What does atopic allergy mean

Who Gets Eczema?

Many people with eczema own family members with the condition. Experts ponder it passes from parents to kids through the genes. Eczema is fairly common.

People with eczema also may own asthma and some types of allergies, such as hay fever. Eczema, asthma, and hay fever are known as «atopic» conditions. These affect people who are overly sensitive to allergens in the environment. For some, food allergiesmay bring these on or make them worse. For others, allergies to animal dander, dust, pollen or other things might be the triggers.

Eczema is not contagious.

Diagnosis

The diagnosis of atopic dermatitis depends on a personal and/or family history of atopy coupled with the clinical signs and symptoms described by Hanifin (Table 1).11 Pruritus and xerosis are key elements; without them, the diagnosis should be questioned.9

Table 1: Hanifin Criteria for Atopic Dermatitis
Major Features (must own 3)

  • Pruritus
  • Typical morphology and distribution
    1. Chronic or chronically relapsing dermatitis
    2. Facial and extensor involvement during infancy and childhood
    3. Flexural lichenification and linearity in adults
    4. Personal or family history of atopy (asthma, allergic rhinoconjunctivitis, atopic dermatitis)
    Minor or Less-Specific Features

    1. Scalp dermatitis (cradle cap)
    2. Ichthyosis, hyperlinearity, keratosis pilaris
    3. Susceptibility to cutaneous infections (especially Staphylococcus aureus and herpes simplex virus)
    4. Periauricular fissures
    5. Cheilitis
    6. Immunoglobulin E (IgE) reactivity (increased serum IgE, radioallergosorbent, or prick test reactivity)
    7. Hand or foot dermatitis
    8. Perifollicular accentuation (especially in pigmented areas)
    9. Xerosis

    Reprinted from Hanifin JM.

    Atopic dermatitis in infants and children. Pediatr Clin North Am 1991; (4)38:763–789. Copyright © 1991 with permission from Elsevier. https://www.sciencedirect.com/journal/pediatric-clinics-of-north-america

    Atopic dermatitis can resemble other types of dermatitis (seborrheic dermatitis, allergic contact dermatitis, irritant contact dermatitis) and dermatophytosis.

    What does atopic allergy mean

    It may be a component of rare genetic diseases such as Netherton syndrome, ichthyosis, and immunodeficiency syndromes (e.g., X-linked agammaglobulinemia, Wiskott-Aldrich syndrome, isolated IgA deficiency, and severe combined immunodeficiency disease). Helpful diagnostic tests include a serum IgE level, serum protein electrophoresis, fungal scraping for potassium hydroxide preparation and culture, and skin biopsy.

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    How Is Eczema Treated?

    If you’re diagnosed with eczema, your doctor might:

    1. prescribe medicines to put on the skin that soothe the redness and irritation, such as creams or ointments that contain corticosteroids (not the same as steroids used by some athletes)
    2. recommend other medicines to take by mouth if the eczema is really bad or you get it a lot

    If someone has severe eczema, ultraviolet light therapy can assist clear up the condition.

    Newer medicines that change the way the skin’s immune system reacts also may help.

    What Are the Signs & Symptoms of Eczema?

    The symptoms of eczema:

    1. can be on any part of the body. But in teens, the itchy patches generally happen where the elbow bends; on the backs of the knees; on the inner wrists and ankles; and on the face, neck, and upper chest.
    2. are mainly dry, itchy skin
    3. can vary fairly a bit from person to person
    4. also include redness, scales, and fluid-filled bumps that become moist and then crust over
    5. tend to come and go.

      When they get worse, it is called a flare-up.

    Some people who own eczema scratch their skin so much it becomes thick, darker, and almost leathery in texture (called lichenification).

    Prevalence

    Atopic dermatitis is a common condition affecting approximately 17% of the population2 with a slight female preponderance (1.3:1 in children). The incidence has increased twofold to threefold since the 1970s. The basis of this increase is not well understood; however, environmental factors appear to frolic an significant role in disease prevalence.

    Factors associated with an increased risk of atopic dermatitis include little family size, higher socioeconomic and educational levels regardless of ethnicity, movement from a rural to urban environment, and increased use of antibiotics (the Western lifestyle).

    This has led to the hygiene hypothesis, which suggests that infections in early childhood (from less-hygienic practices and older siblings) might prevent atopic dermatitis. This hypothesis is supported by evidence that infections induce type-1 helper T cells (TH1), whereas there is a predominance of type-2 helper T cells (TH2) in atopic dermatitis. TH1 responses antagonize the development of TH2 cells, thereby potentially decreasing the incidence of atopic dermatitis.3

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    Summary

    1. Cotter DG, Schairer D, Eichenfield L. Emerging therapies for atopic dermatitis: JAK inhibitors. J Am Acad Dermatol 2018; 78(3 suppl 1):S53–S62.

    2. Leung DY, Bieber T. Atopic dermatitis. Lancet 2003; 361(9352):151–160.
    3. Levy LL, Urban J, King BA. Treatment of recalcitrant atopic dermatitis with the oral Janus kinase inhibitor tofacitinib citrate. J Am Acad Dermatol 2015; 73(3):395–399.
    4. Simpson EL, Flohr C, Eichenfield LF, et al. Efficacy and safety of lebrikizumab (an anti-IL-13 monoclonal antibody) in adults with moderate-to-severe atopic dermatitis inadequately controlled by topical corticosteroids: a randomized, placebo-controlled phase II trial (TREBLE). J Am Acad Dermatol 2018; 78(5):863–871.
    5. It is associated with asthma and airborne allergies (atopic triad).
    6. Rudikoff D, Lebwohl M.

      Atopic dermatitis. Lancet 1998; 351(9117):1715–1721.

    7. Clausen ML, Agner T, Lilje B, Edslev SM, Johannesen TB, Andersen PS. Association of disease severity with skin microbiome and filaggrin gene mutations in adult atopic dermatitis. JAMA Dermatol 2018; 154(3):293–300.
    8. Ruzicka T, Hanifin JM, Furue M, et al; XCIMA Study Group. Anti-interleukin-31 receptor A antibody for atopic dermatitis. N Engl J Med 2017; 376(9):826–835.
    9. Atopic dermatitis is a common childhood condition in every races.
    10. Hanifin JM. Atopic dermatitis in infants and children.

      Pediatr Clin North Am 1991; 38(4):763–789.

    11. Guttman-Yassky E, Silverberg JI, Nemoto O, et al. Baricitinib in adult patients with moderate-to-severe atopic dermatitis: a phase 2 parallel, double-blinded, randomized placebo-controlled multiple-dose study. J Am Acad Dermatol 2018; Feb 1. doi:10.1016/j.jaad.2018.01.018.
    12. Nakagawa H, Nemoto O, Igarashi A, Nagata T. Efficacy and safety of topical JTE-052, a Janus kinase inhibitor, in Japanese adult patients with moderate-to-severe atopic dermatitis: a phase II, multicentre, randomized, vehicle-controlled clinical study.

      Br J Dermatol 2018; 178(2):424–432.

