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Biomedical subjects

Raymond G Slavin

Publications and source records attributed to Raymond G Slavin.

At least 19 recordsLinked to original sources
PubMed2006

Rhinosinusitis: developing guidance for clinical trials.

The Rhinosinusitis Initiative was developed by 5 national societies. The current guidance document is an expansion of the 2004 publication "Rhinosinusitis: Establishing definitions for clinical research and patient care" and provides templates for clinical trials in antimicrobial, anti-inflammatory, and symptom-relieving therapies for the following: (1) acute presumed bacterial rhinosinusitis, (2) chronic rhinosinusitis (CRS) without nasal polyps, (3) CRS with nasal polyps, and (4) classic allergic fungal rhinosinusitis. In addition to the templates for clinical trials and proposed study designs, the Rhinosinusitis Initiative has developed 6 appendices, which address (1) health outcomes, (2) nasal endoscopy and staging of CRS, (3) radiologic imaging, (4) microbiology, (5) laboratory measures, and (6) biostatistical methods.

Chronic Disease↗
PubMed2006

Allergic contact dermatitis.

The pathophysiology of ACD follows an intricate design and results in the characteristic, delayed inflammatory response. Although the astute physician may correctly diagnose ACD from its initial, classic history and presentation, alternative diagnoses should be considered and excluded. Patch testing performed with a relevant panel of contact allergens is the ultimate confirmatory test of ACD. Correctly identifying the inciting allergen permits appropriate personal avoidance. Corticosteroids remain the principal treatment options.

Dermatitis, Allergic Contact↗
PubMed2006

Rhinosinusitis: Developing guidance for clinical trials.

The Rhinosinusitis Initiative was developed by 5 national societies. The current guidance document is an expansion of the 2004 publication, "Rhinosinusitis: Establishing definitions for clinical research and patient care" and provides templates for clinical trials in antimicrobial, anti-inflammatory, and symptom-relieving therapies for the following: (1) acute presumed bacterial rhinosinusitis, (2) chronic rhinosinusitis (CRS) without nasal polyps, (3) CRS with nasal polyps, and (4) classic allergic fungal rhinosinusitis. In addition to the templates for clinical trials and proposed study designs, the Rhinosinusitis Initiative has developed 6 appendices, which address (1) health outcomes, (2) nasal endoscopy and staging of CRS, (3) radiologic imaging, (4) microbiology, (5) laboratory measures, and (6) biostatistical methods.

Chronic Disease↗
PubMed2006

Asthma in older adults: observations from the epidemiology and natural history of asthma: outcomes and treatment regimens (TENOR) study.

BACKGROUND: The Epidemiology and Natural History of Asthma: Outcomes and Treatment Regimens (TENOR) was a 3-year, multicenter, observational study of 4,756 patients 6 years or older with severe or difficult-to-treat asthma by physician evaluation. More than 280 pulmonologist and allergist sites across the United States participated. OBJECTIVE: To compare health care utilization (HCU), medication use, asthma control, and quality of life (QoL) in older (> or =65 years; n = 566) and younger (18-64 years; n = 2,912) adult patients in TENOR. METHODS: Patients had to be under a physician's care for at least 1 year and have high medication use or HCU in the past year. Heavy smokers (> or =30 pack-years) and patients with cystic fibrosis were excluded. RESULTS: Although older patients in TENOR had worse lung function as measured by decreased percent predicted forced expiratory volume in 1 second (FEV1) (P < .001), they had significantly lower HCU compared with younger patients. They also had higher use of inhaled corticosteroids and better QoL than younger patients. Older patients reported fewer problems controlling their asthma (P < .001) but reported worse communication with their physicians (P = .02). CONCLUSIONS: Older patients in TENOR appeared to do better than younger patients, despite having worse lung function. Older patients in TENOR may have received more aggressive care than older asthmatic patients in other studies, based on a higher use of inhaled and oral corticosteroids. Whether differences in treatment or disease influenced other physiologic or inflammatory outcomes that contribute to the disconnect between HCU and FEV1 awaits further study.

