Angioedema:
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
Philadelphia [u.a.]
Saunders
2006
|
| Schriftenreihe: | Immunology and allergy clinics of North America
26,4 |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XV S., S. 604 - 789 Ill., graph. Darst. |
| ISBN: | 1416038094 9781416038092 |
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Datensatz im Suchindex
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| adam_text | ANGIOEDEMA
CONTENTS
Foreword
Rafeul Alam
Preface
Bruce L. Zuraw
Differential Diagnosis of Angioedema
David
Angioedema is a swelling of a defined area that typically lasts for
no longer than a few days. However, allergists will often be con¬
sulted on cutaneous reactions that do not (by history) suggest an¬
gioedema nor appear to be consistent with angioedema. Most of
the conditions that present with swelling are due to dependent
edema, infections, or medication side effects. However, angio¬
edema can be a result of autoimmune conditions that present with
angioedema and not urticaria. A high index of suspicion for other
conditions should help in the differential diagnoses.
Structure and Function of Cl-Inhibitor
Ineke G.A.
Heterozygous deficiency of
ical picture of hereditary angioedema
protease inhibitor (serpin). Cl-IXH is unique among serpins in that
it has a unique
any known protein, in addition to its serpin domain. In this article
thé
chanism of serpins in genera! and discuss the structure and func¬
tion of Cl-IXH in light of these insights. In addition,
consequences of mutations in Cl-IXH as occurring in patients
uho
the unique
VOLUME
Mechanism of Angioedema in First Complement Component
Inhibitor Deficiency
Alvin E. Davis III
Since shortly after the discovery that hereditary angioedema re¬
sulted from deficiency of first complement component (Cl) inhibi¬
tor, the characterization of the mediator of angioedema has been a
major goal. However, because Cl inhibitor regulates activation of
both the contact and complement systems, identification of the
mediator was not immediately accomplished. For a number of
years, some studies appeared to indicate involvement of one sys¬
tem, whereas other studies suggested involvement of the other.
However, the vast majority of the evidence accumulated over the
past several years indicates quite clearly that the major mediator
is bradykinin. Therefore, unregulated contact system activation is
the defect that leads directly to the development of angioedema.
Hereditary Angioedema: The Clinical Syndrome
and its Management in the United States
Michael M. Frank
There have been important breakthroughs in the understanding
and treatment of hereditary anigoedema
normality of the serum protein Cl inhibitor led to purified protein
use to end attacks. Consideration of endocrine functions led to re¬
discovery of impeded
siderations of pathophysiology led to introduction of
aminocaproic and rranexemic acids in prophylaxis and to a resur¬
gence in trials of new therapeutic agents. We have gone from a si¬
tuation where it was not uncommon for patients to have a severe
attack sometime in their lives that led to airway compromise and
possible death to a situation where death from disease is highly
unusual. Thus
medicine.
Acquired Deficiency of the Inhibitor of the First Complement
Component: Presentation, Diagnosis, Course, and Conventional
Management
Lorenza
Andrea Zanichelli, and Marco Cicardi
Acquired deficiency of the inhibitor of the first complement compo¬
nent (Cl-INH) is a rare, potentially life-threatening disease whose
cause, course, and management are not completely defined. This
article analyzes the etiopathogenetic mechanism, the clinical pre¬
sentation, and the relationship between acquired Cl-INH defi¬
ciency and lymphoproliferative disorders. Moreover, the authors
give an overview of the outcome of the disease and the different
therapies proposed to cure it.
CONTENTS
Novel Therapies for Hereditary Angioedema
Bruce L. Zuraw
Advances in our understanding of the molecular mechanisms un¬
derlying hereditary angioedema
ment of new treatment modalities. Five new drugs for the
treatment of
United States. These novel therapeutics can be divided into two
groups: drugs that replace Cl inhibitor (C1INH) functional activity
and drugs that abrogate the bradykinin-mediated increase in vas¬
cular permeability associated with
cludes two plasma-derived C1INH concentrates as well as a
recombinant
group includes an engineered plasma kallikrein inhibitor as well
as a B2 bradykinin receptor antagonist. This article reviews the ra¬
tionale, development, and potential use of these novel therapeutics.
