Physical urticaria
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Physical urticaria Physical urticaria Presentation Transcript

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