DOCSLIB.ORG

Delayed Hypersensitivity Insystemic Lupus

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Delayed Hypersensitivity Insystemic Lupus Ann Rheum Dis: first published as 10.1136/ard.27.4.311 on 1 July 1968. Downloaded from Ann. rheum. Dis. (1968), 27, 311 DELAYED HYPERSENSITIVITY IN SYSTEMIC LUPUS ERYTHEMATOSUS* BY SIDNEY R. BLOCKt, CHARLES B. GIBBS, MARY BETTY STEVENS, AND LAWRENCE E. SHULMAN From The Connective Tissue Division, Department of Medicine, School of Medicine, The Johns Hopkins Hospital, Baltimore, Maryland Systemic lupus erythematosus (SLE) is a disorder of erythematosus or with rheumatoid arthritis and unusual immunological reactivity in which abnor- controls were challenged with a battery of bacterial malities of both humoural and delayed-type hyper- and fungal antigens and calf thymus DNA. No sensitivity are found. Most characteristic of the evidence for heightened delayed hypersensitivity in disease are the multiple circulating antibodies, patients with SLE was found, even with respect to especially antinuclear factors, which have the DNA. In fact, patients with systemic lupus capacity to react with autologous cellular antigens. demonstrated a significant hyporeactivity to inter- However, the relationship of these serum auto- mediate strength PPD (purified protein derivative of the disease (tuberculin)) which, although unexplained, is of antibodies to the tissue manifestation copyright. remains obscure. practical significance in the management of patients Holman (1960) and Friedman, Bardawil, Merrill, with this disease. and Hanau (1960) described a tuberculin-like response to the intradermal injection of autologous Material and Methods and homologous leucocytes in patients with SLE and, Patients.-Twenty patients with SLE and 23 with less frequently, rheumatoid arthritis. Subsequent definite or classical rheumatoid arthritis were obtained workers (Tromovitch and March, 1961; Bennett and from the Connective Tissue Disease and Arthritis Clinics and the in-patient medical service of the Johns http://ard.bmj.com/ Holley, 1961; Azoury, Jones, Derbes, and Gum, Hopkins Hospital. Selection was based solely upon 1966) have confirmed this cutaneous hypersensitivity certainty of clinical diagnosis and the patients' coopera- to leucocytes in the majority of patients with SLE; tion and availability for study. All were women. furthermore, a similar dermal response has been 112 controls were obtained from among female demonstrated after challenge with heterologous patients hospitalized on the medical service. Specifically nuclear antigens, especially calfthymus deoxyribonu- excluded from the control group were patients with cleic acid (DNA) (Azoury and others, 1966; Ores and definite or suspect connective tissue disease, patients with Lange, 1964; Chieregato and Faldarini, 1964; tuberculosis, and potentially anergic individuals such as on September 26, 2021 by guest. Protected Fardal and Winkelmann, 1965). Whether this those with sarcoidosis, Hodgkin's disease, or patients delayed-typed reaction indicates altered cellular receiving cytotoxic drug therapy. hypersensitivity only to nuclear constituents or Skin Test Procedure.-Patients were tested with the reflects a more generalized hyperergic state is not following battery of six antigens: known. It is even possible that the cutaneous (1) Intermediate strength PPD,* 0-0001 mg. per response to leucocyte and nuclear antigens results 0-1 ml.; from a local interaction between antigen and (2) Histoplasmin,* 1 :100 dilution; circulating antinuclear antibody, although the (3) Trichophytin, ** 1:30 dilution; temporal sequence is not that of classical Arthus- (4) Candida albicans extract,** 1:100 dilution; type reactivity. (5) Streptokinase (SK)-Streptodomase (SD),*** 10 The present study was undertaken to investigate units SK and 2- 5 units SD per 0 1 ml; these possibilities. Patients with systemic lupus (6) Calf thymus DNA,**** 0-1 mg. per 0-1 ml., after the method of Ores and Lange (1964). * This work was supported by an Arthritis Foundation Clinical *Parke, Davis & Co. Study Center Grant, and in part by a U.S. Public Service Clinical **Hollister-Stier Laboratories. Research Grant (5 MO 1 FR 35 27) ***Lederle Laboratories, as "Varidase". t Cornell New York Hospital Medical Center, New York, N.Y. ****Mann Research Laboratories. 