CUTANEOUS IMMUNE COMPLEX VASCULITIS, SKIN-LIMITED CUTANEOUS IGA OR IGG/IGM VASCULITIS (Formerly Called: Allergic/Hypersensitivity Vasculitis)
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Apixaban-Induced Cutaneous Hypersensitivity: a Case Series with Evidence of Cross-Reactivity
Volume 26 Number 10| October 2020| Dermatology Online Journal || Letter 26(10):20 Apixaban-induced cutaneous hypersensitivity: a case series with evidence of cross-reactivity Nasro A Isaq1 BS, Whitney M Vinson2 MD, Sahand Rahnama-Moghadam2 MD MS Affiliations: 1Indiana University School of Medicine, Indianapolis, Indiana, USA, 2Department of Dermatology, Indiana University School of Medicine, Indianapolis, Indiana, USA Corresponding Author: Sahand Rahnama-Moghadan MD MS, Department of Dermatology, Indiana University School of Medicine, 545 Barnhill Drive, Emerson Hall 139, Indianapolis, IN 46202, Tel: 317-944-7744, Email: [email protected] Keywords: novel oral anticoagulants (NOACs), apixaban, 2 weeks she developed low-grade fevers, chills, rivaroxaban, drug induced rash, apixaban hypersensitivity nausea, shortness of breath, headaches, and cough. reaction, rivaroxaban cross reactivity, novel oral She was admitted to the hospital where computed anticoagulant induced hypersensitivity reaction, apixaban tomography of the chest demonstrated ground glass induced rash opacities located peripherally within her lungs. Laboratory results showed a decrease in hemoglobin, elevated dsDNA, positive rheumatoid To the Editor: factor, and elevated beta-2 glycoprotein concerning Atrial fibrillation is the most common cardiac arrhythmia affecting more than 2.7 million patients for drug-induced lupus. Her apixaban was held owing to concern for hemorrhage. A in the US [1]. As the population ages, it is predicted bronchoalveolar lavage was performed revealing to affect more than 6-12 million people by 2050 [1]. eosinophilic predominance, suggestive of Patients with atrial fibrillation are at increased risk for eosinophilic pneumonia secondary to a connective thromboembolic events and require anticoagulation therapy to prevent thrombus formation and stroke. tissue disease versus drug reaction. -
Primer the Complement System
View metadata, citation and similar papers at core.ac.uk brought to you by CORE providedMagazine by ElsevierR259 - Publisher Connector vascular permeability and the infection. The second category Primer extravasation of plasma. This is in which there is persistent accompanied by the adhesion of formation of immune complexes is leukocytes to vascular endothelium autoimmune disease, in which, by The complement and their emigration into definition, the antigen is a system surrounding tissue. Complement permanent feature of the host. plays an important part in An understanding of how immune Philip Taylor, Marina inflammation, in helping to recruit complexes cause tissue injury effector cells and in promoting the developed from study of such Botto and Mark Walport killing and clearance of pathogens. diseases in humans and animals, and But complement can be both from the induction of experimental The system of plasma proteins called friend and foe. In some immune complex disease. In these complement was so-named because circumstances the activation of situations, immune complexes were it complements the activity of complement in response to immune shown to cause tissue injury through antibody in the lysis of bacteria. It complexes may cause harm: acutely activation of complement, as opsonin has a central role in host defence in the context of massive (binding to complement receptors on against many micro-organisms and in complement activation occurring in leukocytes) and as the source of the modulation of inflammatory patients with overwhelming Gram- anaphylatoxins (stimulating leukocyte reactions, an activity that has been negative bacterial sepsis, and chemotaxis and degranulation). But illuminated by the study of humans chronically, when an antibody the development of gene-targeted with naturally occurring deficiencies response develops in the context of mice with deficiencies of complement of complement. -
Foundation Block Lecture Three Cell Mediated Immunity
