Allergic Reactions After Vaccination: Translating Guidelines Into Clinical Practice
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Early-Phase GVHD Gene Expression Profile in Target Versus Non
Bone Marrow Transplantation (2013) 48, 284–293 & 2013 Macmillan Publishers Limited All rights reserved 0268-3369/13 www.nature.com/bmt ORIGINAL ARTICLE Early-phase GVHD gene expression profile in target versus non-target tissues: kidney, a possible target? B Sadeghi1, H Al-Chaqmaqchi1, S Al-Hashmi1, D Brodin2, Z Hassan1,3, M Abedi-Valugerdi4, A Moshfegh5 and M Hassan1,3 GVHD is a major complication after allo-SCT. In GVHD, some tissues like liver, intestine and skin are infiltrated by donor T cells while others like muscle are not. The mechanism underlying targeted tropism of donor T cells is not fully understood. In the present study, we aim to explore differences in gene expression profile among target versus non-target tissues in a mouse model of GVHD based on chemotherapy conditioning. Expression levels of JAK–signal transducers and activators of transcription (STAT), CXCL1, ICAM1 and STAT3 were increased in the liver and remained unchanged (or decreased) in the muscle and kidney after conditioning. At the start of GVHD the expression levels of CXCL9, ITGb2, SAA3, MARCO, TLR and VCAM1 were significantly higher in the liver or kidney compared with the muscle of GVHD animals. Moreover, biological processes of inflammatory reactions, leukocyte migration, response to bacterium and chemotaxis followed the same pattern. Our data show that both chemotherapy and allogenicity exclusively induce expression of inflammatory genes in target tissues. Moreover, gene expression profile and histopathological findings in the kidney are similar to those observed in the liver of GVHD mice. Bone Marrow Transplantation (2013) 48, 284–293; doi:10.1038/bmt.2012.120; published online 23 July 2012 Keywords: gene expression; GVHD; kidney; target tissues; mouse model INTRODUCTION none of these reports describe any changes in gene expression Allo-SCT is the treatment of choice for a variety of malignant and profile of non-target tissues like muscle. -
Drug Allergies: an Epidemic of Over-Diagnosis
Drug Allergies: An Epidemic of Over-diagnosis Donald D. Stevenson MD Senior Consultant Div of Allergy, Asthma and Immunology Scripps Clinic Learning objectives • Classification of drug induced adverse reactions vs hypersensitivity reactions • Patient reports of drug induced reactions grossly overstate the true prevalence • The 2 most commonly recorded drug “allergies”: NSAIDs and Penicillin • Accurate diagnoses of drug allergies • Consequences of falsely identifying a drug as causing allergic reactions Classification of Drug Associated Events • Type A: Events occur in most normal humans, given sufficient dose and duration of therapy (85-90%) – Overdose Barbiturates, morphine, cocaine, Tylenol – Side effects ASA in high enough doses induces tinnitus – Indirect effects Alteration of microbiota (antibiotics) – Drug interactions Increased blood levels digoxin (Erythromycin) • Type B: Drug reactions are restricted to a small subset of the general population (10-15%) where patients respond abnormally to pharmacologic doses of the drug – Intolerance: Gastritis sometimes bleeding from NSAIDs – Hypersensitivity: Non-immune mediated (NSAIDs, RCM) – Hypersensitivity: Immune mediated (NSAIDs, Penicillins ) Celik G, Pichler WJ, Adkinson Jr NF Drug Allergy Chap 68 Middleton’s Allergy: Principles and Practice, 7th Ed, Elsevier Inc. 2009; pg 1206 1206. Immunopathologic (Allergic) reactions to drugs (antigens): Sensitization followed by re-exposure to same drug antigen triggering reaction Type I Immediate Hypersensitivity IgE Mediated Skin testing followed -
Allergy, Hypersensitivity, Angioedema, and Anaphylaxis Episode Overview