311 Ann Rheum Dis: first published as 10.1136/ard.27.4.311 on 1 July 1968. Downloaded from 312 ANNALS OF THE RHEUMATIC DISEASES 0 1 ml. of was each antigen injected intradermally in with rheumatoid arthritis and of 48 years for the the volar surface of the forearm. All tests were per- controls. formed simultaneously in each patient. Reactions were read at 24 and 48 hours by two observers, and millimetres of erythema and induration were recorded. The test was Frequency of Positive Tests (Table 11).-No considered positive only when or more five millimetres of difference was found among patients with SLE, induration were present at one or both of these times. rheumatoid arthritis, and controls with respect to Serum Factors.-Immediately before skin testing, the frequency of positive reactors to trichophytin, venous blood was obtained from all patients and controls, Candida albicans extract, streptokinase-strepto- for subsequent determination of antinuclear factor dornase, or histoplasmin. activity. The immunofluorescent technique of Holborow None of the twenty patients with SLE, however, and Johnson (1964) was used, with rat liver sections as showed a response to the source of antigen. The test was considered positive positive intermediate strength when nuclear fluorescence was demonstrated at a serum PPD, while approximately one-quarter of the dilution of 1:10 or greater. In addition, L.E.-cell tests patients with rheumatoid arthritis and one-third of were performed on all patients with SLE by the method the controls had positive tests. This significant of Zinkham and Conley (1956). lack of reactivity to tuberculin could not be explained on the basis of exposure history to tuberculosis. Clinical Data.-After skin test results had been re- Six (30 per cent.) of those with SLE had a known corded, a medical summary was prepared on each exposure to the disease, as did five (22 per cent.) patient, with emphasis on exposure history, features of patients with rheumatoid arthritis and sixteen past and current illness suggesting dis- (14 immunological per cent.) controls. On the other hand, only two orders, and drug therapy. Clinical analyses were performed without knowledge of reactivity to DNA. of these five rheumatoid arthritis patients and four Statements of statistical significance are based on x2 of the sixteen controls with exposure to tuberculosis analysis using Yates' correction. had positive intradermal tests, indicating overall poor correlation between reactivity and epidemio- Results logic data. copyright. As shown in Table I, the patients, all women, Reactivity to DNA was surprisingly low (20 per were predominantly Negroes in the fourth, fifth, and cent.) in patients with SLE, occurring no more sixth decades of life. Patients with SLE formed a frequently in this group than in those with rheuma- significantly younger group, with an average age of toid arthritis (22 per cent.) or controls (18 per cent.). 38 years, as compared to a mean age of 51 for those TABLE I Frequency of Multiple Positive Tests. The num- http://ard.bmj.com/ AGE, SEX AND RACE OF PATIENTS (all females) ber of positive tests per patient was no greater for those with systemic lupus. Only six (30 per cent.) Clinical Diagnosis SLE RA Controls of the SLE patients reacted to three antigens; none Total 20 23 112 reacted to more than three. In contrast, twelve Race Negro 11 10 87 (52 per cent.) of those with rheumatoid arthritis and White 9 13 25 59 (53 per cent.) of the controls had three or more tests to the five bacterial and Less than 20 2 - 3 positive fungal antigens. on September 26, 2021 by guest. Protected 20-29 6 3 16 30-39 3 1 21 Age (yrs) 40-49 3 5 20 50-59 5 7 19 Intensity of Response.