive family history of PD in first- and second-degree relatives (p=0.001; PAR=12.4%), and smoking </=30 pack-years or not smoking (p=0.005; PAR=41.4%). All four variables combined had a PAR=54.1%. CONCLUSIONS: Our final model of PD risk suggests that occupational, environmental lifestyle and, likely, genetic factors, individually and collectively, play a significant role in the etiology of the disease. Clearly, additional risk factors remain to be determined through future research.

Age Factors↗

The relationship between early fever and allergic sensitization at age 6 to 7 years.

BACKGROUND: The hygiene hypothesis suggests that early infections might protect against later allergic sensitization. OBJECTIVE: The purpose of this study was to determine whether fevers before age 1 year were associated with allergic sensitization at age 6 to 7 years. METHODS: Eight hundred thirty-five children from suburban Detroit, Michigan, were enrolled at birth. Clinic records from their first year were abstracted for episodes of fever, antibiotic use, and respiratory infections. Fever was defined as a rectal temperature of 38.3 degrees C (101 degrees F) or greater or its equivalent measured at another site. At age 6 to 7 years, 441 children underwent allergy testing. The primary outcome measures were atopy (>/=1 positive skin prick test result), seroatopy (>/=1 positive allergen-specific IgE level), and allergic sensitization (either seroatopy or atopy). RESULTS: By age 1 year, 207 (46.9%) of the 441 participants had a documented fever. Among children with 0, 1, or 2 or more fevers in the first year, 33.3%, 31.3%, and 26.0% demonstrated atopy at age 6 to 7 years, respectively (P =.504); 43.4%, 39.7%, and 25.0% had seroatopy, respectively (P =.032); and 50.0%, 46.7%, and 31.3% had allergic sensitization, respectively (P =.028). After adjusting for potential confounders, each febrile episode in the first year was associated with reduced odds for allergic sensitization (adjusted odds ratio, 0.69; 95% CI, 0.47-1.00). Febrile upper respiratory tract infections, in particular, were associated with lower odds of allergic sensitization (adjusted odds ratio, 0.55; 95% CI, 0.31-0.97) per episode. CONCLUSION: This study provides direct support for the hygiene hypothesis because children with fevers before age 1 year were less likely to demonstrate allergic sensitivity at age 6 to 7 years.

Adult↗

Family history, dust mite exposure in early childhood, and risk for pediatric atopy and asthma.

BACKGROUND: Dust mite allergen exposure is considered a major determinant of sensitization to these allergens during childhood and a risk factor for pediatric asthma. OBJECTIVE: By using a birth cohort in a setting with a substantial burden of dust mite allergen, we evaluated exposure and risk for outcomes related to allergy and asthma. METHODS: We collected dust from the bedrooms of 428 children born from 1987 to 1989 and measured Der f 1 and Der p 1 (microg/g dust, combined). Follow-up at 6 to 7 years of age included clinical examination, skin prick testing, specific serum IgE measurement, and methacholine challenge. RESULTS: No overall association was evident for any outcome except bronchial hyperresponsiveness (adjusted odds ratio [OR], 0.62; 95% CI, 0.38-1.00; P <.050; and OR, 0.53; CI, 0.27-1.04; P <.065 for dust mite allergen levels > or =2 microg/g and >10 microg/g, respectively). With a parental history of allergy and asthma, there was an association between a positive dust mite skin test (OR, 2.09; CI, 0.93-4.73; P <.076) and dust mite allergen level >10 microg/g. The inverse was true for children without a parental history. Dust mite exposure of >10 microg/g was associated with a decreased risk of current atopic asthma among children with a parental history (OR, 0.39; CI, 0.05-3.13; P <.376), but with increased risk if without a parental history (OR, 1.52; CI, 0.22-10.6; P <.673). CONCLUSION: Parental history is an important independent variable in the relationship between early dust mite exposure and atopic outcomes. Increased exposure during infancy is associated with a higher risk for sensitization in the presence of a positive parental history, but is protective among children of parents without a history of atopic disease.

Antigens, Dermatophagoides↗

Parental history of atopic disease: disease pattern and risk of pediatric atopy in offspring.

BACKGROUND: Family history is an important risk factor for atopic disease. However, most studies assess only limited information on family history. Because atopic disease can exhibit transient or persistent patterns, it may be useful to assess information on patterns of disease within families. This approach has been applied in other diseases, such as cancer, to discriminate between predominantly inherited versus environmentally caused (sporadic) cases. OBJECTIVE: In a cohort of children who were followed from birth until age 6 to 7 years, we examined the relationship between parental onset (ie, childhood and adulthood) and duration of atopic disease (ie, persistent disease) and the risk of pediatric atopic disease. Our hypothesis was that different parental disease patterns would be important to pediatric risk of disease. METHODS: Data from 476 families in the ongoing Childhood Allergy Study in Detroit, Mich, were analyzed by using logistic regression. We examined the association between parental patterns of disease and disease onset in their children. Results Father's disease history, particularly asthma history, was more strongly related to pediatric outcomes than mother's history. Asthma status in the fathers, whether it was childhood-only, adulthood-only, or persistent, was associated with current asthma in the children. Childhood-only and persistent asthma in fathers conferred a higher risk of atopy in the study children, whereas adulthood-only disease did not. There was also a significant relationship between persistent allergy in the father and atopy in the study children. CONCLUSION: Our data support the hypothesis that there are complex inheritance patterns for allergy and asthma. Therefore, a detailed family history of atopy, including childhood and adulthood experiences, is critical to identifying and classifying risk and disease phenotypes.

Adult↗

Relationship between adherence to inhaled corticosteroids and poor outcomes among adults with asthma.

BACKGROUND: Regular use of inhaled corticosteroids (ICSs) can improve asthma symptoms and prevent exacerbations. However, overall adherence is poor among patients with asthma. Objective To estimate the proportion of poor asthma-related outcomes attributable to ICS nonadherence. METHODS: We retrospectively identified 405 adults age 18 to 50 years who had asthma and were members of a large health maintenance organization in southeast Michigan between January 1, 1999, and December 31, 2001. Adherence indices were calculated by using medical records and pharmacy claims. The main outcomes were the number of asthma-related outpatient visits, emergency department visits, and hospitalizations, as well as the frequency of oral steroid use. RESULTS: Overall adherence to ICS was approximately 50%. Adherence to ICS was significantly and negatively correlated with the number of emergency department visits (correlation coefficient [ R ] = -0.159), the number of fills of an oral steroid ( R = -0.179), and the total days' supply of oral steroid ( R = -0.154). After adjusting for potential confounders, including the prescribed amount of ICS, each 25% increase in the proportion of time without ICS medication resulted in a doubling of the rate of asthma-related hospitalization (relative rate, 2.01; 95% CI, 1.06-3.79). During the study period, there were 80 asthma-related hospitalizations; an estimated 32 hospitalizations would have occurred were there no gaps in medication use (60% reduction). CONCLUSIONS: Adherence to ICS is poor among adult patients with asthma and is correlated with several poor asthma-related outcomes. Less than perfect adherence to ICS appears to account for the majority of asthma-related hospitalizations.

Administration, Inhalation↗