Urticaria (Symptoms)
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About Urticaria
Urticaria or hives is a relatively common form of allergic reaction that causes raised red skin welts. Urticaria is also known as nettle rash or uredo. These welts can be 5 mm (0.2 inches) in diameter or more, itch severely, and often have a pale border. Urticaria is generally caused by direct contact with... more 
Urticaria or hives is a relatively common form of allergic reaction that causes raised red skin welts. Urticaria is also known as nettle rash or uredo. These welts can be 5 mm (0.2 inches) in diameter or more, itch severely, and often have a pale border. Urticaria is generally caused by direct contact with an allergenic substance, or an immune response to food or some other allergen.
Pathophysiology
The skin lesions of urticarial disease are caused by an inflammatory reaction in the skin, causing leakage from capillaries in the epidermis, resulting in an edema which persists until the interstitial fluid is absorbed into the surrounding cells.
Urticarial disease is thought to be caused by the release of histamine and other mediators of inflammation (cytokines) from cells in the skin. This process can be the result of an allergic or non-allergic reaction, differing in eliciting mechanism of histamine release.
Allergic urticaria
Histamine and other pro-inflammatory substances are released from mast cells in the skin and tissues in response to the binding of allergen-bound IgE antibodies to high affinity cell surface receptors. Basophils and other inflammatory cells are also seen to release histamine and other mediators, and are thought to play an important role, especially in chronic urticarial diseases.
Non-allergic urticaria
Mechanisms other than allergen-antibody interactions are known to cause histamine release from mast cells. For instance, a diverse group of signaling substances called neuropeptides have been found to be involved in emotionally induced urticaria.
Dominantly inherited cutaneous and neurocutaneous porphyrias (porphyria cutanea tarda, hereditary coproporphyria, variegate porphyria and erythropoietic protoporphyria) have been associated with solar urticaria. Drug-induced solar urticaria should be investigated for porphyrias.
Misconception
The rash derived from poison-ivy is commonly mistaken for urticaria. Poison-ivy is caused by urushiol toxin. This resin can be spread by contact, but it is easily washed off.
Types
Acute urticaria usually show up a few minutes after contact with the allergen and can last a few hours to several weeks. Food allergic reactions typically fit in this category. Common causes of reaction include consumption of shell fish, nuts, eggs, fish, acid derivatives, dye, or a combination of these.
Chronic urticaria refers to hives that persists for 6 weeks or more. There are no visual differences between acute and chronic urticaria. Some of the more severe chronic cases have lasted more than 20 years.
Drug-induced urticaria has been known to result in severe cardiorespiratory failure. The anti-diabetic sulphonylurea glimepiride (trade name Amaryl®), in particular, has been documented to induce allergic reactions manifesting as urticaria. Other cases include dextroamphetamine, aspirin, penicillin, clotrimazole, sulfonamides and anticonvulsants.
Physical urticarias is often categorized into the following.
Aquagenic: Reaction to water (rare)
Cholinergic: Reaction to body heat, such as when exercising or after a hot shower
Cold (Chronic cold urticaria): Reaction to cold, such as ice, cold air or water
Delayed Pressure: Reaction to standing for long periods, bra-straps, belts
Dermatographic: Reaction when skin is scratched (very common)
Heat: Reaction to hot food or objects (rare)
Solar: Reaction to direct sunlight (rare)
Vibration: Reaction to vibration (rare)
Adrenergic: Reaction to adrenaline / noradrenaline (extremely rare)
Related conditions
Angioedema is related to urticaria. In angioedema, the swelling occurs in a lower layer of the dermis than it does in urticaria. This swelling can occur around the mouth, in the throat, in the abdomen, or in other locations. Urticaria and angioedema sometimes occur together in response to an allergen and is a concern in severe cases as angioedema of the throat can be fatal.
Treatment
Urticarias can be very difficult to treat. Most treatment plans for urticaria involve being aware of one's triggers, but this can be difficult since there are several different forms of urticaria and people often exhibit more than one type. Also, since symptoms are often idiopathic there might not be any clear trigger. If one's triggers can be identified then outbreaks can often be managed by limiting one's exposure to these situations.
Drug treatment is typically in the form of Antihistamines such as loratadine (Claritin), hydroxyzine, cetirizine and other H1 receptor antagonists. These are taken on a regular basis to protective effect, lessening or halting attacks.
For some people, H2-receptor antagonists such as cimetidine (Tagamet) and ranitidine (Zantac) can also help control symptoms either protectively or by lessening symptoms when an attack occurs. When taken in combination with a H1 antagonist it has been shown to have a synergistic effect which is more effective than either treatment alone. The use of ranitidine (or other H2 antagonist) for urticaria is considered an off-label use, since these drugs are primarily used for the treatment of peptic ulcer disease (PUD) and gastroesophageal reflux disease (GERD).
Tricyclic antidepressants such as doxepin, also are often potent H1 and H2 antagonists and may have a role in therapy, although side effects limit their use.
For very severe outbreaks, an oral corticosteroid such as Prednisone is sometimes prescribed. However this form of treatment is controversial because of the extensive side effects common with corticosteroids and as such is not a recommended long-term treatment option.
None of these treatments are surefire means of controlling attacks. Some people prove to be treatment resistant, and medications can suddenly cease being as effective as they once were. In these instances, changes to a treatment plan can sometimes help. It can be difficult to determine appropriate medications since some such as loratadine require a day or two to build up to effective levels, and since the condition is intermittent and outbreaks typically clear up without any treatment.