-With no increase in the 60-69 1 6 18 70-79 1 15 frequency of positive reactors to any of the adminis- tered antigens and no greater number of multiple TABLE II FREQUENCY OF POSITIVE REACTORS Total Positive Reactors Clinical Number Diagnosis of PPD* Histoplasmin Trichophytin Candida albicans SK-SD* DNA* Patients I1I No. Per cent. No. Per cent. No. Per cent. No. Per cent. No. Per cent. No. Per cent. SLE 20 0 0 1 5 19 95 14 70 7 35 4 20 RA 23 6 26 4 17 22 96 19 83 8 35 5 22 Controls 112 37 33 17 1 5 106 95 78 70 43 38 20 18 *See text Ann Rheum Dis: first published as 10.1136/ard.27.4.311 on 1 July 1968. Downloaded from DELA YED HYPERSENSITIVITY IN SLE 313 test reactors among those with SLE, the possibility nineteen of the twenty patients had had antinuclear still remained that the intensity of the response was factors detected earlier in their course, and L.E.-cells greater in this group. Shown in Table III are the had been found previously in seventeen.) Seven average millimetres of induration in patients with patients with SLE had never received corticosteroid positive tests. No significant difference in mean therapy; in an additional patient, prednisone had response to any antigen was observed among the been discontinued over 5 years earlier. Only two clinical groups. Moreover, the intensity of the were receiving prednisone in excess of 25 mg. daily. reaction to DNA was uniformly less than the Cutaneous reactivity could not be correlated with response to the bacterial and fungal antigens. any specific clinical or serologic feature ofthe disease. Of the four patients with positive skin tests to DNA, TABLE III only one had active disease. Nephritis was present INTENSITY OF POSITIVE REACTIONS in three of the four, but five patients with nephritis showed no reaction to intradermal DNA. Mean Positive Response (mm.) Three factors, independent of the diagnosis of Clinical Diagnosis PPD* Histo- Tricho- Candida SK-SD* DNA* SLE, remained to be evaluated in relation to plasmin phytin albicans cutaneous reactivity, namely, (1) circulating anti- SLE - lot 17 18 13 6 nuclear antibody, (2) corticosteroid therapy, and (3) RA 9 8 11 13 12 6 Controls 10 8 14 15 12 7 age.
Load more

Recommended publications
  • Difference Between Hypersensitivity and Autoimmunity Key Difference – Hypersensitivity Vs Autoimmunity
    Difference Between Hypersensitivity and Autoimmunity www.differencebetwee.com Key Difference – Hypersensitivity vs Autoimmunity Autoimmunity is an adaptive immune response mounted against self-antigens. In simple terms, when your body is acting against its own cells and tissues, this is called an autoimmune reaction. An exaggerated and inappropriate immune response to an antigenic stimulus is defined as a hypersensitivity reaction. Unlike autoimmune reactions that are triggered only by the endogenous antigens, hypersensitivity reactions are triggered by both endogenous and exogenous antigens. This is the key difference between hypersensitivity and autoimmunity. What is Hypersensitivity? An exaggerated and inappropriate immune response to an antigenic stimulus is defined as a hypersensitivity reaction. The first exposure to a particular antigen activates the immune system and, antibodies are produced as a result. This is called sensitization. Subsequent exposures to the same antigen give rise to hypersensitivity. Few important facts regarding the hypersensitivity reactions are given below They can be elicited by both exogenous and endogenous agents. They are a result of an imbalance between the effector mechanisms and the countermeasures that are there to control any inappropriate execution of an immune response. The presence of a genetic susceptibility increases the likelihood of hypersensitivity reactions. The manner in which hypersensitivity reactions harm our body is similar to the way that the pathogens are destroyed by immune reactions. Figure 01: Allergy According to the Coombs and Gell classification, there are four main types of hypersensitivity reactions. Type I- Immediate Type/ Anaphylactic Mechanism Vasodilation, edema, and contraction of smooth muscles are the pathological changes that take place during the immediate phase of the reaction.
