Your SlideShare is downloading. ×
0
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Physical urticaria
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply
0 Comments
2 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
3,288
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
148
Comments
0
Likes
2
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. Physical urticarias<br />Boonthorn<br />30 December 2009<br />
  • 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. 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. 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. Classification of urticaria<br />EAACI/GA 2LEN/EDF guideline. Allergy 2006: 61: 316–320<br />
  • 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. Dermographism( urticariafactitia )<br />
  • 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 &amp; 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. 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 &amp;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. 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. Diagnostic testing<br />Stroking skin with firm object, eg. tongue blade<br />Provokes typical wheal&amp;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. Dermographism( urticariafactitia )<br />weal response without itch on provocation at 60 g/mm2 (589 kPa) or higher indicates simple dermographism<br />John Wiley &amp; Sons A/S Allergy 2009: 64: 1715–1721<br />
  • 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. 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. 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. 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. 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. 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. 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. 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 &amp; 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. 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. Delayed pressure urticaria<br />John Wiley &amp; Sons A/S Allergy 2009: 64: 1715–1721<br />
  • 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. 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. 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. 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 &amp;gt; antihistamine alone<br />Cyclosporin (3mg/kg/d)4<br />IVIg ( 0.4g/kg/d for 5 d )4 =&amp;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. 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. 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. 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. 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. 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 &amp; Sons A/S Allergy 2009: 64: 1715–1721<br />
  • 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. cholinergic urticaria<br />Hives induced in patient with cholinergic urticaria after running in place for 10 minutes<br />
  • 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. 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. 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. 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 &amp;gt; 0.7ºC =&amp;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. Cholinergic urticaria<br />test is positive if exercise challenge leads to typical rash over 10 min<br />John Wiley &amp; Sons A/S Allergy 2009: 64: 1715–1721<br />
  • 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 &amp;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. 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. =&amp;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. Local heat urticaria<br />Thresholds may allow for determination of<br />disease activity and for assessing response to therapy<br />John Wiley &amp; Sons A/S Allergy 2009: 64: 1715–1721<br />
  • 42. Acquired cold urticaria(cold contact urticaria)<br />Positive ice cube test in a patient with cold urticaria<br />
  • 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. 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 &amp;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. Acquired cold urticaria<br />DDx of ACU<br />F. Siebenhaar et al.Clinical and Experimental Dermatology, 32, 241–245<br />
  • 46. Acquired cold urticaria<br />DDx of ACU<br />F. Siebenhaar et al.Clinical and Experimental Dermatology, 32, 241–245<br />
  • 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&amp;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. etiology<br />Secondary ACU<br />Cryoglobulinemia : <br />secondary to CLL, lymphosarcoma, LCV, HCV infection, and angioimmunoblasticlymphadenopathy<br />Infectious diseases ( virus&amp;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. 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. Acquired cold urticaria<br />John Wiley &amp; Sons A/S Allergy 2009: 64: 1715–1721<br />
  • 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. Pathogenesis<br />hypothesized : presence in skin of precursor molecule , activated by exposure to particular wavelength of light =&amp;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. 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. Solar urticaria<br />John Wiley &amp; Sons A/S Allergy 2009: 64: 1715–1721<br />
  • 68. Treatment<br />Antihistamines : drug of choice<br />Topical &amp; 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. direct skin contact with water<br />Epidemiology<br />rare disorder with &amp;lt; 50 cases ( case report )<br />Female &amp;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. 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. 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. 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. 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. 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. 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. 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 />

×