tag:blogger.com,1999:blog-20572693053781149972024-03-23T06:14:35.590-04:00Allergy Notes<center>Allergy, Asthma and Immunology News by a Board-certified Allergist at Cleveland Clinic Florida</center>Unknownnoreply@blogger.comBlogger1913125tag:blogger.com,1999:blog-2057269305378114997.post-41270215353897640032023-01-12T14:36:00.001-05:002023-01-12T14:54:33.762-05:00SABA/ICS prn combo for asthma: AIRSUPRA (albuterol/budesonide)<p>As of January 2023, AIRSUPRA (albuterol/budesonide), has been approved in the US for the as-needed treatment or prevention of bronchoconstriction and to reduce the risk of exacerbations in people with asthma aged 18 years and older.<br /><br />AIRSUPRA (<b>180mcg albuterol/160mcg budesonide</b>) significantly reduced the risk of severe exacerbations compared to albuterol in patients with moderate to severe asthma when used as an as-needed rescue medication in response to symptoms.<br /><br />Albuterol rescue inhalers available prior to 2023 can alleviate acute symptoms, but do not treat the underlying inflammation in asthma. The approval of AIRSUPRA means that for the first time, adults with asthma in the US have a<b> rescue treatment to manage both their symptoms and the inflammatory</b> nature of their disease.<br /><br />References:<br /><br /><a href="https://www.astrazeneca-us.com/content/az-us/media/press-releases/2023/airsupra-pt027-approved-in-the-us-for-asthma.html">https://www.astrazeneca-us.com/content/az-us/media/press-releases/2023/airsupra-pt027-approved-in-the-us-for-asthma.html</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-16930893545843519932022-09-14T15:09:00.007-04:002022-09-14T15:09:00.180-04:00Allergic diseases and sleep problems in children<p>Allergic rhinitis was associated with a broad range of sleep problems and to a lesser extent in children with asthma and least in children with eczema. <br /><br /><b>Allergic rhinitis</b> was associated with:<br /><br />- sleep routine problems<br />- morning tiredness<br />- night arousals<br />- sleep disordered breathing<br />- restless sleep<br /><br /><b>Asthma</b> was associated with:<br /><br />- sleep routine problems<br />- sleep disordered breathing<br />- restless sleep<br /><br /><b>Eczema</b> was associated with restless sleep.<br /><br />The association between allergic disease and <b>psychological distress was mediated through sleep problems</b>.<br /><br />References:<br /><br /><a href="https://www.annallergy.org/article/S1081-1206(22)00409-4/fulltext">https://www.annallergy.org/article/S1081-1206(22)00409-4/fulltext</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-83578787582050552922022-09-13T15:04:00.005-04:002022-09-13T15:04:00.180-04:00Add-on etanercept as a treatment for Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN)<p>Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is a severe cutaneous adverse reaction to drugs. The disease carries considerable morbidity and mortality. <br /><br />Immunomodulators for SJS/TEN such as systemic corticosteroids and intravenous immunoglobulin (IVIG) have been widely used in clinical practice. <br /><br />Emerging evidence suggested that tumor necrosis factor-α antagonists on SJS/TEN may help.<br /><br />This restrospective review found that add-in of etanercept at the time of initiating conventional therapy could be a superior option to:<br /><br />- accelerate disease recovery<br />- reduce the high dose and total amount of systemic steroids<br /><br />References:<br /><br /><a href="https://www.annallergy.org/article/S1081-1206(22)00441-0/fulltext">https://www.annallergy.org/article/S1081-1206(22)00441-0/fulltext</a><br /><br /><a href="https://www.annallergy.org/article/S1081-1206(22)00579-8/fulltext">https://www.annallergy.org/article/S1081-1206(22)00579-8/fulltext</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-25184921259379409362022-09-12T14:44:00.001-04:002022-09-12T14:44:00.169-04:00Against the hygiene hypothesis as the cause of allergic diseases<p>The article argues against the hygiene hypothesis for causation of allergic diseases:<br /><a href="https://www.annallergy.org/article/S1081-1206(22)00585-3/fulltext">https://www.annallergy.org/article/S1081-1206(22)00585-3/fulltext</a><br /><br />The authors make the case that the basic changes in hygiene, clean water, complete separation of fecal matter from food production, and helminth eradication were complete before most of the major rises in allergic disease. Thus, all the allergic diseases increase occurred “post-hygiene.” <br /><br />The look for another cause: There is one major change that has decreased the severity of 2 allergic diseases, that is <b>air conditioning </b>and the closing of houses so that air exchange rates are as low as 0.6 air changes per hour. This means that only minimal quantities of pollen can enter the houses but also that houses become drier and less hospitable to mites. Both hay fever and asthma have become less severe since 2000. <br /><br />References:<br /><br /><a href="https://www.annallergy.org/article/S1081-1206(22)00585-3/fulltext">https://www.annallergy.org/article/S1081-1206(22)00585-3/fulltext</a><br /><br /><a href="https://www.annallergy.org/article/S1081-1206(22)00504-X/fulltext">https://www.annallergy.org/article/S1081-1206(22)00504-X/fulltext</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-64419531067343745622022-09-10T14:40:00.008-04:002022-09-10T14:40:00.164-04:00Prognostic factors for polyp recurrence in chronic sinusitis<p>Chronic rhinosinusitis with nasal polyps is frequently managed with endoscopic sinus surgery (ESS). Prior studies describe individual clinical variables and eosinophil density measures as prognostic for <br /><br /><b>Polyp recurrence (PR) was found in 39.4%</b> of patients with CRSwNP s/p endoscopic surgery. <br /><br />Polyp recurrence (PR) was associated with:<br /><br />- modified Lund-Mackay (MLM) radiographic score (MLM)<br />- asthma<br />- eosinophil cationic protein<br />- anti–double-stranded DNA IgG<br />- IL-5 <br /><br />A combined model comprised of eosinophil cationic protein, IL-5, pre-ESS MLM, asthma, and anti–double-stranded DNA IgG could accurately predict polyp recurrence (PR).<br /><br />More in JACI:<br /><a href="https://www.jacionline.org/article/S0091-6749(22)00343-8/fulltext">https://www.jacionline.org/article/S0091-6749(22)00343-8/fulltext</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-39859470600779207852022-09-09T14:36:00.009-04:002022-09-09T14:36:00.180-04:00Blood endotypic signatures in atopic dermatitis<p>Atopic dermatitis (AD) is the <b>most common chronic inflammatory skin disease.