CrackCast Show Notes –Allergy and Anaphylaxis – October 2017 www.canadiem.org/crackcast Chapter 109 – Allergy, Hypersensitivity, Angioedema, and Anaphylaxis Episode Overview Key Points: 1. A history of sudden urticarial rash accompanied by respiratory difficulty, abdominal pain, or hypotension, strongly favors the diagnosis of anaphylaxis. 2. Epinephrine is the first-line treatment in patients with anaphylaxis: give it immediately. 3. There are no absolute contraindications to the use of epinephrine in the setting of anaphylaxis. 4. Antihistamines and corticosteroids are second- and third-line agents in the management of anaphylaxis and should not replace or precede epinephrine. 5. Consider prolonged observation or admission for patients who: a. Experience protracted anaphylaxis, hypotension, or airway involvement; b. Receive IV epinephrine or more than two doses of IM epinephrine; c. Or have poor outpatient social support. 6. Patients discharged after an anaphylactic event should be prescribed an EpiPen and instructed on its use. 7. Patients with refractory hypotension may require glucagon (receiving beta-blockage) or a continuous IV epinephrine infusion. 8. Non-histaminergic angioedema (non-allergic angioedema) does not typically respond to epinephrine and antihistamines. New drugs, including berinert, icatibant, ecallantide, and Ruconest have been approved for use in HAE. FFP has been used with varying success in HAE, ACID, and ACE inhibitor–induced angioedema. NOTE: ACID: acquired C1 esterase deficiency (ACED) Core Questions: 1. List the four types of Gell and Coombs classifications of immune reaction and give examples of each 2. List four etiologic agents causing anaphylaxis by immunologic mechanisms 3. List six mediators of anaphylaxis and their physiologic actions and clinical manifestations 4. -
Hypersensitivity Reactions (Types I, II, III, IV)
Hypersensitivity Reactions (Types I, II, III, IV) April 15, 2009 Inflammatory response - local, eliminates antigen without extensively damaging the host’s tissue. Hypersensitivity - immune & inflammatory responses that are harmful to the host (von Pirquet, 1906) - Type I Produce effector molecules Capable of ingesting foreign Particles Association with parasite infection Modified from Abbas, Lichtman & Pillai, Table 19-1 Type I hypersensitivity response IgE VH V L Cε1 CL Binds to mast cell Normal serum level = 0.0003 mg/ml Binds Fc region of IgE Link Intracellular signal trans. Initiation of degranulation Larche et al. Nat. Rev. Immunol 6:761-771, 2006 Abbas, Lichtman & Pillai,19-8 Factors in the development of allergic diseases • Geographical distribution • Environmental factors - climate, air pollution, socioeconomic status • Genetic risk factors • “Hygiene hypothesis” – Older siblings, day care – Exposure to certain foods, farm animals – Exposure to antibiotics during infancy • Cytokine milieu Adapted from Bach, JF. N Engl J Med 347:911, 2002. Upham & Holt. Curr Opin Allergy Clin Immunol 5:167, 2005 Also: Papadopoulos and Kalobatsou. Curr Op Allergy Clin Immunol 7:91-95, 2007 IgE-mediated diseases in humans • Systemic (anaphylactic shock) •Asthma – Classification by immunopathological phenotype can be used to determine management strategies • Hay fever (allergic rhinitis) • Allergic conjunctivitis • Skin reactions • Food allergies Diseases in Humans (I) • Systemic anaphylaxis - potentially fatal - due to food ingestion (eggs, shellfish, -
Arthus Reaction
The Journal of Emergency Medicine, Vol. 56, No. 4, pp. 450–451, 2019 Ó 2018 Elsevier Inc. All rights reserved. 0736-4679/$ - see front matter https://doi.org/10.1016/j.jemermed.2018.12.047 Visual Diagnosis in Emergency Medicine ARTHUS REACTION Mei-Hua Wang, RN,* Alvin Hu,† Yei-Soon Lee, MD,* and Chih-Cheng Lai, MD‡ *Department of Emergency Department, Chi Mei Medical Center, Liouying, Taiwan, †Poznan University of Medical Sciences, Poznan, Poland, and ‡Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Taiwan Reprint Address: Chih-Cheng Lai, MD, Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan CASE REPORT 0–4%), respectively, and a C-reactive protein level of 9.1 mg/L. Blood culture was collected but showed no bac- A 6-year-old boy presented to the emergency department terial growth. Physical examination showed an erythem- (ED) with fever and skin rash (Figure 1) over his left atous skin rash with swelling and severe pain over the thigh. He had just received a combination vaccine with vaccination site. Acetaminophen was given for pain relief diphtheria, tetanus, pertussis, and poliomyelitis (DTaP- and fever. Steroid (methylprednisolone 20 mg every 8 h) IPV) on his left thigh 12 h prior to his visit to the ED. and an antihistamine (cyproheptadine 2 mg three times a His vital signs were body temperature of 36.6C, respira- day) were prescribed for suspected allergic reaction. Af- tory rate of 20 breaths/min, blood pressure of 104/83 mm ter treatment, the fever subsided and the painful swelling Hg, and heart rate of 100 beats/min. -
