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Preeclampsia - Basic, Genomic, and Clinical
von: Shigeru Saito
Springer-Verlag, 2018
ISBN: 9789811058912 , 286 Seiten
Format: PDF, Online Lesen
Kopierschutz: Wasserzeichen
Preis: 117,69 EUR
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Preface
6
Contents
7
Part I: Risk Factors for Preeclampsia
9
1: Risk Factors for Preeclampsia
10
1.1 Introduction
11
1.2 Prevalence
11
1.3 Risk Factors
11
1.3.1 Pregnancy-Specific Factors
11
1.3.1.1 First Pregnancy (Nulliparity)
11
1.3.1.2 New Paternity (Primipaternity Hypothesis)
16
1.3.1.3 Limited Sperm Exposure
16
1.3.1.4 Interval between Pregnancies
17
1.3.1.5 Assisted Reproductive Technology
17
1.3.1.6 Multiple Pregnancy
17
1.3.1.7 Hydatidiform Mole
18
1.3.1.8 Fetal Gender
18
1.3.2 Pre-existing Maternal Conditions
19
1.3.2.1 Older Age
19
1.3.2.2 Higher Body Mass Index or Obesity
19
1.3.2.3 Personal or Family History of Preeclampsia
20
Personal History
20
Family History
21
Paternal Factor (So-Called Dangerous Father)
21
1.3.2.4 Ethnicity or Race
21
1.3.2.5 Pre-existing Hypertension (Chronic Hypertension)
21
1.3.2.6 Pre-existing Diabetes Mellitus (Insulin-Dependent Diabetes Mellitus)
22
1.3.2.7 Pre-existing Renal Disease
22
1.3.2.8 Antiphospholipid Antibody Syndrome
23
1.3.2.9 Systemic Lupus Erythematosus
23
1.3.2.10 Infections
24
1.3.3 Environmental Factors
24
1.3.3.1 High Altitude
24
1.3.3.2 Income
25
1.4 Factors for Preventing Preeclampsia
25
1.4.1 Smoking
25
1.4.2 Summer Births
26
1.4.3 Maternal Physical Activity
26
References
27
Part II: Genetic Background in Preeclampsia
33
2: Genetic Background of Preeclampsia
34
2.1 Introduction
35
2.2 Overview of Genetic Factors in the Pathogenesis of Preeclampsia
35
2.3 Maternal Genetic Factors
37
2.3.1 Vasoactive-Related Gene Polymorphism
37
2.3.2 Coagulation-Related Genes
38
2.3.3 Cytokine-Related Genes
39
2.3.4 Others
39
2.4 Paternal/Fetal Genetic Factors
39
2.4.1 Paternal Genetic Factors
39
2.4.2 Fetal Genetic Factors
39
2.5 HLA Polymorphisms
40
2.6 Maternal and Fetal Genotypes
41
2.7 Genome-Wide Association Studies
42
2.8 Future Directions
43
References
43
Part III: Pathological Findings in Preeclampsia
49
3: Trophoblast Invasion: Remodelling of Spiral Arteries and Beyond
50
3.1 Introduction
51
3.2 Extravillous Trophoblast
51
3.2.1 Interstitial Trophoblast
53
3.2.2 Endoglandular Trophoblast
55
3.2.3 Endovascular Trophoblast
55