</b> AD can be very challenging to manage. <br /><br />AD is characterized by:<br /><br />- dense cutaneous dendritic cell and T-cell infiltrates<br />- increased inflammatory mediators in affected tissues<br />- barrier defects secondary to the downregulation of differentiation proteins and lipids<br /><br />AD is associated with a polarized type 2 immune axis. <br /><br />However, AD is not a homogenous disease. AD may be categorized into <b>multiple clinical phenotypes </b>depending on the underlying molecular signature (endotype).<br /><br />Read more in JACI here:<br /><a href="https://www.jacionline.org/article/S0091-6749(22)00834-X/fulltext">https://www.jacionline.org/article/S0091-6749(22)00834-X/fulltext<br /><br /></a><a href="https://www.jacionline.org/article/S0091-6749(22)00186-5/fulltext">https://www.jacionline.org/article/S0091-6749(22)00186-5/fulltext</a><br /></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-22633418229829581742022-09-08T14:34:00.007-04:002022-09-08T14:34:00.188-04:00Eosinophilic gastrointestinal diseases: updated nomenclature<p><b>Eosinophilic gastrointestinal (GI) diseases (EGIDs)</b> are characterized by tissue eosinophilia and symptoms of esophageal or GI dysfunction. Eosinophilic esophagitis (EoE) diagnostic criteria are well established.<br /><br />The prevalence of non-EoE EGIDs is much lower, and there are no consensus guidelines for diagnosis as of year 2022.<br /><br />Particularly <b>problematic</b> has been variable use of the term<b> eosinophilic gastroenteritis</b> to describe EGIDs involving the stomach, small intestine, large intestine, or groupings of these anatomic sites. <br /><br />EGID is recommended as the umbrella term for pathologic infiltration of the GI tract with eosinophils:<br /><br /><b>- EoE </b>- Esophageal involvement alone is termed EoE<br /><b>- non-EoE EGID</b> - any other location of involvement than esophagus can be termed a non-EoE EGID<br /><br />Individual involved areas of the GI tract should be named specifically, and an “Eo” abbreviation convention should be used.<br /><br />Read more in JACI here:<br /><a href="https://www.jacionline.org/article/S0091-6749(22)00709-6/fulltext">https://www.jacionline.org/article/S0091-6749(22)00709-6/fulltext</a><br /><br /><br /></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-83017016235448258962022-09-07T14:28:00.010-04:002022-09-07T14:28:00.172-04:00Chronic rhinosinusitis: Future treatments review in JACI<p>Chronic rhinosinusitis (CRS) has a major clinical impact and affects 10% of the US population.<br /><br />CRS presents with <b>2 major phenotypes</b>: <br /><br />- CRS with <b>nasal polyps</b> (CRSwNP)<br />- CRS without nasal polyps (CRSsNP)<br /><br /><b>Type 2 endotype</b> (cytokines such as IL-4, IL-5, and IL-13; tissue eosinophilia; and local IgE production) comprises 80% to 90% of patients with CRSwNP and 30% to 50% of patients with CRSsNP in Western countries. <br /><br />CRSwNP in Asia and CRSsNP have more endotypic heterogeneity, with significant subpopulations that have combinations of type 1 (IFN-γ and IL-12), type 2, and type 3 (IL-17 and IL-22) inflammation.<br /><br />Read more in JACI here:<br /><a href="https://www.jacionline.org/article/S0091-6749(22)00760-6/fulltext">https://www.jacionline.org/article/S0091-6749(22)00760-6/fulltext</a><br /><br /><br /></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-61242844931302721672022-09-05T14:17:00.002-04:002022-09-05T14:17:00.177-04:00T2 inflammation biomarkers and cytokines<p>T2 inflammation is characterized by elevations in:<br /><br />- absolute peripheral or sputum eosinophil counts <br />- levels of IgE (total and allergen-specific)<br />- fractional exhaled nitric oxide (FeNO)<br /><br />The 3 above serve as<b> biomarkers</b> of T2 inflammation. <br /><br />T2 inflammation is mediated by key <b>cytokines:</b><br /><br />- IL-4<br />- IL-5<br />- IL-13<br />- thymic stromal lymphopoietin<br />- IL-25<br />- IL-33<br /><br />IL-4 and IL-13 utilize Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathways.<br /><br />There are biologic therapies targeting these T2 cytokines, reviewed in the article below:<br /><a href="https://www.jacionline.org/article/S0091-6749(22)00840-5/fulltext">https://www.jacionline.org/article/S0091-6749(22)00840-5/fulltext</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-82276615595500382022022-09-03T15:50:00.001-04:002022-09-03T15:50:00.176-04:00Aquagenic urticaria<p>Aquagenic urticaria (AquaU) is a rare variant of chronic inducible urticaria. In AquaU wheals occur after skin contact with water. <br /><br />AquaU can be <b>classified as:</b><br /><br />- <b>familial </b>AquaU (FAquaU, <b>18%) </b><br />- <b>acquired </b>AquaU (AAquaU,<b> 82%)</b><br /><br />The use of second-generation H1 antihistamines (2ndAH1) was reported most often to achieve marked improvement in AquaU<br /><br />The use of topical therapies in AquaU has controversial efficiency.<br /><br />More in JACI-IP:<br /><a href="https://www.jaci-inpractice.org/article/S2213-2198(22)00477-9/fulltext">https://www.jaci-inpractice.org/article/S2213-2198(22)00477-9/fulltext</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-35000549987730669432022-09-02T15:41:00.001-04:002022-09-02T15:41:00.173-04:00Personalized Management Strategies in Mast Cell Disorders<p>Mastocytosis is a myeloid neoplasm. It is defined by expansion and focal accumulation of clonal mast cells (MCs) in one or more organs. <br /><br /><b>Mastocytosis has a complex pathology</b> and may be complicated by:<br /><br />- MC activation<br />- bone abnormalities<br />- neurological problems<br />- gastrointestinal symptoms<br />- hematologic progression<br /><br />Mediator-related symptoms can occur in any type of mastocytosis. <br /><br />The World Health Organization divides mastocytosis into <b>several forms:</b><br /><br />- cutaneous<br />- systemic mastocytosis (SM)<br />- MC sarcoma<br /><br />In most patients with SM, somatic mutations in KIT are detected. <br /><br />Patients with indolent SM have a normal to near-normal life expectancy. This is in contrast with patients with advanced SM, including aggressive SM and MC leukemia, who have a poor prognosis. <br /><br />Management of patients with SM is an emerging challenge. It requires a <b>multidisciplinary approach.