Physical urticaria

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Physical urticaria

  1. 1. Physical urticarias<br />Boonthorn<br />30 December 2009<br />
  2. 2. Mechanical<br />Symptomatic dermographism<br />Delayed pressure urticaria<br />Vibratory angio-oedema<br />Thermal<br />Cholinergic urticaria<br />Localized heat urticaria<br />Cold contact urticaria<br />Other<br />Exercise-induced anaphylaxis<br />Solar urticaria<br />Aquagenicurticaria<br />Outline Physical urticarias<br />
  3. 3. Clinical appearance<br />rapid appearance of wheals and/or angioedema<br />wheal consists <br />Central swelling of variable size, almost invariably surrounded by reflex erythema<br />itching or sometimes burning sensations<br />with skin return to normal appearance, usually within 1–24 h<br />Urticaria ( Definition )<br />EAACI/GA 2LEN/EDF guideline. Allergy 2006: 61: 316–320<br />
  4. 4. wheal demonstrates <br />edema of upper and mid-dermis<br />dilatation of postcapillaryvenules and lymphatic vessels of upper dermis<br />Upregulation of endothelial adhesion molecules<br />mixed inflammatory perivascular infiltrate of neutrophils and/or eosinophils, macrophages and T-helper lymphocytes<br />mild to moderate increase of mast cell numbers<br />Urticaria ( histology )<br />EAACI/GA 2LEN/EDF guideline. Allergy 2006: 61: 316–320<br />
  5. 5. Classification of urticaria<br />EAACI/GA 2LEN/EDF guideline. Allergy 2006: 61: 316–320<br />
  6. 6. subset of chronic urticaria.<br />approximately 20% - 30% of chronic urticaria<br />induced by variety of environmental stimuli eg. exercise, temperature changes, cold, heat,pressure, sunlight, vibration, and water<br />physical stimuli are predominant cause of condition<br />incidental factor in case of chronic idiopathic urticaria<br />multiple physical urticarias ( small number )<br />Physical urticarias<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  7. 7. Dermographism( urticariafactitia )<br />
  8. 8. means to‘‘write on the skin’’<br />most common of physical urticarias<br />incidental finding in evaluation of other skin conditions ( AD, CIU, and other PU )<br />rapid onset of cutaneous wheal & flare after experiencing skin pressure<br />Epidemiology<br />Simple dermographism( most common ) approximately 2-5% of general population<br />Symptomatic forms ( much less common ) no prevalence data<br />Dermographism( urticariafactitia )<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  9. 9. Clinical features<br />simple dermographism<br />Wheal provoked by stroking skin with firm object<br />typically appears within 6-7 minutes and begins to fade 15 to 30 minutes later<br />symptomatic dermographism<br />appearing in &lt;5 minutes and lasting 30 minutes<br />red dermographism( variants of symptomatic )<br />Follicular or inflamed and swollen<br />Purposeful stroking ( most common )<br />Unaware inciting event eg. Scratch (dry skin) <br />Severe dermographism ass. With urticariapigmentosa or systemic mastocytosis<br />Dermographism( urticariafactitia )<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  10. 10. Pathogenesis<br />remains uncertain<br />Elevated levels of serum histamine (whealing episode)<br />successful passive transfer serum from dermagraphicpatient transferred dermographismto monkey<br />Suggest IgE-mediated reaction, but no allergen has been identified<br />Dermographism( urticariafactitia )<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  11. 11. Diagnostic testing<br />Stroking skin with firm object, eg. tongue blade<br />Provokes typical wheal&flare response (few mins.)<br />not taking antihistamines<br />Dermographometer ( research )<br />Apply well-defined,reproducible amount of pressure to subject’s skin<br />useful in documenting response to therapy<br />Threshold in simple dermographism:4900 g/cm2<br />in symptomatic dermographismthe threshold is 3200 -3600 g/cm2<br />Dermographism( urticariafactitia )<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  12. 12. Dermographism( urticariafactitia )<br />weal response without itch on provocation at 60 g/mm2 (589 kPa) or higher indicates simple dermographism<br />John Wiley & Sons A/S Allergy 2009: 64: 1715–1721<br />
