hives

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Definition

Hives is an allergic skin reaction causing localized redness, swelling, and itching.

Description

Hives is a reaction of the body's immune system that causes areas of the skin to swell, itch, and become reddened (wheals). When the reaction is limited to small areas of the skin, it is called "urticaria." Involvement of larger areas, such as whole sections of a limb, is called "angioedema."

— Richard Robinson

[Origin unknown.]

For more information on hives, visit Britannica.com.

Definition

Hives are an allergic skin reaction causing localized redness, swelling, and itching.

Description

Hives are a reaction of the body's immune system that causes areas of the skin to swell, itch, and become reddened. (The affected areas are called wheals.) When the reaction is limited to small areas of the skin, it is called urticaria. Involvement of larger areas, such as whole sections of a limb, is called angioedema.

Causes & Symptoms

Causes

Hives are an allergic reaction. The body's immune system is normally responsible for protection from foreign invaders. When it becomes sensitized to normally harmless substances, the resulting reaction is called an allergy. An attack of hives is set off when such a substance, called an allergen, is ingested, inhaled, or otherwise contacted. It interacts with immune cells called mast cells, which reside in the skin, airways, and digestive system. When mast cells encounter an allergen, they release histamine and other chemicals, both locally and into the bloodstream. These chemicals cause blood vessels to become more porous, allowing fluid to accumulate in tissue and leading to the swollen and reddish appearance of hives. Some of the chemicals released sensitize pain-related nerve endings, causing the affected area to become itchy and sensitive.

A wide variety of substances may cause hives in sensitive people. Common culprits include:

• prescription and nonprescription drugs (Aspirin and penicillin are the two most commonly known causes of allergic reactions in adults.)
• nuts, especially peanuts, walnuts, and Brazil nuts
• fish, mollusks, and shellfish
• eggs
• wheat
• milk
• strawberries
• food additives and preservatives
• influenza vaccines
• tetanus toxoid vaccine
• gamma globulin
• bee, wasp, and hornet stings
• bites of mosquitoes, fleas, and scabies.

In addition, hives may also result from the body's response to certain physical conditions, such as emotional stress, rubbing, cold wind, heat contact (prickly heat rash), wearing tight clothing, or exercise after a heavy meal.

Symptoms

Urticaria is characterized by redness, swelling, and itching of small areas of the skin. These patches usually grow and recede in less than a day, but may be replaced by others in other locations. Angioedema is characterized by more diffuse swelling. Swelling of the airways may cause wheezing and respiratory distress. In severe cases, airway obstruction may occur.

Diagnosis

Hives are easily diagnosed by visual inspection. The cause of hives is usually apparent, but may require a careful medical history in some cases.

Treatment

Home Remedies

To deal with the symptoms of hives, an oatmeal bath may help to relieve itching. Chickweed (Stellaria media), applied as a poultice (crushed or chopped herbs applied directly to the skin) or added to bath water, may also help relieve itching.

Nutritional Therapy

Naturopaths or nutritionists will try to determine what allergic substance is causing the reaction and help the patient eliminate or minimize its effects. They may also recommend vitamin C, vitamin B₁₂, and quercetin (a flavonoid) supplements to help control acute or chronic hives.

Homeopathic Therapy

The following homeopathic remedies have been used to relieve itching, redness or swelling associated with hives:

• Urtica urens
• Apis(Apis mellifica)
• Sulfur

Allopathic Treatment

Mild cases of hives are treated with antihistamines, such as diphenhydramine (Benadryl). More severe cases may require such oral corticosteroids prednisone. Topical corticosteroids are not effective. In 2002, the Food and Drug Administration (FDA) approved the allergy drug Claritin for over-the-counter use for patients with urticaria. The drug comes in tablet and syrup form and carries little risk. Its release for over-the-counter use was delayed until the company that manufactures the drug could add instructions for patients about self-diagnosis of hives. They cautioned it should be used only for recurrent hives that had already been diagnosed by a physician, not for acute or severe urticaria. Airway swelling may require emergency injection of epinephrine (adrenaline).

Expected Results

Most cases of hives clear up within one to seven days without treatment, provided the cause (allergen) is found and avoided.

