Autoimmune Disorders E-Book
170,99 €
Mehr erfahren.
- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
Autoimmune Disorders Comprehensive resource on the science of autoimmune disorders, covering causes, treatment, prevention, and the latest research in the field Autoimmune Disorders is an authoritative reference on the science of autoimmune disorders, covering their causes, including infections, vaccine adjuvants, environmental stimuli, and silicone implants, the latest research on the genetics, epigenetics, and immunology of autoimmunity, predictive markers, therapeutic approaches for treatment and prevention, and suggestions for future research directions. This book explores the intricate connections between adjuvants and autoimmune responses, focusing on the emergence of the Autoimmune/Inflammatory Syndrome Induced by Adjuvants (ASIA syndrome), as well as autoimmune connections in areas such as chronic fatigue syndrome, autoantibodies targeting the autonomic system, and small fiber neuropathy. The authors emphasize the profound impact of vaccines on public health, underscoring that their benefits far outweigh potential side effects and exploring the historical context of adjuvants in vaccine development. From tattoos to environmental factors, each chapter adds a unique thread to the tapestry of adjuvants, autoimmune responses, and their interactions. Sample topics covered in Autoimmune Disorders include: * Food additives and dental implants as a trigger of autoimmunity and increased risk of ASIA syndrome as a result of the chemical and social factors * Sustained immune activation in ASIA syndrome as a bridge to lymphomagenesis and how immune checkpoints, metals, and bisphenol connect to autoimmunity * Postural Orthostatic Tachycardia syndrome (POTS), Sick Building syndrome, and Gulf War syndrome (GWS) as parts of ASIA syndrome * Sarcoidosis and Sjögren's syndrome as a proof of concept of hyperstimulation syndrome Autoimmune Disorders is an essential reference on the subject for academics, specialized postgraduate students, and practicing professionals seeking to improve integrated research strategies and foster a deeper understanding of the complex relationship between immunology, public health, and individual well-being.
Sie lesen das E-Book in den Legimi-Apps auf:
Seitenzahl: 964
Veröffentlichungsjahr: 2024
Ähnliche
Table of Contents
Cover
Table of Contents
Title Page
Copyright
List of Contributors
Introduction
References
1 Hyperstimulation of the Immune System
Background
Biomaterials that are lined to hyperstimulation of the immune system (silicone, mesh and heavy metals)
Hyperstimulation syndrome induced by silicone breast implants
Hyperstimulation syndrome induced by mesh
Hyperstimulation syndrome induced by metals
Link among foreign bodies, chronic stimulation, and lymphoproliferative disorders
Studies on silicone, metals, and the risk of lymphoma
References
2 Autoimmune/Inflammatory Syndrome Induced by Adjuvants (ASIA): Genetics, Immunization, and Autoimmunity
Introduction
Genetic background
Immunity
Autoimmunity
Conclusion
References
3 Vaccine Adjuvants: History, Role, Mechanisms of Action, and Side Effects
Introduction
Materials and methods
Etymology of adjuvants
Classification of adjuvants
History of adjuvants
Role and mechanisms of actions of adjuvants
Safety and side effects
Safety and side effects of aluminum‐adjuvanted vaccines
Safety and side effects of emulsion‐adjuvanted vaccines
Safety and side effects of novel adjuvants
Overall synthesis of safety and side effects of adjuvanted vaccines
Conclusions and future directions
References
4 Commonly Used Food Additives Are Nutritional Adjuvants in ASIA Syndrome
Introduction
Gluten is a nutritional adjuvant
Microbial transglutaminase is a potential new adjuvant
Nanoparticle complexes are potential new adjuvants
Food colorants are potential new adjuvants
Emulsifiers are potential new adjuvants
Conclusions
Abbreviations
Author contributions
References
5 Silicone Implant Incompatibility Syndrome
Highlights
Introduction
Silicone as an immunologic adjuvant
Pathophysiological mechanisms of inflammatory/immunological disturbances related to SBI
Silicone implant incompatibility syndrome
Autoimmune diseases in patients with SIIS
Effectivity of SBI explantation in improving symptoms and laboratory findings
SIIS, who might be at risk?
Conclusion
Abbreviations
References
6 Silicone Breast Implants (SBIs) and Autoimmune Dysautonomya
References
7 Autoimmune/Inflammatory Syndrome Induced by Adjuvants (ASIA or Shoenfeld’s Syndrome) Due to Polypropylene Mesh Implants
Introduction
Adverse events associated with mesh implants
ASIA: autoimmune/inflammatory syndrome induced by adjuvants (Shoenfeld's syndrome)
Pathophysiology of ASIA after foreign body implantation
Evidence that mesh can cause ASIA
Biological plausibility of mesh implants as a cause of ASIA
Approaches to causation
Conclusion
References
8 Vaccines, Vaccinosis, and Autoimmunity
Vaccines and their epidemiological, clinical, societal, and economic impact
Conclusion
References
9 Sustained Immune Activation in ASIA Syndrome – A Bridge to Lymphomagenesis
Background
Introduction
Animal model as a proof of concept
Conclusions and future goals
References
10 Chronic Fatigue Syndrome
Introduction
The evolutionary history of “chronic fatigue syndrome”
Conclusion
References
11 Autoantibodies and Autonomic Nervous System
G‐protein‐coupled receptor antibodies: basic facts and historical perspective
Associations between anti‐GPCR antibodies and clinical manifestations of dysautonomia
The autoimmune concept for dysautonomia
Potential treatment strategy of dysautonomia
References
12 Postural Orthostatic Tachycardia Syndrome (POTS) as a Part of ASIA Syndrome
Introduction
POTS and autoantibodies
POTS and chronic inflammation
POTS and other autoimmune diseases
POTS and small‐fiber neuropathy (SFN)
References
13 Role of the Small‐fiber Neuropathy in the Pathogenesis of ASIA Syndrome
Small‐fiber neuropathy: definition and principles of diagnostics
Conclusion
References
14 Tattoo as a Possible Trigger for Autoimmune Syndrome Induced by Adjuvants
Introduction
Tattoo and its components
Sjögren's syndrome and tattoo
Sarcoidosis and tattoo
Postural orthostatic tachycardia syndrome, ASIA syndrome, and tattoo
Similarities between silicone incompatibility syndrome (SIS) and ASIA syndrome following tattoo
Potential therapies for ASIA syndrome following tattoo
Conclusion
References
15 The Sick Building Syndrome as a Part of the Autoimmune (Autoinflammatory) Syndrome Induced by Adjuvant
Introduction
Manifestations of SBS
Development of SBS: potential hazards and sources
Conventional and green buildings
Legal requirements and regulations
SBS and Autoimmune (Autoinflammatory) Syndrome Induced by Adjuvants (ASIA)
Conclusion
References
16 Gulf War Syndrome (GWS) and ASIA Syndrome
Introduction
Etiology and pathogenesis of GWS
GWS in relation to other multisymptom conditions
Conclusion
References
17 Vaccinations in Patients with Autoimmune Diseases
Risk of infection in patients with AIRD
Safety and efficacy of vaccinations in patients with AIRD
References
18 Autoimmune Phenomena in Cancer Patients Treated with Immune Checkpoint Inhibitors
Introduction
Incidence and autoimmune irAEs
Autoimmune diseases
Management and treatment of autoimmune irAEs
Summary
References
19 Heavy Metals in Autoimmune Diseases: Too Much Noise in Autoimmunity
Chapter highlights
Introduction
How metals affect the immune system
Metals and systemic lupus erythematosus
Metals and type 1 diabetes mellitus
Metals and rheumatoid arthritis
Metals and multiple sclerosis
Metals and inflammatory bowel disease (IBD)