Hereditary Angioedema with Normal Cl Inhibitor Activity
Including Hereditary Angioedema with Coagulation Factor
Gene Mutations
Konrad
Until recently it was assumed that hereditary angioedema is a dis¬
ease that results exclusively from a deficiency of the Cl inhibitor. In
2000,
tivity, and protein in plasma were described; all patients were wo¬
men. In many of the affected women, oral contraceptives, hormone
replacement therapy containing estrogens, and pregnancies trig¬
gered the clinical symptoms. Recently, in some families mutations
in the coagulation factor
in the affected women.
Angiotensin-Converting Enzyme Inhibitor-Associated
Angioedema
James Brian Byrd, Albert Adam, and Nancy J. Brown
Angioedema, characterized by swelling of the lips, face, and ton¬
gue, occurs in anywhere from
ing enzyme (ACE) inhibitor users. The incidence is more
common in black Americans than in white Americans, in women
than in men, and in smokers than in
and relapsing nature of ACE inhibitor-associated angioedema
can confound clinical recognition of the adverse event but also pro¬
vides clues to its causes. Defective degradation of vasoactive pep-
tide substrates of ACE, such as bradykinin or substance P, may
contribute via non-ACE pathways to the pathogenesis of ACE in¬
hibitor—associated angioedema.
CONTENTS
Idiopathic
Evangelo
Angioedema is a constellation of syndromes characterized by inter¬
mittent swelling of the deeper layers of the skin or
both). About
urticaria and pruritus. Some angioedema is caused by vasoactive
substances secreted by activated mast cells, eosinophils, or by an
inappropriate activation of the complement and
which may be either hereditary or acquired. However, most cases
of angioedema are idiopathic. Performing a comprehensive history
and physical examination and establishing a close partnership with
the patient are still the most important steps in determining the
cause and treating the condition.
Anaphylactic and Anaphylactoid Causes of Angioedema
Paul A.
Angioedema (and urticaria) are the most common manifestations
of anaphylaxis. While urticaria appears to occur or be recognized
more frequently during acute episodes of anaphylaxis, it is often
absent during fatal anaphylaxis when massive tongue enlargement
or pharyngeal or laryngeal edema is the cause of asphyxiation.
Medications, foods, contrast materials, physical stimuli, and idio¬
pathic anaphylaxis are well-recognized causes of angioedema.
New immunomodulatory therapies also have been associated with
anaphylaxis and angioedema. In the absence of skin test reagents
for detection of anti-penicillin IgE antibodies, graded test-chal¬
lenges should be considered for penicillin-allergic patients who re¬
quire beta-lactam antibiotic therapy. Similar approaches are useful
for aspirin, non-selective NSAIDs, and other medications where
IgE antibodies are not present or cannot be identified.
Су
Episodic Angioedema with Eosinophilia (Gleich s Syndrome)
Aleena Banerji, Peter F. Weller, and Javed Sheikh
Of the various angioedema syndromes, some are thought to be
cytokine-mediated. The authors review the cytokine-associated
angioedema syndromes with a focus on episodic angioedema with
eosinophilia (Gleich s Syndrome) and non-episodic angioedema
with eosinophilia. NERDS (nodules, eosinophilia, rheumatism, der¬
matitis, and swelling), Clarkson Syndrome (idiopathic capillary
leak syndrome), and angioedema associated with aldesleukin (hu¬
man
There is still much to be learned about the pathophysiology, diagno¬
sis, and treatment of patients with these disorders.
Index
CONTENTS
|
| adam_txt |
ANGIOEDEMA
CONTENTS
Foreword
Rafeul Alam
Preface
Bruce L. Zuraw
Differential Diagnosis of Angioedema
David
Angioedema is a swelling of a defined area that typically lasts for
no longer than a few days. However, allergists will often be con¬
sulted on cutaneous reactions that do not (by history) suggest an¬
gioedema nor appear to be consistent with angioedema. Most of
the conditions that present with swelling are due to dependent
edema, infections, or medication side effects. However, angio¬
edema can be a result of autoimmune conditions that present with
angioedema and not urticaria. A high index of suspicion for other
conditions should help in the differential diagnoses.
Structure and Function of Cl-Inhibitor
Ineke G.A.