  13. 13. Treatment<br />Simple dermographism(asymptomatic) : requires no therapy<br />symptomatic dermographism: <br />avoidance of any inciting triggers<br />use of medications <br />skin hydration and emollients ( prevent scratch )<br />H1 antihistamines<br />H2 antihistamine ( IF FAIL H1 alone )<br />UVB light<br />Dermographism( urticariafactitia )<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  14. 14. Dermographism( urticariafactitia )<br />Narrowband ultraviolet B phototherapy is beneficial in antihistamine-resistant symptomatic dermographism: pilot study<br />J Am Acad Dermatol 2008;59:752-7.<br />
  15. 15. Delayed pressure urticaria<br />Pressure swelling provoked by a bra strap<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />
  16. 16. marked subcutaneous swelling after application of sustained pressure stimulus to skin<br />Occur in 30 minutes,typically 4 to 6 hours <br />may persist for up to 48 hours , distinguished from other physical urticarias<br />dependent on degree of pressure, duration of stimulus, body site affected, activity of disease<br />DPU are provoked (distinguished from CIU)<br />Should be considered in all patients with CIU whose disease is unresponsive to antihistamines<br />Delayed pressure urticaria<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />
  17. 17. Epidemiology<br />Incidence<br />2% among 2310 urticaria1<br />37% in 135 pts. In urticaria clinic2<br />Male:female =2:1<br />Onset<br />5-63 yrs. (peak onset 30-40)<br />Duration<br />1-40 yrs. (mean 9yrs.) ,fluctuate condition<br />Delayed pressure urticaria<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />Champion RH. Br J Dermatol 1988;119:427<br />2. Barlow RJ.et al. J Am Acad Dermatol 1993;29: 954– 8.<br />
  18. 18. Clinical features<br />erythema and cutaneous and subcutaneous swelling<br />Edema of hands and feet (difficult to distinguish from idiopathic angioedema)<br />Common triggers<br />Long walks, manual activities using heavy objects, overstaying in standing or sitting position, and wearing tight clothes<br />Local symptoms<br />Burning pain , warm sensation, dysesthesias, stinging, and local tension,True itch is rare <br />Localization of lesions<br />Sites of sustained and constant pressure (e.g., palms, soles, buttocks, and shoulders)<br />Delayed pressure urticaria<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />LawlorF,et al. Br J Dermatol 1989;120:405.<br />CzarnetzskiBM,et al. Br J Dermatol 1984;111:315<br />
  19. 19. Clinical features<br />Time of onset : 30 min.( early) , 4-6 hrs.(most)<br />Duration of lesions <br />mean, 22–38 hours; range, 8–72 hours<br />Systemic symptoms<br />up to 50% of patients, even if rarely relevant: shivering, hyperpyrexia,dizziness, arthralgia, nausea, headache, short breath, and asthenia<br />Elevated ESR (17-71%) , α-1 and total antitrypsin (acute phase reactant)<br />Neutrophilia without eosinophilia<br />Delayed pressure urticaria<br />Dermatologic Therapy, Vol. 22, 2009, S22–S26<br />
  20. 20. Pathogeneis<br />Not known<br />Proposed mechanism<br />Late phase reaction ( timing ,cell infiltrate,histopathology)<br />Type III or other reaction to unknown allergy ( timing, histopathology , but no evidence of vascular damage DIF : negative & normal complement )<br />mast cell (histmine ,leukotriene not major part)<br />IL-6 increase in lesion ( but nonspecific)<br />Eosinophil ( found eosinophilic major basic protein)<br />Upregulation of ELAM-1(6hrs.),VCAM-1(24hrs.)<br />Delayed pressure urticaria<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />
  21. 21. Diagnostic testing<br />Pressure testing ( no standard method)<br />Positive pressure challenge at least 30 min.<br />Usually read pressure test at 6 hrs.<br />Hanging 15-lb weight at end of crepe bandage over shoulder, thigh, or forearms at least 15 minutes ( usful in clinical setting , not for clinical trial )<br />apparatus in (known weight)metal rods are held vertically in place, resting on patient’s back<br />Calibrated dermographometerwith spring loaded tip , press right angle to back lat. to spine (99.4g/mm2) 5,15,33,70(optimal),100 sec.<br />Delayed pressure urticaria<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />
  22. 22. Delayed pressure urticaria<br />John Wiley & Sons A/S Allergy 2009: 64: 1715–1721<br />
  23. 23. Delayed pressure urticaria<br />Pressure instrument adapted from Illig and Kunick with weighted rods resting on a<br />patients’ back.<br />Experimentally produced pressure swelling using pressure instrument<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />
  24. 24. Delayed pressure urticaria<br />calibrated dermographometer. <br />The setting of 10 =pressure of application of 9.75 * 105Pascals. The tip is pressed perpendicularly into the skin and held in place for 5, 15, 30, 70, or 100 seconds<br />Experimentally produced pressure papules using the dermographometer<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />
  25. 25. Treatment<br />Activities cause problem ,be modified or stopped<br />No single effective drug treatment<br />adequate doses of antihistamine eg. Cetirizine 10 mg q 8hrs.1<br />Prednisolone at least 30 mg/d may be used in short period for acute severe exacerbation<br />Aspirin (3900mg/d) not suppress completely<br />colchicine, indomethacin (75mg/d) ineffective<br />Nimesulide+ketotifen improved compared with steroid<br />Delayed pressure urticaria<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />1. Kontou-Fili K, et al. J Am AcadDermatol 1991;24:1090.<br />
  26. 26. Treatment<br />Dapsone 50mg/d ( clear,5pts.)1<br />Sulphasalazine 4g/d ( 2pt.)2<br />Montelukast 10 mg/d for 1 week( 1 pt.)3<br />Montelukast +nonsedate antihistamine eg. Desloratadine &gt; antihistamine alone<br />Cyclosporin (3mg/kg/d)4<br />IVIg ( 0.4g/kg/d for 5 d )4 =&gt;5/8 response<br />Delayed pressure urticaria<br />F. Lawlor, A. Kobza Black / Immunol Allergy Clin N Am 24 (2004) 247–258<br />Gould DJ et al. Br J Dermatol 1991;125:25.<br />Engler RJM et al. Am Au Ast Immunol 1995;74:155<br />Berkun Y et al. Allergy 2000;55:203.<br />Kobza Black A . J Invest Dermatol 2001;6:148<br />
  27. 27. development of pruritus and swelling after application of vibratory stimulus to the skin<br />Epidemiology<br />Reports are rare in literature<br />hereditary vibratory angioedema (AD) (4pt.)<br />sporadic and generally related to occupation<br />Vibratory angioedema<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  28. 28. Clinical features<br />After experiencing appropriate vibratory stimulus, complain of local pruritus, erythema, and swelling arising within few minutes<br />Symptoms peak in severity at 4-6 hours and typically resolve by 24 hours<br />Riding motorcycle, horse, or mountain bike; handling jackhammer; mowing the lawn; toweling; massaging; clapping; and walking<br />severity and duration to be proportional to :<br />intensity and duration of applied vibratory stimulus <br />area of exposed body surface<br />Vibratory angioedema<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  29. 29. Pathogenesis<br />not been satisfactorily elucidated<br />Elevated levels of serum histamine and mast cell degranulation<br />Passive transfer experiments : negative <br />nonimmunologic immediate hypersensitivity reaction<br />Direct mast cell stimulation from vibration may lead to degranulation and local release of histamine<br />Vibratory angioedema<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  30. 30. Diagnostic testing<br />subject’s arm is held on level plane, and a vortex mixer is placed in contact with the skin<br />applied for 5 minutes<br />observed for 5 to 6 hours<br />If positive, develop pruriticerythema and edema around full circumference of the arm<br />Dermatographism and pressure urticaria should be excluded using the appropriate tests<br />Vibratory angioedema<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  31. 31. Vibratory angioedema<br />-vibratory angioedema and weal can be reproduced using a laboratory vortex mixer<br />-measurement of circumference of arm before and after challenge at 3 points (wrist, mid-forearm, elbow) can help define vibration induced swelling<br />John Wiley & Sons A/S Allergy 2009: 64: 1715–1721<br />
  32. 32. Treatment<br />avoidance of specific vibratory stimuli<br />H1 antihistamine<br />using a 5-minute desensitization protocol every 5 to 7 days<br />Vibratory angioedema<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  33. 33. cholinergic urticaria<br />Hives induced in patient with cholinergic urticaria after running in place for 10 minutes<br />