Foundation Block Lecture Five Hypersensitivity Objectives: • To know that hypersensitivity reactions are over and excessive immune responses that can be harmful to body in four different ways • To be familiar with inflammatory processes in type I hypersensitivity reaction that mediates allergic inflammation • To recognize that type II hypersensitivity deals with immune responses against antigens that are integral part of cell membrane and are usually associated with autoimmune disorders • To know that type III hypersensitivity reactions are mediated by immune complexes and cause vasculitis • To describe type IV hypersensitivity is a purely cell mediated immune response associated with chronic inflammation ● Important. ● Extra notes. ● Females notes ● Males notes. What is hypersensitivity? Protective immunity: desirable reaction. Hypersensitivity: undesirable damaging reaction produced by excessive immune reactions. - Undesirable responses can be mediated by: - Antibody binding to antigens (Types I-III). - Cell mediated reaction to chemicals or proteins (Type IV). Types of hypersensitivity: 4 Types of hypersensitivity responses are classified by GEL AND COOMBS (names of scientists) according to the responding mechanisms, NOT the responding antigens: *From 433 team Type I: 1- Also termed as: - Immediate Hypersensitivity. - Allergic reactions. (e.g. asthma and eczema) - Anaphylactic reactions: severe and rapidly progressing systemic forms which can be quickly life threatening. …..............(causes.vasodilation and hypovolemia which causes heart stop then death) 2- Most people will not react to these allergens but some individuals “atopic” respond by producing large amounts of IgE in …........response to those otherwise harmless substances. 3- Non-allergic individuals respond to these allergens by producing IgG antibodies. 4- Features: - Antibody type: IgE - Cellular components: Mast cells, basophiles & eosinophils - Antigens: Also known as allergens ( antigens with low molecular weight & highly soluble). -
Defining Natural Antibodies
PERSPECTIVE published: 26 July 2017 doi: 10.3389/fimmu.2017.00872 Defining Natural Antibodies Nichol E. Holodick1*, Nely Rodríguez-Zhurbenko2 and Ana María Hernández2* 1 Department of Biomedical Sciences, Center for Immunobiology, Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, MI, United States, 2 Natural Antibodies Group, Tumor Immunology Division, Center of Molecular Immunology, Havana, Cuba The traditional definition of natural antibodies (NAbs) states that these antibodies are present prior to the body encountering cognate antigen, providing a first line of defense against infection thereby, allowing time for a specific antibody response to be mounted. The literature has a seemingly common definition of NAbs; however, as our knowledge of antibodies and B cells is refined, re-evaluation of the common definition of NAbs may be required. Defining NAbs becomes important as the function of NAb production is used to define B cell subsets (1) and as these important molecules are shown to play numerous roles in the immune system (Figure 1). Herein, we aim to briefly summarize our current knowledge of NAbs in the context of initiating a discussion within the field of how such an important and multifaceted group of molecules should be defined. Edited by: Keywords: natural antibody, antibodies, natural antibody repertoire, B-1 cells, B cell subsets, B cells Harry W. Schroeder, University of Alabama at Birmingham, United States NATURAL ANTIBODY (NAb) PRODUCING CELLS Reviewed by: Andre M. Vale, Both murine and human NAbs have been discussed in detail since the late 1960s (2, 3); however, Federal University of Rio cells producing NAbs were not identified until 1983 in the murine system (4, 5). -
ANCA--Associated Small-Vessel Vasculitis
ANCA–Associated Small-Vessel Vasculitis ISHAK A. MANSI, M.D., PH.D., ADRIANA OPRAN, M.D., and FRED ROSNER, M.D. Mount Sinai Services at Queens Hospital Center, Jamaica, New York and the Mount Sinai School of Medicine, New York, New York Antineutrophil cytoplasmic antibodies (ANCA)–associated vasculitis is the most common primary sys- temic small-vessel vasculitis to occur in adults. Although the etiology is not always known, the inci- dence of vasculitis is increasing, and the diagnosis and management of patients may be challenging because of its relative infrequency, changing nomenclature, and variability of clinical expression. Advances in clinical management have been achieved during the past few years, and many ongoing studies are pending. Vasculitis may affect the large, medium, or small blood vessels. Small-vessel vas- culitis may be further classified as ANCA-associated or non-ANCA–associated vasculitis. ANCA–asso- ciated small-vessel vasculitis includes microscopic polyangiitis, Wegener’s granulomatosis, Churg- Strauss syndrome, and