Prevention

Preventing hives depends on avoiding the allergen causing them. Analysis of new items in the diet or new drugs taken may reveal the likely source of the reaction. Chronic hives may be aggravated by stress, caffeine, alcohol, or tobacco; avoiding these may reduce the frequency of reactions.

Resources

Books

Jonas, Wayne B., and Jennifer Jacobs., "Skin Rashes." Healing with Homeopathy: The Doctor's Guide. New York, NY: Warner Books, 1996.

Lawlor, G. J., Jr., T.J. Fischer, and D.C. Adelman. Manual of Allergy and Immunology. Boston, MA: Little, Brown and Co., 1995.

Murray, Michael T. and Joseph E. Pizzorno. "Hives." Encyclopedia of Natural Medicine. Revised 2nd ed. Rocklin, CA: Prima Publishing, 1998.

Novick, N. L. You Can Do Something About Your Allergies. NY: Macmillan, 1994.

Periodicals

Franklin, Deanna. "FDA Panel Recommends OTC Approval of Claritin (Urticaria Indication Debated)." Family Practice News (June 15, 2002):26–31.

[Article by: Mai Tran; Teresa G. Odle]

Definition

Hives is an allergic skin reaction causing localized redness, swelling, and itching.

Description

Hives is a reaction of the body's immune system that causes areas of the skin to swell, itch, and become reddened (wheals). When the reaction is limited to small areas of the skin, it is called urticaria. Involvement of larger areas, such as whole sections of a limb, is called angioedema.

Demographics

Many children and adults experience hives at various times during their lives. As hives is not a reportable event, no accurate prevalence statistics are available.

Causes and Symptoms

Hives is an allergic reaction. The body's immune system is normally responsible for protection from foreign invaders. When it becomes sensitized to normally harmless substances, the resulting reaction is called an allergy. An attack of hives is set off when such a substance, called an allergen, is ingested, inhaled, or otherwise contacted. It interacts with immune cells called mast cells, which reside in the skin, airways, and digestive system. When mast cells encounter an allergen, they release histamine and other chemicals, both locally and into the bloodstream. These chemicals cause blood vessels to become more porous, allowing fluid to accumulate in tissue and leading to the swollen and reddish appearance of hives. Some of the chemicals released sensitize pain nerve endings, causing the affected area to become itchy and sensitive.

A wide variety of substances may cause hives in sensitive people, including foods, drugs, and insect bites or stings. Common culprits include:

• nuts, especially peanuts, walnuts, and Brazil nuts
• fish, mollusks, and shellfish
• eggs
• wheat
• milk
• strawberries
• food additives and preservatives
• penicillin or other antibiotics
• flu vaccines
• tetanus toxoid vaccine
• gamma globulin
• bee, wasp, and hornet stings
• bites of mosquitoes, fleas, and scabies

Urticaria is characterized by redness, swelling, and itching of small areas of the skin. These patches usually grow and recede in less than a day but may be replaced by others in other locations. Angioedema is characterized by more diffuse swelling. Swelling of the airways may cause wheezing and respiratory distress. In severe cases, airway obstruction may occur.

When to Call the Doctor

A doctor or other healthcare professional should be called when hives do not spontaneously clear within a day of their appearance or when they include swelling of the throat. If the reactions are severe, as in anaphylactic reaction or shock, immediate medical care is needed.

Diagnosis

Hives are easily diagnosed by visual inspection. The cause of hives is usually apparent but may require a careful medical history in some cases.

Treatment

Mild cases of hives are treated with antihistamines, such as diphenhydramine (Benadryl). More severe cases may require oral corticosteroids, such as prednisone. Topical corticosteroids are not effective. Airway swelling may require emergency injection of epinephrine (adrenaline).

An alternative practitioner will try to determine what allergic substance is causing the reaction and help the person eliminate or minimize its effects. To deal with the symptoms of hives, an oatmeal bath may help to relieve itching. Chickweed (Stellaria media), applied as a poultice (crushed or chopped herbs applied directly to the skin) or added to bath water, may also help relieve itching. Several homeopathic remedies, including Urtica urens and Apis (Apis mellifica), may help relieve the itch, redness, or swelling associated with hives.