Adolescent↗
PubMed2006

Facial angioedema in children due to ladybug (Harmonia axyridis) contact: 2 case reports.

BACKGROUND: Only 9 adult cases of immediate-hypersensitivity reaction to ladybugs, also known as Asian lady beetles (Harmonia axyridis), have been documented in the literature. These patients have all shown symptoms of allergic rhinoconjunctivitis or asthma from exposure to ladybugs. OBJECTIVE: To describe the first pediatric patients with severe allergic facial angioedema requiring emergency department management after exposure to ladybugs. METHODS: Evidence of IgE-mediated hypersensitivity to ladybugs was documented by positive skin prick test reactions, correlating with exposure history. RESULTS: Two cases in preschool boys had similar features, although they were evaluated and tested by 2 different allergists. Both patients developed severe facial or periocular angioedema with no significant respiratory involvement after exposure to ladybugs outside their infested homes. Both patients required an emergency department visit for treatment. Allergy evaluation using ladybug extract for skin prick testing showed markedly positive reactions in both patients. There were no further episodes after environmental control measures were instituted. CONCLUSIONS: Although allergic respiratory or cutaneous reactions to ladybugs are uncommon, a high index of suspicion from exposure history and confirmatory skin testing can be conclusive for the diagnosis.

Angioedema↗
PubMed2005

Rhinosinusitis and pediatric asthma.

Rhinosinusitis is a common disease in patients of all age groups. Rhinosinusitis arises from a variety of infectious and inflammatory mechanisms. There is ample evidence that rhinosinusitis can directly influence asthma. There is also growing evidence that rhinosinusitis may be associated with asthma as different manifestations of the same disorder. A great deal of future research is required to fully elucidate the different mechanisms whereby rhinosinusitis influences or associates with asthma, but it is clear that rhinosinusitis needs to be considered in patients with severe or refractory asthma.

Asthma↗
PubMed2004

HLA-DQB1 *03 in allergic fungal sinusitis and other chronic hypertrophic rhinosinusitis disorders.

BACKGROUND: Many common chronic inflammatory disorders have strong HLA gene associations, particularly with MHC class II. Allergic fungal rhinosinusitis (AFS) and hypertrophic sinus disease (HSD) are chronic sinonasal mucosal inflammatory disorders. Allergic bronchopulmonary aspergillosis, a disorder analogous to AFS, was recently reported to have HLA-MHC class II associations. OBJECTIVE: We sought to determine whether MHC class II is also associated with AFS and HSD. METHODS: HLA DNA genotyping was obtained on 44 patients with AFS and 30 patients with HSD (of which 21 were atopic). RESULTS: Sixty-six percent of patients with AFS carried at least one HLA-DQB1 *03 allele; DQB1 *0301 and DQB1 *0302 were the most frequent allelic variants (odds ratio [OR] vs healthy subjects = 8.22; 95% CI, 4.30-15.73; P < .001; OR vs all patients with HSD = 1.93; 95% CI, 1.09-3.41; P < .01; OR vs atopic patients with HSD = 2.57; 95% CI, 1.46-4.53; P < .001). Of the 31 patients with AFS and positive Bipolaris spicifera cultures, 68% had DQB1 *03, with DQB1 *0301 and DQB1 *0302 being most frequent (OR vs healthy subjects = 8.93; 95% CI, 4.65-17.15; P < .001; OR vs patients with HSD = 2.10; 95% CI, 1.18-3.73; P < .001). Of the 30 patients with HSD, 50% carried DQB1 *03 (OR vs healthy subjects = 4.25; 95% CI, 2.25-8.02; P < .001) but differed in frequencies of DQB1 *03 allelic variants compared with patients with AFS ( P = .0004). For HSD, nonatopic subjects had the highest DQB1 *03 association (OR vs healthy subjects = 8.63; 95% CI, 4.50-16.54; P < .001). DQB1 *03 allelic variants did not correlate with allergy skin test results, atopic status, total serum IgE levels, culture results, asthma, or aspirin-nonsteroidal anti-inflammatory drug hypersensitivity. CONCLUSION: Patients with AFS and HSD have HLA-DQB1 *03 alleles as a risk factor for disease, with AFS having the highest association. However, they differ in DQB1 *03 allelic variant frequencies, suggesting several potential roles for MHC class II in their immunopathogenesis.