Heterozygous deficiency of
ical picture of hereditary angioedema
protease inhibitor (serpin). Cl-IXH is unique among serpins in that
it has a unique
any known protein, in addition to its serpin domain. In this article
thé
chanism of serpins in genera! and discuss the structure and func¬
tion of Cl-IXH in light of these insights. In addition,
consequences of mutations in Cl-IXH as occurring in patients
uho
the unique
VOLUME
Mechanism of Angioedema in First Complement Component
Inhibitor Deficiency
Alvin E. Davis III
Since shortly after the discovery that hereditary angioedema re¬
sulted from deficiency of first complement component (Cl) inhibi¬
tor, the characterization of the mediator of angioedema has been a
major goal. However, because Cl inhibitor regulates activation of
both the contact and complement systems, identification of the
mediator was not immediately accomplished. For a number of
years, some studies appeared to indicate involvement of one sys¬
tem, whereas other studies suggested involvement of the other.
However, the vast majority of the evidence accumulated over the
past several years indicates quite clearly that the major mediator
is bradykinin. Therefore, unregulated contact system activation is
the defect that leads directly to the development of angioedema.
Hereditary Angioedema: The Clinical Syndrome
and its Management in the United States
Michael M. Frank
There have been important breakthroughs in the understanding
and treatment of hereditary anigoedema
normality of the serum protein Cl inhibitor led to purified protein
use to end attacks. Consideration of endocrine functions led to re¬
discovery of impeded
siderations of pathophysiology led to introduction of
aminocaproic and rranexemic acids in prophylaxis and to a resur¬
gence in trials of new therapeutic agents. We have gone from a si¬
tuation where it was not uncommon for patients to have a severe
attack sometime in their lives that led to airway compromise and
possible death to a situation where death from disease is highly
unusual. Thus
medicine.
Acquired Deficiency of the Inhibitor of the First Complement
Component: Presentation, Diagnosis, Course, and Conventional
Management
Lorenza
Andrea Zanichelli, and Marco Cicardi
Acquired deficiency of the inhibitor of the first complement compo¬
nent (Cl-INH) is a rare, potentially life-threatening disease whose
cause, course, and management are not completely defined. This
article analyzes the etiopathogenetic mechanism, the clinical pre¬
sentation, and the relationship between acquired Cl-INH defi¬
ciency and lymphoproliferative disorders. Moreover, the authors
give an overview of the outcome of the disease and the different
therapies proposed to cure it.
CONTENTS
Novel Therapies for Hereditary Angioedema
Bruce L. Zuraw
Advances in our understanding of the molecular mechanisms un¬
derlying hereditary angioedema
ment of new treatment modalities. Five new drugs for the
treatment of
United States. These novel therapeutics can be divided into two
groups: drugs that replace Cl inhibitor (C1INH) functional activity
and drugs that abrogate the bradykinin-mediated increase in vas¬
cular permeability associated with
cludes two plasma-derived C1INH concentrates as well as a
recombinant
group includes an engineered plasma kallikrein inhibitor as well
as a B2 bradykinin receptor antagonist. This article reviews the ra¬
tionale, development, and potential use of these novel therapeutics.
Hereditary Angioedema with Normal Cl Inhibitor Activity
Including Hereditary Angioedema with Coagulation Factor
Gene Mutations
Konrad
Until recently it was assumed that hereditary angioedema is a dis¬
ease that results exclusively from a deficiency of the Cl inhibitor. In
2000,
tivity, and protein in plasma were described; all patients were wo¬
men. In many of the affected women, oral contraceptives, hormone
replacement therapy containing estrogens, and pregnancies trig¬
gered the clinical symptoms. Recently, in some families mutations
in the coagulation factor
in the affected women.
Angiotensin-Converting Enzyme Inhibitor-Associated
Angioedema
James Brian Byrd, Albert Adam, and Nancy J. Brown
Angioedema, characterized by swelling of the lips, face, and ton¬
gue, occurs in anywhere from
ing enzyme (ACE) inhibitor users. The incidence is more
common in black Americans than in white Americans, in women
than in men, and in smokers than in
and relapsing nature of ACE inhibitor-associated angioedema
can confound clinical recognition of the adverse event but also pro¬
vides clues to its causes. Defective degradation of vasoactive pep-
tide substrates of ACE, such as bradykinin or substance P, may
contribute via non-ACE pathways to the pathogenesis of ACE in¬
hibitor—associated angioedema.
