“urticaria from cold -hives welts”

Chronic spontaneous urticaria and angioedema is diagnosed when hives and swelling are present for more than six weeks and when it has been determined that an apparent protracted episode of urticaria is not the result of recurrent episodes of acute urticaria.
The best treatment for hives and angiodema is to identify and remove the trigger, but this is not an easy task. Antihistamines are usually prescribed by your doctor to provide relief from symptoms. Antihistamines work best if taken on a regular schedule prevent hives from forming in the first place.
Saigal K, Valencia IC, Cohen J, Kerdel FA. Hypocomplementemic urticarial vasculitis with angioedema, a rare presentation of systemic lupus erythematosus: rapid response to rituximab. J Am Acad Dermatol. 2003 Nov. 49(5 Suppl):S283-5. [View Abstract]
The British guideline refers to chronic urticaria/angio-oedema; it also lists angio-oedema without weals as a subtype and refers to urticarial vasculitis as a differential diagnosis. Urticarial vasculitis is vasculitis of the skin characterised by inflammation of the small blood vessels rather than urticaria[5]. Causes include infection (hepatitis B/C, glandular fever or streptococcal infection), medication (penicillins, fluoxetine, thiazides, allopurinol, quinolones or carbamazepine), autoimmune disease, paraproteinaemia and malignancy.
Diagnosis is by skin biopsy, taken ideally from a ‘new’ lesion (within 12 h of appearance), which shows a small vessel leucocytoclastic vasculitis involving post-capillary venules, with endothelial cell swelling, a neutrophil cell infiltrate, extravasation of red blood cells and fibrinoid deposits in and around blood vessels [75]. The condition is thought to be mediated via a type III/immune complex hypersensitivity reaction, in which antigen/antibody complexes deposit in vessel walls. This results in complement activation, neutrophil chemotaxis and infiltration and the release of proteolytic neutrophil enzymes, such as collagenases and elastases, which cause tissue damage. Immunofluorescence shows deposition of immunoglobulin and complement.
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Skin biopsy may be performed to confirm urticarial vasculitis. Microscopic findings of early lesions include a neutrophil leukocytoclastic vasculitis, in which there is damage to small vessels in the middle layers of the skin (dermis). In later lesions, a lymphocytic vasculitis may be seen.
Chronic or recurrent urticaria (>6 wk) – Basic laboratory studies should include complete blood count (CBC), erythrocyte sedimentation rate (ESR), thyroid-stimulating hormone (TSH), and antinuclear antibody (ANA) [4]
Usually not. The rash is itchy but normally fades within a day or so and causes no harm. Most people with hives (acute urticaria) do not feel too unwell unless they have a cold or flu that is triggering the rash. The cause of the rash is not known in more than half of cases and it is commonly a one-off event.
Chronic hives can lead to severe discomfort, distress, and possibly depression. Stress, too, can aggravate hives, creating a vicious cycle. Patients who experience symptoms of depression should speak to a doctor.
In brief, the crucial role of C1q in the pathway is its importance as the first protein to start the complement cascade (which ends in the destruction of the invading bacteria or virus), and its ability to link the two important arms of the immune system – the innate immune system: a broad defence system; and the adaptive immune system: the strong immune response capable of remembering previous infections, allowing fast response against recurrent infections, meaning that people with a normal immune system don’t continually catch the same cold or same strain of flu repeatedly.[5]
In every medical reference, you would see them listing stress as one of the potential causes that can trigger hives or angioedema. Studies of groups of people suffering with different levels of urticaria have proven that stress can worsen hives and that it’s possible to get urticaria induced by stress.

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