    13. Gooderham MJ, Hong HC, Eshtiaghi P, Papp KA. Dupilumab: a review of its use in the treatment of atopic dermatitis. J Am Acad Dermatol 2018; 78(3 suppl 1):S28–S36.
    14. Silverberg JI, Thyssen JP, Paller AS, et al. What’s in a name? Atopic dermatitis or atopic eczema, but not eczema alone. Allergy 2017; 72(12):2026–2030.
    15. Laughter D, Istvan JA, Tofte SJ, Hanifin JM.

      The prevalence of atopic dermatitis in Oregon schoolchildren. J Am Acad Dermatol 2000; 43(4):649–655.

    16. MacLean JA, Eidelman FJ. The genetics of atopy and atopic eczema. Arch Dermatol 2001; 137(11):1474–1476.
    17. Bissonnette R, Papp KA, Poulin Y, et al. Topical tofacitinib for atopic dermatitis: a phase IIa randomized trial. Br J Dermatol 2016; 175(5):902–911.
    18. Klein PA, Clark RA. An evidence-based review of the efficacy of antihistamines in relieving pruritus in atopic dermatitis. Arch Dermatol 1999; 135(12):1522–1525.
    19. Associated pruritus is severe and can interfere with social and scholarly activities.
    20. Atopic dermatitis has an increased incidence in industrialized countries.
    21. Ruzicka T: Atopic eczema between rationality and irrationality.

      Arch Dermatol 1998; 134(11):1462–1469.

    22. First-line treatment consists of applying bland emollients, limiting use of soap, and decreasing bath temperature.
    23. Nakatsuji T, Chen TH, Two AM, et al. Staphylococcus aureus exploits epidermal barrier defects in atopic dermatitis to trigger cytokine expression. J Invest Dermatol 2016; 136(11):2192–2200.
    24. Kondo H, Ichikawa Y, Imokawa G.

      Percutaneous sensitization through barrier-disrupted skin elicits a Th2-dominant cytokine response. Eur J Immunol 1998; 28(3):769–779.

    25. Paller AS, Tom WL, Lebwohl MG, et al. Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. J Am Acad Dermatol 2016; 75(3):494–503.e6.
    26. Williams HC. Is the prevalence of atopic dermatitis increasing? Clin Exp Dermatol 1992; 17(6):385–391.
    27. Fonacier L, Spergel J, Charlesworth EN, et al.

      Report of the Topical Calcineurin Inhibitor Task Force of the American College of Allergy, Asthma and Immunology and the American Academy of Allergy, Asthma and Immunology. J Allergy Clin Immunol 2005; 115(6):1249–1253.

    28. Zebda R, Paller AS. Phosphodiesterase 4 inhibitors. J Am Acad Dermatol 2018; 78(3 suppl 1):S43–S52.

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    Outcomes

    Atopic dermatitis is a chronic disease with intermittent flares and spontaneous remissions.

    Approximately 40% to 60% of children with atopic dermatitis own the disease in adulthood, generally manifested as hand dermatitis. More than 75% of children with atopic dermatitis also own asthma or allergic rhinitis.

    With excellent skin care, including the application of appropriate moisturizers, and the use of topical corticosteroids or topical calcineurin inhibitors, most patients with atopic dermatitis do well.

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    What Causes Eczema?

    Doctors don’t know exactly what causes eczema, but they ponder it could be a difference in the way a person’s immune system reacts to things.

    Skin allergies may be involved in some forms of eczema.

    Definition

    Atopic dermatitis (Figure 1) and atopic eczema1 are interchangeable terms for an inflammatory condition of the skin characterized by erythema, pruritus, scaling, lichenification, and papulovesicles. Atopic dermatitis is a distinct condition in persons who are genetically predisposed to developing immunoglobulin (Ig) E-mediated hypersensitivity reactions. It is characterized by the itch-scratch cycle: affected persons own the sensation of itch, followed by scratching and the subsequent creation of a rash. The classic triad of atopy includes atopic eczema, asthma, and allergies.

    A wide range of environmental factors such as contact allergens, stress, food, skin flora, and humidity frolic roles in the development and severity of atopic dermatitis.

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    References

    • Stay cool. Sudden changes in temperature, sweating, and becoming overheated may cause your eczema to kick in.
    • MacLean JA, Eidelman FJ. The genetics of atopy and atopic eczema. Arch Dermatol 2001; 137(11):1474–1476.
    • Don’t scratch. It’s hard to resist, but scratching can make eczema worse and make it harder for skin to heal.

      You might break the skin and let bacteria in, causing an infection.

    • Paller AS, Tom WL, Lebwohl MG, et al. Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. J Am Acad Dermatol 2016; 75(3):494–503.e6.
    • Williams HC. Is the prevalence of atopic dermatitis increasing? Clin Exp Dermatol 1992; 17(6):385–391.
    • Ruzicka T, Hanifin JM, Furue M, et al; XCIMA Study Group. Anti-interleukin-31 receptor A antibody for atopic dermatitis. N Engl J Med 2017; 376(9):826–835.
    • Klein PA, Clark RA.

      An evidence-based review of the efficacy of antihistamines in relieving pruritus in atopic dermatitis. Arch Dermatol 1999; 135(12):1522–1525.

    • Zebda R, Paller AS. Phosphodiesterase 4 inhibitors. J Am Acad Dermatol 2018; 78(3 suppl 1):S43–S52.
    • Silverberg JI, Thyssen JP, Paller AS, et al. What’s in a name?

      What does atopic allergy mean

      Atopic dermatitis or atopic eczema, but not eczema alone. Allergy 2017; 72(12):2026–2030.

    • Cotter DG, Schairer D, Eichenfield L. Emerging therapies for atopic dermatitis: JAK inhibitors. J Am Acad Dermatol 2018; 78(3 suppl 1):S53–S62.
    • Stay away from things that can irritate your skin. Besides your known triggers, some things you may desire to avoid include household cleaners, drying soaps, detergents, and scented lotions. For facial eczema, wash gently with a nondrying facial cleanser or soap substitute, and use facial moisturizers, makeup, and sunscreens that tell «non-comedogenic/oil-free» on the product label.
    • Say yes to cotton. Clothes made of scratchy fabric love wool can irritate your skin.

      Soft cotton clothes are a better bet.

    • Nakagawa H, Nemoto O, Igarashi A, Nagata T. Efficacy and safety of topical JTE-052, a Janus kinase inhibitor, in Japanese adult patients with moderate-to-severe atopic dermatitis: a phase II, multicentre, randomized, vehicle-controlled clinical study. Br J Dermatol 2018; 178(2):424–432.
    • Clausen ML, Agner T, Lilje B, Edslev SM, Johannesen TB, Andersen PS. Association of disease severity with skin microbiome and filaggrin gene mutations in adult atopic dermatitis. JAMA Dermatol 2018; 154(3):293–300.
    • Nakatsuji T, Chen TH, Two AM, et al.

      Staphylococcus aureus exploits epidermal barrier defects in atopic dermatitis to trigger cytokine expression. J Invest Dermatol 2016; 136(11):2192–2200.