</b><br /><br />More in the JACI-IP article below, <b>REMA score</b> and other practical suggestions are listed:<br /><a href="https://www.jaci-inpractice.org/article/S2213-2198(22)00281-1/fulltext">https://www.jaci-inpractice.org/article/S2213-2198(22)00281-1/fulltext</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-79720011466452559212022-09-01T15:32:00.001-04:002022-09-01T15:32:00.189-04:00Nontryptase Urinary and Hematologic Biomarkers of Mast Cell Activation<p>Nontryptase Urinary and Hematologic Biomarkers of Mast Cell Activation include:<br /><br />- <b>urinary metabolites of histamine</b><br />- urine and serum or plasma<b> prostaglandin D2</b><br />- urine or plasma<b> leukotriene E4</b><br /><br /><b>Drawbacks of trytase</b><br /><br />Serum tryptase levels have been the workhorse in diagnosing Mast Cell Activation Disorers. <br /><br />However, tryptase has several drawbacks including the need to obtain acute and baseline samples, which require 2 visits to health care facilities and <b>2 venipunctures. </b><br /><br />In addition, increased baseline tryptase level has been reported in <b>hereditary alpha tryptasemia (HaT). </b><br /><br />More in the JACI-IP article below:<br /><a href="https://www.jaci-inpractice.org/article/S2213-2198(22)00282-3/fulltext">https://www.jaci-inpractice.org/article/S2213-2198(22)00282-3/fulltext</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-26763079499048176432022-08-31T15:22:00.001-04:002022-08-31T15:22:00.160-04:00Tryptase Genotyping for Diagnosis of Mast Cell Disorders: consder the test if serum tryptase level exceeds 6.5 ng/mL<p>Tryptase levels in serum can be used for diagnosis and management of:<br /><br />- <b>clonal</b> mast cell disorders such as mastocytosis<br />- severe mast cell–dependent<b> systemic reactions</b> such as anaphylaxis<br /><br /><b>Hereditary α-tryptasemia (HαT)</b><br /><br />The majority of individuals with elevated basal serum tryptase levels have increased <b>TPSAB1 gene </b>encoding α-tryptase. This defines hereditary α-tryptasemia (HαT). HaT affects nearly 6% of the general population. <br /><br /><b>When to check for TPSAB1 gene?</b><br /><br />The presence or absence of HαT should be determined when defining what is an abnormal serum tryptase level. <br /><br />Symptomatic individuals undergoing evaluation for a mast cell–associated disorder with a baseline serum t<b>ryptase level exceeding 6.5 ng/mL should be considered for tryptase genotyping</b> in order to screen for HαT. <br /><br />More in the JACI-IP article below:<br /><a href="https://www.jaci-inpractice.org/article/S2213-2198(22)00489-5/fulltext">https://www.jaci-inpractice.org/article/S2213-2198(22)00489-5/fulltext</a><br /><br /></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-78702424766277022992022-08-30T15:15:00.003-04:002022-08-30T15:15:00.176-04:00Genetic Testing in the Diagnosis and Prognostication of Systemic Mastocytosis<p>Mastocytosis is a group of rare and heterogeneous diseases. They are characterized by an increased accumulation of abnormal mast cells in various organs/tissues. <br /><br />The pathogenesis of mastocytosis is linked to the presence of KIT-activating mutations. <br /><br />In systemic mastocytosis (SM), the most frequent mutation is <b>KIT p.D816V</b>. The presence of KIT p.D816V is one of the minor diagnostic criteria for systemic mastocytosis (SM). <br /><br />Allele-specific quantitative PCR and droplet digital PCR are the most sensitive lab tests for KIT p.D816V.<br /><br />KIT p.D816V multilineage involvement is associated with a worse prognosis. <br /><br />Mutations in <b>genes other than KIT</b> are frequently identified in systemic mastocytosis (SM). Those mutations have a negative prognosis. <br /><br />More details in the JACI-IP article below:<br /><br /><a href="https://www.jaci-inpractice.org/article/S2213-2198(22)00239-2/fulltext">https://www.jaci-inpractice.org/article/S2213-2198(22)00239-2/fulltext</a></p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-86195446273699311272022-08-29T14:57:00.001-04:002022-08-29T14:57:00.168-04:00Mast cell activation disorders (MCADs) <b>Mast cell activation (MCA)</b> is common and occurs in a <b>number of conditions,</b> including:<br /><br />- IgE-dependent and independent allergic reactions<br />- atopic disorders<br />- autoimmune processes<br />- mastocytosis<br /><br />In a subset of patients with mast cell activation (MCA), no underlying disease and no known trigger are found. This is clearly a challenge for both patients and physicians.<br /><br />When the symptoms of mast cell activation (MCA) are severe, systemic, and recurrent, and accompanied by a diagnostic increase in the serum tryptase level or other mast cell mediators, an MCA syndrome (MCAS) may be diagnosed. <br /><br />In patients with MCA syndrome (MCAS), the symptoms typically respond to medications suppressing mast cell activation, mediator production in mast cells, or mediator effects. <br /><br />Diagnostic consensus criteria must be fulfilled to diagnose MCAS. This is clear. The criteria were listed in prior JACI articles and are also available by using the search function of this website. <br /><br />In other patients, MCA may be local, less severe, or less acute. They do not have MCAS if the criteria are not fulfilled.<br /><br />The JACI-IP article linked below discusses MCA disorders (MCADs) and:<br /><br />- confirmed MCAS<br />- MCAD not fulfilling MCAS criteria<br />- suspected MCAD that is not present<br />- discrimination between overt MCAD and predisposing conditions, such as atopic states, mastocytosis, and hereditary alpha tryptasemia (HaT)<br /><br />References:<br /><br /><a href="https://www.jaci-inpractice.org/article/S2213-2198(22)00493-7/fulltext">https://www.jaci-inpractice.org/article/S2213-2198(22)00493-7/fulltext</a><br /><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-66869654338155374552022-03-31T14:17:00.005-04:002022-03-31T14:19:40.828-04:00Cardiovascular risks with Tixagevimab and Cilgavimab (Evusheld)
The FDA has a specific warning about Evusheld - it should be include in the informed consent, esp. since the prophylaxis use is off-label:
<p> <p/>
<b>Warnings/Precautions</b><p> <p/>
<b>Concerns related to adverse effects:</b><p> <p/>
Cardiovascular events: A higher rate of serious cardiovascular adverse events, including myocardial infarction, was observed among recipients of tixagevimab and cilgavimab, compared to placebo. All patients who experienced cardiac events had cardiac risk factors and/or a history of cardiovascular disease, and there was no clear temporal pattern. Consider potential risk and benefit in patients with a history of cardiovascular disease and advise patients to seek immediate medical attention if they experience signs/symptoms of a cardiovascular event (FDA 2021).<p> <p/>
In the post-hoc analysis of PROVENT, the incidence of <b>serious cardiac adverse events (eg, myocardial infarction, cardiac failure, arrhythmia) was higher in the antibody group than in the placebo group (0.6% vs 0.2%)</b>. One person who received the antibodies died of a myocardial infarction. There was no clear temporal relationship between antibody administration and cardiac adverse events.