3.2.3.1 Endoarterial Trophoblast
57
3.2.3.2 Endovenous Trophoblast
58
3.2.4 Endolymphatic Trophoblast
58
3.3 General Considerations on Trophoblast Invasion
58
3.3.1 Deep Invasion
59
3.3.2 Shallow Invasion in the First Trimester
59
3.4 Preeclampsia and Shallow Invasion
60
3.4.1 Placental Blood Flow
61
3.4.2 Preeclampsia and Placental Hypoxia
62
3.4.2.1 Effect of Shallow Trophoblast Invasion
62
3.4.2.2 Placental Perfusion and Oxygenation
62
References
63
Part IV: Pathophysiology of Preeclampsia
66
4: Immunological Maladaptation
67
4.1 Introduction
68
4.2 Role of the Immune System
69
4.3 Epidemiological Evidence of Impaired Tolerance in Preeclampsia
70
4.4 Immunological Changes in Preeclampsia
71
4.4.1 Macrophages and Monocytes
71
4.4.2 Dendritic Cells (DCs)
72
4.4.3 NK Cells
74
4.4.4 Th1/Th2/Th17/Treg Balance
75
4.5 The Immune-Mediated Pathophysiology of Preeclampsia
76
4.6 Immunological Findings in Animal Models of Preeclampsia
78
4.7 Challenges in Treating Preeclampsia with Immune Cells or Immunomodulators
79
References
81
5: Glucose Intolerance and Insulin Resistance: Relevance in Preeclampsia
87
5.1 Introduction
87
5.2 Preeclampsia and the Glucose Tolerance Defect
89
5.3 Preeclampsia Presents a Risk for Future Diabetes Development
91
5.4 Perspective
93
References
96
6: Placental Adenosine Signaling in the Pathophysiology of Preeclampsia
101
6.1 Introduction
102
6.2 Metabolism of Adenosine and Adenosine Signaling via Adenosine Receptors
102
6.3 Detrimental Roles of Adenosine Signaling in Various Chronic Disease States
104
6.4 Evidence Associated with Adenosine Signaling and PE
105
6.4.1 Increased Levels of Adenosine in Maternal and Fetoplacental Circulation in PE Patients
105
6.4.2 Expression of Adenosine Receptors in the Placenta of PE Patients
106
6.5 Identification of Enhanced Placental Adenosine Signaling as a Novel Pathogenic Factor for PE
106
6.5.1 Generation of Genetically Engineered Pregnant Mouse with Placenta-Specific Elevation of Adenosine
106
6.5.2 Dams with Elevated Placental Adenosine Displayed Key Features of PE
108
6.5.3 ADORA2B Activation Is Responsible for the Features of PE Induced by Placental Excess Accumulation of Adenosine
108
6.5.4 Human Evidence of the Accumulated Placental Adenosine and Its Underlying Mechanisms Contributing to PE
109
6.5.5 Elevated CD73 Underlies Increased Placental Adenosine and Contributes to Pathophysiology of PE via ADORA2B Activation