  34. 34. “generalized heat urticaria”<br />precipitated by increase in core body temp.<br />Common triggers : exercise, strong emotions, bathing in hot water, ingestion of spicy or hot foods<br />Epidemiology<br />5% of all cases of chronic urticaria<br />30% of all cases of physical urticaria<br />onset : during second or third decade of life<br />Male = female<br />Cholinergic urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  35. 35. Clinical features<br />Numerous punctate wheals (1–3 mm) surrounded by large flares<br />tingling, itching, or burning sensation of skin before appearance of hives<br />typically begin on trunk and neck and spread distally to involve face and extremities<br />Systemic symptoms ( rare cases ) eg. hypotension, angioedema, and bronchospasm<br />must be differentiated from exercise-induced anaphylaxis (only appear with exercise)<br />Cholinergic urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  36. 36. Cholinergic urticaria<br />demonstrated<br />Postulated<br />Pathogenesis not been fully elucidated<br />increased number of muscarinic receptors in areas that demonstrate hives<br />Elevated levels of histamine (during attack)<br />neurogenic reflex<br />type I allergy to own sweat<br />abnormal cutaneous response in presence of cholinergic agents<br />associated with hypohidrosis<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  37. 37. Diagnostic testing<br />intradermal injection of 0.01 mg of methacholine in 0.1 mL saline produces local area of hives ( positive 1/3 , not used to rule out)<br />Specific provocative challenges ( but not specific )<br />Best diagnostic tool : submerged partially in hot water bath at 40ºC until core body temp. increased &gt; 0.7ºC =&gt; genealizedurticaria ( aquagenic can produce only submerge portion )<br />Cholinergic urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  38. 38. Cholinergic urticaria<br />test is positive if exercise challenge leads to typical rash over 10 min<br />John Wiley & Sons A/S Allergy 2009: 64: 1715–1721<br />
  39. 39. Treatment<br />Identification and avoidance of known triggers<br />Medical therapy <br />Oral antihistamines<br />Ketotifen<br />anabolic steroid danazol (reserved only for severe cases refractory to antihistamines)<br />Beta-blocker ( use with extreme caution )<br />Prognosis<br />Favorable ( only 1/3 persist &gt; 10yrs. )<br />Average duration 7.5 yrs. ( 3-16 yrs. )<br />Cholinergic urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  40. 40. warm stimulus :direct contact with skin<br />result in formation of wheal within minutes<br />must be differentiated from cholinergic urticaria and solar urticaria<br />Pathogenesis :<br />histamine release (mast cell cause of condition)<br />Passive transfer experiments : negative<br />Diagnostic testing<br />application of test tube containing water at 44ºC to arm for 4-5 mins. =&gt;localized hive develop within few mins.<br />Temp test<br />Treatment<br />antihistamines and oral cromolyn not been effective<br />Desensitization using hot baths successful in 1pt.<br />Local heat urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  41. 41. Local heat urticaria<br />Thresholds may allow for determination of<br />disease activity and for assessing response to therapy<br />John Wiley & Sons A/S Allergy 2009: 64: 1715–1721<br />
  42. 42. Acquired cold urticaria(cold contact urticaria)<br />Positive ice cube test in a patient with cold urticaria<br />
  43. 43. development of weal-and-flare type skin reactions and ⁄ or angiooedema after exposure of the skin to cold<br />Fourth commonest type of longlastingurticaria<br />occur minutes after the skin is exposed to cold air, liquids or objects<br />extensive cold contact may result in generalized urticarial symptoms +/- systemic reactions<br />endangered by drowning when swimming in cold water <br />suffocation due to pharyngeal angiooedema after consuming cold foods and beverages<br />Acquired cold urticaria<br />F. Siebenhaar et al.Clinicaland Experimental Dermatology, 32, 241–245<br />
  44. 44. Epidemiology<br />most frequently affects young adults<br />Mean duration : 4–5 years<br />remission or at least improvement of symptoms in 50% of patients within 5 years<br />Women &gt; men (twice)<br />Incidence<br />0.05% of urticaria<br />5.2 - 33.8% of physical urticaria<br />Varies depending on study and geographical region, i.e. higher incidences with cold climate<br />Acquired cold urticaria<br />F. Siebenhaar et al.Clinical and Experimental Dermatology, 32, 241–245<br />
  45. 45. Acquired cold urticaria<br />DDx of ACU<br />F. Siebenhaar et al.Clinical and Experimental Dermatology, 32, 241–245<br />
  46. 46. Acquired cold urticaria<br />DDx of ACU<br />F. Siebenhaar et al.Clinical and Experimental Dermatology, 32, 241–245<br />
