Dermatologic diseases: Urticaria, Contact dermatitis Flashcards
What is the definition of chronic urticaria?
Presence of urticaria for at least six weeks
What is the pathogenesis of CU?
Mast cell degranulation can occur via IgE independent pathways.
Basophils/mast cells are triggered by the following mechanism:
- IgE binds to the α-subunit of its high-affinity receptor, FcɛRI, on mast cells and basophils and, if present at high concentrations, can activate these cells regardless of the specific antigen. We used to look for specific auto antigens like anti TPO but this has not made any clinical difference yet in phenotyping.
- In addition, the cross-linking of IgE by their respective allergens, autoallergens and IgG anti-IgE antibodies can lead to mast cell and basophil activation and mediator release in allergic, autoallergic and autoimmune urticaria, respectively.
- IgG autoantibodies to IgE and FcɛRI were the first autoantibodies described in the context of autoimmune CSU. Most studies report that 20–50% of patients with CSU have these autoantibodies This is type IIb in CSU.
Management of CU?
Second generation H1 antagonists are the first line treatment.
Allergic contact dermatitis: What is the most common form? What is the reaction caused by?
Toxicodendron dermatitis, formerly known as Rhus dermatitis, also known as poison ivy, poison oak, and poison sumac, is the most common form of allergic contact dermatitis seen in pediatric and adult patients in US.
Reaction is caused by urushiol, oleoresin oil found in the sap that oozes easily from any crushed part of the plant.
What foods are cross reactive with oleoresin oil?
Mango, as well as cashew nut shells and Ginkgo tree fruit pulp can cause similar reactions to that of Toxicodendron dermatitis because of cross reactivity of the oleoresin oil.
Allergic contact dermatitis to plants causes
- Anacardiaceae family of plants causes the most cases of plant dermatitis= Toxicodendron dermatitis, formerly known as Rhus dermatitis, also known as poison ivy, poison oak, and poison sumac.
- Plants from Rutaceae family including orange, grapefruit, lemon and lime are common sensitizers and are seen quite often in food preparers and barworkers.
What is hypocomplementemic urticarial vasculitis syndrome (HUVS)
- Chronic urticarial rash which may bruise or become purpuric and hypocomplementemia
- Biopsy leukocytoclastic vasculitis
- Arthralgia and/or arthritis; uveitis, episcleritis, and /or conjunctivitis
- Proteinuria, hematuria, renal insufficiency, and/or glomerulonephritis
- Abdominal pain, nausea, vomiting, and/or diarrhea
- Positive anti-C1q antibodies.
- Lung involvement in HUVS includes coughing, hemoptysis, shortness of breath, pleural effusions, and COPD
History for allergic contact dermatits
- Delayed-type eczematous dermatitis
- Wear jewelry, apply nail polish, or dye her hair?
- Skin cream or wash (scented or unscented)?
Most frequent causes of allergic contact dermatitis with a periocular/periorbital distribution
- Metal (nickel, gold)- nickel products in jewelry and cosmetics
- Fragrances
- Preservatives
- Antibiotics
- Paraphenylenediamine (hair dyes or in hairstylists)
- Thimerosal
- Acrylates- distribution of rash especially along hand and nail bed, along with eyelid dermatitis may suggest involvement of nail polish/acrylic nails
(Products label “unscented” can contain fragrances along with masking scents or odor-neutralizing chemical and is not synonymous with products labeled “fragrance-free.”)
Management of allergic contact dermatitis
- Patch testing may be helpful in deciphering the potential sensitizer
- Avoidance of sensitizing agents
- Use of fragrance-free (not unscented) products such as petrolatum
- Low-potency topical steroid ointment or topical calcineurin inhibitor
If indicated by history or physicial exam in chronic urticaria, what are some limited laboratory testing that can be included?
CBC with differential
ESR and/or CRP
Liver enzyme
TSH
H. pylori infection
Mastocytosis
Malignancy
Skin biopsy (refractory CU, vasculitis suspected, other nonurticarial immunologic skin diseases are a consideration)
What is contact urticaria (clinical features and testing)
Clinical presentation
- Contact urticaria appears w/in 30min of exposure (vs. allergic contact dermatitis)
- Systemic symptoms can be seen (GI and nasopharyngeal) ?on ingestion
- Plant- and animal-derived proteins most common causes in workplace
- Bakers and agricultural workers highest risk
- Cooks, butchers, restaurant personnel, veterinarians, hairdressers, florists, and forestry workers also affected
- Foods implicated: meats, fish, eggs, fruits, vegetables, and flour and associated enzymes (α-amylase)
Investigations
- Percutaneous testing
- Open testing: Apply small amt of presumed offending agent to normal skin on volar aspect of forearm, observe for 20-60 minutes for wheal-and-flare
- Consider serum specific IgE but many protein allergens not identified yet
- Oral challenge can differentiate from IgE-mediated food allergy (esp if systemic symptoms)
Contact dermatitis from methylisothiazolinone
A chemical preservative found in many water-based products such as sunscreen, cosmetics, hair products, liquid soap, laundry products, premoistened facial wipes and baby wipes
Contact dermatitis from sporting goods such as tennis rackets, building construction, and vehicle parts; distribution of rash is on hands
Bisphenol A is often found in sporting goods such as tennis rackets, building construction, and vehicle parts; therefore, favoring the distribution of the rash is on the hands
Contact dermatitis from shoes and leather with rash distribution on dorsum of feet
Potassium dichromate is found in shoes and leather so the rash distribution is usually on the dorsum of the feet.