Treatment of<unk>  angioedema is separated into two main parts. First controlling acute symptoms during angioedema attacks is crucial for preventing and lowering the risk of mortality. Second, managing AAE chronically with prophylactic treatment is important to improve prognosis and quality of life. Both pharmacologic therapies (i.e. medications) and symptom management can be used in both acute and chronic treatment of AAE. Pharmacologic treatment in acute situations consists of replacing the enzyme concentrate that is<unk> nt or dysfunctional in this disease process. In life threatening situations, including cases of oral and pharyngeal swelling, it is important to manage these symptoms and to protect the airways in order to lower the risk of mortality. Typical treatments for anaphylaxis and allergic reactions, such as epinephrine, corticosteroids, and antihistamines, are often used in acute cases of AAE with variable resolution.<unk> -INH concentrates are available in intravenous (IV) and intramuscular (IM) methods of delivery.<unk> -INH concentrate therapy has shown considerable efficacy (or effect) in acute and prophylactic treatments of hereditary angioedema, but has varying levels of efficacy in AAE. For prophylaxis, clinicians focus on controlling underlying underlying disorders, such as those mentioned under causes, that could be contributing to AAE pathophysiology. Beyond controlling comorbidities, angioedema is usually managed through medications to prevent attacks and to reduce the number of attacks.<unk> -INH concentrate can be used to replace deficient or abnormal<unk> -INH enzyme with considerable efficacy. The following list of medical therapies have been used for prophylaxis, including androgens, tranexamic acid, and monoclonal antibody such as rituximab. These agents all have varying roles, efficacy, and potential risks through their use.
Acquired C1 esterase inhibitor deficiency
Hereditary angioedema
Terminal complement pathway deficiency
Type IV hypersensitivity
IgG4-related skin disease
Complement 3 deficiency
Type III hypersensitivity
Complement 2 deficiency