  47. 47. Pathogenesis<br />Still remain largely unclear<br />Postulate autoimmune mechanism<br />interaction of IgEautoAbwith cold-dependent skin Ag <br />Cold temperatures presumably encourage interaction of IgM or IgG anti-IgEAb with IgE attached to mast cells, activate mast cells (primary target cell) and cause mediator release ( histamine,PGD2,PAF,neutrophil&eosinophil chemotactic factor<br />Acquired cold urticaria<br />A.A. Wanderer, H.M. Hoffman / Immunol Allergy Clin N Am 24 (2004) 259–286<br />
  48. 48. etiology<br />Secondary ACU<br />Cryoglobulinemia : <br />secondary to CLL, lymphosarcoma, LCV, HCV infection, and angioimmunoblasticlymphadenopathy<br />Infectious diseases ( virus&bact.)<br />infectious mononucleosis ,Syphilis , rubeola, varicella, hepatitis , and respiratory viral infections <br />Leukocytoclasticvasculitis<br />Miscellaneous: insect stings, drugs(eg. Penicillin ,oral contraceptive, ACEI), neoplasms<br />Acquired cold urticaria<br />A.A. Wanderer, H.M. Hoffman / Immunol Allergy Clin N Am 24 (2004) 259–286<br />
  49. 49. Diagnostic testing<br />first aim <br />To confirm ACU by performing simple cold-provocation testing<br />positive immediate cold-stimulation test (CST):<br />development of urticarial skin lesions at sites of cold challenge<br />most common : application of ice cube to skin<br />Second<br />Determine disease activity and monitor response to therapeutic interventions<br />threshold testing for critical cold-stimulation times and ⁄ or temperatures (Peltier effect based electronic device)<br />Acquired cold urticaria<br />Clinical and Experimental Dermatology, 32, 241–245<br />
  50. 50. Acquired cold urticaria<br />John Wiley & Sons A/S Allergy 2009: 64: 1715–1721<br />
  51. 51. Acquired cold urticaria<br />CSTT performed with beakers filled with ice slurry.<br />Confluent wheals appear after 2- and 4-minute applications of cold stimulus to separate skin sites. minimum time of cold stimulus (CSTT) was 2 minutes for this patient.<br />A.A. Wanderer, H.M. Hoffman / Immunol Allergy Clin N Am 24 (2004) 259–286<br />
  52. 52. Acquired cold urticaria<br />Peltier effect-based electronic device (TempTest) for<br />diagnosing and monitoring ACU symptoms. (a,d) Control unit<br />with ⁄ without applicator; (b) applicator with 12 stimulators;<br />(c) example of use<br />Clinical and Experimental Dermatology, 32, 241–245<br />
  53. 53. Acquired cold urticaria<br />Critical temperature thresholds (CTTs) and their changes in ACU are correlated with disease severity and with changes in ACU activity, respectively. ACU severity (a, n = 16)<br />changes in disease activity (b, n = 19) were assessed in patients with ACU using a three-item and a five-item Likert scale, respectively<br />British Journal of Dermatology 2010 162, pp198–200<br />
  54. 54. Treatment<br />Avoidance of cold<br />prevent ACU symptoms,serious events<br />Threshold testing help to recognize and control cold exposure in daily life<br />Symptomatic therapy<br />antihistamines : most effective symptomatic therapeutic option to prevent and reduce reactions <br />Required high dose antihistamine(4*)<br />insufficiently treated patients with severe ACU are at risk of developing life-threatening complications<br />Acquired cold urticaria<br />Clinical and Experimental Dermatology, 32, 241–245<br />
  55. 55. If insufficient response to antihistamines, consider concomitant use of leucotrieneantagonists,ciclosporin,corticosteroidsor anti-IgE<br /><ul><li>Curative therapy</li></ul>antibiotic therapy (should be considered)<br />high doses of penicillin [e.g. oral phenoxymethylpenicillin1 MU ⁄ day for 2–4 weeks or intramuscular benzylpenicillin 1 MU ⁄ day for 20 days and tetracyclines over 2–4 weeks (e.g.doxycycline200 mg ⁄ day for 3 weeks)<br />Acquired cold urticaria<br />Clinical and Experimental Dermatology, 32, 241–245<br />
  56. 56. Further treatment options<br />induction of cold tolerance (effective method), needs to be done very cautiously under supervision because of risk of systemic reactions, required high patient compliance <br />Treatment with topical capsaicin,reportedto prevent ACU symptoms<br />results in depletion of neuropeptidesfrom sensory nerve fibres (pathogeneticrole remains to be clarified in detail )<br />Acquired cold urticaria<br />Clinical and Experimental Dermatology, 32, 241–245<br />