drug-induced vasculitis. Better definition criteria and advancement in the technologies make these diagnoses increasingly common. Features that may aid in defining the spe- cific type of vasculitic disorder include the type of organ involvement, presence and type of ANCA (myeloperoxidase–ANCA or proteinase 3–ANCA), presence of serum cryoglobulins, and the presence of evidence for granulomatous inflammation. Family physicians should be familiar with this group of vasculitic disorders to reach a prompt diagnosis and initiate treatment to prevent end-organ dam- age. Treatment usually includes corticosteroid and immunosuppressive therapy. (Am Fam Physician 2002;65:1615-20. Copyright© 2002 American Academy of Family Physicians.) asculitis is a process caused These antibodies can be detected with indi- by inflammation of blood rect immunofluorescence microscopy. -
Multiple Myeloma Baseline Immunoglobulin G Level and Pneumococcal Vaccination Antibody Response
Journal of Patient-Centered Research and Reviews Volume 4 Issue 3 Article 5 8-10-2017 Multiple Myeloma Baseline Immunoglobulin G Level and Pneumococcal Vaccination Antibody Response Michael A. Thompson Martin K. Oaks Maharaj Singh Karen M. Michel Michael P. Mullane Husam S. Tarawneh Angi Kraut Kayla J. Hamm Follow this and additional works at: https://aurora.org/jpcrr Part of the Immune System Diseases Commons, Medical Immunology Commons, Neoplasms Commons, Oncology Commons, Public Health Education and Promotion Commons, and the Respiratory Tract Diseases Commons Recommended Citation Thompson MA, Oaks MK, Singh M, Michel KM, Mullane MP, Tarawneh HS, Kraut A, Hamm KJ. Multiple myeloma baseline immunoglobulin G level and pneumococcal vaccination antibody response. J Patient Cent Res Rev. 2017;4:131-5. doi: 10.17294/2330-0698.1453 Published quarterly by Midwest-based health system Advocate Aurora Health and indexed in PubMed Central, the Journal of Patient-Centered Research and Reviews (JPCRR) is an open access, peer-reviewed medical journal focused on disseminating scholarly works devoted to improving patient-centered care practices, health outcomes, and the patient experience. BRIEF REPORT Multiple Myeloma Baseline Immunoglobulin G Level and Pneumococcal Vaccination Antibody Response Michael A. Thompson, MD, PhD,1,3 Martin K. Oaks, PhD,2 Maharaj Singh, PhD,1 Karen M. Michel, BS,1 Michael P. Mullane,3 MD, Husam S. Tarawneh, MD,3 Angi Kraut, RN, BSN, OCN,1 Kayla J. Hamm, BSN3 1Aurora Research Institute, Aurora Health Care, Milwaukee, WI; 2Transplant Research Laboratory, Aurora St. Luke’s Medical Center, Aurora Health Care, Milwaukee, WI; 3Aurora Cancer Care, Aurora Health Care, Milwaukee, WI Abstract Infections are a major cause of morbidity and mortality in multiple myeloma (MM), a cancer of the immune system. -
Immune-Pathophysiology and -Therapy of Childhood Purpura
Egypt J Pediatr Allergy Immunol 2009;7(1):3-13. Review article Immune-pathophysiology and -therapy of childhood purpura Safinaz A Elhabashy Professor of Pediatrics, Ain Shams University, Cairo Childhood purpura - Overview vasculitic disorders present with palpable Purpura (from the Latin, purpura, meaning purpura2. Purpura may be secondary to "purple") is the appearance of red or purple thrombocytopenia, platelet dysfunction, discolorations on the skin that do not blanch on coagulation factor deficiency or vascular defect as applying pressure. They are caused by bleeding shown in table 1. underneath the skin. Purpura measure 0.3-1cm, A thorough history (Table 2) and a careful while petechiae measure less than 3mm and physical examination (Table 3) are critical first ecchymoses greater than 1cm1. The integrity of steps in the evaluation of children with purpura3. the vascular system depends on three interacting When the history and physical examination elements: platelets, plasma coagulation factors suggest the presence of a bleeding disorder, and blood vessels. All three elements are required laboratory screening studies may include a for proper hemostasis, but the pattern of bleeding complete blood count, peripheral blood smear, depends to some extent on the specific defect. In prothrombin time (PT) and activated partial general, platelet disorders manifest petechiae, thromboplastin time (aPTT). With few exceptions, mucosal bleeding (wet purpura) or, rarely, central these studies should identify most hemostatic nervous system bleeding; -
DIFFERENTIAL DIAGNOSIS of Hypersensitivity Vasculitis