      What does atopic allergy mean

    • Simpson EL, Flohr C, Eichenfield LF, et al. Efficacy and safety of lebrikizumab (an anti-IL-13 monoclonal antibody) in adults with moderate-to-severe atopic dermatitis inadequately controlled by topical corticosteroids: a randomized, placebo-controlled phase II trial (TREBLE). J Am Acad Dermatol 2018; 78(5):863–871.
    • Moisturize! A scent-free moisturizer will prevent your skin from becoming irritated and cracked. Moisturize every day, ideally twice or three times a day. The best time to apply moisturizer is after the skin has been soaked in a bath or shower, then patted dry gently.

      Ointments (such as petroleum jelly) and creams are best because they contain a lot of oil. Lotions own too much water to be helpful.

    • Bissonnette R, Papp KA, Poulin Y, et al. Topical tofacitinib for atopic dermatitis: a phase IIa randomized trial. Br J Dermatol 2016; 175(5):902–911.
    • Kondo H, Ichikawa Y, Imokawa G. Percutaneous sensitization through barrier-disrupted skin elicits a Th2-dominant cytokine response.

      Eur J Immunol 1998; 28(3):769–779.

    • Laughter D, Istvan JA, Tofte SJ, Hanifin JM. The prevalence of atopic dermatitis in Oregon schoolchildren. J Am Acad Dermatol 2000; 43(4):649–655.
    • Fonacier L, Spergel J, Charlesworth EN, et al. Report of the Topical Calcineurin Inhibitor Task Force of the American College of Allergy, Asthma and Immunology and the American Academy of Allergy, Asthma and Immunology.

      J Allergy Clin Immunol 2005; 115(6):1249–1253.

    • Leung DY, Bieber T. Atopic dermatitis. Lancet 2003; 361(9352):151–160.
    • Guttman-Yassky E, Silverberg JI, Nemoto O, et al. Baricitinib in adult patients with moderate-to-severe atopic dermatitis: a phase 2 parallel, double-blinded, randomized placebo-controlled multiple-dose study. J Am Acad Dermatol 2018; Feb 1. doi:10.1016/j.jaad.2018.01.018.
    • Hanifin JM. Atopic dermatitis in infants and children. Pediatr Clin North Am 1991; 38(4):763–789.
    • Take your meds. Follow your doctor’s directions for every medicines.
    • Ruzicka T: Atopic eczema between rationality and irrationality.

      Arch Dermatol 1998; 134(11):1462–1469.

    • Rudikoff D, Lebwohl M. Atopic dermatitis. Lancet 1998; 351(9117):1715–1721.
    • Gooderham MJ, Hong HC, Eshtiaghi P, Papp KA. Dupilumab: a review of its use in the treatment of atopic dermatitis. J Am Acad Dermatol 2018; 78(3 suppl 1):S28–S36.
    • Use warm water. Too much exposure to boiling water can dry out your skin, so take short warm — not boiling — showers and baths and wear gloves if your hands will be in water for endless periods of time.

      Gently and thoroughly pat your skin dry, using a soft towel.

    • Levy LL, Urban J, King BA. Treatment of recalcitrant atopic dermatitis with the oral Janus kinase inhibitor tofacitinib citrate. J Am Acad Dermatol 2015; 73(3):395–399.
    • Unwind.Stress can aggravate eczema, so attempt to relax.

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    en españolTodo sobre el eccema

    How Is Eczema Diagnosed?

    There is no specific test used to diagnose eczema. A doctor will glance at the rash and enquire about your symptoms and past health, as well as your family’s health.

    If you or your family members own any atopic conditions, that’s an significant clue.

    The doctor will desire to law out other conditions that can cause skin inflammation. The doctor might recommend that you see a dermatologist or an allergist.

    How Can I Deal With Eczema?

    There’s no cure for eczema. But you can assist prevent a flare-up:

    1. Stay cool. Sudden changes in temperature, sweating, and becoming overheated may cause your eczema to kick in.
    2. Stay away from things that can irritate your skin. Besides your known triggers, some things you may desire to avoid include household cleaners, drying soaps, detergents, and scented lotions.

      For facial eczema, wash gently with a nondrying facial cleanser or soap substitute, and use facial moisturizers, makeup, and sunscreens that tell «non-comedogenic/oil-free» on the product label.

    3. Take your meds. Follow your doctor’s directions for every medicines.
    4. Don’t scratch. It’s hard to resist, but scratching can make eczema worse and make it harder for skin to heal. You might break the skin and let bacteria in, causing an infection.
    5. Moisturize! A scent-free moisturizer will prevent your skin from becoming irritated and cracked. Moisturize every day, ideally twice or three times a day.

      The best time to apply moisturizer is after the skin has been soaked in a bath or shower, then patted dry gently. Ointments (such as petroleum jelly) and creams are best because they contain a lot of oil. Lotions own too much water to be helpful.

    6. Say yes to cotton. Clothes made of scratchy fabric love wool can irritate your skin. Soft cotton clothes are a better bet.
    7. Use warm water. Too much exposure to boiling water can dry out your skin, so take short warm — not boiling — showers and baths and wear gloves if your hands will be in water for endless periods of time. Gently and thoroughly pat your skin dry, using a soft towel.
    8. Unwind.Stress can aggravate eczema, so attempt to relax.

    What Is Eczema?

    Eczema (pronounced: EK-zeh-ma) is a condition where the skin becomes red, scaly, irritated, and itchy.

    There are numerous types of eczema, but atopic dermatitis (pronounced: ay-TOP-ik der-muh-TIE-tis) is one of the most common. To numerous people, the terms «eczema» and «atopic dermatitis» mean the same thing.

    Pathophysiology

    Atopic dermatitis is a type I IgE-mediated hypersensitivity reaction, but the exact etiology is unknown. The pathogenesis is multifactorial and involves a complicated immunologic cascade, including disruption of the epidermal barrier, IgE dysregulation, defects in the cutaneous cell-mediated immune response, and genetic factors.

    The major elements in immune dysregulation are Langerhans’ cells, inflammatory dendritic epidermal cells, monocytes, macrophages, lymphocytes, mast cells, and keratinocytes, every of which interact through an intricate cascade of cytokines leading to a predominance of TH2 cells over TH1 cells.4 The TH2 cytokines, interleukin (IL)-4, IL-5, IL-10, and IL-13, are increased in the skin, and there is a corresponding decrease in TH1 cytokines, mainly interferon-gamma and IL-2.

    Patients with atopic dermatitis often own dry, sensitive skin due to changes in the epidermis, which serves as a barrier to the environment by maintaining the water balance of the skin.

    Essential fatty acids (EFAs), such as linoleic and linolenic acid, are significant components of the epidermal barrier. In atopic dermatitis, delta-desaturase activity is deficient,5 which leads to decreased linoleic and linolenic acid metabolites. Loss of EFAs results in increased transepidermal water loss and subsequent xerosis (dryness). The EFAs form the substrate of the inflammatory mediators (prostaglandins and leukotrienes), resulting in a secondary deficiency of prostaglandin E1.

    Defects in the epidermal barrier also lead to increased susceptibility to atopens (atopic allergens such as home dust mites, grass, or pollen).