    [Show full text]
  • Food Fact Sheet: Food Allergy and Food Intolerance
    Food Fact Sheet: Food Allergy and Food Intolerance Having to avoid certain foods in your diet can be difficult. But there are a few simple things you can do to help you manage your food allergies - allowing you to stay safe, continue to participate in fun activities and enjoy your food. What is the difference between food allergy and food intolerance? For some people, eating certain foods can lead to an unpleasant and sometimes dangerous physical reaction. The term used to describe all types of reactions to foods is ‘food hypersensitivity’. A 'food allergy' is a reaction involving the immune system (the body’s defence against foreign bodies). Those that do not involve the immune system are often called a ‘food intolerance’. It is important to identify and manage foods that trigger any symptoms in an appropriate way. Food allergy Proteins within foods can trigger immediate (within two hours) or delayed symptoms (up to several days later). Immediate food allergy (IgE mediated food allergy) Immediate reactions to foods occur when your immune system reacts to a normally harmless protein in food, due to the creation of Immunoglobulin E (IgE). This results in the release of chemicals (e.g. histamine) which trigger allergic symptoms. These symptoms are usually in the skin (itching/swelling), or gut (vomiting, diarrhoea). Other symptoms can include breathing problems and in rare cases an extreme allergic reaction called anaphylaxis. Delayed food allergy (non IgE mediated food allergy) Delayed reactions to foods still involve your immune system, but there is a different type of immune reaction involved. Symptoms typically occur in the gut (vomiting, diarrhoea, constipation) and/or the skin (atopic eczema).
    [Show full text]
  • 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.
    [Show full text]
  • 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,
    [Show full text]
  • Microbiology Chapter 19 Outline
    Microbiology Chapter 19 Outline Introduction (p. 515) 1. Hay fever, transplant rejection, and autoimmunity are examples of harmful immune reactions. 2. Immunosuppression is inhibition of the immune system. 3. Superantigens activate many T cell receptors that can cause adverse host responses. Hypersensitivity (pp. 516–526) 1. Hypersensitivity reactions represent immunological responses to an antigen (allergen) that lead to tissue damage rather than immunity. 2. Hypersensitivity reactions occur when a person has been sensitized to an antigen. 3. Hypersensitivity reactions can be divided into four classes: types I, II, and III are immediate reactions based on humoral immunity, and type IV is a delayed reaction based on cell-mediated immunity. Allergies and the Microbiome (p. 516) 4. Childhood exposure to microbes may decrease development of allergies. Type I (Anaphylactic) Reactions (pp. 516–522) 5. Anaphylactic reactions involve the production of IgE antibodies that bind to mast cells and basophils to sensitize the host. 6. The binding of two adjacent IgE antibodies to an antigen causes the target cell to release chemical mediators, such as histamine, leukotrienes, and prostaglandins, which cause the observed allergic reactions. 7. Systemic anaphylaxis may develop in minutes after injection or ingestion of the antigen; this may result in circulatory collapse and death. 8. Localized anaphylaxis is exemplified by hives, hay fever, and asthma. 9. Skin testing is useful in determining sensitivity to an antigen. 10. Desensitization to an antigen can be achieved by repeated injections of the antigen, which leads to the formation of blocking (IgG) antibodies. Microbiology Chapter 19 Outline Type II (Cytotoxic) Reactions (pp. 522–524) 11.
    [Show full text]
  • Allergens Toolkit Introduction the Number of People That Suffers Food Allergy Or Food Intolerance to Some Products Is Increasing
    The International Nut and Dried Fruit Council (INC) is the leading international organization on health, nutrition, statistics, food safety, and international standards and regulations regarding nuts and dried fruits. INC Members include more than 800 nut and dried fruit sector companies from over 70 countries. International Nut and Dried Fruit Council C/de la Fruita Seca 4 · Polígon Tecnoparc 43204 Reus, Spain [email protected] www.nutfruit.org World consumption of nuts keeps growing and giving reasons for optimism. In season 2018/2019, world tree nut production has been estimated at 4.5 million metric tons, 50% up from a decade ago, and peanuts at more than 37 million MT. Health-driven consumer trends have made waves in recent years becoming largely responsible for securing this positive performance. Allergens Toolkit Introduction The number of people that suffers food allergy or food intolerance to some products is increasing. Approximately 15 million people in the United States have food allergies. The Food Allergy Research & Resource Program (FARRP) currently estima- tes the prevalence of IgE-mediated food allergies in the United States at 3.5 - 4.0% of the overall population (1). In children, it increased by 50 percent between 1997 and 2011. As for nuts, it is estimated that the prevalence of peanut and tree nut allergy in U.S. children more than tripled between 1997 and 2008 (2). In Europe, the prevalence of food allergy/intolerance in adults is approximately 5% (3). But first, it is necessary to clarify the difference between these two concepts: food allergy and food intolerance. What is a Food Allergy? Food allergies are caused by an adverse immune reaction (hypersensitivity) to certain food proteins, an abnormal response to a food induced by the body's immune system.