Adolescent↗
PubMed2004

Nonoccupationally induced allergy to monkey.

BACKGROUND: A previous study described 2 patients with occupationally induced asthma caused by exposure to monkey. We describe a patient who developed asthma, rhinitis, and conjunctivitis owing to sensitivity to a pet monkey. The patient had a long history of upper and lower allergic airway disease. When 2 pet macaque monkeys were introduced into the home, the patient noticed increasing coughing, wheezing, and shortness of breath. During a particularly long exposure to the monkey in a car, the patient developed severe wheezing, rhinitis, and conjunctival edema. OBJECTIVE: To demonstrate that a nonoccupational exposure to monkey can lead to allergic sensitivity. METHODS: Commercially obtained macaque monkey hair was defatted in acetone and extracted. A total of 5 microg/mL of extract protein was adsorbed onto microtiter plates, and an alkaline phosphatase enzyme-linked immunosorbent assay was performed on serum samples from 4 individuals: 2 controls, 1 individual with suspected sensitivity, and the patient. A positive result was an optical density greater than twice that of the control. RESULTS: The patient's serum had an optical density greater than twice that of the control. The antibody levels of 2 control subjects-the patient's wife and one of the investigators-were elevated but not positive. The investigator had manifested asthma after exposure. CONCLUSIONS: This is the first report of sensitivity to monkey occurring in a nonoccupational setting.

Animals↗
PubMed2004

Fresh frozen plasma in the treatment of resistant angiotensin-converting enzyme inhibitor angioedema.

BACKGROUND: Angioedema, particularly of the head and neck, is a well-recognized adverse effect of angiotensin-converting enzyme (ACE) inhibitors. Most cases respond to conventional therapy, including antihistamines and corticosteroids. Severe episodes may require epinephrine and intubation. OBJECTIVE: To report the case of a patient with ACE inhibitor-induced angioedema treated with fresh frozen plasma (FFP). METHODS: The patient is a 43-year-old, white woman who first received the ACE inhibitor ramipril in March 2002. After 3 weeks, she developed angioedema of her lips and fingers, which resolved with antihistamines, corticosteroids, and one dose of epinephrine. A low dose of ramipril was restarted 4 days later, which was increased throughout 4 days. In late August 2002, she developed severe upper lip and tongue edema recalcitrant to conventional therapy. Her C1 esterase inhibitor level was normal. RESULTS: After 4 days of treatment with antihistamines, corticosteroids, epinephrine, antileukotrienes, cyclosporine, and intravenous immunoglobulins, the patient's tongue swelling continued to recur and became more severe. Two units of intravenous FFP was given, with rapid improvement and no further recurrence of tongue swelling. CONCLUSIONS: In our patient, FFP was highly successful in the treatment of resistant, life-threatening angioedema due to an ACE inhibitor. The benefit of FFP in this setting might be due to the effect of kininase II in breaking down accumulated bradykinin.

Adult↗
PubMed2003

MHC restriction in allergic bronchopulmonary aspergillosis.

Allergic bronchopulmonary aspergillosis (ABPA) is a rare complication in patients with asthma but more common in patients with cystic fibrosis. In the presence of the fungus Aspergillus fumigatus (Af) in the lower respiratory tract, patients mount a heightened IgG and IgE humoral response specific for Af antigens. Studies on ABPA have suggested a pathogenic role for antigen specific CD4+ Th2 like T lymphocytes producing increased levels of IL-4 and IL-5. MHC class II genes coding for highly polymorphic HLA molecules have been shown to be the likely candidates for controlling immune responses to common allergens. However there has been a lack of information on the pathophysiological role of HLA genes in the development of ABPA. This review describes an association between HLA- class II alleles and the specific responses to Af antigen (Asp f 1) in ABPA. These studies focused on MHC restriction and distribution of HLA- class II alleles in two groups of unrelated North American Caucasian patients with cystic fibrosis and/or asthma. One group consisted of patients with a confirmed diagnosis of ABPA and a second group of patients with Af sensitivity but no ABPA. HLA association studies revealed that the predisposition to develop ABPA is associated with HLA-DR2 and DR5, and possibly DR4 or DR7. A strong association of HLA-DR antigens with ABPA reflects that HLA-DR molecules may present disease-causing peptides. On the other hand a significant association of HLA-DQ2 with Af sensitive nonABPA indicates the involvement of HLA-DQ molecules in protection. A combination of these genetic factors determines the outcome of ABPA in patients with cystic fibrosis and asthma.