Metals and systemic sclerosis
Metals and thyroid disease
Metals and Sjögren disease
Metals and autoimmune/inflammatory syndrome induced by adjuvants
Conclusion
References
20 The Role of Bisphenol A in ASIA Syndrome
Introduction
Bisphenol A
Exposure to BPA in health care
Pathophysiological mechanisms of BPA‐induced autoimmunity
Direct mechanisms of BPA action on autoimmunity
The role of BPA in autoimmune diseases
Conclusion
References
21 Sarcoidosis and Autoimmune Inflammatory Syndrome Induced by Adjuvants: Is There a Connection?
Introduction
ASIA signs in sarcoidosis
Major criteria
Typical biopsy
Minor criteria
Sarcoidosis models
Discussion
References
22 Sjögren's Syndrome as a Proof of Concept of the Hyperstimulation Syndrome
Introduction
SjS as a classic example of ASIA syndrome
Hyperstimulation of the immune system in SjS
The role of infections
Epstein–Barr virus
Hepatitis C virus
Other infections
Vaccines
Silicone and silica
Immune checkpoint inhibitors
Hormonal imbalance
The crossroad between immune hyperstimulation, SjS, and neoplasms
Conclusions
Abbreviations
References
23 Gluteal Biopolymer Injections as a Case of ASIA Syndrome
Introduction and overview
In vitro cell effects of biopolymers
Clinical consequences of the cosmetic application of biopolymers
ASIA syndrome and gluteal biopolymers
Authors’ experience with patients with biopolymers in the gluteal area and ASIA syndrome
Therapeutic approach
Conclusions
References
24 The Chemical and Social Landscape of the Modern World and Increased Risk of ASIA
Introduction
Diseases related to increased intestinal permeability
Environmental toxicants and loss of epithelial tight junction fidelity
Early‐life stress, vulnerability to psychosocial stress, and role of the HPA axis
Role of the gut‐brain axis and intestinal microbiome
Animal models of chronic inflammation
Conclusions
References
25 Oil Injections and ASIA Syndrome
Introduction
Epidemiology
Etiology
Pathogenesis
Clinical manifestation
Diagnostic approach
Treatment
Conclusions
References
26 Metals in Dental Implants as a Trigger of Autoimmunity
References
27 Conclusions: State of the Art and Prospects
Index
End User License Agreement
List of Tables
Chapter 2
Table 2.1 Mechanism of adjuvant‐induced autoimmunity.
Chapter 3
Table 3.1 An overview of major vaccine adjuvants.
Chapter 4
Table 4.1 Nutritional adjuvants fulfill the diagnostic criteria of the ASIA...
Chapter 7
Table 7.1 Fibromyalgia 2016 criteria.
Table 7.2 Criteria for the diagnosis of autoimmune/inflammatory syndrome in...
Chapter 9
Table 9.1 Major and minor criteria for the diagnosis of the ASIA syndrome....
Table 9.2 Lymphoma in autoimmune diseases.
Table 9.3 The lipophilic nature of adjuvants
a
(similar to lipophilic drugs)...
Chapter 11
Table 11.1 The autoantibodies directed against G‐protein‐coupled receptors ...
Chapter 13
Table 13.1 Main known causes of the small‐fiber neuropathy.
Table 13.2 Main symptoms of the small‐fiber neuropathy.
Table 13.3 Additional instrumental methods of small‐fiber neuropathy diagno...
Chapter 15
Table 15.1 Prevalence percentage of symptoms associated with sick building ...
Table 15.2 The prevalence of clinical manifestations: MMF, silicone‐related...
Chapter 16
Table 16.1 Prevalence of ASIA syndrome clinical manifestations in veterans ...
Chapter 20
Table 20.1 The pathophysiological mechanisms of BPA action in the developme...
Chapter 21
Table 21.1 Suspected organic and inorganic triggers of sarcoidosis developm...
Table 21.2 Clinical manifestations of sarcoidosis typical for autoimmune di...
Table 21.3 Features of lymphocytic populations in sarcoidosis and autoimmun...
Table 21.4 Detection of various autoantibodies in sarcoidosis patients in v...
Table 21.5 Distribution of HLA‐DRB1 genotypes in sarcoidosis patients.
Chapter 23
Table 23.1 Diverse complications by filler type.
Table 23.2 Main characteristics of studies including patients with biopolym...
Table 23.3 Clinical characteristics of patients, biopolymer extraction, sur...
Table 23.4 Shoenfeld's criteria for ASIA syndrome.
Chapter 25
Table 25.1 Clinical manifestations of ASIA associated with mineral oil.
List of Illustrations
Chapter 4
Figure 4.1 A schematic presentation of five frequently used food additives a...
Chapter 5
Figure 5.1 Commonly associated clinical manifestations in patients with SIIS...
Figure 5.2 Clinical entities related with chronic immune activation due to s...
Chapter 7
Figure 7.1 Mesh‐induced ASIA (autoinflammatory/autoimmunity syndrome induced...
Figure 7.2 Schematic illustration of the process of autoimmunity development...
Figure 7.3 Pathogenesis of mesh‐related ASIA. In genetically predisposed ind...
Chapter 11
Figure 11.1 Clinical manifestations of dysautonomia.
Figure 11.2 In genetically predisposed patients, triggers such as infection,...
Chapter 13
Figure 13.1 Small‐fiber neuropathy in patients with post‐COVID‐19 syndrome, ...
Chapter 14
Figure 14.1 Images from our patient's extensive tattoos.
Chapter 16
Figure 16.1 Schematic illustration of Gulf War syndrome progression: environ...
Chapter 19
Figure 19.1 The effects of heavy metals on the immune system.
Abbreviations
:...