    When such allergens contact atopic skin, they stimulate TH2 lymphocytes to produce cytokines such as IL-4, IL-5, and IL-13, which in turn promote an increase in IgE synthesis.6 Atopic dermatitis patients often own high levels of IgE antibodies due to home dust mites and other allergens. Eliminating these allergens from the environment, an extremely hard undertaking, can improve atopic dermatitis.

    Defective cell-mediated immunity leads to increased susceptibility to numerous bacterial, viral, and fungal infections of the skin. Children with atopic dermatitis are particularly susceptible to severe, widespread herpes simplex virus infection (eczema herpeticum)—a systemic and potentially fatal infection that primarily affects areas of athletic atopic eczema.

    Widespread infections with human papillomavirus (warts) and molluscum contagiosum are also common in children with atopic dermatitis.

    In Dermatology, the microbiome includes resident microorganisms of the skin and plays an significant role in regulating immunity. In comparison to patients with normal skin, patients with atopic dermatitis protest an altered microbiome in affected areas. There are even detectable environmental differences in the non-inflamed skin of atopic patients.7 Additionally, unaffected patients carry Staphylococcus epidermidis on their skin that acts to improve any immune defense against microbes.

    Most patients with atopic dermatitis not only own a compromised skin barrier but are also colonized with Staphylococcus aureus (S aureus). Studies support that this bacterium further worsens the inflammatory response and may be coupled with a decrease in antimicrobial defense.8

    Numerous factors exacerbate or trigger atopic dermatitis, including colonization with S aureus, stress, anxiety, systemic illness, and xerosis. The most common trigger is S aureus colonization.

    More than 90% of patients with atopic dermatitis own S aureus colonization of lesional skin, and more than 75% own colonization of uninvolved skin.9 Staphylococci exacerbate atopic dermatitis by 2 mechanisms: acting as superantigens by stimulating an augmented T cell response—thereby exacerbating the skin disease—and promoting increased production of IgE. IgE has anti–S aureus properties and helps control colonization and infection in normal persons. In atopic dermatitis patients, the elevated IgE levels contribute to immune dysregulation. Treatment with topical or oral antistaphylococcal antibiotics (or both) decreases the colonization of the skin and often leads to improvement.

    Family studies support a genetic basis for atopic dermatitis.

    When both parents are atopic, their offspring own a 70% risk for atopic dermatitis5; the risk of inheritance is higher if the mom is atopic. The mode of inheritance appears to be complicated and likely involves several genes. To date, no specific single gene has been identified as a unique marker for atopic dermatitis or atopy.10

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    Signs and Symptoms

    Atopic dermatitis is a chronic disease with periods of remissions and exacerbations. Three age-related stages exist: the infantile stage (up to 2 years old), the childhood stage (from 2 to 12 years), and the adult stage (puberty onward).

    The manifestations vary with age, even in the same patient. Every stages are characterized by xerosis, fissures, pruritus, and lichenification. The main differentiating factor is the area of involvement.

    The infantile stage is characterized by pruritic, red, eczematous plaques on the cheeks and extensor extremities. Secondary impetiginization, with honey-colored crust, is common in infants. Scalp involvement can resemble seborrheic dermatitis. The diaper area is spared.

    The childhood stage is primarily a papular dermatitis affecting the flexural areas, especially the antecubital and popliteal fossa, wrists, ankles, and neck. Thickened, lichenified plaques with excoriation (Figures 2 to 4) are common.

    In darker-pigmented children, follicular papules may be the only manifestation. Hypopigmentation and hyperpigmentation can happen, which can cause grand anxiety in parents. Pityriasis alba, characterized by hypopigmented, scaly patches on the face, is commonly seen. Keratosis pilaris, or spiny hair follicles, commonly affects the posterior aspects of the upper arms and the anterior thighs.

    The adult stage is unpredictable.

    Affected patients may own had only a few outbreaks since infancy or they may own had a chronic, relapsing course. Hand dermatitis is common and may be the only manifestation of adult atopic dermatitis, which can lead to significant disability. Love affected children, adults also commonly own lichenification of the flexures and facial dermatitis.

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    Treatment

    Atopic dermatitis tends to be a chronic relapsing disease.

    The goals of therapy should be to reduce the number and severity of flares and to increase the number of disease-free periods. The mainstay of treatment for atopic dermatitis is hydrating the skin with the regular use of emollients and suppressing cutaneous inflammation with topical corticosteroids. Topical calcineurin inhibitors own become an significant adjunctive therapy. For severe disease, especially during acute flares, systemic corticosteroids may be necessary. Secondary infections require treatment with topical or oral antibiotics, or both.

    Oral antihistamines can assist decrease pruritus. In severe, recalcitrant cases, phototherapy or systemic immunosuppressive medications may be necessary.

    Most patients with atopic dermatitis require hydration though the liberal use of bland emollients, which serve to hydrate the stratum corneum and maintain the lipid barrier. Sufficient emollients applied liberally several times a day may be enough to significantly reduce the disease activity of atopic dermatitis. Parents of infants and toddlers should apply a bland emollient to the entire body with each diaper change. Older children should apply bland emollients in the morning, after school, and at bedtime.

    Bathing should be limited to brief, cool showers once daily. Soap, which dries and irritates the skin, should be avoided, but tender lipid-free cleansers are beneficial.

    Corticosteroids suppress lymphocyte activity in the skin, thereby decreasing inflammation. Patients can use a low-potency topical steroid (hydrocortisone or desonide) for day-to-day control of mild disease and a medium-potency steroid (triamcinolone acetonide, fluticasone, or fluocinolone) for more severe flares. Low-potency topical steroids are suitable for infants and for intertriginous and sensitive areas (face, genitals); more potent steroids should be avoided on these sites.

    Severe, widespread disease can require systemic corticosteroids. Because of the well-known side effects of systemic corticosteroids (e.g., adrenal suppression, osteoporosis, hypertension, diabetes, obesity, striae), their use should be limited to patients with severe disease.

    Topical calcineurin inhibitors (tacrolimus, pimecrolimus) are effective alternatives to the chronic use of topical corticosteroids. Topical calcineurin inhibitors bind calcineurin and block the activation of T cells by cytokines, thus halting the inflammatory cascade that leads to atopic dermatitis. Topical calcineurin inhibitors are especially suitable for more delicate areas such as the face and genitals because they do not carry the risks of atrophy, telangiectasias, and striae associated with the chronic use of steroids.

    Reports own surfaced suggesting a possible risk of lymphoma associated with high-dose oral pimecrolimus in animal studies,12 prompting the US Food and Drug istration to put out a black box warning advising against the use of topical calcineurin inhibitors in children younger than 2 years. However, there are no data to support an increased risk of lymphoma with topical treatment in humans.12 Topical calcineurin inhibitors should be used for a limited time and only on affected skin. They should not be used as a daily moisturizer, first-line therapy, or preventive therapy.

    The pruritus associated with atopic dermatitis can be severe and often interferes with school, work, and sleep.

