<unk>  angioedema is diagnosed through a supportive clinical examination usually in addition to laboratory evaluation. The clinical history consists of recurrent angioedema episodes, symptom onset after 30 years of age, and negative family history of hereditary angioedema. Laboratory evaluation typically consists of complement studies, genotyping, and/or checking for antibodies against<unk> INH. The most useful complement studies obtained are as follows: * C4 level * C3 level *<unk>  INH antigenic level *<unk>  INH function *<unk> q level To help confirm cases of<unk>  angioedema, the following pattern of complement studies are observed: low C4 level, low<unk> -INH protein level, low<unk> q level, and decreased<unk> -INH protein function.This figure provides a diagnostic approach to<unk><unk>  deficiency. Using the diagnostic approach mentioned here and in the figure shown above,<unk>  angioedema is categorized into subtypes for targeted management. The following subtypes include: AAE-I, AAE-II, sex-hormone dependent AAE, and drug-induced AAE. AAE-I subtype groups paraneoplastic syndrome or B-cell malignancies that lead to destruction of the<unk> -INH enzyme causing<unk>  angioedema. AAE-II subtype groups autoimmune disorders, such as systemic lupus, causing<unk>  angioedema. Sex-hormone dependent AAE is associated with case reports of individuals with abnormally elevated estrogen levels or in cases where physiologically elevated estrogen is expected as in pregnancy. Drug-induced AAE can be triggered by certain medications, including ACE<unk> s or angiotensin receptor blockers. Furthermore, additional laboratory testing can be done to consider other causes of swelling that appear similar to angioedema. Some of the common differential diagnoses for angioedema include: allergic reactions, contact dermatitis, skin and soft tissue infections (i.e. cellulitis), lymphedema, and foreign body aspiration.
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