    [Show full text]
  • Transfusion-Associated Graft-Versus-Host Disease
    Vox Sanguinis (2008) 95, 85–93 © 2008 The Author(s) REVIEW Journal compilation © 2008 Blackwell Publishing Ltd. DOI: 10.1111/j.1423-0410.2008.01073.x Transfusion-associatedBlackwell Publishing Ltd graft-versus-host disease D. M. Dwyre & P. V. Holland Department of Pathology, University of California Davis Medical Center, Sacramento, CA, USA Transfusion-associated graft-versus-host disease (TA-GvHD) is a rare complication of transfusion of cellular blood components producing a graft-versus-host clinical picture with concomitant bone marrow aplasia. The disease is fulminant and rapidly fatal in the majority of patients. TA-GvHD is caused by transfused blood-derived, alloreactive T lymphocytes that attack host tissue, including bone marrow with resultant bone marrow failure. Human leucocyte antigen similarity between the trans- fused lymphocytes and the host, often in conjunction with host immunosuppression, allows tolerance of the grafted lymphocytes to survive the host immunological response. Any blood component containing viable T lymphocytes can cause TA-GvHD, with fresher components more likely to have intact cells and, thus, able to cause disease. Treatment is generally not helpful, while prevention, usually via irradiation of blood Received: 13 December 2007, components given to susceptible recipients, is the key to obviating TA-GvHD. Newer revised 18 May 2008, accepted 21 May 2008, methods, such as pathogen inactivation, may play an important role in the future. published online 9 June 2008 Key words: graft-versus-host, immunosuppression, irradiation, transfusion. along with findings due to marked bone marrow aplasia. Introduction Because of the bone marrow failure, the prognosis of TA- Transfusion-associated graft-versus-host disease (TA-GvHD) GvHD is dismal.
    [Show full text]
  • Angioedema in the Emergency Department: a Practical Guide to Differential Diagnosis and Management Jonathan A
    Bernstein et al. International Journal of Emergency Medicine (2017) 10:15 International Journal of DOI 10.1186/s12245-017-0141-z Emergency Medicine REVIEW Open Access Angioedema in the emergency department: a practical guide to differential diagnosis and management Jonathan A. Bernstein1*, Paolo Cremonesi2, Thomas K. Hoffmann3 and John Hollingsworth4 Abstract Background: Angioedema is a common presentation in the emergency department (ED). Airway angioedema can be fatal; therefore, prompt diagnosis and correct treatment are vital. Objective of the review: Based on the findings of two expert panels attended by international experts in angioedema and emergency medicine, this review aims to provide practical guidance on the diagnosis, differentiation, and management of histamine- and bradykinin-mediated angioedema in the ED. Review: The most common pathophysiology underlying angioedema is mediated by histamine; however, ED staff must be alert for the less common bradykinin-mediated forms of angioedema. Crucially, bradykinin-mediated angioedema does not respond to the same treatment as histamine-mediated angioedema. Bradykinin-mediated angioedema can result from many causes, including hereditary defects in C1 esterase inhibitor (C1-INH), side effects of angiotensin-converting enzyme inhibitors (ACEis), or acquired deficiency in C1-INH. The increased use of ACEis in recent decades has resulted in more frequent encounters with ACEi-induced angioedema in the ED; however, surveys have shown that many ED staff may not know how to recognize or manage bradykinin-mediated angioedema, and hospitals may not have specific medications or protocols in place. Conclusion: ED physicians must be aware of the different pathophysiologic pathways that lead to angioedema in order to efficiently and effectively manage these potentially fatal conditions.