Chapter 20
Figure 20.1 The effects of BPA on innate immune responses.
Figure 20.2 BPA effects on T‐lymphocytes and cytokine production.
Chapter 21
Figure 21.1 ASIA criteria in sarcoidosis.
Figure 21.2 Stages of the course of sarcoidosis within the ASIA syndrome.
Chapter 22
Figure 22.1 Proposed etiopathogenetic mechanisms from genetic susceptibility...
Chapter 23
Figure 23.1. Butterfly wings design technique. (a) Preoperative markings are...
Figure 23.2. Foreign body modeling reaction as a precursor of ASIA syndrome....
Figure 23.3. Clinical case of a woman with biopolymer injection, magnetic re...
Figure 23.4. Timeline of a patient with some toxic risk factors and biopolym...
Chapter 25
Figure 25.1 Graphical abstract. SSc, systemic sclerosis; RA, rheumatoid arth...
Figure 25.2 (a) Injection of mineral oil in buttocks and migration to thighs...
Figure 25.3 (a) Mild ASIA‐MO observed after injection in both breasts. (b) S...
Guide
Cover
Table of Contents
Title Page
Copyright
List of Contributors
Introduction
Begin Reading
Index
End User License Agreement
Pages
iii
iv
vii
viii
ix
x
xi
xii
xiii
xiv
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79
80
81
82
83
84
85
86
87
88
89
91
92
93
94
95
96
97
98
99
100
101
102
103
104
105
106
107
108
109
110
111
112
113
114
115
117
118
119
120
121
122
123
124
125
126
127
129
130
131
132
133
134
135
137
138
139
140
141
142
143
144
145
146
147
148
149
150
151
152
153
155
156
157
158
159
160
161
162
163
164
165
166
167
168
169
170
171
172
173
174
175
176
177
178
179
180
181
182
183
184
185
186
187
188
189
190
191
192
193
194
195
196
197
198
199
201
202
203
204
205
206
207
208
209
210
211
212
213
214
215
216
217
218
219
220
221
222
223
225
226
227
228
229
230
231
232
233
234
235
236
237
238
239
240
241
242
243
244
245
246
247
248
249
250
251
252
253
254
255
256
257
258
259
260
261
262
263
264
265
266
267
268
269
270
271
272
273
274
275
276
277
278
279
280
281
283
284
285
286
287
288
289
290
291
292
293
294
295
296
297
298
299
300
301
302
303
305
306
307
308
309
310
311
312
313
314
315
316
317
318
319
320
321
323
324
325
326
327
328
329
330
331
332
333
334
335
336
337
338
339
340
341
342
343
345
346
347
348
349
350
351
352
353
Autoimmune Disorders
Adjuvants and Other Risk Factors in Pathogenesis
EDITED BY
Abdulla Watad
Rheumatology Unit and Zabludowicz Center for Autoimmune DiseasesSheba Medical CenterTel Aviv UniversityTel-HashomerIsrael
Nicola Luigi Bragazzi
Laboratory for Industrial and AppliedMathematics (LIAM)Department of Mathematics and StatisticsYork UniversityTorontoCanada Postgraduate School of Public HealthDepartment of Health Sciences (DISSAL)University of GenoaGenoaItaly
Yehuda Shoenfeld
Reichman UniversityHerzliyaIsrael Zabludowicz Center for AutoimmuneDiseases (Founder)Sheba Medical CenterTel-HashomerIsrael
This edition first published 2024© 2024 John Wiley & Sons Ltd.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions.
The right of Abdulla Watad, Nicola Luigi Bragazzito, and Yehuda Shoenfeld be identified as the authors of the editorial material in this work has been asserted in accordance with law.
Registered OfficesJohn Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, USAJohn Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK
For details of our global editorial offices, customer services, and more information about Wiley products visit us at www.wiley.com.
Wiley also publishes its books in a variety of electronic formats and by print‐on‐demand. Some content that appears in standard print versions of this book may not be available in other formats.
Trademarks: Wiley and the Wiley logo are trademarks or registered trademarks of John Wiley & Sons, Inc. and/or its affiliates in the United States and other countries and may not be used without written permission. All other trademarks are the property of their respective owners. John Wiley & Sons, Inc. is not associated with any product or vendor mentioned in this book.
Limit of Liability/Disclaimer of WarrantyWhile the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.
Library of Congress Cataloging‐in‐Publication DataNames: Watad, Abdulla, editor. | Bragazzi, Nicola Luigi, editor. | Shoenfeld, Yehuda, 1948‐ editor.Title: Autoimmune disorders : adjuvants and other risk factors in pathogenesis / edited by Abdulla Watad, Nicola Luigi Bragazzi, Yehuda Shoenfeld.Other titles: Autoimmune disorders (Watad)Description: Hoboken, NJ : Wiley, 2024. | Includes bibliographical references and index.Identifiers: LCCN 2024007509 (print) | LCCN 2024007510 (ebook) | ISBN 9781119858416 (hardback) | ISBN 9781119858423 (adobe pdf) | ISBN 9781119858447 (epub)Subjects: MESH: Autoimmune Diseases—etiology | Autoimmune Diseases—physiopathology | Adjuvants, Immunologic—adverse effectsClassification: LCC RC600 (print) | LCC RC600 (ebook) | NLM QW 545 | DDC 616.97/8—dc23/eng/20240325LC record available at https://lccn.loc.gov/2024007509LC ebook record available at https://lccn.loc.gov/2024007510
Cover Design: WileyCover Image: © Ruslan Batiuk /Adobe Stock Photos
List of Contributors
Rojas‐Villarraga Adriana
Research Institute
Fundación Universitaria de Ciencias de la Salud (FUCS)
Bogotá
Colombia
María Alejandra Martínez‐Ceballos
Fundación Oftalmológica Nacional
Bogotá
Colombia
School of Medicine and Health Sciences
Universidad del Rosario
Bogotá
Colombia
Howard Amital
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Sackler Faculty of Medicine
Tel Aviv University
Tel Aviv
Israel
Department of Internal Medicine ‘B’
Sheba Medical Center
Tel‐Hashomer
Israel
Carina Benzvi
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Elena Bartoloni Bocci
Reumatologia
Dipartimento di Medicina e Chirurgia
Università di Perugia
Perugia
Italy
Vânia Borba
Internal Medicine Departmente
Rehaklik Dussnang AG
Dussnang
Thurgau
Switzerland
Nicola Luigi Bragazzi
Laboratory for Industrial and Applied Mathematics (LIAM)
Department of Mathematics and Statistics
York University
Toronto
Canada
Postgraduate School of Public Health
Department of Health Sciences (DISSAL)
University of Genoa
Genoa
Italy
Dana Butnaru
Department of Clinical Immunology
Hospital Clínico San Carlos
Complutense University of Madrid
Madrid
Spain
María P. Cruz‐Domínguez
Internal Medicine Department
Unidad Médica de Alta Especiad
Hospital de Especialidades
“Dr. Antonio Fraga Mouret”
Centro Médico Nacional
“La Raza”. Instituto Mexicano del Seguro Social
México City
México
Internal Medicine Department
División de Estudios de Posgrado
Facultad de Medicina
Universidad Nacional Autónoma de México
México City
México
Paula David
Department of Internal Medicine ’B’
Sheba Medical Center
Tel‐Hashomer
Israel
Arad Dotan
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Sackler Faculty of Medicine
Tel Aviv University
Tel Aviv
Israel
Michael Ehrenfeld
Sackler Faculty of Medicine
Tel Aviv University
Tel Aviv
Israel
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Natalia Gavrilova
Federal State Budget Educational Institution of Higher Education “St. Petersburg State University”
University Emb.