Prognosis

Most cases of hives clear up within one to seven days without treatment, providing the cause (allergen) is found and avoided.

Prevention

Preventing hives depends on avoiding the allergen causing them. Analysis of new items in the diet or new drugs taken may reveal the likely source of the reaction. Chronic hives may be aggravated by stress, caffeine, alcohol, or tobacco; avoiding these may reduce the frequency of reactions.

Nutritional Concerns

Hives may be triggered or worsened by caffeine or alcohol (in adults), or specific allergenic foods, which depend entirely on the patient. Avoiding these substances may reduce the occurrence of hives.

Parental Concerns

Parents should monitor their children to ensure that any attack of hives does not involve the throat area. Young children should be encouraged not to stratch their skin too vigorously. If hives are a recurrent problem, parents should keep track of the foods the child eats in an attempt to discover the allergen.

Resources

Books

Duvic, Madeleine. "Urticaria, Drug Hypersensitivity Rashes, Nodules and Tumors, and Atrophic Diseases." In Cecil Textbook of Medicine, 22nd ed. Edited by Lee Goldman et al. Philadelphia: Saunders, 2003, pp. 2475–85.

Frank, Michael M. "Urticaria and Angioedema." In Cecil Textbook of Medicine, 22nd ed. Edited by Lee Goldman et al. Philadelphia: Saunders, 2003, pp. 1610–3.

Leung, Donald Y. M. "Urticaria and Angioedema (Hives)." In Nelson Textbook of Pediatrics, 17th ed. Edited by Richard E. Behrman et al. Philadelphia: Saunders, 2003, pp. 778–80.

Yancy, Kim B., and Thomas J. Lawley. "Immunologically Mediated Skin Disorders." In Harrison's Principles of Internal Medicine, 15th ed. Edited by Eugene Braunwald et al. New York: McGraw-Hill, 2001, pp. 331–5.

Periodicals

Beltrani, V. S. "Urticaria: reassessed." Allergy and Asthma Proceedings 25, no. 3 (2004): 143–9.

Clarke, P. "Urticaria." Australian Family Physician 33, no. 7 (2004): 501–3.

Dice, J. P. "Physical urticaria." Immunology and Allergy Clinics of North America 24, no. 2 (2004): 225–46.

Grattan, C. E. "Autoimmune urticaria." Immunology and Allergy Clinics of North America 24, no. 2 (2004): 163–81.

Lawlor, F., and A. K. Black. "Delayed pressure urticaria." Immunology and Allergy Clinics of North America 24, no. 2 (2004): 247–58.

Rumbyrt, J. S., and A. L. Schocket. "Chronic urticaria and thyroid disease." Immunology and Allergy Clinics of North America 24, no. 2 (2004): 215–23.

Sheikh, J. "Advances in the treatment of chronic urticaria." Immunology and Allergy Clinics of North America 24, no. 2 (2004): 317–34.

Organizations

American Academy of Dermatology. 930 N. Meacham Road, PO Box 4014, Schaumburg, IL 60168–4014. Web site: www.aad.org/.

American Academy of Pediatrics. 141 Northwest Point Blvd., Elk Grove Village, IL 60007–1098. Web site: www.aap.org/.

Web Sites

"Hives." MedlinePlus. Available online at www.nlm.nih.gov/medlineplus/ency/article/000845.htm (accessed January 6, 2005).

"Hives (Urticaria)." San Francisco State University Student Health Service. Available online at www.sfsu.edu/~shs/skinclinic/urticaria.htm (accessed January 6, 2005).

"Urticaria (Hives)." American Osteopathic College of Dermatology. Available online at www.aocd.org/skin/dermatologic_diseases/urticaria.html (accessed January 6, 2005).

[Article by: L. Fleming Fallon, Jr., MD, DrPH]

A condition characterized by the sudden appearance of red, raised areas on the skin that itch severely. Hives may be caused by an allergic reaction (see allergy) to foods or other substances.

A condition characterized by the sudden and temporary appearance of large areas of painless swelling in the subcutaneous tissue or submucosa, with or without pruritus. Caused by immunological reactions, usually immediate type hypersensitivities. Sometimes referred to as angioneurotic edema.

• hereditary a. — in humans, the periodic occurrence of angioedema caused by a deficiency of the complement regulatory protein.