While the disease is obviously physiological in origin, psychological treatments such as stress management can sometimes lessen severity and occurrence. Additionally, methods similar to psychological pain management can be used to shift focus away from the uncomfortability and itchiness during an attack.
Pathophysiology
The skin lesions of urticarial disease are caused by an inflammatory reaction in the skin, causing leakage from capillaries in the epidermis, resulting in an edema which persists until the interstitial fluid is absorbed into the surrounding cells.
Urticarial disease is thought to be caused by the release of histamine and other mediators of inflammation (cytokines) from cells in the skin. This process can be the result of an allergic or non-allergic reaction, differing in eliciting mechanism of histamine release.
Allergic urticaria
Histamine and other pro-inflammatory substances are released from mast cells in the skin and tissues in response to the binding of allergen-bound IgE antibodies to high affinity cell surface receptors. Basophils and other inflammatory cells are also seen to release histamine and other mediators, and are thought to play an important role, especially in chronic urticarial diseases.
Non-allergic urticaria
Mechanisms other than allergen-antibody interactions are known to cause histamine release from mast cells. For instance, a diverse group of signaling substances called neuropeptides have been found to be involved in emotionally induced urticaria.
Dominantly inherited cutaneous and neurocutaneous porphyrias (porphyria cutanea tarda, hereditary coproporphyria, variegate porphyria and erythropoietic protoporphyria) have been associated with solar urticaria. Drug-induced solar urticaria should be investigated for porphyrias.
Misconception
The rash derived from poison-ivy is commonly mistaken for urticaria. Poison-ivy is caused by urushiol toxin. This resin can be spread by contact, but it is easily washed off.
Types
Acute urticaria usually show up a few minutes after contact with the allergen and can last a few hours to several weeks. Food allergic reactions typically fit in this category. Common causes of reaction include consumption of shell fish, nuts, eggs, fish, acid derivatives, dye, or a combination of these.
Chronic urticaria refers to hives that persists for 6 weeks or more. There are no visual differences between acute and chronic urticaria. Some of the more severe chronic cases have lasted more than 20 years.
Drug-induced urticaria has been known to result in severe cardiorespiratory failure. The anti-diabetic sulphonylurea glimepiride (trade name Amaryl®), in particular, has been documented to induce allergic reactions manifesting as urticaria. Other cases include dextroamphetamine, aspirin, penicillin, clotrimazole, sulfonamides and anticonvulsants.
Physical urticarias is often categorized into the following.
Aquagenic: Reaction to water (rare)
Cholinergic: Reaction to body heat, such as when exercising or after a hot shower
Cold (Chronic cold urticaria): Reaction to cold, such as ice, cold air or water
Delayed Pressure: Reaction to standing for long periods, bra-straps, belts
Dermatographic: Reaction when skin is scratched (very common)
Heat: Reaction to hot food or objects (rare)
Solar: Reaction to direct sunlight (rare)
Vibration: Reaction to vibration (rare)
Adrenergic: Reaction to adrenaline / noradrenaline (extremely rare)
Related conditions
Angioedema is related to urticaria. In angioedema, the swelling occurs in a lower layer of the dermis than it does in urticaria. This swelling can occur around the mouth, in the throat, in the abdomen, or in other locations. Urticaria and angioedema sometimes occur together in response to an allergen and is a concern in severe cases as angioedema of the throat can be fatal.
Treatment
Urticarias can be very difficult to treat. Most treatment plans for urticaria involve being aware of one's triggers, but this can be difficult since there are several different forms of urticaria and people often exhibit more than one type. Also, since symptoms are often idiopathic there might not be any clear trigger. If one's triggers can be identified then outbreaks can often be managed by limiting one's exposure to these situations.
Drug treatment is typically in the form of Antihistamines such as loratadine (Claritin), hydroxyzine, cetirizine and other H1 receptor antagonists. These are taken on a regular basis to protective effect, lessening or halting attacks.
For some people, H2-receptor antagonists such as cimetidine (Tagamet) and ranitidine (Zantac) can also help control symptoms either protectively or by lessening symptoms when an attack occurs. When taken in combination with a H1 antagonist it has been shown to have a synergistic effect which is more effective than either treatment alone. The use of ranitidine (or other H2 antagonist) for urticaria is considered an off-label use, since these drugs are primarily used for the treatment of peptic ulcer disease (PUD) and gastroesophageal reflux disease (GERD).
Tricyclic antidepressants such as doxepin, also are often potent H1 and H2 antagonists and may have a role in therapy, although side effects limit their use.
For very severe outbreaks, an oral corticosteroid such as Prednisone is sometimes prescribed. However this form of treatment is controversial because of the extensive side effects common with corticosteroids and as such is not a recommended long-term treatment option.
None of these treatments are surefire means of controlling attacks. Some people prove to be treatment resistant, and medications can suddenly cease being as effective as they once were. In these instances, changes to a treatment plan can sometimes help. It can be difficult to determine appropriate medications since some such as loratadine require a day or two to build up to effective levels, and since the condition is intermittent and outbreaks typically clear up without any treatment.
While the disease is obviously physiological in origin, psychological treatments such as stress management can sometimes lessen severity and occurrence. Additionally, methods similar to psychological pain management can be used to shift focus away from the uncomfortability and itchiness during an attack.
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