  57. 57. exercise is only trigger in exercise-induced anaphylaxis<br />isolated entity ,association with food ingestion, medication use, and menstruation<br />Epidemiology<br />Age of onset from 4-74 yrs. (mean,24.7 yrs.)<br />Female 71% of population<br />50% had personal Hx of atopy<br />Exercise–induced anaphylaxis<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  58. 58. Clinical features<br />prodromal phase ( fatigue, warmth, pruritus, and erythema ) <br />progress to large hives that become confluent and eventually appear as angioedema<br />develops into systemic anaphylaxis with cardiovascular (hypotension, syncope), respiratory (wheezing, stridor), and gastrointestinal (colic, nausea, vomiting) symptoms. Once fully developed, attacks last 30 minutes to 4 hours<br />late phase : manifests as headache, fatigue, and warmth and could last from 24 to 72 hours<br />Exercise–induced anaphylaxis<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  59. 59. Clinical feature<br />most commonly triggered by jogging, brisk walking, dancing, and aerobic sports<br />Other factors : menstruation , use of aspirin and NSAIDs, and exposure to cold weather<br />Reaction variable , not reproducible in same activity<br />Variant type : punctate wheal , triggered only by exercise and not by elevations in core body Temp.<br />food-dependent, exercise-induced anaphylaxis<br />Exercise–induced anaphylaxis<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  60. 60. Pathogeneis<br />elevations in levels of serum histamine and tryptase during attacks<br />cause of the mast cell degranulation remains uncertain. Postulated reactions may be IgE mediated<br />priming phenomenon may be at work , with food, medications, or other stimuli acting as necessary cofactors<br />Exercise–induced anaphylaxis<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  61. 61. Diagnostic testing<br />Exercise testing is method of choice<br />running on treadmill or using a stationary bicycle with incremental increases in exertion<br />Passive warming tests to rule out cholinergic urticaria with systemic symptoms <br />difficult to reproduce<br />false-negative challenges are common<br />Testing may need to be repeated on multiple occasions to prove the diagnosis<br />Exercise–induced anaphylaxis<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  62. 62. Treatment<br />identify and avoid any specific foods, medications, or other associated factors<br />carry self-injectable epinephrine at all times<br />exercise with a partner who is trained to use epinephrine<br />avoid exercising within 4 - 6 hours of eating<br />not exercising during extremely hot, humid, or cold weather or during an allergy season <br />Antihistamine therapy : only partial benefits in preventing exercise-induced anaphylaxis and not prevent severe attack<br />Long term F/U : stable (46%),decrease (47%)<br />Exercise–induced anaphylaxis<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  63. 63. direct exposure of the skin to sunlight<br />Epidemiology<br />0.4% of urticaria<br />higher incidence in women <br />mean age at initial presentation 35 years (range, 17–71 years)<br />risk factors for solar urticaria, such as patient age, atopic history, and wavelength of light<br />Solar urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  64. 64. Clinical features<br />classic wheals<br />only erythema, itching, or a sensation of burning<br />DDx with sunburn ( more rapid,only minutes)<br />limitation of physical findings to areas of the body exposed to direct sunlight<br />Severity increases with intensity of sun exposure<br />anaphylactic reactions are possible if exposed body surface area is large enough<br />disappearance of urticaria within 24 hours<br />Solar urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  65. 65. Pathogenesis<br />hypothesized : presence in skin of precursor molecule , activated by exposure to particular wavelength of light =&gt;photoallergen<br />Origin of precursor molecule not been determined <br />Type I ( abn. Precursor molecule not found in healthy )<br />Type II ( common precursor molecule ,found in all )<br />passive transfer is not always successful<br />eliminated by removing horny layer of the skin<br />Solar urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  66. 66. Diagnostic testing<br />Phototesting<br />exposed to varying wavelengths using a monochromatic light source, and threshold dose, which induces erythema or urticaria<br />exposure to other light sources, eg. natural sunlight, high-intensity UV light, or slide-projector light, induced symptoms<br />Solar urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  67. 67. Solar urticaria<br />John Wiley & Sons A/S Allergy 2009: 64: 1715–1721<br />