<p> <p/>
<b>The trial incidence of serious cardiac events was 0.6% with Evusheld</b> according to JAMA (https://jamanetwork.com/journals/jama/fullarticle/2788354)<p> <p/>
As a comparioson, the AMI risk with IVIG is limited to case reports, here is an example and a review:
<a href="https://pubmed.ncbi.nlm.nih.gov/16288078">https://pubmed.ncbi.nlm.nih.gov/16288078</a>/<p> <p/>
Again, from the FDA (<a href="https://www.fda.gov/media/154701/download">https://www.fda.gov/media/154701/download</a>): <p> <p/>
“Cardiovascular Events: A higher proportion of subjects who received EVUSHELD versus placebo reported myocardial infarction and cardiac failure serious adverse events. All of the subjects with events had cardiac risk factors and/or a prior history of cardiovascular disease, and there was no clear temporal pattern. A causal relationship between EVUSHELD and these events has not been established. <p> <p/>
Consider the risks and benefits prior to initiating EVUSHELD in individuals at high risk for cardiovascular events, and
advise individuals to seek immediate medical attention if they experience any signs or symptoms suggestive of a cardiovascular event. (5.3)”
<p> <p/>
Of note, among the PROVENT trail participants less than 1% had an immunodeficiency disorder, therefore, strictly speaking, the effect of Tixagevimab and Cilgavimab (Evusheld) in patients with immunodeficiency disorders was not studies in this trial.<p> <p/>
<b>References</b>:<p> <p/>
<a href="https://jamanetwork.com/journals/jama/fullarticle/2788354">https://jamanetwork.com/journals/jama/fullarticle/2788354</a><p> <p/>
<a href="https://www.fda.gov/media/154702/download">https://www.fda.gov/media/154702/download</a><p> <p/><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-37177194929656083822021-06-03T14:58:00.014-04:002021-06-03T15:05:04.876-04:00The idea of “local allergic rhinitis” now returns as “local food allergy” in IBS patients<p><img src="https://docs.google.com/drawings/d/1SzYf8Um-c7gy_g7GyK061f3J3t9M5o9QzerwCGRDpe4/pub?w=476&h=346" /> </p><p>Adverse Food Reactions (<a href="https://docs.google.com/drawings/d/1SzYf8Um-c7gy_g7GyK061f3J3t9M5o9QzerwCGRDpe4/edit?usp=sharing">click to enlarge the image</a>).
</p><p><b>Up to 20% of people develop gastrointestinal (GI) symptoms following a meal.</b> Millions of people have chronic symptoms labeled as functional gastrointestinal pain or irritable bowel syndrome (IBS), with no clearly identifiable cause. </p><p><b>The gut–brain axis theory </b>is an attempt to explain IBS symptoms. Overly sensitive nerves in the GI tract react to normal functions, such as stretching and motility, that now feel painful. During periods of stress (e.g., anxiety or GI infection), symptoms may flare up. </p><p>Mast cells and mediators (neurotropic substances) may be involved in visceral hypersensitivity. </p><p><b>A new hypothesis is that GI mast cells</b> stimulated by food-induced local IgE may be the cause of IBS symptoms.
It is possible that a GI bacterial infection can break tolerance to a food antigen. The immune response toward that antigen can lead to increased GI permeability and pain when exposure to the antigen happens again. </p><p><b>In a study of 12 patients with IBS </b>there was no evidence of systemic IgE against common foods. However, when the same common allergens were injected into the rectal mucosa, every patient with IBS had a localized reaction to at least one of the antigens. </p><p> This test is not applicable to real-life patients yet. No one will be injecting antigens into the rectal mucosa in an allergy clinic near you anytime soon.
Examination of mast cells in GI biopsy specimens is not routinely performed. </p><p>Prolonged and high doses of a histamine H1 receptor antagonist (antihistamines) may reduce visceral hypersensitivity, symptoms, and abdominal pain in patients with IBS. </p><p>This recent NEJM commentary (see references below) attempts to expand the term “food allergy” beyond only systemic IgE-mediated reactions. Adverse food reaction is the more appropriate term in my opinion. Adverse food reactions can be IgE-mediated, cell mediated, mixed, not mediated by the immune system, etc.