Angioedema
Classification and external resources
ICD-10	D84.1 , T78.3
ICD-9	277.6, 995.1
OMIM	606860 106100 610618
DiseasesDB	13606
MedlinePlus	000846
eMedicine	emerg/32 med/135 ped/101
MeSH	D000799

Angioedema (BE: angiooedema) is the rapid swelling (edema) of the dermis, subcutaneous tissue,^[1] mucosa and submucosal tissues. It is very similar to urticaria, but urticaria, commonly known as hives, occurs in the upper dermis.^[1]

In the past, angioedema was referred to by the term angioneurotic edema, which wrongly implied that the phenomenon was due to neurosis.

Cases where angioedema progresses rapidly should be treated as a medical emergency as airway obstruction and suffocation can occur. Epinephrine may be lifesaving when the cause of angioedema is allergic. In the case of hereditary angioedema, treatment with epinephrine has not been shown to be helpful.

Contents 1 Classification 2 Signs and symptoms 3 Diagnosis 4 Pathophysiology 5 Therapy 5.1 Allergic angioedema 5.2 Drug induced angioedema 5.3 Hereditary angioedema 5.4 Acquired angioedema 6 History 7 See also 8 References 9 External links

Classification

Apart from the common form, mediated by allergy, it has been reported as a side effect of some medications, in particular ACE inhibitors. Additionally, there are three autosomal dominant inherited forms known, due to mutations in the genes that control the clotting cascade, including the SERPING1 gene, which results in deficiency of the blood protein C1-inhibitor (type I HAE) and the F12 gene, which controls Factor XII (type III HAE). There is an additional type in which C1 levels are normal but C1 function is decreased (type II HAE). All three forms are called hereditary angioedema (HAE) or occasionally by the outdated term "hereditary angioneurotic edema" (HANE). In all forms of HAE, swelling may also occur in the digestive tract and other organs. It is life-threatening when it involves the larynx due to the potential for asphyxiation.

Signs and symptoms

The skin of the face, normally around the mouth, and the mucosa of the mouth and/or throat, as well as the tongue, swell up over the period of minutes to several hours. The swelling can also occur elsewhere, typically in the hands. The swelling can be itchy. There may also be slightly decreased sensation in the affected areas due to compression of the nerves. Urticaria (hives) may develop simultaneously.

In severe cases, stridor of the airway occurs, with gasping or wheezy inspiratory breath sounds and decreasing oxygen levels. Intubation is required in these situations to prevent respiratory arrest and risk of death.

Sometimes, there has been recent exposure to an allergen (e.g. peanuts), but more often the cause is either idiopathic (unknown) or only weakly correlated to allergen exposure.

In hereditary angioedema, there is often no direct identifiable cause, although mild trauma, including dental work and other stimuli, can cause attacks.^[2] There is usually no associated itch or urticaria, as it is not an allergic response. Patients with HAE can also have recurrent episodes (often called "attacks") of abdominal pain, usually accompanied by intense vomiting, weakness, and in some cases, watery diarrhea, and an unraised, non-itchy splotchy/swirly rash. These stomach attacks can last anywhere from 1–5 days on average, and can require hospitalization for aggressive pain management and hydration. Abdominal attacks have also been known to cause a significant increase in the patient's white blood cell count, usually in the vicinity of 13-30,000. As the symptoms begin to diminish, the white count slowly begins to decrease, returning to normal when the attack subsides. As the symptoms and diagnostic tests are almost indistinguishable from an acute abdomen (e.g. perforated appendicitis) it is possible for undiagnosed HAE patients to undergo laparotomy (operations on the abdomen) or laparoscopy (keyhole surgery) that turns out to have been unnecessary.

HAE may also cause swelling in a variety of other locations, most commonly the limbs, genitals, neck, throat, and face. The pain associated with these swellings varies from mildly uncomfortable to agonizing pain, depending on its location and severity. Predicting where and when the next episode of edema will occur is impossible. Most patients have an average of one episode per month, but there are also patients who have weekly episodes or only one or two episodes per year. The triggers can vary and include infections, minor injuries, mechanical irritation, operations or stress. In most cases, edema develops over a period of 12–36 hours and then subsides within 2–5 days.

