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This article is part of a Supplement: Volume 6 Supplement 2
This article is part of a Supplement: Volume 6 Supplement 2
This article is part of a Supplement: Volume 6 Supplement 2
This article is part of a Supplement: Volume 6 Supplement 2
Osteopontin (OPN) is a multifunctional cytokine that has been primarily investigated in Th1 diseases. Recently, it has also been implicated in Th2-mediated allergic diseases, such as asthma. The expression of ...
Little information is available on the effect of allergen-specific immunotherapy on airway responsiveness and markers in exhaled air. The aims of this study were to assess the safety of immunotherapy with puri...
Despite over a century of clinical use and a well-documented record of efficacy and safety, a growing minority in society questions the validity of vaccination and fear that this common public health intervent...
Eosinophilic esophagitis (EoE) is characterized by the inflammation of the esophagus and the infiltration of eosinophils into the esophagus, leading to symptoms such as dysphagia and stricture formation. Syste...
We published the Canadian 2003 International Consensus Algorithm for the Diagnosis, Therapy, and Management of Hereditary Angioedema (HAE; C1 inhibitor [C1-INH] deficiency) and updated this as Hereditary angio...
Advances in understanding the pathophysiology and mechanism of swelling in hereditary angioedema (HAE) has resulted in the development of multiple new drugs for the acute and prophylactic treatment of patients...
Hereditary angioedema (C1 inhibitor deficiency, HAE) is associated with intermittent swellings which are disabling and may be fatal. Effective treatments are available and these are most useful when given earl...
Manifestation of acute edema in hereditary angioedema (HAE) is characterized by interindividual and intraindividual variability in symptom expression over time. Flexible therapy options are needed.
C1-inhibitor (C1-INH) deficiency is a rare blood disorder resulting in angioedema attacks that are debilitating and may be life-threatening. Prophylaxis and therapy of events has changed since our first Canadi...
Hereditary angioedema is a rare disorder with a genetic background involving mutations in the genes encoding C1-INH and of factor XII. Its etiology is unknown in a proportion of cases. Recurrent edema formatio...
Hereditary angioedema (HAE) resulting from the deficiency of the C1 inhibitor (C1-INH) is a rare, life-threatening disorder. It is characterized by attacks of angioedema involving the skin and/or the mucosa of...
Women with hereditary angioedema (HAE) are more likely to be symptomatic that men. Hormonal factors (puberty, contraception, pregnancy,....) play a significant role in the precipitation or worsening of the con...
The clinical, biochemical and genetic features of the conditions known as estrogen-dependent inherited angioedema, estrogen-associated angioedema, hereditary angioedema with normal C-1 inhibitor, type III angi...
Until recently it was assumed that hereditary angioedema is a disease that results exclusively from a genetic deficiency of the C1 inhibitor. In 2000, families with hereditary angioedema, normal C1 inhibitor a...
Acquired angioedema (AAE) is characterized by acquired deficiency of C1 inhibitor (C1-INH), hyperactivation of the classical pathway of human complement and angioedema symptoms mediated by bradykinin released ...
Primary immune deficiency disorders (PIDs) are a group of diseases associated with a genetic predisposition to recurrent infections, malignancy, autoimmunity and allergy. The molecular basis of many of these d...
Hereditary Angioedema (HAE) is a rare, autosomal dominant (AD) disorder caused by a C1 esterase inhibitor (C1-inh) deficiency or qualitative defect. Treatment of HAE in many parts of the world fall short and c...
The current geriatric population in the United States accounts for approximately 12% of the total population and is projected to reach nearly 20% (71.5 million people) by 2030[1]. With this expansion of the numbe...
T cell disorders have been poorly understood until recently. Lack of knowledge of underlying molecular mechanisms together with incomplete data on long term outcome have made it difficult to assess prognosis a...
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
This article is part of a Supplement: Volume 6 Supplement 1
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