HIGHLIGHTS FROM MEDICAL GRAND ROUNDS renal disease also is rare. However, certain types of kidney posure to an exogenous antigen such as a drug, serum, disease are associated with a higher incidence of hyper- toxin, or to an infection. Typically, the onset of vasculitis uricemia and gout, including chronic lead nephropathy, occurs 7 to 10 days after exposure to the antigen. The polycystic disease, amyloidosis, analgesic nephropathy, characteristic rash presents as palpable purpura, although and medullary cystic disease. Hypertension and its ulcers, nodules, bullae, or urticaria also may develop in therapy are associated with an increased incidence of some patients. hyperuricemia and gout. On biopsy, the lesions display polymorphonuclear The management of concurrent marked hyper- leukocytes and associated leukocytoclasis, but the in- uricemia and chronic renal disease is directed to preser- filtrates may be predominantly mononuclear. Im- vation of renal function, blood pressure control, and munofluorescent studies often show deposition of com- reduction of the serum uric acid. Uric acid homeostasis plement and immunoglobulins in vessel walls, and other can be achieved by maintaining urine flow (>2 L/d), techniques may show soluble immune complexes and restricting dietary purines and excessive alcohol, and, if evidence of complement activation; however, these needed, allopurinol in the lowest dose that can main- laboratory findings are neither universal nor necessary for tain a near-normal serum uric acid. Therapy should the diagnosis. start with 50 mg/d and increase in 50-mg increments The clinical course is usually self-limited. Varying until the level is under control. Generally, the dosage is degrees of fever, malaise, and weight loss may occur and 100 mg/d for every 30 cc/min of GFR. -
Suppression of Immune Complex-Induced Inflammation by the Chemotactic Factor Inactivator
Suppression of immune complex-induced inflammation by the chemotactic factor inactivator. K J Johnson, … , T P Anderson, P A Ward J Clin Invest. 1977;59(5):951-958. https://doi.org/10.1172/JCI108717. Research Article Small amounts (10(-10) mol) of purified human chemotactic factor inactivator (CFI) suppress leukocytic infiltration, permeability changes, and hemorrhage associated with acute immune complex-induced injury in rats. The reversed passive dermal Arthus reaction and acute immune complex-induced alveolitis in rats have served as the model systems of inflammation. The mechanism of inhibition does not appear to relate to interference with formation and deposition of immune complexes, or with fixation of complement in vitro or iv vivo. Human CFI inhibits in vitro the chemotactic activity generated in complement-activated rat serum. The inhibitory effects of human CFI are not seen if it is first heat inactivated. The data provide the first direct support for the conclusion that CFI has anti-inflammatory activity. Find the latest version: https://jci.me/108717/pdf Suppression of Immune Complex-Induced Inflammation by the Chemotactic Factor Inactivator KENT J. JOHNSON, THOMAS P. ANDERSON, and PETER A. WARD From the Department of Pathology, University of Connecticut Health Center, Farmington, Connecticut 06032 A B S T RA C T Small amounts (10-10 mol) of purified fested by skin tests (7-10). These observations have human chemotactic factor inactivator (CFI) suppress suggested that CFI is an important regulator of the leukocytic infiltration, permeability changes, and inflammatory response. In this communication direct hemorrhage associated with acute immune complex- evidence is presented to show that purified human CFI induced injury in rats. -
Teledermatology and Common Dermatology Issues in the Hospitalized Patient
Teledermatology and Common Dermatology Issues in the Hospitalized Patient Patricia Meyer, DNP, CRNP, FNP‐BC, AGACNP‐BC, NE‐BC The Rise of Teledermatology Improve Shortage of Ability for dermatology dermatology dermatologist to access providers see more patients • Obtaining a CC, HPI, ROS, Allergies, Med list , PMH, Social and Family Hx • A problem‐focused exam • Digital imaging • Uploading of‐ CC, HPI, ROS, Allergies, Med list , PMH, Social and Family Hx, Physical exam, and digital images via secure computer site • Onsite person to obtain BX if needed Teledermatology What is Involved After Info is Uploaded • Dermatologist will form differential diagnosis • Suggest a work up • Formulate and assessment and plan Teledermatology What is Involved • Medication list, prescription and over‐the‐counter drugs • History of past reactions to drugs or foods, topicals, soaps, detergents • Any recent illness ? Exposure to others with similar s/s • Any concurrent infections, metabolic disorders, or immunocompromise, or hx of History Needed autoimmune issues, hx of CA? • Any note in correlation with medication administration and rash onset? • How was medication administered? • Improvement if medication stopped and symptom reoccurrence if medication restarted? Worrisome • Mucous membrane erosions • Blisters Physical Exam • Nikolsky sign Features and • Confluent erythema symptoms • Angioedema and tongue swelling • Palpable purpura • Skin necrosis • Lymphadenopathy • High fever, dyspnea, or hypotension HJ is a 82 year old male, who was admitted from SNF, due to abd pain. HJ is being treated for diverticulitis with Cipro and Flagyl. Teledermatolgy is consulted due to a “rash.” Per the patient’s RN , “it is unclear if this is a new drug rash”. Upon further review with patient he states that he has had this rash for some time “it is very itchy and often keeps me up at night .” He denies any worsening or improving factors. -
Immunoglobulin M Memory B Cell Decrease in Inflammatory Bowel Disease
European Review for Medical and Pharmacological Sciences 2004; 8: 199-203 Immunoglobulin M memory B cell decrease in inflammatory bowel disease A. DI SABATINO, R. CARSETTI**, M.M. ROSADO**, R. CICCOCIOPPO, P. CAZZOLA, R. MORERA, F.P. TINOZZI*, S. TINOZZI*, G.R. CORAZZA Gastroenterology Unit and *Department of Surgery, IRCCS Policlinico S. Matteo, University of Pavia – Pavia (Italy) **Research Center Ospedale Bambino Gesù – Rome (Italy) Abstract. – Background & Objectives: Abbreviation list Memory B cells represent 30-60% of the B cell pool and can be subdivided in IgM memory and CAI = Clinical activity index switched memory. IgM memory B cells differ from CDAI = Crohn’s disease activity index switched because they express IgM and their fre- quency may vary from 20-50% of the total memo- Ig = Immunoglobulin ry pool. Switched memory express IgG, IgA or IgE and lack surface expression of IgM and IgD. Switched memory B cells derive from the germi- nal centres, whereas IgM memory B cells, which require the spleen for their survival and/or gener- Introduction ation, are involved in the immune response to en- capsulated bacteria. Since infections are one of the most frequent comorbid conditions in inflam- Several studies have focused on the mecha- matory bowel disease, we aimed to verify whether nisms that regulate T cell survival, differenti- IgM memory B cell pool was decreased in ation and activation in inflammatory bowel Crohn’s disease and ulcerative colitis patients. disease1,2, but very little is known about B Patients & Methods: Peripheral blood sam- ples were obtained from 22 Crohn’s disease pa- cells and their function. -
Understanding the Immune System: How It Works
Understanding the Immune System How It Works U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES NATIONAL INSTITUTES OF HEALTH National Institute of Allergy and Infectious Diseases National Cancer Institute Understanding the Immune System How It Works U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES NATIONAL INSTITUTES OF HEALTH National Institute of Allergy and Infectious Diseases National Cancer Institute NIH Publication No. 03-5423 September 2003 www.niaid.nih.gov www.nci.nih.gov Contents 1 Introduction 2 Self and Nonself 3 The Structure of the Immune System 7 Immune Cells and Their Products 19 Mounting an Immune Response 24 Immunity: Natural and Acquired 28 Disorders of the Immune System 34 Immunology and Transplants 36 Immunity and Cancer 39 The Immune System and the Nervous System 40 Frontiers in Immunology 45 Summary 47 Glossary Introduction he immune system is a network of Tcells, tissues*, and organs that work together to defend the body against attacks by “foreign” invaders. These are primarily microbes (germs)—tiny, infection-causing Bacteria: organisms such as bacteria, viruses, streptococci parasites, and fungi. Because the human body provides an ideal environment for many microbes, they try to break in. It is the immune system’s job to keep them out or, failing that, to seek out and destroy them. Virus: When the immune system hits the wrong herpes virus target or is crippled, however, it can unleash a torrent of diseases, including allergy, arthritis, or AIDS. The immune system is amazingly complex. It can recognize and remember millions of Parasite: different enemies, and it can produce schistosome secretions and cells to match up with and wipe out each one of them.