Diagnosis

The diagnosis is made on the clinical picture. Routine blood tests (complete blood count, electrolytes, renal function, liver enzymes) are typically performed. Mast cell tryptase levels may be elevated if the attack was due to an acute allergic (anaphylactic) reaction. When the patient has been stabilized, particular investigations may clarify the exact cause; complement levels, especially depletion of complement factors 2 and 4, may indicate deficiency of C1-inhibitor. HAE type III is a diagnosis of exclusion consisting of observed angioedema along with normal C1 levels and function.

The hereditary form (HAE) often goes undetected for a long time, as its symptoms resemble those of more common disorders, such as allergy or intestinal colic. An important clue is the failure of hereditary angioedema to respond to antihistamines or steroids, a characteristic that distinguishes it from allergic reactions. It is particularly difficult to diagnose HAE in patients whose episodes are confined to the gastrointestinal tract. Besides a family history of the disease, only a laboratory analysis can provide final confirmation. In this analysis, it is usually a reduced complement factor C4, rather than the C1-INH deficiency itself, that is detected. The former is used during the reaction cascade in the complement system of immune defense, which is permanently overactive due to the lack of regulation by C1-INH.

Pathophysiology

Bradykinin plays a critical role in all forms of hereditary angioedema.^[3] This peptide is a potent vasodilator and increases vascular permeability, leading to rapid accumulation of fluid in the interstitium. This is most obvious in the face, where the skin has relatively little supporting connective tissue, and edema develops easily. Bradykinin is released by various cell types in response to numerous different stimuli; it is also a pain mediator. Dampening or inhibiting bradykinin has been shown to relieve HAE symptoms.

Various mechanisms that interfere with bradykinin production or degradation can lead to angioedema. ACE inhibitors block ACE, the enzyme that among other actions, degrades bradykinin. In hereditary angioedema, bradykinin formation is caused by continuous activation of the complement system due to a deficiency in one of its prime inhibitors, C1-esterase (aka: C1-inhibitor or C1INH), and continuous production of kallikrein, another process inhibited by C1INH. This serine protease inhibitor (serpin) normally inhibits the association of C1r and C1s with C1q to prevent the formation of the C1-complex, which - in turn - activates other proteins of the complement system. Additionally, it inhibits various proteins of the coagulation cascade, although effects of its deficiency on the development of hemorrhage and thrombosis appear to be limited.

There are three types of hereditary angioedema:

• Type I - decreased levels of C1INH (85%);
• Type II - normal levels but decreased function of C1INH (15%);
• Type III - no detectable abnormality in C1INH, occurs in an X-linked dominant fashion and therefore mainly affects women; it can be exacerbated by pregnancy and use of hormonal contraception (originally described by Bork et al. in 2000, exact frequency uncertain).^[4] It has been linked with mutations in the factor XII gene.^[5]

Angioedema can be due to antibody formation against C1INH; this is an autoimmune disorder. This acquired angioedema is associated with the development of lymphoma.

Consumption of foods which are themselves vasodilators such as alcohol or cinnamon can increase the probability of an angioedema episode in susceptible patients. If the episode occurs at all after the consumption of these foods, its onset may be delayed overnight or by some hours, making the correlation with their consumption somewhat difficult. In contrast, consumption of bromelain in combination with turmeric may be beneficial in reducing symptoms. ^[6]

The use of ibuprofen or aspirin may increase the probability of an episode in some patients. The use of acetaminophen typically has a smaller, but still present, increase in the probability of an episode.

Therapy

Allergic angioedema

In allergic angioedema, avoidance of the allergen and use of antihistamines may prevent future attacks. Cetirizine is a commonly prescribed antihistamine for angioedema. Some patients have reported success with the combination of a nightly low dose of cetirizine to moderate the frequency and severity of attacks, followed by a much higher dose when an attack does appear. Severe angioedema cases may require desensitization to the putative allergen, as mortality can occur. Chronic cases require steroid therapy, which generally leads to a good response.

