Urticaria is a common disorder that affects 15-20% of the population at some time. Lesions are characterised by a transient , pruritic , patch eruption that consists of lightly erythematous papules or wheals. When conditions are protracted , urticaria is annoying to the victim and challenging for the physician . Foods , drugs and many other agents may cause urticaria by inducing mediator release from mast cells in the skin . Identification of the precipitating agent is crucial for effective treatment of urticaria.

Urticarial lesions----raised erythematous , intensely pruritis (itch)

-the thigh vasculitis lesions are indurated and residual pigmentation is likely.

-Angioedema ( involvement of dermis and subcutaneous / submucosal tissue) of the lips can last several days and forewarns of possible pharyngeal and pulmonary involvement .

 Pathogenesis:-Histamine is a key mediator in urticaria, and its realease from mast cells by a variety of stimuli manifests in urticaria. classically the 6 "i's" 1) ingestants ie foods,2) injectants ie drugs 3) insect stings ,4) inhalants, 5) infections 6 ) internal diseases. Foods and drugs are common etiologic agents and can cause urticaria by several mechanisms. additionally factors thats associated with increased incidence of urticaria includes heat , fever , exercise , menstrual changes , and emotional stress . Cutaneous punch biopsy may show dilatation of venules , edema , mast cell degranulation and infiltration of mononuclear cells or or eosinophils or both .

Immunologic Mechanisms		Diagnostic Tests
-IgE-mediated requires prior sensitization to enviornmental antigens-6 I's Ingestantats ( food) ie fish ,shrimps, berries, nuts , eggs. Injectants ( drugs) ie. penicillins, sulphonamides Insect stings ie bees , wasp , hornets, yellow jackets Inhalants ie pollen , spores, animal dander caused by autoantibody to IgE receptorsAnaphalotoxin (C5-c3a)-mediated Infections ie hepatitis,Epstein-Barr virus,streptococcus *? sinus, dental Tb etc. Internal Disease ie. Stemic rheumatic disease, neoplastic disorders, transfusion reactions.   Non-immunologic mechanisms Direct mass-cell effects Drugs ie opiate derivatives, dextran , radigraphic contrast media foods ie. shellfish , strawberries Effect on Aracidonic acid metabolism Drugs ie, aspirin and other non-steroidal antiinflammatories undetermined ? dust mites --food addatives, food dye's, preservatives.		Complete blood count with differential. Chemistry profile Erythocyte sedimentation rate T4,TSH measurements Urinalysis, urine culture ANA ( anti-nuclear antibody) Radiographic (X-rays)-chest , sinus , dental , panorex. Selective tests:- Cryoglobulin . hepatitis and Syphylis serology, Rheumatoid factor, Serum complement, Serum IgE, IgM Skin biopsy*( if ESR is elevated, to exclude urticarial vasculitis ). Stools - ova & parasites

Classification :- Acute or Chronic

Acute:- Hives persists less than 4-6 weeks( usually 2 - 4 days) fish ,shrimps, berries, nuts , eggs. food additives ( tartrazin dyes, benzoic acid deravatives{sodium benzoate , 4-hydroxybenzoic acid. } certain medications ie. aspirin nonsteroidal anti-inflammatory drugs. or radiocontrast media. Antibiotics( eg. penicillin , sulphonamides). Often an atopic individual

Chronic:- persisting greater than 6 weeks More than 75% have an idiopathic disorder. More common in middle aged womenSpecific sometimes associated disorders includes fungal infections ( candida albicans) parasitic or bacterial infection.

Diagnosis- a detailed history , with special emphasis on drug ingestion , dietary intake and other provocative or exacerbating factors is most important . a careful review of systems with emphasis on connective tissue disorders, endocrine and neoplastic conditions may uncover etiologic factors. Extent of severity should be obtained. I am reminded of a patient -middle aged female with h/o of severe bronchospasm and urticaria who I never actually witnessed symptoms during any visit but who semmed allergic to most every thing ? even sunlight who one day by chance I passed her -seeing her in a car with rolled up windows doing a cigarette- she never showed to my office again but about 1 year later I had to relate story to a dermatologist seeing her who had his own significant misgivings about her lucid history but she had slipped AND MENTIONED MY NAME- just pointing out how vital the history plays along with medical accumen! The physical examination should include notation of the morphology and distribution of the urticarial lesions and coexisting angioedema. A complete exam should be done -exclusion of subclinical infections (eg. sinusitis , urinary tract infection apical dental abscess fungal infections of skin hair or vagina.etc.Provacative tests to elicit urticaria may be performed when indicated by the history and characteristics of the urticarial eruptions. Lab test may not be indicated if a definitive agent is identified . where food ingestion is suspected related elimination diet with reintroduction of one food at a time may be of value in targeting offending agent. . When vasculitis is suspected by history of burning sensation in the skin ESR , skin bniopsy for histology and immunoflorescence examination should be performed.

Urticarial Vasculitis Differentiating chronic idiopathic urticaria and urticarial vasculitis is important as theraputic approaches may be different . Typically urticarial vasculitisis charcterised as follows:- lesions show central clearing or have dusky appearance individual lesions last longer than 24 hours associated systemic symptoms (eg arthralgia, fever , uvitis , episcleritis , hematuria, wheezing , chest pain , diarrhea.raynaud's phenomenon.

Urticaria in systemic iliness Infection:- Viral hepatitis A, Hepatitis B , mononucleosis, coxsackie virus Bacterial ( Streptococcus-bacterial Sinus, dental , urinary tract Fungal candidaa, dermatophytosis parasitic ( ascaris , trichinosis, giardiasis) Spirochaete(syphyllis lyme disea.se ) Connective tissue disorder:- Systemic lupus erythematosus Sjorgen Syndrome Rheumatic fever Juvenile rheumatoid arthritis Necrotizing vasculitis Polymyositis Endocrine Disordes:- Hyperthyroidism Hypothyroidism Hypoparathyroidism Neoplastic Disorders Lymphoma Leukemia Carcinoma( colorectal , lung , ovarian , liver) Myeloma Other:- Pregnancy Urticarial vasculitis Macroglobulinemia		Management severe attacks may merit sc epinephrine 0.3cc(1:1000) Identified causative agents should be limited from repeat exposure Antihistamine act by occupying the receptor sites on effector cells to exclusion of agonists.They do not however alter the course of the disease.Basically there are H1 and H2 blockers-additionally some are without sedating effects.Drugs includes benadryl , piriton , periactin,claritin Atarax, cimetidine. Beta agonist ie. salbutomol brethine may be useful adjunctively Also tricyclic antidepressants ie. Sinequan may be used. Other therapies ie capasaicin or local anaesthetics can suppress wheal and flare reactions in local heat urticaria. Systemic corticosteroids are useful in severe acute urticaria. Many times I actually implement H1,H2 blockers + sytemic steroids as an initial protocol of therapy for up to 3 weeks when reports of of other basic management strategies have not seemed effective. Still other therapies may be tried in refractory cases . These includes nifedipine , (adalat) ketotifen(Zaditen) cyclosporine (sandimmune) plasmapharesis and ultrvioletB photheraphy.
Jesus is lord of all call upon His great name!!!

to be continued.