Urticarias, erythemas, purpuras

Question 1

EAC pathogenesis

Answer 1

• reaction pattern or ‘hypersensitivity’, peripheral migration thought to reflect localized production of proinflammatory cytokines and vasoactive peptides
• Infectious: dermatophytes, fungi (Candida, Penicillum in blue cheese), viral (pox, EBV, VZV), bacteria (pseudomonas), parasites, ectoparasites
• Drugs: diuretics, NSAIDs, antimalarials, finasteride, amitryptiline, rituximab
• Other: Crohns, pregnancy, autoimmune endocrinopathies, HES, neoplasms (PEACE: paraneoplastic EAC eruption)
• Association only found in 1/3 of patients

Question 2

EAC clinical

Answer 2

• expand centrifugally and have central clearing
• can get to ~ 6 cm
• can be polycyclic, or simple festooned bands
• Superficial form: minimally elevated, trailing scale +/- pruritus, very rarely vesicles at periphery
• Deep form: advancing edges are elevated, no scale or pruritus
• Resolution: no scarring, but PIH, and rarely purpura
• Can persist for weeks to months

Question 3

EAC histo

Answer 3

• Superficial:
  
  • Mild spongiosis and microvesiculation with focal parakeratosis
  • Superficial perivascular lymphohistiocytic infiltrate
  • These correspond to scale on the inner margin
  • Coat-sleeving: inflammatory cells form a fairly tight aggregate around vessels
  • Rarely, eosinophils (maybe when from drug?)
  • Advancing edges - oedema
• Deep:
  
  • Epidermis unremarkable
  • Mononuclear cell infiltrate with sharply demarcated perivascular arrangement in mid-lower dermis

Question 4

EAC Rx

Answer 4

• Treat underlying condition if identified
• Topical steroids
• Topical antipruritics and sedating antihistamine
• Case reports: tacrolimus, calipotriene, NBUVB, oral metronidazole, etanercept, interferon alpha