Drug induced angioedema

ACE inhibitors can induce angioedema.^[7][8][9] ACE inhibitors block the enzyme ACE so that it can no longer degrade bradykinin; thus bradykinin accumulates and causes angioedema.^[7][8] This complication appears more common in African-Americans.^[10] In patients with ACE inhibitor angioedema, the drug needs to be discontinued and an alternate treatment needs to be found, such as an angiotensin II receptor blocker (ARB)^[11] which has a similar mechanism but does not affect bradykinin. However, this is controversial as there are small studies that have shown that patients with ACE inhibitor angioedema can develop it with ARBs as well.^[12][13]

Hereditary angioedema

In hereditary angioedema, specific stimuli that have previously led to attacks may need to be avoided in the future. It does not respond to antihistamines, corticosteroids, or epinephrine.

Acute treatment

The aim of acute treatment is to halt progression of the edema as quickly as possible, which can be life-saving, particularly if the swelling is in the larynx. In Germany, most acute treatment consists of C1-INH concentrate from donor blood, which must be administered intravenously. In an emergency, fresh frozen blood plasma, which also contains C1-INH, can also be used. However, in most European countries, C1-INH concentrate is only available to patients who are participating in special programmes. Fresh frozen plasma (FFP) can be used as an alternative to C1-INH concentrate.

Long-term prophylaxis

Patients in whom episodes occur at least once a month or who are at high risk of developing laryngeal edema require long-term prophylaxis. This often involves male sex hormones (androgens), which increase production of C1-INH in the liver through an as yet unknown mechanism. Danazol is the most commonly used.^[14] The dose should be kept as low as possible because of its frequent adverse effects. The use of androgens is particularly problematic in children and they must not be taken during pregnancy. Several cases in which patients developed benign liver tumours during treatment with danazol resulted in the substance being taken off the market in Germany at the beginning of 2005.^{[citation needed]}

As an alternative, drugs known as fibrinolysis inhibitors, such as tranexamic acid, are used, although their effect is comparatively weak and their potential for side effects is questionable.^{[citation needed]}

Short-term prophylaxis

Short-term prophylaxis is normally administered before surgery or dental treatment. In Germany, C1-INH concentrate is used for this and given 1-11/2 hours before the procedure. In countries where C1-inhibitor concentrate is not available or only available in an emergency (laryngeal edema), high-dose androgen treatment is administered for 5–7 days.

Long-term prophylaxis

In those with frequent or unpredictable attacks, regular infusions of plasma or inhibitor concentrate may be used.^{[citation needed]} C1-INH concentrate is not available in the US, so sometimes fresh frozen plasma is used. C1inh concentrate is currently under late-stage development for both acute and prophylactic use.^{[citation needed]}

New treatment options

Clinical development of several new active substances, which intervene in the disease process in different ways, is currently ongoing.

Ecallantide is a peptide inhibitor of kallikrein that has received orphan status for HAE and has shown positive results in phase III trials.^[15]

Icatibant (marketed as Firazyr) is a selective bradykinin receptor antagonist, which has been approved in only Europe and not in the USA.^[16] After initial borderline results this drug was shown to be effective in phase III trials.^[17]

Pharming, a Dutch biotechnology company, is developing a recombinant C1 inhibitor for acute attacks of hereditary angioedema.^{[citation needed]}

Cinryze [1] has been approved by the FDA in October 2008

No studies have been done on these agents in relation to HAE type III.^{[citation needed]}

Acquired angioedema

In acquired angioedema, HAE types I and II, and non-histaminergic angioedema, antifibrinolytics such as tranexamic acid or ε-aminocaproic acid may be effective. Cinnarizine may also be useful because it blocks the activation of C4 and can be used in patients with liver disease while androgens cannot[2].

History

Dr Heinrich Quincke first described the clinical picture of angioedema in 1882,^[18] though there had been some earlier descriptions of the condition.^[19][20][21]

Sir William Osler remarked in 1888 that some cases may have a hereditary basis; he coined the term hereditary angio-neurotic edema.^[22]

See also

• Hereditary angioedema
• Gleich's syndrome (unexplained angioedema with high eosinophil counts)
• Drug-induced angioedema

