UpToDate خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده:
4
September 2025
| Anaphylaxis (including generalized allergic reaction) | Urticaria | Angioedema disorders (including ACEI use and rare C1 inhibitor deficiency) | |
| Onset | Minutes to 1 hour (rarely several hours). | Days to weeks, but can occur in minutes to hours if IgE mediated (eg, food, medications). | Hours, peaking at 24 to 36 hours. |
| Clinical course | Variable and unpredictable, may progress within minutes to respiratory or cardiovascular compromise and death, may be mild and resolve spontaneously. Generalized allergic reactions may actually be early anaphylaxis and progress to airway compromise or systemic findings. | Most episodes of acute urticaria improve within 1 to 2 weeks. | Gradually resolves over 1 to 3 days. |
| Skin findings | Urticaria, flushing/generalized erythema, pruritus; skin findings can be absent in severe cases. | Intensely pruritic urticaria; flushing/generalized erythema can also occur. One-third of patients have urticaria with angioedema*. | Not present (this is a key differentiating factor). |
| Associated symptoms | Dyspnea, throat tightness, hoarse voice, conjunctival erythema, nasal congestion, sneezing, bronchospasm, cough, chest tightness, hypotension, syncope, altered mental status, crampy abdominal pain, vomiting, uterine cramping. | Systemic findings typically not present: If they are, treat as anaphylaxis. | ACEI-associated angioedema – Systemic symptoms typically not present. C1 inhibitor deficiency – Can have crampy abdominal pain/vomiting if bowel wall involvement. |
| Angioedema locations | Lips, tongue, face, uvula, and/or larynx. | Urticaria can affect skin anywhere on the body. When accompanied by angioedema or presenting as isolated angioedema, face, lips, extremities, and/or genitals are often involved. | ACEI-associated angioedema – Commonly affects lips, tongue, or sometimes face, but other sites (eg, larynx) may rarely be affected. C1 inhibitor deficiency – Can affect larynx, intestinal walls, or skin (although usually not all at once). |
| Mediators | Multiple – Histamine, tryptase, platelet-activating factor, nitric oxide, arachidonic acid metabolites. | Histamine. | Bradykinin. |
| Testing | Tryptase.¶ | Typically not helpful.Δ | For ACEI-associated angioedema – None. For suspected C1 inhibitor deficiency – C1 inhibitor level and function and C4.◊ |
| First-line treatment | Epinephrine; IV fluids if hypotensive. | Antihistamines. | For all – Airway management as necessary. For ACEI-associated angioedema – Discontinue ACEI. For known or suspected C1 inhibitor deficiency – Multiple possible therapies.§ |
| Second-line treatment | Antihistamines, glucocorticoids, bronchodilators. | Glucocorticoids. |
ACEI: angiotensin-converting enzyme inhibitor; IgE: immunoglobulin E; IV: intravenous.
* When angioedema occurs with urticaria, it is assumed to be histamine mediated.
¶ Refers to UpToDate table on tryptase collection for timing and collection of sample.
Δ If a food is the suspected trigger, blood tests for IgE specific to that food may be sent (eg, IgE to milk, shrimp, etc). Testing for most other triggers (medications, insect venoms, exercise, etc) is best performed in consultation with an allergist as part of follow-up care. Refer to UpToDate algorithm on evaluation of new-onset urticaria.
◊ Note that C1 inhibitor deficiency can be hereditary or acquired (usually after age 40 years). A low C4 may be seen in most of these disorders and is a reasonable screening test. However, there are also angioedema disorders in which complement studies are normal and diagnosis is more complicated. In addition, use of an ACEI can "unmask" these disorders, such that a patient may develop angioedema as a result of both ACEI use and an underlying disorder. For this reason, it is important to refer patients with repeated episodes of angioedema to an allergy/immunology specialist for further evaluation.
§ Hereditary angioedema therapies include C1 inhibitor concentrate, icatibant, ecallantide, and fresh-frozen plasma.
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