This gastrointestinal tissue–IgE-specific allergic response, if mast cell mediated, is more accurately described as a mixed IgE-/cell-mediated reaction. Eosinophilic esophagitis (EoE) may be in the same category. </p><p>The ovalbumin-specific IgE antibodies identified by Aguilera-Lizarraga et al. were detectable only in colonic tissue. This is very similar to the previously described “local allergic rhinitis”: local application of the allergen induces local sIgE and mediators. </p><p>It is too soon to jump to the conclusion that IBS is a food-induced “allergic” disorder. It may still be food induced as many patients will verify. However, the application of the term “food allergy” to IBS in this case may not be helpful, especially for the same patients that need nothing more than a relief of the GI symptoms that may severely affect their quality of life. A follow-up with a gastroenterologist is recommended for patients with IBS. </p><p>References: </p><p><a href="https://www.nejm.org/doi/full/10.1056/NEJMcibr2104146?query=TOC">https://www.nejm.org/doi/full/10.1056/NEJMcibr2104146?query=TOC</a> </p><p><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5225338/">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5225338/</a> </p><p><a href="https://pubmed.ncbi.nlm.nih.gov/33442055/">https://pubmed.ncbi.nlm.nih.gov/33442055/</a>
</p><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-17584942311169035882020-07-25T07:00:00.000-04:002020-07-25T07:00:13.571-04:00Modifiable risk factors for the development of allergy (#ACAAI19 Twitter summary)<br />
Dr. Ellis @DrAnneEllis: Next up we have Dr. Syed Ashad - Risk factors for developing allergic disease - Lessons from the Isle of Wight.<br />
<br />
The Isle of Wight cohort has 1536 parents and 495 children.<br />
<br />
Modifiable risk factors for the development of atopy:<br />
Obesity<br />
Smoking<br />
Pollution<br />
Acetaminophen <br />
Air Pollution<br />
Breast feeding <br />
Microbiome<br />
<br />
Carina Venter PhD RD @VenterCarina Love this data from the Isle of Wight. - obesity trajectories and asthma risk<br />
<a href="https://twitter.com/VenterCarina/status/1193536142337069056">https://twitter.com/VenterCarina/status/1193536142337069056</a><br />
<br />
Michael R. Rupp, MD @Docallergy: Obesity is a huge problem with some association with asthma. Time of influence is in the first few years of life. Maternal smoking and obesity seem to have the most increased risk for wheeze. Multigenerational smoking can increase DNA methylation and pass through generations to children increasing risk for wheeze even if child doesn’t smoke. <br />
<br />
PARS is the best way to predict asthma<br />
<a href="https://pars.research.cchmc.org/">https://pars.research.cchmc.org/</a><br />
<br />
Dr. Ellis @DrAnneEllis: Childhood obesity in the Isle of Wight study - <b>if child is obese at the age of 4, highly likely to have persistent obesity. </b><br />
<br />
Risk factors for childhood obesity - maternal obesity, maternal smoking - leads to a significant risk of asthma by age 18.<br />
<br />
If both the mother and the grandmother were smokers, even more dramatic effect on the risk of asthma in the child.<br />
<br />
<b>Smoking by the grandmother induced epigenetic changes present in the index child. </b><br />
<br />
<b>Traffic related air pollution (TRAP) in the Isle of Wight study shown to lead to a number of epigenetic alterations affecting a number of tissues. </b><br />
<br />
Microbiome analysis from children in the Isle of Wight cohort showed Enterobacteriaceae strongly associated at the family level with eczema, bacteroidetes predominated in 4 of 6 samples from infants without eczema. <br />
<br />
Acetaminophen use in adolescence associated with an increased risk of wheezing/asthma in the IoW study. Breastfeeding for at least 4 months led to improved lung function at age 10 and 18yo. <br />
<br />
<b>Preschool wheeze is common. Only 1/3rd of these early wheezers will go on to develop asthma, however. </b><br />
<br />
Family history of asthma, chest infections, positive allergy skin test and absence of nasal symptoms are major risk factors for wheezy infants to go onto develop asthma.<br />
<br /><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-18157484404505965982020-07-24T08:30:00.000-04:002020-07-24T08:30:05.320-04:00Cannabis allergy (#ACAAI19 Twitter summary)Atoosa Kourosh @AllergyHealth: 30% of patients with true cannabis allergy will test negative to Can S 3 so it’s good to send component testing from http://pirllab.com and <br />
@thermofisher<br />
<br />
Nicole Ramsey @IDnibbler Xolair effective for cannabis allergy in a police officer who was unable to avoid exposure at work. Children with asthma can be allergic to MJ smoked by their parents. This has been proven by basophil activation test in a recent report. Short term mj smoking acts like a bronchodilator (such as albuterol) but long term effects are more obstructive or COPD-like. No sig change in PFTs or CXR however vs cigarette use. <br />
<br />
E-cigarette use causes significant pulmonary toxicity. Marijuana smoking is actually worse for you than nicotine cigarettes. Vaping and e-cigarette use is increasing nicotine addiction NOT decreasing it, as was originally intended. <br />
<br />
Since recreational use was legalized in CO, mj use remained the same and alcohol and cigarette use has decreased. <br />
<br />
LTP syndrome can be seen associated with MJ exposure. Kiwi banana avocado are also implicated in OAS. <br />
<br />
Atoosa Kourosh @AllergyHealth: We are seeing more allergic reactions to marijuana products. Several Allergens identified in Cannabis thus far but reaction to Can S 3 may be predictive of systemic reaction and plant food syndrome to peach, peanut, apple. Important to distinguish between symptoms of cannabis ingestion and allergic reaction. <br />
<br />
Nicole Ramsey @IDnibbler: Important point for allergists skin testing marijuana in states where it is recreationally legal. It is still federally illegal so could cause issues with your institution. <div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-9089760956738637272020-07-23T08:00:00.000-04:002020-07-23T08:00:02.462-04:00Primary Immunodeficiency Disease (PIDD) (#ACAAI19 Twitter summary)Dr Alexei Gonzalez @alexeigonzmd: ESID data: between 5-66% of patients with CVID will develop Lund disease; 1/4 will have ILD.<br />
<br />
GLILD has three pathologic patterns: granulomas, lymphocytic interstitial pneumonitis, and follicular bronchiolitis. GLILD future treatment: RTX x 4 cycles followed by 18 months of AZA or MMF. GLILD: steroids are 50% ineffective - consider dual immunosuppressive therapy. <br />
<br />
Sasha Alvarado, DO @sashaaalvarado: Elena Perez, MD: <b>29% of patients with CVID have autoimmune manifestations.</b><br />
<br />
