UrticariaThe diagnostic challenge of hivesRichard J. Sveum, MD VOL 100 / NO 2 / AUGUST 1996 / POSTGRADUATE MEDICINE This is the second of five articles on allergy Preview : Patients who present with hives are often hoping their physician can tell them what caused the condition. In acute cases, that is often possible, but unfortunately, the majority of chronic cases are idiopathic. In this article, Dr Sveum puts the spotlight on urticaria. He stresses the importance of taking a careful medical history and describes treatment options. U rticaria is part of a more severe allergic reaction called anaphylaxis, in which hypotension or respiratory distress can be present. When a patient presents with flaring or reddened skin and wheals, prompt evaluation is needed. Once the physician is sure anaphylaxis is not occurring, the next step is to proceed with careful history taking. Urticaria, commonly known as hives, is a vascular reaction in the upper dermis, marked by the development of wheals on virtually any area of the body. Acute urticaria is defined as hives that last for less than 6 weeks (1); when the hives last for more than 6 weeks, however, the condition is considered chronic. Chronic urticaria can be particularly frustrating to diagnose and treat, since most cases are idiopathic. Fortunately, the condition can often be controlled with appropriate medical management.
Mechanisms
Mast cells can be activated by specific IgE antibodies attached to receptors on the surface of the cells or by a non-IgE mechanism mediated by neurotransmitters or other cell products (table 1). A recent report (2) described a group of patients with chronic urticaria who had IgG autoantibodies directed against the high-affinity IgE receptor. These autoantibodies can also trigger the release of mediators from mast cells.
Causes
In chronic urticaria, the cause is most often idiopathic. The condition can sometimes be associated with endocrine abnormalities, especially hyperthyroidism. A recent report (4) suggested that in some patients thyroid antibodies may be an important factor. Occasionally, chronic urticaria is a symptom of a more serious underlying disease, so it is important not to miss any associated systemic illnesses (table 4).
Clinical features
Diagnosis
Physical examination can confirm the presence of urticarial lesions and provide an opportunity to look for coexisting systemic diseases. A history of urticaria following exposure to physical triggers can be confirmed with a challenge. Stroking the skin or challenging with physical agents such as ice or light can establish the diagnosis of physical urticaria. Laboratory testing has to be considered from the standpoint of cost-effectiveness but usually includes a complete blood cell count with differential, erythrocyte sedimentation rate, and urinalysis. Skin testing for specific IgE antibodies is sometimes helpful, as are skin biopsy (especially if one suspects vasculitis [bruising, hives for more than 24 hours, or nonblanching urticaria]), examination of stool for ova and parasites, chest and sinus roentgenograms, measurement of liver enzyme levels, and tests for fluorescent antinuclear antibodies and cryoglobulins.
Treatment
The management of chronic urticaria is more challenging (table 5). It is best to warn patients with chronic urticaria that they may be dealing with this condition for 1 to 2 years, so that they know not to expect an immediate resolution. Nonsedating antihistamines, including terfenadine (Seldane), astemizole (Hismanal), loratadine (Claritin), and now cetirizine hydrochloride (Zyrtec), can be helpful in mild cases. Since histamine stimulation of the H2 histamine receptor can sometimes contribute to symptoms, a 10-day trial of either cimetidine (Tagamet) or ranitidine hydrochloride (Zantac) is suggested.
In some patients whose chronic urticaria is particularly difficult to control, tricyclic antidepressants such as doxepin hydrochloride (Adapin, Sinequan) can be used for their antihistaminic properties. Only in the most resistant cases should use of oral corticosteroids be considered. Prednisone (1 to 2 mg/kg per day in divided doses) is given for 5 to 7 days or until remission, and then the dosage may be tapered.
Angioedema
Angioedema without urticaria is classified as either hereditary or acquired. In hereditary angioedema, there is an abnormality of a serum protein, the C1 esterase inhibitor. Eighty-five percent of the time the abnormality is a deficiency, that is, antigenic measurement shows the amount of C1 esterase inhibitor to be decreased. Fifteen percent of the time the C1 esterase inhibitor is present in normal levels but has an abnormal function. Acquired angioedema can be due to an underlying malignancy that consumes the C1 esterase inhibitor or to the presence of autoantibodies. When a patient has angioedema, the family history becomes important, since hereditary angioedema is an autosomal dominant condition. Management of angioedema involves, first and foremost, the maintenance of an airway in an acute episode. Management of the chronic form mostly revolves around prophylaxis, in which androgens, such as danazol (Danocrine), have been used to increase the C1 esterase inhibitor levels. If surgery is required and androgens cannot be used, C1 esterase inhibitor can be infused with fresh frozen plasma.
Summary
Treatment of chronic urticaria generally involves the use of antihistamines first. Corticosteroids are to be avoided, if possible. References
Dr Sveum is a consultant, department of allergy, Park Nicollet Clinic, and clinical associate professor of medicine and pediatrics, University of Minnesota Medical School-Minneapolis. Mailing address: Richard J. Sveum, MD, Park Nicollet Clinic, 3800 Park Nicollet Blvd, Minneapolis, MN 55416. Symposium
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