    [Show full text]
  • Human Antibody-Dependent Cellular Cytotoxicity
    Human Antibody - Dependent Cellular Cytotoxicity ISOLATION AND IDENTIFICATION OF A SUBPOPULATION OF PERIPHERAL BLOOD LYMPHOCYTES WHICH KILL ANTIBODY-COATED AUTOLOGOUS TARGET CELLS ARNOLD M. BRIER, LEONARD CHESS, and STUART F. SCIHLOSSMIAN From the Departmetnt of Medicitnc, Beth Israel Hospital, atnd Division of Tumor Immunology, Sidney Farber Catncer Center, and Department of Medicine, Harvard Medical School, Boston, Massachtusetts 02115 A B S T R A C T Antibody-dependent cellular cytotoxicity rabbit gam1ma globulin, but not by rabbit F (ab)2 anti- (ADCC), has been shown to be independent in vitro hunmain F (ab)2 or media. This supports the contention of thymus-derived lymphocytes, but the precise nature previously suggested in studies usiing unfractionated of the effector lymphocyte has not been fully clarified. lmniphocyte populations that the ADCC effector cell rec- To further study the identity of the ADCC effector cell ognizes the Fc portion of the antibody mzolecule. The type(s), peripheral blood leukocvtes were purified by variable and low level of activity noted in the Jg(+) Ficoll-Hypaque density centrifugation and fractionated populations is unexplained but possibly due to a variable into surface immunoglobulin-positive [Jg(+)] and sur- population of null cell-derived Ig(+) lmphocytes face immunoglobulin-niegative [Ig (-) ] populations by within the Nhole Ig(+) population. In conclusioin, these chromatographic separation on Sephadex G-200 anti- experimlenits demonstrate that, in vitro, the major human immunoglobulin columns. After column fraction- ADCC effector activity of circulating hulmian peripheral ation, the ADC( effector activity against antibody- blood lymnphocytes resides in the Ig(-), E(-), EAC- coated autologous lymphocytes was predominantl-y and (±) subpopulatioin terImed 'null cells." Since it has been consistently found in the Jg(-) fractioin.
    [Show full text]
  • Diseases of the Immune System 813
    Chapter 19 | Diseases of the Immune System 813 Chapter 19 Diseases of the Immune System Figure 19.1 Bee stings and other allergens can cause life-threatening, systemic allergic reactions. Sensitive individuals may need to carry an epinephrine auto-injector (e.g., EpiPen) in case of a sting. A bee-sting allergy is an example of an immune response that is harmful to the host rather than protective; epinephrine counteracts the severe drop in blood pressure that can result from the immune response. (credit right: modification of work by Carol Bleistine) Chapter Outline 19.1 Hypersensitivities 19.2 Autoimmune Disorders 19.3 Organ Transplantation and Rejection 19.4 Immunodeficiency 19.5 Cancer Immunobiology and Immunotherapy Introduction An allergic reaction is an immune response to a type of antigen called an allergen. Allergens can be found in many different items, from peanuts and insect stings to latex and some drugs. Unlike other kinds of antigens, allergens are not necessarily associated with pathogenic microbes, and many allergens provoke no immune response at all in most people. Allergic responses vary in severity. Some are mild and localized, like hay fever or hives, but others can result in systemic, life-threatening reactions. Anaphylaxis, for example, is a rapidly developing allergic reaction that can cause a dangerous drop in blood pressure and severe swelling of the throat that may close off the airway. Allergies are just one example of how the immune system—the system normally responsible for preventing disease—can actually cause or mediate disease symptoms. In this chapter, we will further explore allergies and other disorders of the immune system, including hypersensitivity reactions, autoimmune diseases, transplant rejection, and diseases associated with immunodeficiency.
