Canine Atopic Dermatitis Flashcards

1
Q

what are the results of uncontrolled atopic dermatitis?

A
  1. recurrent multidrug-resistant staph infections and malassezia dermatitis
  2. recurrent otitis externa
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2
Q

describe practice guidelines for canine AD

A
  1. treatment of acute flares of cAD:
    -glucocorticoids
    -oclacitinib
    -cytopoint
  2. treatment of chronic stages of cAD:
    -glucocorticoids
    -oclacitinib
    -cyclosporine
    -cytopoint
  3. prevent recurrences of cAD:
    -allergen immunotherapy
    -food elimination/diet trials

issues with current guidelines (from 2015)
-cAD dogs can at the same time exhibit both acute/subacute flares and chronic skin lesions at different body locations!
-atopic dermatitis is a chronic disease
-cAD dogs have different disease severities so not one drug fits all

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3
Q

describe the different phenotypes of cAD

A

phenotype 1: severe itch, but mild skin lesions

phenotype 2: generalized skin lesions plus lots of itch

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4
Q

describe the guidelines for cAD treatment

A
  1. ID and address flare factors:
  2. symptomatic treatment of itch and/or inflammation
  3. prevention of AD flares
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5
Q

compare AIT to symptomatic therapy for cAD

A

AIT: the only disease modifying therapy!
-ID relevant allergens through intradermal/serologic testing
-then SQ, sublingual, intralymphatic or recomvbinant allergen AIT

symptomatic management: once stop drugs, symptoms return!
-glucocorticoids
-cyclosporine
-oclacitinib
-lokivetmab
-antihistamines
-other

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6
Q

why are drugs shown as equal in clinical efficacy in studies but not in real life?

A
  1. drug wash-outs before start of study lead to population bias
    -milder AD phenotypes also often included in studies
  2. studies require 50% improvement in itch and clinical scores
  3. multiple biases in head to head studies between drugs because of different drug dosages/frequencies/duration of therapy
    -there is currently no optimal/standard drug dosage or therapy for EVERY case of cAD!
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7
Q

describe general length and use of glucocorticoids

A

-in most studies, glucocorticoids are tapered after an initial 7 days

-but severely inflamed and itchy skin needs longer duration of oral GCs (2-4 weeks SID then taper)

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8
Q

describe the general effective length and use of cyclosporine

A

-better changes in pruritis scores when given daily for 6 weeks but

-often tapered to every 2-3 days after 30 days due to expense

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9
Q

describe oclacitinib and lokivetmab efficacy in cAD

A
  1. in real life, many dogs are not controlled with these drugs
  2. many animals not able to achieve reduction in pruritis
    -oclacitinib saw rebound after tapering to once daily admin
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10
Q

sum up the current treatment guidelines for cAD

A
  1. topical anti-inflammatory/itchy therapy remains the mainstay for human and canine AD
  2. current canine AD guidelines do NOT provide a defined first line agent algorithm for practitioners or which systemic agent to select
  3. current symptomatic drugs are considered equal in efficacy for therapy but real life practice shows differences between agents
  4. further characterization of clinical phenotypes in cAD and clinical responses to different symptomatic drugs is needed
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11
Q

describe reactive versus proactive

A

reactive therapy: get control/induction of remission
-anti-inflammatory therapy (2x daily) until no visible skin lesions

  1. proactive therapy: keep control/maintenance of remission
    -low dose, continuous intermittent application of anti-inflammatory therapy to previously affected AD skin
    -mainstay of treatment of every human patient
  2. why?
    -nonlesional AD skin: macroscopically no AD skin lesions visible BUT is always molecularly active and will cause a disease flare (microscopic inflammation) due to tissue resident memory T cells
  3. which agents used?
    -humans: tacrolimus
    -canine: triamcinolone spray, hydrocortisone spray, mometasone furoate cream/ointment (topical glucocorticoids)
    -topical glucocorticoids alone reduce itch and clinical lesions!!
    -topical glucocorticoids also improve efficacy of systemic agents like JAK inhibitors, lokivetmab
  4. how use:
    -majority of patients with topical intermittent (tuesday/saturday per week) proactive glucocorticoid therapy to previously affected AD skin remained controlled at 12-14 weeks
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12
Q

sum up reactive/proactive therapy for AD

A
  1. topical anti-inflammatory/itch therapy remains mainstay
  2. proactive topical glucocorticoid therapy can extend AD remission for several month
  3. topical glucocorticoids improve efficacy of oclacitinib
  4. main limitation of proactive steroid topical therapy is lack of long-term safety
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13
Q

describe the concept of reactive/proactive systemic therapy in cAD

A

the breadth of target immune inhibition determines the timing of their use!

broadest to narrowest:
-glucocorticoids: rapid improvement and broad targeting for reversal of cAD inflammation in short-term use!/reactive treatment
-cyclosporine
-ilunocitinib
-oclacitinib
-lokivetmab (cytopoint): more proactive treatment to keep control

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14
Q

how would you handle a refractory cAD case?/how to select a drug?

A

ex.) 5 months of daily lokivetmab + oclacitinib + topical antiseptic shampoo/spray/oral cephalexin

how to choose a drug:
-phase 1: reactive therapy; choose drugs for itch/inflammation + secondary complications (broader range: glucocorticoids, cyclosporine, ilunocitinib) until subclinical remission

-phase 2: proactive topical therapy twice weekly with topical glucocorticoids + re-usage of agent like injectable lokivetmab

-if super refractory, start cyclosporine in phase 1 and continue as needed through phase 2 or switch to injectable lokivetmab JAK inhibitors (systemic control through phase 2 is difference)

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