    Despite a lack of objective data to support their use, antihistamines are commonly used to break the itch-scratch-itch cycle.13 Nonsedating antihistamines such as fexofenadine, cetirizine, loratadine, and desloratadine can assist offset daytime itching without somnolence. Sedating antihistamines such as diphenhydramine or hydroxyzine are often helpful for nighttime pruritus.

    Patients with atopy own an abnormal tolerance to S aureus colonization of the skin, which can exacerbate the dermatitis. Affected patients should use lipid-free antibacterial cleansers.

    For open wounds, a topical antibiotic such as mupirocin can assist to prevent secondary impetiginization (Figures 5 and 6). An oral antibiotic with S aureus coverage and excellent skin penetration, such as amoxicillin-clavulanic acid, cephalexin, or azithromycin, is necessary for extensive excoriations and impetigo.

    In severe, recalcitrant cases, ultraviolet (UV) light treatments (UVB or psoralen plus UVA [PUVA]) and immunosuppressive medications (e.g., methotrexate, cyclosporine, azathioprine, mycophenolate mofetil) may be helpful.13 These should be used extremely cautiously and with shut monitoring and should be reserved for the most severe cases.

    Allergic contact dermatitis from topical medications, cosmetics, or metals should be considered in patients with recalcitrant disease.

    Evaluation by an environmental dermatologist and an allergist, including patch, pinprick, and serum radioallergosorbent testing, may be warranted. Topical medications that are known sensitizers, such as lidocaine, doxepin cream, and diphenhydramine cream, as well as topical antibiotics such as neomycin, should be strictly avoided. Allergic contact dermatitis to topical steroids should be considered in any patient who fails to improve or worsens with the use of topical steroids.

    A multitude of new treatments are currently available or under investigation for atopic dermatitis. These range from oral to topical agents and each has an significant inflammatory target.

    Key components of this TH2-mediated disease include cytokines such as IL-4, IL-5, IL-13, and IL-31. Dupilumab binds a subunit of the IL-4 receptor and therefore blocks IL-4 and IL-13. This medication is approved for the treatment of moderate-to-severe atopic dermatitis and there are ongoing long-term studies.14

    Similarly, lebrikizumab is an IL-13 antibody in trial that has demonstrated efficacy in atopic patients who were still using topical corticosteroids; continued studies are needed.15

    IL-31 seems to frolic a role in atopic dermatitis and itch development.

    Nemolizumab (CIM331) targets the IL-31 receptor A and has been shown to decrease itch sensation among affected patients in early reports.16

    A related approach includes targeting Janus kinase (JAK) signaling, which plays an significant role in immune function and is involved in inflammatory skin conditions including chronic itch. While further investigation remains necessary, early data show JAK inhibitors (jakinibs) to be a promising therapy option.17 JAK assists in the function and effect of various TH2 cytokines discussed above. Baricitinib, an inhibitor of JAK1 and JAK2, has been shown to reduce atopic dermatitis and itch in patients who continued to use topical corticosteroids.18 Additional JAK1 inhibitors currently under study include PF-04965842 and ABT-494 (upadacitinib).17

    While the JAK pathway was first targeted with oral tofacitinib citrate (a JAK1 and JAK3 inhibitor)19, topical preparations are in trial including topical tofacitinib.20 In addition, the efficacy and safety of a topical JAK inhibitor called JTE-052—which notably inhibits JAK1, JAK2, JAK3, and tyrosine kinase 2—has been reported with promising results.21 Topical ruxolitinib studies are underway as well.17

    Lastly, crisaborole, a topical phosphodiesterase 4 inhibitor, is approved for patients with mild-to-moderate atopic dermatitis and has demonstrated efficacy.22 Targeting this pro-inflammatory molecule has led to the development of other phosphodiesterase 4 inhibitors.23

    With novel therapies emerging, it is necessary to continue investigation into the efficacy and safety of these various systemic and topical treatments.

    Furthermore, studies are overall lacking in the pediatric population. Nonetheless, the future for the treatment of atopic dermatitis is encouraging and rapidly expanding.

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    What Else Should I Know?

    If you live with eczema, tune in to what triggers it and how to manage it. For example, if you discover that some types of makeup irritate your skin, enquire a dermatologist to recommend brands that are less likely to do so.

    Your self-esteem doesn’t own to suffer because you own eczema, and neither does your social life!

    Getting involved in your school and extracurricular activities can be a grand way to get your mind off the itch.

    Don’t forget to exercise. It’s a grand way to blow off stress — attempt walking, bike riding, swimming, or another sport that keeps your skin cool and dry while you work out.

    8.00 Skin Disorders

    A. What skin disorders do we assess with these listings?

    We use these listings to assess skin disorders that may result from hereditary, congenital, or acquired pathological processes.

    The kinds of impairments covered by these listings are: Ichthyosis, bullous diseases, chronic infections of the skin or mucous membranes, dermatitis, hidradenitis suppurativa, genetic photosensitivity disorders, and burns.

    B. What documentation do we need?

    When we assess the existence and severity of your skin disorder, we generally need information about the onset, duration, frequency of flare-ups, and prognosis of your skin disorder; the location, size, and appearance of lesions; and, when applicable, history of exposure to toxins, allergens, or irritants, familial incidence, seasonal variation, stress factors, and your ability to function exterior of a highly protective environment.

    To confirm the diagnosis, we may need laboratory findings (for example, results of a biopsy obtained independently of Social Security disability evaluation or blood tests) or evidence from other medically acceptable methods consistent with the prevailing state of medical knowledge and clinical practice.

    C. How do we assess the severity of your skin disorder(s)?

    We generally base our assessment of severity on the extent of your skin lesions, the frequency of flare-ups of your skin lesions, how your symptoms (including pain) limit you, the extent of your treatment, and how your treatment affects you.

    1. Extensive skin lesions.

    Extensive skin lesions are those that involve multiple body sites or critical body areas, and result in a extremely serious limitation. Examples of extensive skin lesions that result in a extremely serious limitation include but are not limited to:

    a. Skin lesions that interfere with the motion of your joints and that extremely seriously limit your use of more than one extremity; that is, two upper extremities, two lower extremities, or one upper and one lower extremity.

    b. Skin lesions on the palms of both hands that extremely seriously limit your ability to do fine and gross motor movements.

    c. Skin lesions on the soles of both feet, the perineum, or both inguinal areas that extremely seriously limit your ability to ambulate.

    2. Frequency of flare-ups.

    If you own skin lesions, but they do not meet the requirements of any of the listings in this body system, you may still own an impairment that prevents you from doing any gainful activity when we consider your condition over time, especially if your flare-ups result in extensive skin lesions, as defined in C1 of this section. Therefore, if you own frequent flare-ups, we may discover that your impairment(s) is medically equal to one of these listings even though you own some periods during which your condition is in remission.

    We will consider how frequent and serious your flare-ups are, how quickly they resolve, and how you function between flare-ups to determine whether you own been unable to do any gainful activity for a continuous period of at least 12 months or can be expected to be unable to do any gainful activity for a continuous period of at least 12 months. We will also consider the frequency of your flare-ups when we determine whether you own a severe impairment and when we need to assess your residual functional capacity.