    [Show full text]
  • Late Post-Operative Occurrence of Dentin Hypersensitivity in Adult Patients Following Allogeneic Hematopoietic Stem Cell Transplantation—A Preliminary Report
    International Journal of Environmental Research and Public Health Article Late Post-Operative Occurrence of Dentin Hypersensitivity in Adult Patients Following Allogeneic Hematopoietic Stem Cell Transplantation—A Preliminary Report Agnieszka Bogusławska-Kapała 1 , Barbara Kocha ´nska 2 , Ewa Rusyan 3 , Grzegorz Władysław Basak 4 and Izabela Struzycka˙ 1,* 1 Department of Comprehensive Dental Care, Medical University of Warsaw, 02-091 Warsaw, Poland; [email protected] 2 Department of Conservative Dentistry, Medical University of Gda´nsk,80-210 Gda´nsk,Poland; [email protected] 3 Department of Conservative Dentistry, Medical University of Warsaw, 02-091 Warsaw, Poland; [email protected] 4 Department of Hematology, Oncology and Internal Medicine, Medical University of Warsaw, 02-091 Warsaw, Poland; [email protected] * Correspondence: [email protected] Abstract: Allogeneic hematopoietic stem cell transplantation (alloHSCT) is one of the most commonly performed transplantation procedures nowadays. Despite the significant progress made in the Citation: Bogusławska-Kapała, A.; treatment, alloHSCT is still associated with numerous complications also affecting the oral cavity. Kocha´nska,B.; Rusyan, E.; Basak, One of them is dentin hypersensitivity (DH)—a sharp, short-term pain that occurs when stimuli act G.W.; Struzycka,˙ I. Late on exposed dentin. Various authors point out that DH may result in a significantly lower quality of Post-Operative Occurrence of Dentin life, among other things by impeding the consumption of food as well as causing difficulties in daily Hypersensitivity in Adult Patients oral hygiene. The aim of the study was a preliminary analysis of the incidence rate and severity of following Allogeneic Hematopoietic Stem Cell Transplantation—A DH pain in adult patients during late period after alloHSCT.
    [Show full text]
  • Management of Systemic Anti-Cancer Therapy Reactions in Adults
    000 – GUIDELINES FOR THE MANAGEMENT OF SYSTEMIC ANTI-CANCER THERAPY REACTIONS IN ADULTS Broad Recommendations / Summary These guidelines are to help practitioners prevent, recognise and successfully treat the incidence of reaction/anaphylaxis from systemic anti-cancer therapy. The guidelines have been adapted from the former North East Yorkshire and Humber Clinical Alliance (Cancer) NEYHCA CEG – Guidelines for the Management of Chemotherapy Induced Anaphylaxis in Adults, version 2.2a January (2014) - formally HYCCN. NEYHCA has since ceased to exist as has administration or version control facilitation. Therefore, the adapted, updated guidelines are to rebrand and publish directly onto the local HEY Trust Intranet Site and linked to the Queens Centre for Oncology and Haematology; Cancer Services and Chemotherapy CNS Team Website to ensure up to date best practice. Previous terminology relating to cytotoxic chemotherapy is now under the contemporary term of Chemobiological Systemic Anti-Cancer Therapy, referred to as SACT within the text and includes all classifications of intravenous anti-cancer agents including biological, immunological and hormone therapies in line with up to date evidence and classifications. 1 000 – GUIDELINES FOR THE MANAGEMENT OF SYSTEMIC ANTI-CANCER THERAPY REACTIONS IN ADULTS 1 PURPOSE / LEGAL REQUIREMENTS / BACKGROUND The purpose of these guidelines is to inform all Health Care Professionals (HCP) of their responsibility to avoid, recognise and successfully manage the incidence of reaction/anaphylaxis during Chemobiological systemic anti-cancer therapy (SACT). It remains the responsibility of the practitioner to interpret the application of the guidelines, be aware of best possible practice whilst taking account of local circumstances and the needs and wishes of individual patients.
    [Show full text]