  68. 68. Treatment<br />Antihistamines : drug of choice<br />Topical & systemic steroids : used if antihistamines are insufficient<br />Desensitization ( last only few days )<br />PUVA ( more long lasting protection , greater long-term adverse effect )<br />Plasmapharesis +/- PUVA (may depend on characteristics of specific photoallergen at work<br />Longterm F/U : 25% complete resolution , 32% improved , 35% unchange , 8% worsened<br />Solar urticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  69. 69. direct skin contact with water<br />Epidemiology<br />rare disorder with &lt; 50 cases ( case report )<br />Female &gt; male<br />Age of onset : at or slightly after puberty<br />Familial occurrences have been reported <br />personal or family Hx of atopy occasionally reported<br />Aquagenicurticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  70. 70. Clinical features<br />small, punctuate (1–3 mm), perifollicular wheals may occur on all parts of body, although generally not on palms and soles ( Indistinguishable from cholinergic urticaria )<br />Wheals appear rapidly after direct contact with any source of water (ie, distilled, tap, or saline) not influenced by temperature or pH <br />fade within 30 - 60 minutes<br />Alcohol and other organic solvents applied to skin do not lead to wheal formation<br />Aquagenicurticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  71. 71. Clinical features<br />Systemic symptoms are rare<br />refractory period lasting several hours<br />primary differential diagnoses : <br />cholinergic urticaria ( Exercise, sweating, heat, and strong emotions )<br />aquagenicpruritus (occurs on skin contact with water but lacks visible cutaneous manifestations)<br />Aquagenicurticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  72. 72. Pathogenesis<br />still is poorly understood<br />postulated that water interacted with sebum to form substance capable of acting as direct mast cell degranulation<br />Enhancing ability of water to penetrate stratum corneum increases the wheal-provoking effects of water (complete removal of stratum corneum , rather than preventing urticaria, worsen reaction)<br />Activation of cholinergic pathway (ability of the acetylcholine antagonist scopolamine to suppress wheal formation ( some study not suppress)<br />Methacholine injection : negative<br />Aquagenicurticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  73. 73. Diagnostic testing<br />standard test : application of water compress at 35ºC ( room temp.) to upper body for 30 minutes<br />extremities, are affected less commonly in aquagenicurticaria<br />Certain areas of skin with thickened epidermal layer may be less desirable for testing because of reduced penetration of water<br />rule out other physical urticarias ( cholinergic and cold-induced urticaria )<br />Aquagenicurticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  74. 74. Treatment<br />Antihistamine therapy : variable response<br />Barrier method : application of petrolatum ointment<br />UVB light treatment twice a week<br />PUVA therapy<br />Anabolic steroid stanozol<br />Aquagenicurticaria<br />J.P. Dice / Immunol Allergy Clin N Am 24 (2004) 225–246<br />
  75. 75. conclusion<br />Pathogenesis for these disorders remains unclear<br />sensitivity by the mast cell to environmental stimuli<br />future research is needed <br />conditions share the features of rapid onset and relatively short duration (except delayed pressure urticaria)<br />there is enough variability in presentation<br />
  76. 76. Diagnostic testing should be completed for several of these conditions in each patient Because of occasional overlap of triggers and occasional coexistence of multiple physical urticarias, <br />Treatment <br />generally avoidance of known triggers <br />use of antihistamines for prophylaxis<br />Other modalities are occasionally effective<br />Life-threatening,systemicsymptoms are rare (except in exercise-induced anaphylaxis) but must be considered<br />Self-injectableepinephrine should be provided to any patient at risk<br />conclusion<br />

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