Lisa Forbes, MD: Whole exome sequencing is preferred, but commercial labs offer accessible PID panels, and there are many experts who are happy to collaborate with private practitioners on variants of unknown significance. <br />
<br /><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-52499455384105501372020-07-22T08:00:00.000-04:002020-07-22T08:00:02.071-04:00Case Simulation for the Education on Anaphylaxis Management (#ACAAI19 Twitter summary)<br />
Dr. Ellis @DrAnneEllis: Gearing up to moderate/facilitate my new favourite workshop "Hands On - The use of Case Simulation for the Education of Allergic Emergencies - Spotlight on Anaphylaxis".<br />
<br />
Simulation for Anaphylaxis Management is a tremendous tool. Studies has shown simulation to be more effective than classroom training and increases closed loop communication, teamwork skills, confidence in managing life-threatening events. <br />
<br />
Direct observations of simulated emergencies allows detection of critical errors with risk of real harm to a real patient. <br />
<br />
Technicians with high fidelity simulators can be the "voice of the patient". Cyanosis, wheezing, rashes can emerge on the mannequin. <br />
<br />
In one study - only half of trainees in an internal medicine program going through a simulation scenario of anaphylaxis recognized the diagnosis, only half of those gave epinephrine. <br />
<br />
In another study, epinephrine dosing errors were noted in 46 - 94% of participants. <br />
<br />
<a href="https://twitter.com/MDMagazine/status/1193253170996056064">https://twitter.com/MDMagazine/status/1193253170996056064</a><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-78440696864608718692020-07-21T07:30:00.000-04:002020-07-21T07:30:05.998-04:00Food challenges in infants (#ACAAI19 Twitter summary)Dr. Ellis @DrAnneEllis Dr. Justin Greiwe - Best practices for oral food challenges on infants - which patients and when?<br />
<br />
<b>Food allergy is a family disease, not an individual problem. </b><br />
<br />
Huge social and psychological consequences to a food allergy diagnosis - some children will be home schooled, not allowed to go to sleep overs or birthday parties, avoid airplanes/sporting events. So we have to get this diagnosis right! Oral food challenges are the Gold standard for diagnosing food allergy - they are underutilized in clinical practice, unfortunately.<br />
<br />
Why perform an oral food challenge?<br />
Make the diagnosis<br />
Monitor for resolution<br />
Assess the status of tolerance to cross-reactive foods<br />
Relieve parental or patient anxiety<br />
Determine if patient is a candidate for oral immunotherapy<br />
<br />
The Ultimate Goal is to accurately identify patients who will benefit from oral food challenge - it does require ingestion of a meal-sized portion of tested food prepared in usual state.<br />
<br />
Kevin Parks MD @kparksmd Dr Greiwe: a test does not define allergy. We've heard this so many times yet clinical decision-making hasn't caught up... history + exam + tests = data needed to assess food allergy.<br />
<br />
Carina Venter PhD RD @VenterCarina No need to avoid food allergens during pregnancy or lactation for prevention. <br />
<br />
Dr. Ellis @DrAnneEllis Testing via skin prick test or in vitro tests have advantages and pitfalls<br />
IgE to Ara H2 is a strong predictor of peanut allergy. High IgE levels of Gal d1 and Bos d8 associated with more persist allergy to egg and milk, respectively. Skin prick testing to food has a high negative predictive value but overall positive predictive challenge of only ~50%. <br />
<br />
Many factors can affect the accuracy of a specific IgE - clear history of previous reaction - if IgE 0.36 to 2 kU/L, 44% of patients passed a challenge despite that history. <br />
<br />
Younger age important -lower levels of allergen specific IgE have increased clinical relevance in young children - having concomitant environmental allergy can artificially drive up the food specific IgE level. <br />
<br />
A survey of US allergist showed that 92% of practitioner felt there was a need to perform OFC in their practice, but a minority actually did them. <br />
<br />
ACGME requirements now dictate that Allergy Fellows in Training need to participate in a minimum of 5 oral food challenges. <br />
<br />
Late phase and biphasic anaphylactic reactions very rare following oral food challenge - my editorial opinion is because of the rapid administration of epinephrine at the first sign of concerns anaphylaxis symptoms during an OFC. <br />
<br />
RDN @PeanutFarmers @PeanutRD And Dr. Greenhawt mentioned yesterday that quality of life improves regardless of whether individual passes or does not pass the oral food challenge. <br />
<br />
Kevin Parks MD @kparksmd Broad panel in vitro food-specific IgE tests are NEVER a good idea! <br />
<br />
In survey of allergists the 3 top reasons OFC's are not performed were lack of time, lack of staff, and lack of office space - not safety.<br />
<br />
Dr. Ellis @DrAnneEllis Issues unique to infant challenges:<br />
Appropriate portion sizes for age<br />
Appropriate vehicles/food forms<br />
Mixing vehicles infant has previously tolerate<br />
Allow ample time to feed!!<br />
<br />
Subtle clues for infant reactions - ear picking, tongue rubbing, putting hand in mouth more than usual, neck scratching, change in general demeanor (quiet/withdrawn, clingy, fussy).<br />
<br />
Stopping Criteria for OFC have been published. Don't be a cowboy, known when to quit. <br />
<br />
Critical to do an oral challenge before enrolling someone on oral immunotherapy. Don't go through the burden of OIT if the disease isn't there.<br />
<br />
Katherine Anagnostou @PedAllergyDoc <b>As food OIT develops there will be a high need and demand for oral food challenges. </b><br />
<br />
Dr. Ellis @DrAnneEllis Exacerbations of skin disease related to food do exist, but nowhere near as commonly as patients/public believe.<br />
<br />
Use the failed oral food challenge as a teaching point both during and after the reaction - our responsibility as allergists to reduce anxiety and fear - instill healthy respect for food without crippling parent and children. Instill Confidence not Fear in our food allergy patients - Empowerment not Despair. Ensure that food allergy does not define the patient. <br />
<br />
Kevin Parks MD @kparksmd Primary teaching points for families with food allergy: confidence rather than fear, empowerment rather than despair. Lowering the psychosocial cost of food allergy should be a primary goal. Passing a food challenge should be followed by including the food in the child's diet. Recent data suggests they don't. Follow up is key. <br />
<br />
Dr. Ellis @DrAnneEllis Dr. Benjamin Prince now discussing Practical Aspects of Infant (and toddler) oral food challenges.<br />
<br />