Reaction by Staphylococcal Protein a Cell Superantigen: Elicitation of An
In Vivo Inflammatory Response to a Prototypic B Cell Superantigen: Elicitation of an Arthus Reaction by Staphylococcal Protein A This information is current as Lisa M. Kozlowski, Weiping Li, Michael Goldschmidt and Arnold of October 1, 2021. I. Levinson J Immunol 1998; 160:5246-5252; ; http://www.jimmunol.org/content/160/11/5246 Downloaded from References This article cites 50 articles, 28 of which you can access for free at: http://www.jimmunol.org/content/160/11/5246.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on October 1, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 1998 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. In Vivo Inflammatory Response to a Prototypic B Cell Superantigen: Elicitation of an Arthus Reaction by Staphylococcal Protein A1 Lisa M. Kozlowski,2* Weiping Li,* Michael Goldschmidt,† and Arnold I. Levinson3* Staphylococcal protein A (SpA) is representative of a new class of Ags, the B cell superantigens (SAgs). -
Prevalence and Impact of Reported Drug Allergies Among Rheumatology Patients
diagnostics Article Prevalence and Impact of Reported Drug Allergies among Rheumatology Patients Shirley Chiu Wai Chan , Winnie Wan Yin Yeung, Jane Chi Yan Wong, Ernest Sing Hong Chui, Matthew Shing Him Lee, Ho Yin Chung, Tommy Tsang Cheung, Chak Sing Lau and Philip Hei Li * Division of Rheumatology and Clinical Immunology, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong; [email protected] (S.C.W.C.); [email protected] (W.W.Y.Y.); [email protected] (J.C.Y.W.); [email protected] (E.S.H.C.); [email protected] (M.S.H.L.); [email protected] (H.Y.C.); [email protected] (T.T.C.); [email protected] (C.S.L.) * Correspondence: [email protected]; Tel.: +852-2255-3348 Received: 28 October 2020; Accepted: 7 November 2020; Published: 9 November 2020 Abstract: Background: Drug allergies (DA) are immunologically mediated adverse drug reactions and their manifestations depend on a variety of drug- and patient-specific factors. The dysregulated immune system underpinning rheumatological diseases may also lead to an increase in hypersensitivity reactions, including DA. The higher prevalence of reported DA, especially anti-microbials, also restricts the medication repertoire for these already immunocompromised patients. However, few studies have examined the prevalence and impact of reported DA in this group of patients. Methods: Patients with a diagnosis of rheumatoid arthritis (RA), spondyloarthritis (SpA), or systemic lupus erythematosus (SLE) were recruited from the rheumatology clinics in a tertiary referral hospital between 2018 and 2019. Prevalence and clinical outcomes of reported DA among different rheumatological diseases were calculated and compared to a cohort of hospitalized non-rheumatology patients within the same period. -
COVID-19 Vaccine and Allergy
COVID Vaccine and Allergy Stephanie Leonard, MD Associate Clinical Professor Department of Pediatric Allergy & Immunology January 20, 2020 Safe and Impactful • Proper Screening COVID Vaccine • Monitoring Administration • Clinical Assessment • Vaccine Adverse Event Reporting System (VAERS) detected 21 cases of anaphylaxis after administration of a reported 1,893,360 first doses of the Pfizer-BioNTech COVID-19 vaccine • 11.1 cases per million doses (0.001%) • 1.3 cases per million for flu vaccines • 71% occurred within 15 min of vaccination, 86% within 30 minutes • Range = 2–150 minutes • Of 20 with follow-up info, all had recovered or been discharged home. • 17 (81%) with h/o allergies to food, vaccine, medication, venom, contrast, or