109
6.6 Conclusion and Future Direction
110
References
111
7: Obesity, Adipokines, and Lipokines
115
7.1 Overview
115
7.2 Obesity
116
7.3 Adipokine
117
7.3.1 Tumor Necrosis Factor
118
7.3.2 Leptin
118
7.3.3 Adiponectin
119
7.3.4 Resistin
119
7.3.5 Plasminogen Activator Inhibitor
119
7.3.6 Monocyte Chemoattractant Protein-1
120
7.3.7 Visfatin
120
7.3.8 Interleukin-6
120
7.3.9 Apelin
121
7.4 Lipokine
121
7.4.1 Free Fatty Acids
121
7.4.2 Palmitoleate (Palmitoleic Acid)
122
7.4.3 Retinol-Binding Protein 4
122
7.4.4 Adipocyte Fatty Acid-Binding Protein
122
References
123
8: Autophagy in Preeclampsia
127
8.1 Introduction
128
8.2 The Role of Autophagy in Reproduction
128
8.3 The Role of Autophagy on Trophoblast Functions
131
8.4 The Role of Autophagy in Preeclampsia or FGR: Pros and Cons
133
8.5 Protein Aggregation in Preeclampsia
135
8.6 Cautions for Estimating Autophagy in the Placenta
135
8.7 Future Directions for Autophagy Research on Preeclampsia
137
References
138
9: Animal Models in Preeclampsia
143
9.1 Introduction
144
9.2 Pathology
144
9.3 Animal Models
145
9.3.1 What Kind of Animals?
145
9.3.2 Immune Response
145
9.3.2.1 Administration of Low-Dose Endotoxin
147
9.3.2.2 IL-4 and IL-12 Administration: Th1/Th2 Imbalance Model
147
9.3.2.3 Cytokine Administration/Reduction Models (TNF?, IL-6, IL-10)
147
9.3.2.4 Autoantibodies to Angiotensin II Type I Receptors (AT1-AAs)
147
9.3.3 Trophoblast Invasion
148
9.3.3.1 Doxycycline-Administrated Model
148
9.3.3.2 Storkhead Box 1 (STOX1)
148
9.3.4 Oxygen Dysregulation
148
9.3.4.1 Reduced Uterine Perfusion Pressure (RUPP) Model
148
9.3.4.2 Hypoxia-Inducible Factor 1? (HIF-1?)-Related Models
149
9.3.5 Anti-angiogenesis
150
9.3.5.1 sFLT1 Model Animals
150
9.3.5.2 sENG Model
150
9.3.6 Preexisting Hypertension Model/Spontaneous Model
151
9.3.6.1 Renin Angiotensin-Related Models of Preeclampsia
151
9.3.6.2 The BPH/5 Mouse
151
9.3.7 Others
151
9.3.7.1 Insulin-Induced Models of Preeclampsia
151
9.3.7.2 Stress-Induced Model Animals
152
9.3.7.3 N?-Nitro-l-Arginine Methyl Ester Hydrochloride (l-NAME)-Treated Rat
153
9.3.7.4 Adenosine-Related Placental Dysfunction Model
153
9.4 Challenges and Future Directions
153
References
154
10: The Differences Between Early- and Late-Onset Pre-eclampsia
158
10.1 Introduction: What Is Pre-eclampsia?
159
10.2 Definitions of Early- and Late-Onset Pre-eclampsia
160
10.3 Clinical Features of Early- and Late-Onset Pre-eclampsia
161
10.3.1 Differences in Short-Term Outcomes and Risk of Recurrence
161
10.3.2 Differences in Long-Term Health Outcomes
161
10.4 Epidemiology of Early- and Late-Onset Pre-eclampsia Rates and Risk Factors
162
10.5 Previous Pathophysiological Understanding of Early- and Late-Onset Pre-eclampsia
163
10.6 Two Placental Pathways to Pre-eclampsia
165
10.7 The New Two-Stage Model in Relation to Early- and Late-Onset Pre-eclampsia
168
References
170
Part V: Prediction of Preeclampsia
174
11: sFlt-1/PLGF
175
11.1 Introduction
176
11.2 Anti-angiogenesis Is an Important Mechanism in the Pathogenesis of Preeclampsia
176
11.3 Diagnosis of Preeclampsia with the Use of Angiogenetic Factors
182
11.4 Angiogenic Factors and Prediction of Preeclampsia
186
11.4.1 Early Prediction of Preeclampsia and Screening in the First Trimester
186
11.4.2 Short-Term Prediction in the Second and Third Trimester
188
11.5 The sFlt-1/PlGF Ratio and Clinical Decision-Making
190
References
192
12: Ambulatory Blood Pressure Measurement and Home Blood Pressure Measurement
199