Oral food challenges are a necessary procedure for any allergist who is going to be diagnosing food allergy.<br />
<br />
Sometimes getting the patient to eat can be the most difficult and frustrating part of the challenge. <br />
<br />
The good news about infant OFCS- most reactions are mild and cutaneous, only a few cases have required epinephrine in the RCTs. <br />
<br />
Before you begin - counsel the family on how to prepare and what to expect - review what medications to stop and more importantly which ones not to stop (Asthma meds!). Send a written reminder prior to the day of challenge; reschedule if the child appears to be getting sick. Obtain written informed consent on the day of the oral food challenge.<br />
<br />
Pre-draw up the medications that may be needed to treat a reaction; obtain baseline weight, vital signs and detailed physical exam.<br />
<br />
A 5 yr retrospective chart review of children seen for peanut allergy who had 2 different skin prick tests at two different times - 2mm difference on average after 5 to 8 months (got bigger).<br />
<br />
Important to consider both protein content and total volume of food. Protein content should mirror a normal meal sized portion.<br />
<br />
Initial dose is usually base on overall risk of reaction - lower risk 5-10% of total dose, higher risk -0.1-1% of total dose.<br />
<br />
<b>Most clinic oral food challenges involve 4 to 6 doses;</b> consider more gradual initial doses in patients planning on undergoing OIT later. <br />
<br />
How much time between doses? typically 10 to 30 min - shorter time for lower SPT/sIgE, longer time with higher SPT/sIgE, history of wheeze/asthma or past severe reaction. <br />
<br />
For the non-verbal patient it is critical to perform a good baseline physical exam and vitals.<br />
<br />
Tips for feeding infants and toddlers - Vehicles are EXTREMELY important - applesauce, pudding, yogurt, ice cream, juices, baby food often successful. Encourage the family to bring favorite foods that can be combined with the challenge food. Encourage the family to try foods with similar textures at home prior to the challenge (e.g. the muffin for a baked egg or milk challenge without the egg or milk).<br />
<br />
Minimize skin contact with food as much as possible.<br />
<br />
Provide several food options at one time - a Bamba stick, a serving of peanut butter and a Reese's pieces to choose from, for example. Nut butters are the best way to do tree nut challenge as that's the source with the highest amount of protein compared to nutella for e.g. or almond milk for e.g. <br />
<br />
Kevin Parks MD @kparksmd Feeling less like a loser allergist after this talk. Lots of kids who pass food challenge/have negative SPT/sIgE tests, green light to reintroduce the food at home, they come back a year later having NOT eaten the food! Good to hear the FA experts fight the same battle.<br />
<br />
Dr. Ellis @DrAnneEllis Its why it's now 'part of the deal'. If the patient doesn't promise to eat the food after the challenge, I won't offer it. My 2 yr wait list for the oral challenges can't allow for this to happen.<br />
<br />
Dr. Ellis @DrAnneEllis now Dr. Jay Lieberman - Prevention and Management of Infant Anaphylaxis. Foods are clearly the most common trigger for infant anaphylaxis. Food triggers in infants may vary by country/region - Peanut most common in Tennessee, whereas as Milk most common in Massachusetts. <br />
<br />
If we are to prevent food induced anaphylaxis we must do our best to prevent food allergy - the Addendum guidelines for early introduction of peanut based on results from the LEAP trial are well known. There will be reactions in the low risk population. Not a lot - but they will happen. LEAP doesn't prevent ALL peanut allergy, just significantly reduces the risk. <br />
<br />
Kevin Parks MD @kparksmd Lieberman: infant food challenges are annoying, "they suck", but we have to own them. It's our deal. <br />
<br />
KristinSokolMD @kristinkrasnow If we are not doing oral food challenges, even in our infant patients, we are doing a disservice to our patients. - Dr. Leiberman.<br />
<br />
Dr. Ellis @DrAnneEllis There is universal agreement that epinephrine is the first line therapy for anaphylaxis in infants. Dose is 0.01mg/kg (as will any other age group). One of the challenges of using an epinephrine autoinjector in an infant, however, is that they may be at risk for an intraosseous injection based on the needle length from ultrasound study.<br />
<br />
Very important to hold the child still when administering an epinephrine auto injector - grasp the thigh firmly to avoid lacerations , pinch up the skin to ensure intramuscular injection. Remember dosing of epinephrine is weight based not age based! <br />
<br />
Kevin Parks MD @kparksmd currently available 0.15mg epi AI's (US market) may hit bone in nearly 1/2 of infants based on skin-to-bone distance. We don't know the physiologic effects of intraosseous injection of epi vs IM or SC.<br />
<br />
Dr. Ellis @DrAnneEllis Consider rephrasing a "failed" oral challenge as a "B+" - look what you WERE able to eat, not focusing on that the entire amount of food was not eaten. <br />
<br />
Before you order any test for food allergy - ask your self (and the parents!) what you are going to do with the information. False positive tests are common. Greenhawt now doesn't allow parents to make their own muffins for baked challenges to ensure no cross-contamination with other food allergens.<br />
<br />
No other specialty owns food allergy, drug allergy or anaphylaxis. We owe it to our patients to do the best for their allergic needs!<div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-13031535844650375092020-07-20T07:00:00.000-04:002020-07-20T07:00:06.245-04:00Asthma (#ACAAI19 Twitter summary)Dr. Ellis @DrAnneEllis Professor Stephen Holgate - Asthma - Inflammation is the Symptom not the Cause. <br />
<br />
Epithelial injury and airway remodeling are a common feature of even mild asthma. <br />
<br />
Beyond allergen exposure, there are many other environmental factors contributing to airway inflammation in asthma - air pollution (especially diesel exhaust) tops the list. Air pollution now accepted as a causal factor in asthma development, symptoms and mortality. Ambient black carbon particles reach the fetal side of the human placenta. <br />
<br />
Holgate: the <b>asthmatic epithelium behaves like a non-healing wound. </b><br />
<br />
Gene signatures from the airways of "wheezers" vs non atopic control show predominant presence of Type 2 inflammation pathways as well as repair molecules. <br />
<br />
Targeting alarmins such as TSLP, IL25 and 33 may be the future as you are striking at the "top of the chain" rather than all the downstream effects. <br />
<br />
