Quality of life is lower in adults labeled with childhood-onset food allergy than in those with adult-onset food allergy.

BACKGROUND: Immunoglobulin E-mediated food allergy (FA) affects children and adults with variable age of onset. Phenotype and quality of life (QoL) differences between childhood-onset FA (COFA) and adult-onset FA (AOFA) are not known. OBJECTIVE: To identify phenotypic and QoL differences between AOFA and COFA. METHODS: A cross-sectional study of adults (≥18 years old) seen at Northwestern Memorial HealthCare clinics between 2002 and 2017 with an International Classification of Diseases ninth and tenth revision diagnosis of FA. Subjects completed a FA history survey and a FA QoL questionnaire. FA characteristics and QoL scores were compared between groups. RESULTS: Among 294 consented subjects, 202 had a clinical history consistent with labeled immunoglobulin E-mediated FA. The onset of FA symptoms occurred before age 18 years (COFA) in 80 subjects and after age 18 years in 122 (AOFA) subjects. Shellfish reactions were most common in AOFA-labeled subjects (28%), whereas tree nut reactions were the most common in COFA-labeled subjects (55%) compared with other triggers. Hives (68% vs 52%, P = .03), facial swelling (69% vs 50%, P = .009), wheezing (56% vs 29%, P < .001), and vomiting (41% vs 22%, P = .005) were more often observed in COFA compared with AOFA. Total QoL was significantly reduced in COFA compared with AOFA (3.6 vs 3.0, P = .003) along with specific domains related to the following: allergen avoidance and dietary restriction (3.7 vs 3.1, P = .006), emotional impact (3.9 vs 3.2, P = .003), and risk of accidental exposure (3.6 vs 2.8, P = .001). CONCLUSION: There are differences in specific food triggers and symptoms in adult-onset and childhood-onset labeled FA. Adults labeled with childhood-onset FA have reduced QoL.

Factors associated with negative histamine control for penicillin allergy skin testing in the inpatient setting.

BACKGROUND: Identification of factors adversely affecting the utility of allergy skin testing is important in optimizing patient care. Inpatient penicillin skin test data from 1997 through 2007 demonstrate that up to 20% of attempted penicillin skin tests are indeterminate owing to a negative histamine test response, despite exclusion of H1 antagonists. Critical illness, vasopressors, steroid use, and psychotropic medications have been postulated to influence outcomes, but large studies are lacking. OBJECTIVE: To identify factors associated with a negative histamine test response for the inpatient setting. METHODS: Fifty-two cases were identified with a negative histamine response after penicillin skin testing in the absence of antihistamine therapy for 72 hours before testing. One hundred twenty-five controls with a normal histamine response were randomly selected from same population. Independent variables assessed included stay in the intensive care unit (ICU), skin color, diabetes, age, use of vasopressors, H2 blocker, steroids, other immunosuppressive drugs, thyroid replacement, proton pump inhibitors, diuretics, 5 categories of psychotropic medications, and amiodarone. RESULTS: Mean age was 68 years for cases vs 60 years for controls (P = .002). Bivariate analysis showed ICU stay was more frequent in cases than in controls (73.1% vs 33.6%, P < .001). Regression analysis yielded odds ratios (ORs) of 8.18 (95% confidence interval 3.22-20.76) for ICU status, 3.76 (1.30-10.92) for systemic corticosteroids, and 4.90 (1.17-20.62) for H2 blockers as associated with lack of histamine response. For every additional year in age, there was increase in the OR of 1.04 (1.01-1.07). CONCLUSION: Regression analysis supports ICU stay during skin testing as associated with a high OR for a negative histamine response independent of age. Systemic corticosteroids, H2 blockers, and older age are associated with a significant OR for a negative histamine response. This is one of largest studies on factors associated with a negative histamine response for the inpatient setting and has significant implications for clinical practice.

Management of rhinosinusitis: an evidence based approach.

PURPOSE OF REVIEW: The most recent recommendations for the management of both acute (ARS) and chronic rhinosinusitis (CRS) based on the strongest data available for each treatment modality are summarized in this review. The clinical relationships between CRS and its comorbidities are also discussed. RECENT FINDINGS: The most promising advances in rhinosinusitis management involve the use of mAbs (anti-IgE, anti-IL-5, anti-IL-4Rα) in trials of CRS with nasal polyposis. Otherwise, the mainstays of treatment for both ARS and CRS have largely remained the same over the past several years. SUMMARY: The treatment of ARS primarily involves symptomatic control with intranasal corticosteroids and nasal saline irrigation; antibiotics should be reserved for the patients who are believed to have bacterial rhinosinusitis. Treating CRS effectively involves using intranasal corticosteroids and irrigation, systemic corticosteroids, and potentially systemic antibiotics. Biologics (mAbs) have shown benefit in clinical studies. Providers should also be aware of concomitant disease processes that may afflict patients with CRS.

Hypertrophic scar cells fail to undergo a form of apoptosis specific to contractile collagen-the role of tissue transglutaminase.

Failure of apoptosis has been postulated to cause the hypercellularity and thus excess scar-tissue formation of hypertrophic scars (HTS). Here, we have examined the susceptibility of fibroblasts derived from normal or HTS to apoptosis induced during collagen-gel contraction, a wound-healing model. Normal scar (NS) fibroblasts underwent significant apoptosis (>40% total) in contractile collagen, whereas apoptosis was not detected in HTS cells. This inability was specific to apoptosis induced by contractile collagen because apoptosis could be induced using diverse modalities. Since chronic fibrotic tissue is known to be excessively cross-linked, we next examined whether collagen matrix that had been conditioned by HTS fibroblasts became refractory to enzymatic breakdown and indeed, found that it is resistant to breakdown by both collagenase D and matrix metalloproteinase-2. Newly formed extracellular matrix is stabilized by the enzyme, tissue transglutaminase, which we demonstrated to be overexpressed by HTS fibroblasts in vivo and in vitro. Reducing tissue transglutaminase activity in collagen gels containing HTS fibroblasts permitted induction of apoptosis on gel contraction, whereas increasing enzymic activity in NS cell-containing gels completely abrogated collagen-contraction-induced-apoptosis. Together, these observations show that HTS fibroblasts exhibit resistance to a specific form of apoptosis elicited by contraction of collagen gels, and that this phenomenon is dependent on excess activity of cell surface tissue transglutaminase.