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Angioedema also known by its eponymic term “Quincke's edema” and old term “angioneurotic edema” is characterized as rapid swelling or edema (fluid accumulation) of the skin, mucosa and submucosal tissues. It is most often mediated by allergy and has been reported as an adverse drug reaction particularly ACE (angiotensin converting enzyme) inhibitors. The inherited form of angioedema which is due to deficiency of the blood protein C1- esterase inhibitor is called hereditary angioedema (HAE) or hereditary angio-neurotic edema (HANE). The angioedema that is due to antibody formation against C1INH (C1-esterase inhibitor) is an autoimmune disorder known as acquired angioedema which is associated with the development of lymphoma.

Angioedema Skin diseases

Angioedema is similar to hives or wheals, but the lesions are much bigger in size and form at a deeper layer of the skin. Typically, the skin of the face, around the mouth, the mouth’s mucosa as well as the tongue and sometimes even the throat swell up over a period of few minutes to several hours. The swelling may be accompanied by itchiness typically in the hands but can be elsewhere in the body. Sometimes there may also be slight decreased sensation in the affected areas due to nerve compression.

The most dangerous and life threatening situation is when swelling in the inner part of the throat occur because it can lead to blockage of air flow into the lungs. Therefore, in cases where the angioedema progresses rapidly, this should be treated as a medical emergency which necessitates acute medical care. The etiology of angioedema might also been a recent allergen exposure (e.g. peanuts), and hives tend to develop at the same time, but most often the cause is idiopathic or unknown. In some susceptible patients, there is increase probability of an angioedema episode with consumption of foods, beverages which are likely considered to be vasodilators such as alcohol, cinnamon and use of certain medications such as ibuprofen, aspirin and acetaminophen.

On the other hand, hereditary angioedema has no direct identifiable cause, although mild trauma and other external stimuli may also trigger the episodic attack. There is usually no associated itchiness or hives formation among patients with hereditary angioedema but this syndrome may have accompanying attacks of recurrent abdominal pain, sometimes leading to an unnecessary laparotomy (surgical incision of the abdomen). An increased incidence of autoimmune disease is likewise noted among these individuals (e.g. systemic lupus erythematosus, glomerulonephritis and hypothyroidism) due to altered complement system activity. Diagnosis of angioedema is essentially based on the clinical picture presented by the affected person. The following tests may be performed once the patient has been stabilized namely: complement levels, C1-inhibitor and complement factors 2 and 4 (showing depleted levels which may indicate the presence of hereditary angioedema). Allergy tests (e.g. skin test, patch test) are an additional test to determine if there is a need to avoid allergens in the future to prevent attacks of angioedema.

The pharmacologic treatment for cases of allergic angioedema is the use of antihistamines but still avoidance of the allergen if already determined is of prime importance to prevent future attacks. Cetirizine (Zyrtec) is the commonly prescribed non-sedating antihistamine for angioedema. Severe angioedema cases may require desensitization to the allergen to avoid mortality in the future. Chronic cases require long-term steroid therapy which typically leads to a good response although prolonged steroid intake is avoided as much as possible because of its serious side effects (e.g. Cushing syndrome). If the cause of angioedema is due ACE inhibitor use then to avoid the side effects just discontinue the medication.

In hereditary angioedema, if there is a known specific stimulus that has previously triggered the attacks then it must be avoided in the future. Some severe cases of hereditary angioedema receive danazol (an androgen) and a replacement therapy with C1-esterase inhibitor to relieve symptoms. In cases of acquired (autoimmune) and non-histaminergic angioedema, antifibrinolytics (e.g. tranexamic acid or ε-aminocaproic acid) may be effective. To prevent death in life threatening cases especially when there is closing of the airways, an emergency intubation and immediate treatment with epinephrine and antihistamines is needed.

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