7‐9
Saint Petersburg
Russia
St Petersburg State University Hospital
Saint Petersburg
Russia
Roberto Gerli
Reumatologia
Dipartimento di Medicina e Chirurgia
Università di Perugia
Perugia
Italy
Montealegre Giovanni
Fundación Universitaria de Ciencias de la Salud (FUCS)
Hospital San José
Bogotá
Colombia
Gilad Halpert
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Department of Molecular Biology
Ariel University
Ariel
Israel
Abihai Lucas Hernández
Internal Medicine Department
Unidad Médica de Alta Especiad
Hospital de Especialidades
“Dr. Antonio Fraga Mouret”
Centro Médico Nacional
“La Raza”. Instituto Mexicano del Seguro Social
México City
México
Hadas Hodadov
Sackler Faculty of Medicine
Tel Aviv University
Tel Aviv
Israel
Eitan Israeli
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Luis J. Jara
Research Division
Instituto Nacional de Rehabilitación
Mexico City
México
E. Kamaeva
Federal State Budget Educational Institution of Higher Education “St. Petersburg State University”
University Emb.
7‐9
Saint Petersburg
Russia
Michael Kirby
Department of Molecular Biology and Adelson School of Medicine
Ariel University
Ariel
Israel
Igor Kudryavtsev
Almazov National Medical Research Centre
The Research Department
Saint Petersburg
Russia
Department of Immunology
Institution of Experimental Medicine
Petersburg State University
Saint Petersburg
Russia
Zora Lazurova
4th Department of Internal Medicine
Pavol Jozef Šafárik University
Kosice
Slovakia
Iana Leineman
Department of Therapy
Rheumatology
Examination of Temporary Disability and Quality of Medical Care Named After E.E. Eichwald
North‐Western State Medical University Named After I.I.Mechnikov
Saint Petersburg
Russia
Aaron Lerner
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Campus Ariel
Ariel University
Ariel
Israel
M. Lukashenko
Federal State Budget Educational Institution of Higher Education “St. Petersburg State University”
University Emb.
7‐9
Saint Petersburg
Russia
Naim Mahroum
International School of Medicine
Istanbul Medipol University
Istanbul
Turkey
Anna Malkova
Laboratory of the Mosaic of Autoimmunity
St. Petersburg State University
Saint Petersburg
Russia
Gabriela Medina
Internal Medicine Department
Unidad Médica de Alta Especiad
Hospital de Especialidades
“Dr. Antonio Fraga Mouret”
Centro Médico Nacional
“La Raza”. Instituto Mexicano del Seguro Social
México City
México
Internal Medicine Department
División de Estudios de Posgrado
Facultad de Medicina
Universidad Nacional Autónoma de México
México City
México
Alberto Ordinola‐Navarro
Internal Medicine Department
Unidad Médica de Alta Especiad
Hospital de Especialidades
“Dr. Antonio Fraga Mouret”
Centro Médico Nacional
“La Raza”. Instituto Mexicano del Seguro Social
México City
México
Internal Medicine Department
División de Estudios de Posgrado
Facultad de Medicina
Universidad Nacional Autónoma de México
México City
México
Mohammed Osman
Division of Rheumatology
Department of Medicine
University of Alberta
Edmonton
Alberta
Canada
Asher Pardo
Department of Occupational and Environmental Health
School of Public Health ‐ Tel Aviv University and the Institute for Occupational Safety and Hygiene
Tel Aviv
Israel
Carlo Perricone
Reumatologia
Dipartimento di Medicina e Chirurgia
Università di Perugia
Perugia
Italy
Albert Pinhasov
Department of Molecular Biology and Adelson School of Medicine
Ariel University
Ariel
Israel
Gabriel M. Ramírez
Rheumatology Department
Hospital General de México
“Dr. Eduardo Liceaga”
México City
México
Uribe Rosa
Antioquia’s Clinic
Itagüí
Colombia
Varvara Ryabkova
Laboratory of the Mosaic of Autoimmunity
Department of Pathology
Saint Petersburg State University
Saint Petersburg
Russia
Department of Hospital Therapy Named after Academician M.V. Chernorutskii
Research Institute of Rheumatology and Allergology
Pavlov First Saint Petersburg State Medical University
Saint Petersburg
Russia
Isa Seida
International School of Medicine
Istanbul Medipol University
Istanbul
Turkey
Kassem Sharif
Department of Gastroenterology
Sheba Medical Centre
Tel‐Hashomer
Israel
Sackler Faculty of Medicine
Tel Aviv University
Tel Aviv
Israel
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Elena Shmerkin
Department of Molecular Biology and Adelson School of Medicine
Ariel University
Ariel
Israel
Yehuda Shoenfeld
Reichman University
Herzliya
Israel
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
L. Soprun
Federal State Budget Educational Institution of Higher Education “St. Petersburg State University”
University Emb.