References

1. ^ ^{a b} angioedema at Dorland's Medical Dictionary
2. ^ Bork K, Barnstedt SE (August 2003). "Laryngeal edema and death from asphyxiation after tooth extraction in four patients with hereditary angioedema". J Am Dent Assoc 134 (8): 1088–94. PMID 12956349. http://jada.ada.org/cgi/pmidlookup?view=long&pmid=12956349. 
3. ^ Bas M, Adams V, Suvorava T, Niehues T, Hoffmann TK, Kojda G (2007). "Nonallergic angioedema: role of bradykinin". Allergy 62 (8): 842–56. doi:10.1111/j.1398-9995.2007.01427.x. PMID 17620062. 
4. ^ Bork K, Barnstedt SE, Koch P, Traupe H (2000). "Hereditary angioedema with normal C1-inhibitor activity in women". Lancet 356 (9225): 213–7. doi:10.1016/S0140-6736(00)02483-1. PMID 10963200. 
5. ^ Cichon S, Martin L, Hennies HC, et al. (2006). "Increased activity of coagulation factor XII (Hageman factor) causes hereditary angioedema type III". Am. J. Hum. Genet. 79 (6): 1098–104. doi:10.1086/509899. PMID 17186468.  Full text at PMC: 965459
6. ^ University of Maryland Medical Center. Angioedema. http://www.umm.edu/altmed/articles/angioedema-000011.htm
7. ^ ^{a b} Sabroe RA; Black AK (Feb 1997). "Angiotensin-converting enzyme (ACE) inhibitors and angio-oedema". British Journal of Dermatology 136 (2): 153-8. PMID 9068723. 
8. ^ ^{a b} Israili ZH; Hall WD (1 Aug 1992). "Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy. A review of the literature and pathophysiology". Annals of Internal Medicine 117 (3): 234-42. PMID 1616218. 
9. ^ Kostis JB; Kim HJ; Rusnak J; Casale T; Kaplan A; Corren J; Levy E (25 Jul 2005). "Incidence and characteristics of angioedema associated with enalapril". Archives of Internal Medicine 165 (14): 1637-42. PMID 16043683. 
10. ^ Brown NJ; Ray WA; Snowden M; Griffin MR (Jul 1996). "Black Americans have an increased rate of angiotensin converting enzyme inhibitor-associated angioedema". Clinical Pharmacologic Therapy 60 (1): 8-13. PMID 8689816. 
11. ^ Dykewicz, MS (Aug 2004). "Cough and angioedema from angiotensin-converting enzyme inhibitors: new insights into mechanisms and management". Current Opinions in Allergy & Clinical Immunology 4 (4): 267-70. PMID 15238791. 
12. ^ Malde B; Regalado J; Greenberger PA (Jan 2007). "Investigation of angioedema associated with the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers". Annals of Allergy, Asthma, and Immunology 98 (1): 57-63. PMID 17225721. 
13. ^ Cicardi M; Zingale LC; Bergamaschini L; Agostoni A (26 Apr 2004). "Angioedema associated with angiotensin-converting enzyme inhibitor use: outcome after switching to a different treatment". Archives of Internal Medicine 164 (8): 910-3. PMID 15111379. 
14. ^ Gelfand JA, Sherins RJ, Alling DW, Frank MM (1976). "Treatment of hereditary angioedema with danazol. Reversal of clinical and biochemical abnormalities". N. Engl. J. Med. 295 (26): 1444–8. PMID 792688. 
15. ^ Lehmann A (August 2008). "Ecallantide (DX-88), a plasma kallikrein inhibitor for the treatment of hereditary angioedema and the prevention of blood loss in on-pump cardiothoracic surgery". Expert Opin Biol Ther 8 (8): 1187–99. doi:10.1517/14712598.8.8.1187. PMID 18613770. 
16. ^ Jerini AG (2008-07-15). "Jerini Receives European Commission Approval for Firazyr (Icatibant) in the Treatment of HAE - Press release". http://jerini.com/cms/en/05-news-events/05-01-corporate-news/05-01-07-newsarchive-2008/08-07-15_EU_Approval.php. Retrieved 2008-07-28. 
17. ^ Bernstein JA (January 2008). "Hereditary angioedema: a current state-of-the-art review, VIII: current status of emerging therapies". Ann. Allergy Asthma Immunol. 100 (1 Suppl 2): S41–6. PMID 18220151. 
18. ^ Quincke H (1882). "Über akutes umschriebenes Hautödem". Monatsh Prakt Derm 1: 129–131. 
19. ^ synd/482 at Who Named It?
20. ^ Marcello Donati. De medica historia mirabili. Mantuae, per Fr. Osanam, 1586
21. ^ J. L. Milton. On giant urticaria. Edinburgh Medical Journal, 1876, 22: 513-526.
22. ^ Osler W (1888). "Hereditary angio-neurotic oedema". Am J Med Sci 95: 362–67. doi:10.1097/00000441-188804000-00004. 