pets. • 4 with no h/o any allergies • 7 with h/o anaphylaxis • Rabies vaccine • Flu vaccine • 19 (90%) diffuse rash or generalized hives Allergic Reactions Including Anaphylaxis After Receipt of the First Dose of Pfizer-BioNTech COVID-19 Vaccine — United States, December 14–23, 2020. MMWR Morb Mortal Wkly Rep 2021;70:46–51. Early Signs of Anaphylaxis • Respiratory: sensation of throat closing*, stridor, shortness of breath, wheeze, cough • Gastrointestinal: nausea*, vomiting, diarrhea, abdominal pain • Cardiovascular: dizziness*, fainting, tachycardia, hypotension • Skin/mucosal: generalized hives, itching, or swelling of lips, face, throat *these can be subjective and overlap with anxiety or vasovagal syndrome Labs that can help assess for anaphylaxis • Tryptase, serum (red top tube) • C5b-9 terminal complement complex Level, serum (SC5B9) (lavender top EDTA tube) Emergency Supplies Management of anaphylaxis at a COVID-19 vaccination site • If anaphylaxis is suspected, take the following steps: • Rapidly assess airway, breathing, circulation, and mentation (mental activity). -
Unlocking the Non-Ige-Mediated Pseudo-Allergic Reaction Puzzle with Mas-Related G-Protein Coupled Receptor Member X2 (MRGPRX2)
cells Review Unlocking the Non-IgE-Mediated Pseudo-Allergic Reaction Puzzle with Mas-Related G-Protein Coupled Receptor Member X2 (MRGPRX2) Mukesh Kumar, Karthi Duraisamy and Billy-Kwok-Chong Chow * School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Hong Kong, China; [email protected] (M.K.); [email protected] (K.D.) * Correspondence: [email protected]; Tel.: +852-2299-0850; Fax: +852-2559-9114 Abstract: Mas-related G-protein coupled receptor member X2 (MRGPRX2) is a class A GPCR ex- pressed on mast cells. Mast cells are granulated tissue-resident cells known for host cell response, allergic response, and vascular homeostasis. Immunoglobulin E receptor (Fc"RI)-mediated mast cell activation is a well-studied and recognized mechanism of allergy and hypersensitivity reac- tions. However, non-IgE-mediated mast cell activation is less explored and is not well recognized. After decades of uncertainty, MRGPRX2 was discovered as the receptor responsible for non-IgE- mediated mast cells activation. The puzzle of non-IgE-mediated pseudo-allergic reaction is unlocked by MRGPRX2, evidenced by a plethora of reported endogenous and exogenous MRGPRX2 ag- onists. MRGPRX2 is exclusively expressed on mast cells and exhibits varying affinity for many molecules such as antimicrobial host defense peptides, neuropeptides, and even US Food and Drug Administration-approved drugs. The discovery of MRGPRX2 has changed our understanding of mast cell biology and filled the missing link of the underlying mechanism of drug-induced MC degranulation and pseudo-allergic reactions. These non-canonical characteristics render MRGPRX2 Citation: Kumar, M.; Duraisamy, K.; Chow, B.-K.-C. -
Immunological Exercises.Pdf
Immunological Exercises Short Notes 1. Smallpox and Edward Jenner 2. Humoral Immunity and Cellular Immunity 3. Acquired Immunity 4. 2019-nCoV/SARS-CoV-2, COVID-19 5. Programmed cell death (apoptosis) 6. GALT (Gut-associated lymphoid tissue) 7. MIS (Mucosal lymphoid system) 8. APCs (antigen presenting cells) 9. Epitopes or antigenic determinants 10. T cell and B cell Epitopes 11. Common Ag and Cross Reaction 12. Heterophilic Ag and Autoantigen 13. Hapten 14.TD-Ag and TI-Ag 15. Heterophilic Ag and Autoantigen 16. Immunoglobulin (Ig) and Antibody (Ab) 17. Ig Isotype and Ig Allotype 18. Ig idotype 19. Monoclonal Ab and Polyclonal Ab 20. Neutralization 21. Opsonization 22. CDRs and VH 23. Fab and Fc 24. Noncovalent forces 25. Ig subtypes and sIgA 26. PAMPs/DAMPs (pathogen/danger/damage-associated molecular patterns) 27. PRRs (Pattern-recognition receptors) 28. NKG2D, MIC, KIR KLR 29. TLRs (Toll-like receptors ) 30. Regulatory T cells (Tregs), Tr1, Th3 31. Immunoregulation 32. Central T Cell Tolerance 33. Peripheral tolerance 34. Positive selection and Negative selection 35. Immune tolerance and Dizygotic twin cows 36. CD28 and B7 molecules 37. Activation-induced cell death (AICD) 38. NK cells and T cells 39. DCs and macrophages (Ms) 40. TCR-CD3 complex 1 41. Mature B cells 42. Recombination signal sequence (RSS) 43. MHC restriction 44. GM-CSF and INF- 45. Cytokine storm/cytokine release syndrome (CRS) 46. Affinity maturation 47. ITIM (immunoreceptor tyrosine-based inhibitory motif) and ITAM 48. BCR (B cell receptor) and TCR (T cell receptor) 49. CDRs, complementary-determining regions 50. Monoclonal antibody(mAb) 51. -