    3. Symptoms (including pain).

    Symptoms (including pain) may be significant factors contributing to the severity of your skin disorder(s).

    We assess the impact of symptoms as explained in §§ 404.1521, 404.1529, 416.921, and 416.929 of this chapter.

    4. Treatment.

    We assess the effects of medication, therapy, surgery, and any other form of treatment you get when we determine the severity and duration of your impairment(s). Skin disorders frequently reply to treatment; however, response to treatment can vary widely, with some impairments becoming resistant to treatment.

    Some treatments can own side effects that can in themselves result in limitations.

    a. We assess the effects of continuing treatment as prescribed by determining if there is improvement in the symptoms, signs, and laboratory findings of your disorder, and if you experience side effects that result in functional limitations. To assess the effects of your treatment, we may need information about:

    i.

    The treatment you own been prescribed (for example, the type, dosage, method, and frequency of istration of medication or therapy);

    ii. Your response to the treatment;

    iii. Any adverse effects of the treatment; and

    iv. The expected duration of the treatment.

    b. Because treatment itself or the effects of treatment may be temporary, in most cases sufficient time must elapse to permit us to assess the impact and expected duration of treatment and its side effects.

    Except under 8.07 and 8.08, you must follow continuing treatment as prescribed for at least 3 months before your impairment can be sure to meet the requirements of a skin disorder listing. (See 8.00H if you are not undergoing treatment or did not own treatment for 3 months.) We consider your specific response to treatment when we assess the overall severity of your impairment.

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    D. How do we assess impairments that may affect the skin and other body systems?

    When your impairment affects your skin and has effects in other body systems, we first assess the predominant feature of your impairment under the appropriate body system.

    Examples include, but are not limited to the following.

    1. Tuberous sclerosis primarily affects the brain. The predominant features are seizures, which we assess under the neurological listings in 11.00, and developmental delays or other mental disorders, which we assess under the mental disorders listings in 12.00.

    2. Malignant tumors of the skin (for example, malignant melanomas) are cancers, or neoplastic diseases, which we assess under the listings in 13.00.

    3. Autoimmune disorders and other immune system disorders (for example, systemic lupus erythematosus (SLE), scleroderma, human immunodeficiency virus (HIV) infection, and Sjögren’s syndrome) often involve more than one body system.

    We first assess these disorders under the immune system disorders listings in 14.00. We assess SLE under 14.02, scleroderma under 14.04, Sjögren’s syndrome under 14.10, and HIV infection under 14.11.

    4. Disfigurement or deformity resulting from skin lesions may result in loss of sight, hearing, lecture, and the ability to chew (mastication). We assess these impairments and their effects under the special senses and lecture listings in 2.00 and the digestive system listings in 5.00. Facial disfigurement or other physical deformities may also own effects we assess under the mental disorders listings in 12.00, such as when they affect mood or social functioning.

    E. How do we assess genetic photosensitivity disorders?

    1. Xeroderma pigmentosum (XP). When you own XP, your impairment meets the requirements of 8.07A if you own clinical and laboratory findings showing that you own the disorder. (See 8.00E3.) People who own XP own a lifelong hypersensitivity to every forms of ultraviolet light and generally lead extremely restricted lives in highly protective environments in order to prevent skin cancers from developing. Some people with XP also experience problems with their eyes, neurological problems, mental disorders, and problems in other body systems.

    2. Other genetic photosensitivity disorders.

    Other genetic photosensitivity disorders may vary in their effects on diverse people, and may not result in an inability to engage in any gainful activity for a continuous period of at least 12 months. Therefore, if you own a genetic photosensitivity disorder other than XP (established by clinical and laboratory findings as described in 8.00E3), you must show that you own either extensive skin lesions or an inability to function exterior of a highly protective environment to meet the requirements of 8.07B.

    You must also show that your impairment meets the duration requirement.

    By inability to function exterior of a highly protective environment we mean that you must avoid exposure to ultraviolet light (including sunlight passing through windows and light from unshielded fluorescent bulbs), wear protective clothing and eyeglasses, and use opaque wide spectrum sunscreens in order to avoid skin cancer or other serious effects. Some genetic photosensitivity disorders can own extremely serious effects in other body systems, especially special senses and lecture (2.00), neurological (11.00), mental (12.00), and neoplastic (13.00). We will assess the predominant feature of your impairment under the appropriate body system, as explained in 8.00D.

    3.

    Clinical and laboratory findings.

    a. General. We need documentation from an acceptable medical source to establish that you own a medically determinable impairment. In general, we must own evidence of appropriate laboratory testing showing that you own XP or another genetic photosensitivity disorder. We will discover that you own XP or another genetic photosensitivity disorder based on a report from an acceptable medical source indicating that you own the impairment, supported by definitive genetic laboratory studies documenting appropriate chromosomal changes, including abnormal DNA repair or another DNA or genetic abnormality specific to your type of photosensitivity disorder.

    b. What we will accept as medical evidence instead of the actual laboratory report. When we do not own the actual laboratory report, we need evidence from an acceptable medical source that includes appropriate clinical findings for your impairment and that is persuasive that a positive diagnosis has been confirmed by appropriate laboratory testing at some time prior to our evaluation. To be persuasive, the report must state that the appropriate definitive genetic laboratory study was conducted and that the results confirmed the diagnosis. The report must be consistent with other evidence in your case record.

    F. How do we assess burns?

    Electrical, chemical, or thermal burns frequently affect other body systems; for example, musculoskeletal, special senses and lecture, respiratory, cardiovascular, renal, neurological, or mental. Consequently, we assess burns the way we assess other disorders that can affect the skin and other body systems, using the listing for the predominant feature of your impairment. For example, if your soft tissue injuries are under continuing surgical management (as defined in 1.00M), we will assess your impairment under 1.08. However, if your burns do not meet the requirements of 1.08 and you own extensive skin lesions that result in a extremely serious limitation (as defined in 8.00C1) that has lasted or can be expected to final for a continuous period of at least 12 months, we will assess them under 8.08.

    G. How do we determine if your skin disorder(s) will continue at a disabling level of severity in order to meet the duration requirement?

    For every of these skin disorder listings except 8.07 and 8.08, we will discover that your impairment meets the duration requirement if your skin disorder results in extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

    By persist, we mean that the longitudinal clinical record shows that, with few exceptions, your lesions own been at the level of severity specified in the listing. For 8.07A, we will presume that you meet the duration requirement. For 8.07B and 8.08, we will consider every of the relevant medical and other information in your case record to determine whether your skin disorder meets the duration requirement.

    H. How do we assess your skin disorder(s) if your impairment does not meet the requirements of one of these listings?

    1. These listings are only examples of common skin disorders that we consider severe enough to prevent you from engaging in any gainful activity. For most of these listings, if you do not own continuing treatment as prescribed, if your treatment has not lasted for at least 3 months, or if you do not own extensive skin lesions that own persisted for at least 3 months, your impairment cannot meet the requirements of these skin disorder listings. (This provision does not apply to 8.07 and 8.08.) However, we may still discover that you are disabled because your impairment(s) meets the requirements of a listing in another body system or medically equals the severity of a listing.