7‐9
Saint Petersburg
Russia
St Petersburg State University Hospital
Saint Petersburg
Russia
Anna Starshinova
Almazov National Medical Research Centre
The Research Department
Saint Petersburg
Russia
Efrosiniia Talalai
Sackler Faculty of Medicine
Tel Aviv University
Tel Aviv
Israel
Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Jan Willem Cohen Tervaert
Division of Rheumatology
Department of Medicine
University of Alberta
Edmonton
Alberta
Canada
Emeritus Professor of Medicine and Immunology
Maastricht University
Maastricht
The Netherlands
Milena Tocut
Department of Internal Medicine C
Wolfson Medical Center
Holon
Israel
Sackler Faculty of Medicine
Tel Aviv University
Tel Aviv
Israel
Olga Vera‐Lastra
Internal Medicine Department
Unidad Médica de Alta Especiad
Hospital de Especialidades
“Dr. Antonio Fraga Mouret”
Centro Médico Nacional
“La Raza”. Instituto Mexicano del Seguro Social
México City
México
Internal Medicine Department
División de Estudios de Posgrado
Facultad de Medicina
Universidad Nacional Autónoma de México
México City
México
Abdulla Watad
Rheumatology Unit and Zabludowicz Center for Autoimmune Diseases
Sheba Medical Center
Tel‐Hashomer
Israel
Sackler Faculty of Medicine
Tel Aviv University
Tel Aviv
Israel
Section of Musculoskeletal Disease
Leeds Institute of Molecular Medicine
University of Leeds
Leeds
UK
Department of Internal Medicine ‘B’
Sheba Medical Center
Tel‐Hashomer
Israel
Institute of Oncology
Sheba Medical Center
Tel‐Hashomer
Israel
Piotr Yablonskiy
Laboratory of the Mosaic of Autoimmunity
St. Petersburg State University
Saint Petersburg
Russia
St. Petersburg Research Institute of Phthisiopulmonology
Saint Petersburg
Russia
Gisele Zandman‐Goddard
Department of Internal Medicine C
Wolfson Medical Center
Holon
Israel
Sackler Faculty of Medicine
Tel Aviv University
Tel Aviv
Israel
Yulia Zinchenko
St. Petersburg Research Institute of Phthisiopulmonology
Saint Petersburg
Russia
Introduction
“The Autoimmune/Inflammatory Syndrome Induced by Adjuvants (ASIA)” is a term introduced by one of the editors of this book, Prof. Yehuda Shoenfeld, to characterize a cluster of autoimmune and inflammatory disorders incited by exposure to various adjuvants [1]. These adjuvants can be encountered in diverse contexts, including vaccinations, silicone implants, and other materials, culminating in a spectrum of symptoms and medical conditions [2]. Given its relatively recent emergence in the medical landscape, with its introduction in 2011, ASIA remains a complex and evolving syndrome, with many facets yet to be fully elucidated. However, an accumulating body of evidence underscores the potential of specific adjuvants to incite autoimmune and inflammatory responses in susceptible individuals, often associated with HLA‐DRB1 genetic factors [3]. Consequently, growing apprehension surrounds the safety of adjuvants integrated into certain vaccines and medical products. It is imperative to underscore that vaccines play a pivotal role in safeguarding public health. Over the years, they have played an instrumental role in eradicating lethal diseases such as smallpox, significantly reducing the prevalence of maladies such as measles and polio. Vaccines operate by invigorating the immune system to mount a defense against specific pathogens, all while sparing the individual from the disease itself. This herd immunity not only extends protection to vaccinated individuals but also shields the broader community, including those who cannot receive vaccines themselves. While vaccines can indeed elicit rare side effects, the immense benefits they confer decisively outweigh the associated risks, making them an indispensable tool in the preservation of public health. This book serves as a comprehensive exploration of ASIA and the diverse adjuvants capable of inciting autoimmune and inflammatory responses. We embark on a journey to decipher the substances implicated in ASIA syndrome, the array of symptoms and conditions it encompasses, and the current state of research in this realm. Our narrative commences by delving into the role of adjuvants in vaccines and the controversies regarding their safety. Though infrequent, some individuals exhibit heightened susceptibility to autoimmune and inflammatory reactions prompted by adjuvants in vaccines, culminating in an array of conditions including Guillain–Barré syndrome, multiple sclerosis, and lupus. We further scrutinize the involvement of silicone implants in the initiation of autoimmune and inflammatory responses. For years, silicone has been a cornerstone of breast implants [4], and though the safety of these implants has been subject to scrutiny [5], the connection between silicone and autoimmune maladies remains enigmatic. Nevertheless, a mounting body of evidence underscores that silicone exposure can incite autoimmune and inflammatory reactions, giving rise to conditions such as silicone implant syndrome, which can manifest with symptoms including fatigue, joint pain, and more. Beyond vaccines and silicone, we cast a spotlight on other adjuvants capable of inciting autoimmune and inflammatory reactions, encompassing commonly employed materials such as aluminum, prevalent in vaccines, and additional substances such as mesh and metals. We also conduct an exploration of autoimmune dysautonomia, a condition that has garnered substantial attention in recent years. Finally, we engage in a comprehensive discussion surrounding the diagnosis and treatment of ASIA as well as the prevailing controversies that encircle this syndrome. It is important to note that skepticism still pervades some medical circles regarding the existence of ASIA, with its symptoms and linkage to adjuvants often escaping recognition. Nonetheless, with an escalating awareness and an expanding body of research, the reality of ASIA as a genuine phenomenon affecting numerous individuals is becoming increasingly evident. In summation, this book aspires to provide an exhaustive overview of ASIA and the manifold adjuvants capable of triggering autoimmune and inflammatory responses. Our hope is that this volume will raise awareness about this intricate syndrome and empower individuals to make informed decisions regarding their health and the medical products they encounter.
References
1. Shoenfeld, Y. and Agmon‐Levin, N. (2011). 'ASIA' – autoimmune/inflammatory syndrome induced by adjuvants.
J. Autoimmun.
36 (1): 4–8.
2. Seida, I., Alrais, M., Seida, R. et al. (2023). Autoimmune/inflammatory syndrome induced by adjuvants (ASIA): past, present, and future implications.
Clin. Exp. Immunol.
uxad033.
3. Arango, M.‐T., Perricone, C., Kivity, S. et al. (2017). HLA‐DRB1 the notorious gene in the mosaic of autoimmunity.
Immunol. Res.
65 (1): 82–98.
4. Watad, A., Rosenberg, V., Tiosano, S. et al. (2018). Silicone breast implants and the risk of autoimmune/rheumatic disorders: a real‐world analysis.
Int. J. Epidemiol.
47 (6): 1846–1854.
5. Watad, A., Bragazzi, N.L., Amital, H., and Shoenfeld, Y. (2019). Hyperstimulation of Adaptive Immunity as the Common Pathway for Silicone Breast Implants, Autoimmunity, and Lymphoma of the Breast.
Isr. Med. Assoc. J.
21 (8): 517–519.