External links

• International Patient Organization for C1 inhibitor Deficiencies
• Israeli HAE Patient Organization
• European HAE information portal
• Online Symptom Diary for Patients with Hereditary Angioedema
• US Hereditary Angioedema Association
• UK Patient organisation for HAE
• All About HAE

v • d • e Immune disorders: Lymphoid and complement immunodeficiency (D80-D85, 279) Primary Antibody/humoral (B) Hypogammaglobulinemia X-linked agammaglobulinemia · Transient hypogammaglobulinemia of infancy Dysgammaglobulinemia IgA deficiency · IgG deficiency · IgM deficiency · Hyper IgM syndrome (2, 3, 4, 5) · Wiskott-Aldrich syndrome · Hyper-IgE syndrome Other Common variable immunodeficiency · ICF syndrome Cell-mediated (T) thymic hypoplasia: hypoparathyroid (Di George's syndrome) · euparathyroid (Nezelof syndrome, Ataxia telangiectasia) peripheral: Purine nucleoside phosphorylase deficiency · Hyper IgM syndrome (1) Severe combined (B+T) x-linked: X-SCID autosomal: Adenosine deaminase deficiency · Omenn syndrome · ZAP70 deficiency · Bare lymphocyte syndrome Acquired AIDS Lymphocytopenia Idiopathic CD4+ lymphocytopenia Complement deficiency C1-inhibitor (Angioedema/Hereditary angioedema) · Complement 2 deficiency lymphocyte navs: cells/physio, immunodeficiency/immunoproliferative immunoglobulin/neoplasia, proc

v • d • e Consequences of external causes (T66-T88, 990-999) Temperature/radiation elevated: Hyperthermia · Heat syncope · Radiation poisoning reduced: Hypothermia · Immersion foot · Chilblain Air Hypoxia/Asphyxia · Barotrauma (Aerosinusitis, Decompression sickness) · Altitude sickness/Chronic mountain sickness Food Starvation Maltreatment Physical abuse · Sexual abuse · Psychological abuse Emesis Motion sickness · Seasickness · Airsickness · Space adaptation syndrome Other Electric shock · Anaphylaxis · Angioedema Hypersensitivity (Allergy, Arthus reaction) Subcutaneous emphysema Certain early complications of trauma embolism (Air, Fat) Crush syndrome/Rhabdomyolysis Contracture/Volkmann's contracture/Compartment syndrome Complications of surgical and medical care transfusion reactions: Transfusion hemosiderosis · TRALI · TACO · TA-GvHD · FNHTR · Acute/Delayed hemolytic transfusion reaction other: Serum sickness · Malignant hyperthermia · Herxheimer reaction · Graft-versus-host disease · Tumor lysis syndrome

v • d • e Pathology: hemodynamics Decreases Thrombus/thrombosis Renal vein thrombosis Ischemia Brain ischemia · Ischaemic heart disease Infarction general: Anemic infarct · Hemorrhagic infarct regional: Myocardial infarction · Splenic infarction · Cerebral infarction Increases Hemorrhage general Bruise/Hematoma: Petechia · Purpura · Ecchymosis regional: head (Epistaxis, Hemoptysis, Intracranial hemorrhage, Hyphema) · torso (Hemothorax, Hemopericardium) · abdomen (Gastrointestinal bleeding, Haemobilia, Hemoperitoneum, Hematocele, Hematosalpinx ) · joint (Hemarthrosis) Edema general: Anasarca · Angioedema/Lymphedema · Exudate/Transudate regional: Cerebral edema · Pulmonary edema · Hydrothorax · Ascites/hydroperitoneum · Hydrosalpinx Other Hyperemia

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