    (See §§ 404.1526 and 416.926 of this chapter.) We may also discover you disabled at the final step of the sequential evaluation process.

    2. If you own not received ongoing treatment or do not own an ongoing relationship with the medical community despite the existence of a severe impairment(s), or if your skin lesions own not persisted for at least 3 months but you are undergoing continuing treatment as prescribed, you may still own an impairment(s) that meets a listing in another body system or that medically equals a listing. If you do not own an impairment(s) that meets or medically equals a listing, we will assess your residual functional capacity and proceed to the fourth and, if necessary, the fifth step of the sequential evaluation process in §§ 404.1520 and 416.920 of this chapter.

    When we decide whether you continue to be disabled, we use the rules in §§ 404.1594 and 416.994 of this chapter.

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    8.01 Category of Impairments, Skin Disorders

    8.02 Ichthyosis, with extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

    8.03 Bullous disease (for example, pemphigus, erythema multiforme bullosum, epidermolysis bullosa, bullous pemphigoid, dermatitis herpetiformis), with extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

    .

    8.04 Chronic infections of the skin or mucous membranes, with extensive fungating or extensive ulcerating skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

    8.05 Dermatitis (for example, psoriasis, dyshidrosis, atopic dermatitis, exfoliative dermatitis, allergic contact dermatitis), with extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

    8.06 Hidradenitis suppurativa, with extensive skin lesions involving both axillae, both inguinal areas or the perineum that persist for at least 3 months despite continuing treatment as prescribed.

    8.07 Genetic photosensitivity disorders, established as described in 8.00E.

    A. Xeroderma pigmentosum. Consider the individual disabled from birth.

    B. Other genetic photosensitivity disorders, with:

    1. Extensive skin lesions that own lasted or can be expected to final for a continuous period of at least 12 months,

    OR

    2. Inability to function exterior of a highly protective environment for a continuous period of at least 12 months (see 8.00E2).

    8.08Burns, with extensive skin lesions that own lasted or can be expected to final for a continuous period of at least 12 months (see 8.00F).

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    What is allergy?

    Allergy is an immunological hypersensitivity mediated by immunoglobulin E antibody (IgE). It is not a disease itself, but a mechanism leading to diseases such as rhinoconjunctivitis, urticaria, asthma and anaphylaxis. A normally harmless substance — love pollen, food or cat saliva — will cause the immune system to defend the body against it. In an allergic reaction the mast cells release a chemical called histamine, which is the primary cause for the allergic symptoms.

    Allergies can be seen in numerous organs, but most commonly they affect the skin and mucous membranes, as these are the barriers between the body and the exterior environment.

    Pollen allergy causes itching in the eyes and a runny nose. Contact allergies can induce a rash. Food allergies cause itching in the mouth as well as abdominal pain and vomiting. The most severe allergic reaction is anaphylaxis. It can rapidly lead to a life-threatening condition where blood pressure drops and breathing may be obstructed because of throat swelling.

    Allergy often starts at an early age. In most cases it persists through the life, but the symptoms may decrease, and some people outgrow their allergy entirely.

    Sometimes other reactions are incorrectly referred to as allergy.

    For example, irritating or toxic substances can cause symptoms in the skin or abdomen that resemble an allergic reaction. Occasionally, sensitivity to certain foods, such as lactose intolerance, is also being called allergy. However, only the immune-mediated hypersensitivity is true allergy.

    Allergy starts with a sensitization phase that doesn’t yet cause allergic symptoms, but wires the immune system to recognize the allergen. The actual allergic reaction is launched upon the next encounter of the allergen and every time after that.

    Canine atopic dermatitis is love a trickster in a fairy tale-always causing chaos.

    But let's talk about a more practical helpful of magic. After every, you don't need to be Houdini to get pet owners to cheer for your successful treatment of their itchy pets. It is true that an estimated 10% to 15% of dogs suffer from atopic dermatitis; and the actual number is probably considerably higher. Atopic dermatitis typically manifests as pruritus and erythema, but some dogs develop recurrent pyoderma or otitis externa instead. Here's how to take the intrigue out of canine atopic dermatitis-no secret key or sleight of hand required.

    We're talking about a long-term relationship here!

    In his CVC presentation, Dr.

    Darin Dell explained the importance of a supportive relationship with owners of atopic dogs and of asking what they can handle-you're in it for the endless haul! Hear it here:

    No magic pill

    No single therapy is 100% effective at treating atopic dermatitis. Most patients need a core therapy and one or two supportive therapies. Four core allergy therapies that are safe for long-term use are 1) immunotherapy, 2) cyclosporine, 3) oclacitinib and 4) canine atopic dermatitis immunotherapeutic (CADI).

    Immunotherapy

    Immunotherapy, the gold standard of allergy therapy, is the only treatment that changes the immune system's response to allergies rather than suppressing the immune system or dulling the clinical signs.

    Immunotherapy can prevent new allergies from developing. It is also the only therapy that could potentially cure a patient. However, the cure rate is low, and most dogs require immunotherapy for life.1

    Onset of action: Six to 12 months for significant benefit

    Side effects: No major side effects (anaphylaxis can happen but is rare)

    Tips

    Both istration routes (subcutaneous injections and sublingual drops) are effective. The best choice is the one that the owner will comply with.

    Because of the slow onset of action, numerous patients need an additional core therapy when beginning immunotherapy.

    Dogs should get immunotherapy for a year before you and the owner discuss whether it is worth continuing.

    Cyclosporine

    Cyclosporine (Atopica-Elanco) treats allergy signs by suppressing IL-2, T helper cells, and T suppressor cells.2

    Onset of action: Four to six weeks for full effect

    Side effects: Mild vomiting and diarrhea are the most common.

    Hypertrichosis, gingival hyperplasia or immunosuppression is possible.

    Tips

    To assist prevent vomiting, owners can freeze capsules, give the medication with a little meal, divide the dose throughout the day, or start with a low dose and ramp up to the target dose over two weeks.

    Since cyclosporine does not provide immediate relief. I combine it with a corticosteroid during the first two or three weeks of treatment.3

    Do not taper cyclosporine until the desired response has been reached. It is best to taper slowly by eliminating one dose a week until every-other-day dosage is achieved or clinical signs relapse.

    If a relapse occurs, the client should return to the previously effective dosing regimen. An inability to taper does not indicate treatment failure; some dogs require daily therapy endless term.

    Oclacitinib

    Oclacitinib (Apoquel-Zoetis) treats allergy signs by blocking IL-31-the cytokine linked to the feeling of itch-and suppressing IL-2, IL-4, IL-6 and IL-13.

    Onset of action: One or two days, but some dogs improve within 30 minutes. I own had a few patients not reply for five to seven days.

    Side effects: Decreased hematopoiesis and immune suppression are potential side effects, especially at higher dosages and in dogs less than 12 months of age.

    Published safety studies own thus far found minimal changes on hematologic tests at maintenance dosing. Vomiting and diarrhea were the most common side effects in clinical studies. 4,5 However, I own had a couple patients develop vomiting severe enough to stop the medication.