1Hyperstimulation of the Immune System
Hadas Hodadov1 and Abdulla Watad1,2,3,4,5
1Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
2Department of Medicine ‘B’, Sheba Medical Center, Tel‐Hashomer,, Israel
3Rheumatology Unit and Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel‐Hashomer, Israel
4Section of Musculoskeletal Disease, Leeds Institute of Molecular Medicine, University of Leeds, Leeds, UK
5Institute of Oncology, Sheba Medical Center, Tel‐Hashomer,, Israel
Background
The immune system safeguards living organisms against constant assaults from both external and internal environments, detecting a wide variety of pathogens, cancer cells, and drugs (i.e., "nonself") and distinguishing them from the organism's own healthy tissue ("self") [1]. Two main subsections constitute the immune system: innate immunity, which provides immediate though incomplete protection against intruders and, at best, has only short‐term memory; and adaptive immunity, offering a tailored response to each stimulus by learning to recognise previously encountered molecules [2]. Dysfunction of the immune system can lead to autoimmune diseases, autoinflammatory disorders, and cancer. Autoimmunity results from a complex interplay between genetic predisposition and environmental factors [3]. Adjuvants are molecules capable of triggering an immune response against specific or nonspecific antigens [4]. Biomaterials are routinely employed to address various conditions in nearly every medical specialty. However, certain substances within this category have been reported to possess adjuvanticity, thereby potentially accelerating or initiating autoimmune phenomena [5].
Biomaterials that are lined to hyperstimulation of the immune system (silicone, mesh and heavy metals)
Biomaterials play a pivotal role in addressing various healthcare issues, including tissue engineering, drug delivery, and medical implants. Their significance lies in the broad potential of these materials to offer support (i.e., scaffolds), allow modifications of chemical properties, and protect biologically active products (i.e., cells, proteins, and chemicals). Biomaterials encompass a diverse range of compounds with varying functions and structural features, ranging from naturally occurring biological macromolecules to fully synthetic coatings [6]. However, a noteworthy aspect, though rare, is that certain biomaterials can chronically stimulate the immune system, resulting in excessive inflammation, fibrotic encapsulation, impaired healing, tissue destruction, or even rejection of medical devices [5]. The implantation of biomaterial elicits a host reaction that determines the integration outcome and the biological response of the implant. Upon implantation, the material interacts with the blood, causing protein adsorption to the biomaterial surface and the development of a temporary matrix that forms on and around the biomaterial. This matrix serves as the initial thrombus at the tissue‐material interface. Protein adsorption and fibrin‐predominant temporary matrix formation are closely linked in their mechanistic responses [7]. Injury to vascularized connective tissue initiates inflammatory responses by the innate immune system, leading to thrombus formation. The temporary matrix contributes components to foreign body reactions and wound healing. Cytokines, growth factors, mitogens, and other bioactive materials within the matrix create a rich environment of activating and inhibiting substances capable of modulating macrophage activity, along with the proliferation of other cell populations involved in inflammatory and wound‐healing responses. Following the initial blood‐material interactions and temporary matrix formation, both acute and chronic inflammation responses ensue [8].
Hyperstimulation syndrome induced by silicone breast implants
One significant biomaterial is silicone, a polymeric compound forming rubber‐like materials used in various applications, including dental procedures, medical implants, and insulation. Silicone breast implants (SBIs), introduced in 1962, have been widely implanted in millions of individuals [9]. While there was an earlier perception that silicone is a biologically inert material, this notion has been refuted, with reported immunological effects induced by silicone. Silicone gel particles can migrate outside the outer shell post‐rupture, and even migration through an intact shell has been demonstrated, known as "gel bleed" [10]. Silicon‐containing particles captured by macrophages induce the release of IL‐1, activate the NALP3 inflammasome and B cells, leading to an imbalance of regulatory T cells, responder T cells, and Th17 cells [11]. Animal studies have demonstrated that SBIs induce an adjuvant effect, increasing susceptibility to autoimmune/rheumatic disorders. The mechanisms by which SBIs induce autoimmune phenomena are numerous, involving dysregulation of both innate and adaptive immunity in individuals genetically predisposed to autoimmunity [9]. In recent years, inconsistent findings on the safety of SBIs have emerged. A large population‐based study involving over 24,000 women with SBIs and approximately 100,000 age‐matched controls revealed a significantly increased risk of autoimmune disease in women with SBIs, with an adjusted odds‐ratio (OR) of 1.22 ([95% CI 1.18–1.26], p < 0.001). The risk was even higher (OR > 1.5, p < 0.05) in specific conditions such as sarcoidosis, systemic sclerosis, and Sjögren's syndrome [11]. Other studies have linked carrying SBIs with systemic clinical symptoms suggestive of rheumatic disorders, including fatigue, weakness, musculoskeletal pain, morning stiffness, and dry eyes and mouth [12]. Plausible mechanisms explaining the link between SBIs and autoimmune phenomena have been proposed, as supported by animal model studies. For example, injecting silicone gel in NZB mice induced proteinuria and autoimmune hemolytic anemia [13], while implanting silicone gel or silicone oil in MRL lpr/lpr mice increased anti‐Ds‐DNA antibodies [14]. In a rat model study, five genes (Fes, Aif1, Gata3, Tlr6, and Tlr2) were identified as hub genes likely linked to the immune responses induced by silicone. Four of these genes (Aif1, Gata3, Tlr6, and Tlr2) have been associated with autoimmunity as target genes or disease markers [15]. Thus, SBIs may trigger immune responses, with various immune reactions detected after silicone implantation.
Hyperstimulation syndrome induced by mesh
Mesh, a loosely woven sheet, constitutes another crucial biomaterial, with the commonly used polypropylene (PP) mesh being a strong yet flexible synthetic implant. PP, the second most widely manufactured type of plastic globally, finds application in various products such as furniture, electronic components, and medical devices [16]. Utilized since the 1960s for hernia repair surgeries and since the 1990s for urinary incontinence and pelvic organ prolapse, PP implants have enhanced surgical outcomes and reduced recurrence risks. Initially considered an inert plastic, chemically inactive to minimize patient complications, a contrasting notion has emerged, suggesting mesh‐related complications, particularly the body's immunological reaction to the implanted material [17]. Some researchers propose that PP mesh may induce a systemic autoimmune inflammatory disorder, akin to women with SBIs induced by adjuvants. PP implants elicit a rapid and effective acute inflammatory response followed by a chronic body reaction. Local inflammatory reactions after mesh insertion may lead to systemic upregulation of inflammatory mediators, primarily regulated by monocytes and macrophages at the implant tissue interface. These cells, known to produce various cytokines, particularly IL‐6, play a crucial role in the acute phase of the inflammatory process, regulating local and systemic responses [18]. One theory explaining the chronic foreign body response to mesh involves oxidative processes, with oxidation causing PP degradation, resulting in chronic inflammation and a subsequent systemic autoimmune inflammatory disorder. Supporting evidence for mesh acting as an adjuvant includes the appearance of systemic autoimmune symptoms shortly after mesh placement and the remission of symptoms after mesh removal [19]. A recent study evaluated patients with implanted PP for the development of systemic illness. Thirty‐nine out of 40 patients presented with chronic fatigue, and 38 of 40 patients had myalgia, both occurring shortly after surgery. All patients fulfilled the diagnostic criteria for ASIA syndrome. In 45% of patients, there was a diagnosis of a well‐established autoimmune disease, suggesting that PP mesh implants increase the risk of developing autoimmune diseases by acting as an adjuvant [20].