12.1 Introduction
199
12.2 Ambulatory Blood Pressure Measurements
202
12.3 Home Blood Pressure Measurements
203
12.4 Summary
204
References
206
13: MicroRNA
209
13.1 MicroRNAs
210
13.2 Placenta-Derived MicroRNAs
211
13.3 Placenta-Derived Exosomes
213
13.3.1 Placental miRNAs Are Released from the Villous Trophoblast into Maternal Circulation via Exosomes
213
13.3.2 Placenta-Derived Exosomes in Maternal Blood during Normal Pregnancy
214
13.4 Abnormal Expression of miRNAs in the Preeclamptic Placenta
215
13.5 Placenta-Derived Exosomes in Maternal Blood as Predictive Markers for PE
215
13.6 Placenta-Specific miRNAs in Maternal Blood as Predictive Markers for PE
216
13.7 Future Prospects
219
References
219
Part VI: Therapy
225
14: Novel Therapies for Preeclampsia
226
14.1 Introduction
226
14.2 Soluble Anti-Aangiogenic Factors in the Pathogenesis of Maternal Syndrome
227
14.3 Angiogenic Biomarkers
229
14.4 Targeted Therapeutics
230
References
233
15: Pravastatin for Preeclampsia Prevention and Treatment
237
15.1 Lessons from the Mouse
238
15.1.1 Pravastatin Prevents Adverse Pregnancy Outcomes in a Mouse Model of Antiphospholipid Syndrome (APS)
238
15.1.2 Pravastatin Prevents the Onset of Preeclampsia in Mouse Models
240
15.2 C1q KO and CBA/J × DBA/2 Mouse Models
241
15.3 sFlt-1-Induced Mouse Models
242
15.4 From Mice to Women: Pilot Clinical Studies
243
References
247
16: Prevention and Treatment of Stroke and Eclampsia
250
16.1 Introduction
251
16.2 Eclampsia
251
16.2.1 Epidemiology and Pathophysiology
251
16.2.2 Treatment and Prevention
252
16.2.2.1 Initial Emergent Care
252
16.2.2.2 Anticonvulsive Therapy
252
16.2.2.3 Antihypertensive Therapy
254
16.2.2.4 Discriminating Between Eclampsia and Stroke
254
16.2.2.5 Collaboration with Neurosurgeons
255
16.2.2.6 Hypertension During Labor (Labor-Onset Hypertension, LOH)
255
16.2.2.7 HBPM: A Tool for Predicting Eclampsia/Stroke
258
16.2.2.8 Verification of the Validity of the Expression “Eclampsia”
259
16.3 Pregnancy-Associated Stroke
259
16.3.1 Epidemiology and Outcomes
259
16.3.2 Treatment and Prevention
260
16.3.2.1 Cerebral Hemorrhaging
260
16.3.2.2 Subarachnoid Hemorrhaging (SAH)
260
16.3.2.3 Cerebral Infarction
261
16.3.2.4 Cerebral Venous Sinus Thrombosis (CVST)
261
16.3.2.5 Moyamoya Disease
262
16.3.2.6 Arteriovenous Malformations (AVM)
262
16.4 Case Presentation
262
16.4.1 Case 1: Eclampsia During Labor with Labor-Onset Hypertension
262
16.4.2 Case 2: Antepartum Cerebral Hemorrhaging
263
16.4.3 Case 3: Cerebral Hemorrhaging During Labor
263
16.5 Challenges and Future Directions
264
References
264
Part VII: The Risk of Cardiovascular Events in Preeclamptic Cases
268
17: Cardiovascular Disease Following Hypertensive Pregnancy
269
17.1 Introduction
270
17.2 Evidence for Long-Term Cardiovascular Risk
271
17.3 Other Long-Term Risks of Hypertensive Pregnancy
273
17.3.1 Cognitive Dysfunction
273
17.3.2 Chronic Kidney Disease
274
17.3.3 Diabetes
275
17.3.4 Venous Thromboembolism
275
17.3.5 Cancer
275
17.3.6 Cardiovascular Disease in the Offspring
275
17.4 Mechanisms by Which Pre-eclampsia Is Related to Cardiovascular Disease
276
17.4.1 Metabolic Syndrome
276
17.4.2 Sympathetic Nervous System
277
17.4.3 Effects of Pre-eclampsia upon the Heart
278
17.4.4 Changes in Vasculature
278
17.5 Opportunities to Prevent Cardiovascular Complications of Pre-eclampsia and Gestational Hypertension
279
17.5.1 Recognition of Risk
279
17.5.2 Lifestyle, Exercise and Drug Therapy
281
References
282