Animals↗
PubMed2003

Occupational rhinitis.

This article aims to define occupational rhinitis, classify its various causes, review the steps in its diagnosis, and describe its nonpharmacologic and pharmacologic principles of management. Occupational rhinitis frequently coexists with asthma but also occurs alone. Although it does not have the same impact as occupational asthma, occupational rhinitis causes distress, discomfort, and work inefficiency. By concentrating on the patient's workplace, the clinician has an opportunity to practice preventive medicine: to recognize substances in the patient's micro- and macroenvironment that are causing the problems and then to intervene by altering the environment or removing the patient from the environment.

Asthma↗
PubMed2003

Occupational rhinitis.

OBJECTIVE: To define occupational rhinitis, classify its various causes, review the steps in diagnosis, and describe the nonpharmacologic and pharmacologic management principles. DATA SOURCES: A review of MEDLINE articles in English on occupation rhinitis for January 1, 1970, through December 31, 2001, was performed. In addition, references were identified from bibliographies of relevant articles and books. STUDY SELECTION: The expert opinion of the author was used to select the relevant articles for the review. RESULTS: Occupational rhinitis is the episodic, work-related occurrence of sneezing, nasal discharge, and nasal obstruction. It frequently coexists with asthma but may present alone. Occupational rhinitis can be caused by heightened olfactory awareness, nonspecific inflammation of the nose, exposure to a high concentration of irritating and soluble chemical gases, or IgE mechanisms. The history and physical examination are the most important components to the workup of the patient. A site visit to the specific work area may give helpful insights to the patients' exposure. In the case of IgE-mediated allergic occupational rhinitis, skin testing or serologic testing may be useful. Greater objectivity to the diagnosis can be obtained through nasal challenge and the rapidly developing technique of rhinomanometry. Nonpharmacologic management (environmental control) and pharmacotherapy, such as that used in allergic rhinitis, should both be instituted. CONCLUSIONS: Although it does not have the same impact as occupational asthma, occupational rhinitis causes distress, discomfort, and work inefficiency. Attention to principles of management involving nonpharmacologic and pharmacologic measures will spare the patient the symptoms of occupational rhinitis.

Humans↗
PubMed2002

T-cell receptor bias in patients with allergic bronchopulmonary aspergillosis.

CD4(+) Th2 helper cell mediated immune responses have been shown to play a crucial role in the pathogenesis of ABPA. HLA and TCR are the candidate genes, which can influence the specificity of these responses. We have previously established a strong association of HLA DR2/5 in ABPA susceptibility. The study was designed to determine whether allergen specific T cell express a limited usage of T cell receptor (TCR) Vbeta gene repertoire in ABPA and to find an association of susceptible HLA-DR determinants with the identified TCR gene segments. TCR Vbeta typing was performed on antigen specific T cell lines from 14 ABPA and 12 nonABPA patients. The majority of ABPA patients (86%) expressed allergen specific T cells with Vbeta13 genes indicating its role in susceptibility, whereas in nonABPA controls, Vbeta1 genes T cell repertoires were predominantly expressed. The unrestricted pattern of Vbeta gene amplification seen before antigen stimulation suggests an oligoclonal expansion of a specific T cell population in response to the allergen Asp f 1 in ABPA and nonABPA patients. The increased usage of Vbeta13 in ABPA and Vbeta1 in nonABPA indicates their importance in susceptibility and resistance, respectively.

Allergens↗