About Drug Side-Effects and Allergies
About drug side-effects and allergies Introduction This leaflet has been produced to provide you with information about side-effects of medicines and drug allergies, and the differences between the two. There are a variety of ways in which people can experience adverse reactions to medications, whether prescribed or bought 'over-the-counter'. Most of these effects are not an 'allergy'. Contrary to what most people think, only small amounts (5-10%) of all adverse drug reactions are caused by a drug allergy. It is important to tell the doctor or healthcare professional looking after you about any drug allergies or side-effects to drugs you may have/or had as this may affect your current treatment. It is important to know the difference between a drug allergy and side-effect because saying you have a drug allergy when in fact it is a side-effect may unnecessarily restrict the treatment choices available to treat your condition. What should I be aware of when taking my medicines? Many medicines can cause side-effects e.g. some medicines may affect your sight or co-ordination or make you sleepy, which may affect your ability to drive, perform skilled tasks safely. The information leaflet provided with your medicine will list any side effects which are known to be linked to your medicine. All medications have side-effects because of the way they work. The majority of people get none, or very few, but some people are more prone to them. The most common side-effects are usually nausea, vomiting, diarrhoea (or occasionally constipation), tiredness, rashes, itching, headaches and blurred vision. -
LECTURE: 10 Title: IMMUNOLOGICAL MECHANISM in TISSUE DAMAGE TYPE-III IMMUNE-COMPLEX MEDIATED HYPERSENSITIVITY
LECTURE: 10 Title: IMMUNOLOGICAL MECHANISM IN TISSUE DAMAGE TYPE-III IMMUNE-COMPLEX MEDIATED HYPERSENSITIVITY LEARNING OBJECTIVES: The student should be able to: • Define type III hypersensitivity reactions. • Identify the role of the immune complex in type III reactions, and indicate which cause more damage small or large immune complexes, and locate the possible deposition of each complex. • Compare type III and type I reactions. • List some of the immune complex diseases: - Autoimmune diseases: ♦ Systemic lupus erythematosus (SLE). ♦ Rheumatoid arthritis (RA). ♦ Hyperthyroidism. - Infectious agents: ♦ Infectious mononucleosis. ♦ Meningitis. ♦ Viral hepatitis (Chronic stage). ♦ Poststreptococcal glomerulonephritis. ♦ Streptokinase (bacterial enzymes) in cardiac patients. - Drugs: ♦ Sulfonamides + penicillin. • Determine either type III reactions act locally or systematically. • Explain the mechanism of local immune complex deposition and give one example. • Explain the mechanism of generalized immune complex deposition, and give one example. • Explain the main target organ (s) for type III reactions. • Describe the mechanism of activation of type III reaction. • List a diagnostic method, and some examples of clinical features of type III such as: - Arthus reactions (Local immune complex-deposition). - Serum sickness (Systemic immune complex-deposition). LECTURE REFRENCE: 1. TEXTBOOK: ROITT, BROSTOFF, MALE IMMUNOLOGY. 6th edition. Chapter 23. pp. 357-367. 2. HANDOUT. Hypersensitivity – Type III Immune complexes are formed every time antibody meets antigen and are removed by the mononuclear phagocyte system following complement activation. Persistence of antigen from continued infection or in autoimmune disease can lead to immune-complex disease. Immune complexes can form both in the circulation, leading to systemic disease, and at local sites such as the lung. Complement helps to disrupt antigen-antibody bonds and keeps immune complexes soluble.