CONTENTS
Idiopathic
Evangelo
Angioedema is a constellation of syndromes characterized by inter¬
mittent swelling of the deeper layers of the skin or
both). About
urticaria and pruritus. Some angioedema is caused by vasoactive
substances secreted by activated mast cells, eosinophils, or by an
inappropriate activation of the complement and
which may be either hereditary or acquired. However, most cases
of angioedema are idiopathic. Performing a comprehensive history
and physical examination and establishing a close partnership with
the patient are still the most important steps in determining the
cause and treating the condition.
Anaphylactic and Anaphylactoid Causes of Angioedema
Paul A.
Angioedema (and urticaria) are the most common manifestations
of anaphylaxis. While urticaria appears to occur or be recognized
more frequently during acute episodes of anaphylaxis, it is often
absent during fatal anaphylaxis when massive tongue enlargement
or pharyngeal or laryngeal edema is the cause of asphyxiation.
Medications, foods, contrast materials, physical stimuli, and idio¬
pathic anaphylaxis are well-recognized causes of angioedema.
New immunomodulatory therapies also have been associated with
anaphylaxis and angioedema. In the absence of skin test reagents
for detection of anti-penicillin IgE antibodies, graded test-chal¬
lenges should be considered for penicillin-allergic patients who re¬
quire beta-lactam antibiotic therapy. Similar approaches are useful
for aspirin, non-selective NSAIDs, and other medications where
IgE antibodies are not present or cannot be identified.
Су
Episodic Angioedema with Eosinophilia (Gleich's Syndrome)
Aleena Banerji, Peter F. Weller, and Javed Sheikh
Of the various angioedema syndromes, some are thought to be
cytokine-mediated. The authors review the cytokine-associated
angioedema syndromes with a focus on episodic angioedema with
eosinophilia (Gleich's Syndrome) and non-episodic angioedema
with eosinophilia. NERDS (nodules, eosinophilia, rheumatism, der¬
matitis, and swelling), Clarkson Syndrome (idiopathic capillary
leak syndrome), and angioedema associated with aldesleukin (hu¬
man
There is still much to be learned about the pathophysiology, diagno¬
sis, and treatment of patients with these disorders.
Index
CONTENTS |
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| index_date | 2024-07-02T16:26:10Z |
| indexdate | 2024-07-09T20:52:24Z |
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| series2 | Immunology and allergy clinics of North America |
| spelling | Angioedema guest ed. Bruce L. Zuraw Philadelphia [u.a.] Saunders 2006 XV S., S. 604 - 789 Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Immunology and allergy clinics of North America 26,4 Angioneurotic Edema Angioneurotic edema Immunologie (DE-588)4026637-0 gnd rswk-swf Angiom (DE-588)4262670-5 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Angiom (DE-588)4262670-5 s Immunologie (DE-588)4026637-0 s b DE-604 Zuraw, Bruce L. Sonstige oth Immunology and allergy clinics of North America 26,4 (DE-604)BV000645505 26,4 Digitalisierung UB Regensburg application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=015419420&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Angioedema Immunology and allergy clinics of North America Angioneurotic Edema Angioneurotic edema Immunologie (DE-588)4026637-0 gnd Angiom (DE-588)4262670-5 gnd |
| subject_GND | (DE-588)4026637-0 (DE-588)4262670-5 (DE-588)4143413-4 |
| title | Angioedema |
| title_auth | Angioedema |
| title_exact_search | Angioedema |
| title_exact_search_txtP | Angioedema |
| title_full | Angioedema guest ed. Bruce L. Zuraw |
| title_fullStr | Angioedema guest ed. Bruce L. Zuraw |
| title_full_unstemmed | Angioedema guest ed. Bruce L. Zuraw |
| title_short | Angioedema |
| title_sort | angioedema |
| topic | Angioneurotic Edema Angioneurotic edema Immunologie (DE-588)4026637-0 gnd Angiom (DE-588)4262670-5 gnd |
| topic_facet | Angioneurotic Edema Angioneurotic edema Immunologie Angiom Aufsatzsammlung |
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