Hyperstimulation syndrome induced by metals
Metals and metal alloys, combinations of metal elements, have been widely utilized as medical implants for over a century across various medical specialties. They find application in a diverse range of medical devices, from solid metal implants in orthopedics to bioelectronics such as pacemakers or neurostimulators [21]. These metal implants are chosen as biomedical materials due to their numerous advantages over other materials, including high mechanical strength, good electrical conductivity, durability, and excellent biological compatibility. Ideally, metal implants should not cause any undesired reactions; however, interactions between the implant and the surrounding tissue can lead to complications, including infection, inflammation, and foreign body response. While heavy metals and their salts have previously been demonstrated to play a role in causing allergic diseases, recent evidence suggests their key involvement in the induction or exacerbation of autoimmune diseases [22]. The mechanism by which heavy metals trigger autoimmunity is not fully understood, but its comprehension is not necessary for establishing an association between them. Manifestations of autoimmunity may include the production of autoantibodies, an increase in serum IgG and IgE, polyclonal activation of B and T lymphocytes, infiltration of destructive inflammatory cells into different target organs, and the deposition of immune complexes in vascular sites [22]. Another suggested mechanism is that metal compounds may exert toxic effects on the immune system, leading to the malfunctioning of the system as a whole. Despite an incomplete understanding of the mechanism, there is a growing notion supported by extensive research that the interaction of metals with the immune system may lead to immunodysregulation, resulting in autoimmune diseases [23].
Link among foreign bodies, chronic stimulation, and lymphoproliferative disorders
Following acute inflammation, chronic inflammation at the implant site is characterized by the presence of mononuclear cells, including monocytes and lymphocytes. An implant may continue to elicit a chronic inflammatory response lasting for months or longer, marked by a broader immune cell infiltration, encompassing both myeloid and lymphoid cells. After the resolution of acute and chronic inflammatory responses, granulation tissue, identified by the presence of macrophages, infiltration of fibroblasts, and neovascularization, is observed in the new healing tissue [5]. It is hypothesized that any breast implant, whether saline or silicone, may release silicone corpuscles over time. Factors such as trauma causing microfractures, exposure to temperature or pressure, ultraviolet radiation, oxidation, and chemical reactions can accelerate this process. When the permeability of the elastomer is impaired, the physiological seroma in the space between the elastomer surface and the fibrous capsule reacts and transports the resulting polydimethylsiloxane compound from the implant surface, encountering the fibrous capsule [24]. The fibrous capsule acts as a physiological protective barrier against products from the intracapsular environment. If met with silicone particles, regardless of the mechanism, an immune response may be generated, potentially leading to a silicone‐induced granuloma. If the fibrous capsule ruptures and exposes its contents to the extracapsular space, the immune reaction can trigger a systemic immune response [24]. Some patients may develop an autoimmune reaction to silicone components. A common finding related to silicone implant complications is a silicone‐induced granuloma of the breast implant capsule (SIGBIC). Histologically, SIGBIC is formed by extracellular and/or intracellular silicone, numerous histiocytes, chronic granulomatous inflammatory infiltrate with multinucleated giant cells, and an infiltrate of mixed lymphocytes – T and B without atypia [25]. Another rare but serious complication is anaplastic large cell lymphoma (ALCL), a subtype of non‐Hodgkin lymphoma of T cells [26]. An association between ALCL and saline and silicone implants exists. The first case of ALCL associated with breast implants was published in 1997 [27], and by 2011, the Food and Drug Administration published a statement confirming 60 cases of ALCL associated with prostheses. ALCL affects the fibrous capsule around the implant, rarely appears as a solid mass, and does not involve the breast parenchyma. As in SIGBIC, the mechanism of ALCL may involve an immune response induced by the silicone material in the implant, leading to an immune overreaction and monoclonal neoplasia with activated T lymphocytes. Additionally, in saline or silicone implants, the capsules may be responsible for chronic local inflammation with T‐cell activation and clonal expansion [28]. Furthermore, in case of capsular disruption, silicone‐containing particles are transported to the regional lymph nodes, causing a marked adjuvant effect. Silica particles induce a type‐2 inflammatory response characterized by an increase in IgE and IgG1 and chronic activation of T cells [25]. The pathophysiology of ALCL and SIGBIC is very similar, with the only difference being the monoclonal neoplasia induced by the activation of T lymphocytes in ALCL, prompting consideration of whether ALCL is an evolution of SIGBIC. Clinically, ALCL may present as fluid filling within the intracapsular space (seroma), while SIGBIC is most often present as an intracapsular mass. Both conditions usually have an excellent prognosis once the fibrous capsule is excised and the implant is removed [28].
Studies on silicone, metals, and the risk of lymphoma
Due to evidence on breast implant‐associated ALCL, some reports propose a possible development of ALCL in relation to other implants, such as metal. Examples include ALCL associated with a stainless‐steel fixation plate for tibial fracture repair or after the placement of dental implants [29, 30]. Chronic inflammation and antigenic stimulation caused by the presence of implants (such as silicone, metal, or others) are suggested as possible neoplastic triggers. Resembling lymphomas associated with other inflammatory conditions, implant‐associated lymphomas are believed to share similar features, including development after prolonged inflammation, localization to a confined body space, and a latency period until the development of lymphoid malignancy. This can be attributed to ongoing inflammation and chronic stimulation of adaptive immune cells with polyclonal activation, which may result in monoclonality and ultimately lead to the development of lymphoma in genetically susceptible hosts [21]. The relationship between SBIs and lymphoma can be demonstrated by the well‐established link between Epstein–Barr virus (EBV) infection and the risk of lymphoma. The pathogenesis of EBV‐associated lymphomas involves dysregulation between inflammatory and inflammation‐neutralizing processes, leading to the production of radical oxygen species that can cause the impairment of critical oncogenic pathways, such as p53, promoting lymphomagenesis and eventually lymphomas [31]. As mentioned, silicone particles are capable of infiltrating lymph nodes, not only local but also distal ones, and enhancing antigen‐specific immune reactions. Thus, the presence of SBIs is comparable to latent infection, with EBV leading to chronic nonspecific stimulation of adaptive immunity, polyclonal activation, monoclonal activation, and eventually, the development of lymphoma.
References
1 Nicholson, L.B. (2016). The immune system.
Essays Biochem.
60 (3): 275–301.
2 Yatim, K.M. and Lakkis, F.G. (2015). A brief journey through the immune system.
Clin. J. Am. Soc. Nephrol.