Kevin Parks MD @kparksmd Stephen Holgate MD on asthma: the airway epithelium is damaged by irritants, infections, and allergens - suggesting that epithelial targets may be a more optimistic therapeutic paradigm in asthma. Holgate making a good case for epithelium as a cause. <br />
<br />
Dr. Ellis @DrAnneEllis Starting off the day with my favorite speaker ever. Dr. Paul O'Byrne - Dean of <br />
@MacHealthSci and asthma expert and scholar and gentleman!<br />
<br />
Drs Hurd and Lenfant founded GINA - 25 years ago- A strategy document, not a guideline - meant to be used anywhere in the world.<br />
<br />
GINA describes the <b>control-based asthma management cycle - Diagnosis first - must confirm it is actually asthma one is trying to treat. </b><br />
<br />
GINA describes asthma management from Step 1 to 5 - Step 1 and 2 are the biggest group of patients who can/should be managed by primary care.<br />
<br />
The biggest problem with Asthma management? <b>Despite the safety of inhaled corticosteroids, adherence to therapy is abysmal - 40% of patients in one study never filled more than one refill </b>of the ICS/LABA there were given. <br />
<br />
Short acting beta agonists (SABAs) are the most widely used asthma medication worldwide - despite the fact that <b>SABAs have been shown to worsen asthma control, enhance EIB, promote airway inflammation and overuse is associated with increased mortality. </b><br />
<br />
SYMGA trials, published in @NEJM aimed to show the efficacy and safety of using an ICS paired with a fast acting LABA - to be used on an add needed basis.<br />
<br />
Regular use of budesonide led to more well controlled asthma weeks compared to PRN Symbicort - but adherence in the trial was 80% - not real world experience. No difference in exacerbations between PRN Symbicort and regular budesonide. More important finding IMO!<br />
<br />
Michael R. Rupp, MD @Docallergy Study showed that<b> at 1 year patients with moderate asthma less than 10% filled Rx as directed</b>. ADHERENCE IS KEY! <br />
<br />
Dr. Ellis @DrAnneEllis Benefit in Asthma exacerbation risk for PRN Symbicort was seen with an 83% reduction in steroid exposure.<br />
<br />
Patients in SYGMA 1 used, typically, 1 dose of reliever every 2 weeks - almost no one used the maximum 8 inhalations per day. Not a single patient who used 8 inhalations of Symbicort per day went on to have a severe exacerbation compared to 9% of patients using the same amount of SABA. <br />
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The PRACTICAL study from New Zealand completely mirrored the results of the SYGMA2 Study (but was government funded rather than via @AstraZenecaCA). Exacerbations were significantly reduced by PRN Symbicort. <br />
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These trials led to GINA making one of the largest changes in their recommendations. <b>As needed low dose ICS/formoterol now the prefered reliever medication for asthma - across all Steps</b> - not just mild/moderate. <br />
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Implications for practice - Adherence to maintenance therapy is poor, overuse of SABAs worsen most asthma outcomes, <b>Symbicort 80 mcg reliever therapy that contains an ICS is superior to SABAs for all asthma outcomes</b>. Off label in USA. <br />
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Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-75292053471220891612020-07-19T07:00:00.000-04:002020-07-19T07:00:03.632-04:00Alpha-gal Food allergy (#ACAAI19 Twitter summary)Dr. Ellis @DrAnneEllis Pork kidney allergy is driven by alpha-gal allergy. Co-authors such as exercise needed to elicit reactions.<br />
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Jason K Lee @lee_jasonk <b>19% of Forrest workers and hunters have alpha gal IgE</b>, not all react clinically. <br />
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Dr. Dave Stukus @AllergyKidsDoc Fascinating story about ‘red meat’ allergy at #ACAAI19. Different than traditional food allergy:<br />
-Delayed onset hours later<br />
-Caused by sugar (alpha-gal) not protein<br />
-Most people not allergic to other foods<br />
-Sensitization caused by lone star tick bite<br />
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Kevin Parks MD @kparksmd dose response relationship between tick exposure and reactivity. more tick bites = increased likelihood of alpha-gal allergy. NOT just caused by Lone Star tick (as was originally thought based on the geography of initial cases).<br />
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Dr. Ellis @DrAnneEllis while the Lone Star tick is what we in North America associate with a cause of alpha gal allergy, many different ticks world wide have been associated. Amblyomma testudarium tick bites associated with alpha gal sensitization, for example. <br />
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Jason K Lee @lee_jasonk The antigen in alpha gal maybe an inherent tick protein and not from external. There is boosting of igE if bitten repeatedly by ticks. Waning of igE over time. May not need to avoid meat all the time with alpha gal. Possible desensitization can occur (case report level evidence). <br />
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Kevin Parks MD @kparksmd Recurrent tick bites boost alpha-gal reactivity. Avoiding ticks categorically can result in loss of sensitization, and tolerance to beef, pork, lamb. <div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-2057269305378114997.post-83466601176577647062020-07-18T07:00:00.000-04:002020-07-18T07:00:06.606-04:00Eosinophilic esophagitis (#ACAAI19 Twitter summary)Kevin Parks MD @kparksmd Presidential Plenary at #ACAAI19 Matt Rank MD on EoE: how long do we continue topical glucocorticoids in responders? Very low quality of evidence, but the committee recommends continuing treatment in responders. In our Oregon experience, adherence is low in responders.<br />
Dr Rank: <b>very few studies compare TCS vs PPI in EoE. In the 2 trials that attempt to address this, no significant difference in outcomes between the treatement groups</b> were observed<b>. </b>No comment yet about the value of PPI as a steroid-sparing strategy (but I bet he'll address it). <br />
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Gerald Lee MD @DrGerryLee @MatthewRankMD presents a forest plot of the response of EoE to PPI - very heterogeneous, leading to the conditional recommendation of PPI. <b>Biomarkers are sorely needed to predict response to therapy, especially since biopsy is how efficacy is measured!</b><div class="blogger-post-footer"><p> </p>
Posted at <a href="http://allergynotes.blogspot.com/">Allergy Notes</a>. Stay updated and <a href="http://feeds.feedburner.com/AllergyNotes">subscribe</a>, follow us on <a href="http://twitter.com/Allergy">Twitter</a> and connect on <a href="http://www.facebook.com/AllergyNotes">Facebook</a>.</div>Unknownnoreply@blogger.com0