10 (7): 1274–1281.
3 Brodin, P. and Davis, M.M. (2017). Human immune system variation.
Nat. Rev. Immunol.
17 (1): 21–29.
4 Watad, A., Sharif, K., and Shoenfeld, Y. (2017). The ASIA syndrome: basic concepts.
Mediterr. J. Rheumatol.
28 (2): 64–69.
5 Anderson, J.M., Rodriguez, A., and Chang, D.T. (2008). Foreign body reaction to biomaterials.
Semin. Immunol.
20 (2): 86–100.
6 Mariani, E., Lisignoli, G., Borzì, R.M., and Pulsatelli, L. (2019). Biomaterials: foreign bodies or tuners for the immune response?
Int. J. Mol. Sci.
20 (3): 636.
7 Veiseh, O. and Vegas, A.J. (2019). Domesticating the foreign body response: recent advances and applications.
Adv. Drug Deliv. Rev.
144: 148–161.
8 Higgins, D.M., Basaraba, R.J., Hohnbaum, A.C. et al. (2009). Localized immunosuppressive environment in the foreign body response to implanted biomaterials.
Am. J. Pathol.
175 (1): 161–170.
9 Hajdu, S.D., Agmon‐Levin, N., and Shoenfeld, Y. (2011). Silicone and autoimmunity: silicone and autoimmunity.
Eur. J. Clin. Investig.
41 (2): 203–211.
10 Maijers, M.C., de Blok, C.J.M., Niessen, F.B. et al. (2013). Women with silicone breast implants and unexplained systemic symptoms: a descriptive cohort study.
Neth. J. Med.
71 (10): 534–540.
11 Watad, A., Rosenberg, V., Tiosano, S. et al. (2018). Silicone breast implants and the risk of autoimmune/rheumatic disorders: a real‐world analysis.
Int. J. Epidemiol.
47 (6): 1846–1854.
12 Balk, E.M., Earley, A., Avendano, E.A., and Raman, G. (2016). Long‐term health outcomes in women with silicone gel breast implants: a systematic review.
Ann. Intern. Med.
164 (3): 164.
13 McDonald, A.H., Schneider, M., Gudenkauf, L. et al. (1998). Silicone gel enhances the development of autoimmune disease in New Zealand black mice but fails to induce it in BALB/cAnPt mice.
Clin. Immunol. Immunopathol.
87 (3): 248–255.
14 Schaefer, C.J. and Wooley, P.H. (1999). The influence of silicone implantation on murine lupus in MRL lpr/lpr mice.
J. Rheumatol.
26 (10): 2215–2221.
15 Huang, X., Zhou, Y., Liu, W. et al. (2017). Identification of hub genes related to silicone‐induced immune response in rats.
Oncotarget
8 (59): 99772–99783.
16 Kowalik, C.R., Zwolsman, S.E., Malekzadeh, A. et al. (2022). Are polypropylene mesh implants associated with systemic autoimmune inflammatory syndromes? A systematic review.
Hernia
26 (2): 401–410. 12 [cited 2022 Mar 2].
https://link.springer.com/10.1007/s10029-021-02553-y
.
17 Dias, E.R.M., Pivetta, L.G.A., de Carvalho, J.P.V. et al. (2021). Autoimmune [auto‐inflammatory] syndrome induced by adjuvants (ASIA): case report after inguinal hernia repair with mesh.
Int. J. Surg. Case Rep.
84: 106060.
18 Di Vita, G., Patti, R., Sparacello, M. et al. (2008). Impact of different texture of polypropylene mesh on the inflammatory response.
Int. J. Immunopathol. Pharmacol.
21 (1): 207–214.
19 Chughtai, B., Sedrakyan, A., Mao, J. et al. (2017). Is vaginal mesh a stimulus of autoimmune disease?
Am. J. Obstet. Gynecol.
216 (5): 495.e1–495.e7.
20 Tervaert, J.W.C. (2018). Autoinflammatory/autoimmunity syndrome induced by adjuvants (Shoenfeld’s syndrome) in patients after a polypropylene mesh implantation.
Best Pract. Res. Clin. Rheumatol.
32 (4): 511–520.
21 U.S Food & Drug Administration (FDA) (2019). Biological responses to metal implants.
22 Mishra, K.P. (2020). Heavy metals exposure and risk of autoimmune diseases: a review.
Arch. Immunol. Allergy
3 (2): 22–26.
23 Pollard, K.M. (2015). Environment, Autoantibodies, and Autoimmunity.
Front. Immunol.
6: 60. 11 [cited 2022 Mar 2];6.
http://journal.frontiersin.org/Article/10.3389/fimmu.2015.00060/abstract
.
24 de Faria Castro Fleury, E., D’Alessandro, G.S., and Lordelo Wludarski, S.C. (2018). Silicone‐induced granuloma of breast implant capsule (SIGBIC): histopathology and radiological correlation.
J Immunol Res
2018: 1, 9.
25 de Fleury, E.F.C. (2020). Synchronous breast implant associated anaplastic large cell lymphoma (BIA‐ALCL) and silicone induced granuloma of breast implant capsule (SIGBIC): What to learn.
Radiol. Case Rep.
15 (10): 1736–1742.
26 Kim, B., Predmore, Z.S., Mattke, S. et al. (2015). Breast implant–associated anaplastic large cell lymphoma: updated results from a structured expert consultation process.
Plast. Reconstr. Surg. Glob. Open
3 (1): e296.
27 Keech, J.A. and Creech, B.J. (1997). Anaplastic T‐cell lymphoma in proximity to a saline‐filled breast implant.
Plast. Reconstr. Surg.
100 (2): 554–555.
28 de Fleury, E.F.C., Rêgo, M.M., Ramalho, L.C. et al. (2017). Silicone‐induced granuloma of breast implant capsule (SIGBIC): similarities and differences with anaplastic large cell lymphoma (ALCL) and their differential diagnosis.
Breast Cancer (Dove Med. Press)
9: 133–140.
29 Palraj, B., Paturi, A., Stone, R.G. et al. (2010). Soft tissue anaplastic large T‐cell lymphoma associated with a metallic orthopedic implant: case report and review of the current literature.
J. Foot and Ankle Surg.
49 (6): 561–564.
30 Yoon, H.‐J., Choe, J.‐Y., and Jeon, Y.K. (2015). Mucosal CD30‐positive T‐cell lymphoproliferative disorder arising in the oral cavity following dental implants: report of the first case.
Int. J. Surg. Pathol.
23 (8): 656–661.
31 Bizjak, M., Selmi, C., Praprotnik, S. et al. (2015). Silicone implants and lymphoma: the role of inflammation.
J. Autoimmun.
65: 64–73.