    Tips

    A twice-a-day dosage is recommended for the first two weeks and then once daily thereafter. I own had some patients whose skin worsened when the frequency was reduced to daily, but eventually, these dogs did get back to the desired level of relief with the daily dosage.

    Calculate the low and high finish of the dose range using 0.4 to 0.6 mg/kg instead of using the dosing chart provided.

    Editor's note: Apoquel has been in the news-but despite shortage issues in the past, Zoetis announced it's now in fully supply.

    Discover more coverage here.

    CADI

    CADI (Zoetis) is a once-a-month injection of a monoclonal antibody that targets IL-31. It is available through most veterinary dermatologists and some general practitioners.

    Onset of action: One or two days, but some dogs feel itch relief as soon as 30 minutes.

    Side effects: None

    Tips

    It is safe for puppies and dogs with other health problems.

    CADI is beneficial for dogs with owners who may not see well enough to give a pill or may forget to give it every day.

    We do not know what clinical effect CADI will own on allergic otitis, recurrent pyoderma or allergy-related erythema since it only targets the cytokine linked to itch.

    A magical(ish) treatment strategy

    Every allergen patient is different-different allergies, primary signs, and secondary problems-so every treatment needs to be diverse, too.

    Nevertheless, your treatment strategy should be consistent.

    Step 1. Provide adequate flea control. Any allergy (e.g. flea, food, seasonal) can cause other allergies to get worse-it can kick start inflammation. So ensure that fleas are a nonissue by making certain these dogs are receiving appropriate flea control.

    Step 2. Eliminate infections. Eliminating infections reduces pruritus and inflammation while also improving the patient's odor and appearance.

    Dogs with allergies may be slower to reply to antibiotics than dogs without allergies are, so check progress after three weeks of antibiotic therapy but treat until infections are gone.

    Step 3. Rebuild the epidermal barrier with ceramides. When the epidermal barrier is intact, there is less allergen exposure, less risk of infection and less pruritus. You can discover ceramides in shampoos, sprays, conditioners and spot-on products.

    Step 4. Conscientiously select a core treatment. First and foremost, the best treatment is the one that the owner will actually ister correctly.

    Beyond that, consider the patient's underlying medical conditions, the severity of the allergy, and the primary signs.

    Step 5. Add supportive therapy as needed. These therapies include antibacterial and antipruritic shampoos, wipes and sprays as well as oral antihistamines, oral essential fatty acids and topical ceramides. Reevaluate your supportive therapy after a month and then on an on-going basis, as the patient's needs will likely change over time.

    Editor's note: It may not be as obvious as the ancient rabbit out the cap, but successful treatment of atopic dermatitis can be magic for the human-animal bond.

    For more ideas, tools and tips, check out the dvm360 dermatology toolkit.

    References

    1. Dell L. Darin, Griffin CE, Thompson LA, et al. Owner assessment of therapeutic interventions for canine atopic dermatitis: a long-term retrospective analysis. Vet Dermatol 2012;23:228.

    2. Guaguere E, Steffan J, Olivry T. Cyclosporin A: a new drug in the field of canine dermatology. Vet Dermatol 2004;15:61-74.

    3. Dip R, Carmichael J, Letellier I, et al.

    Concurrent short-term use of prednisolone with cyclosporine A accelerates pruritus reduction and improvement in clinical scoring in dogs with atopic dermatitis. BMC Vet Res 2013;9:173.

    4. Cosgrove SB, Wren JA, Cleaver DM, et al. A blinded, randomized, placebo-controlled trial of the efficacy and safety of the Janus kinase inhibitor oclacitinib (Apoquel) in client-owned dogs with atopic dermatitis. Vet Dermatol 2013;24,587-597.

    5.

    Zoetis, Apoquel package insert, February 2013.

    Darin Dell, DVM, DACVD

    Animal Dermatology Clinic

    3901 East 82nd St.

    Indianapolis, IN 46240

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    en españolTodo sobre el eccema

    How Is Eczema Diagnosed?

    There is no specific test used to diagnose eczema. A doctor will glance at the rash and enquire about your symptoms and past health, as well as your family’s health. If you or your family members own any atopic conditions, that’s an significant clue.

    The doctor will desire to law out other conditions that can cause skin inflammation.

    The doctor might recommend that you see a dermatologist or an allergist.

    How Can I Deal With Eczema?

    There’s no cure for eczema. But you can assist prevent a flare-up:

    1. Stay cool. Sudden changes in temperature, sweating, and becoming overheated may cause your eczema to kick in.
    2. Stay away from things that can irritate your skin. Besides your known triggers, some things you may desire to avoid include household cleaners, drying soaps, detergents, and scented lotions. For facial eczema, wash gently with a nondrying facial cleanser or soap substitute, and use facial moisturizers, makeup, and sunscreens that tell «non-comedogenic/oil-free» on the product label.
    3. Take your meds. Follow your doctor’s directions for every medicines.
    4. Don’t scratch. It’s hard to resist, but scratching can make eczema worse and make it harder for skin to heal.

      You might break the skin and let bacteria in, causing an infection.

    5. Moisturize! A scent-free moisturizer will prevent your skin from becoming irritated and cracked. Moisturize every day, ideally twice or three times a day. The best time to apply moisturizer is after the skin has been soaked in a bath or shower, then patted dry gently. Ointments (such as petroleum jelly) and creams are best because they contain a lot of oil. Lotions own too much water to be helpful.
    6. Say yes to cotton. Clothes made of scratchy fabric love wool can irritate your skin. Soft cotton clothes are a better bet.
    7. Use warm water. Too much exposure to boiling water can dry out your skin, so take short warm — not boiling — showers and baths and wear gloves if your hands will be in water for endless periods of time.

      Gently and thoroughly pat your skin dry, using a soft towel.

    8. Unwind.Stress can aggravate eczema, so attempt to relax.

    What Is Eczema?

    Eczema (pronounced: EK-zeh-ma) is a condition where the skin becomes red, scaly, irritated, and itchy. There are numerous types of eczema, but atopic dermatitis (pronounced: ay-TOP-ik der-muh-TIE-tis) is one of the most common. To numerous people, the terms «eczema» and «atopic dermatitis» mean the same thing.

    Pathophysiology

    Atopic dermatitis is a type I IgE-mediated hypersensitivity reaction, but the exact etiology is unknown.

    The pathogenesis is multifactorial and involves a complicated immunologic cascade, including disruption of the epidermal barrier, IgE dysregulation, defects in the cutaneous cell-mediated immune response, and genetic factors.

    The major elements in immune dysregulation are Langerhans’ cells, inflammatory dendritic epidermal cells, monocytes, macrophages, lymphocytes, mast cells, and keratinocytes, every of which interact through an intricate cascade of cytokines leading to a predominance of TH2 cells over TH1 cells.4 The TH2 cytokines, interleukin (IL)-4, IL-5, IL-10, and IL-13, are increased in the skin, and there is a corresponding decrease in TH1 cytokines, mainly interferon-gamma and IL-2.

    Patients with atopic dermatitis often own dry, sensitive skin due to changes in the epidermis, which serves as a barrier to the environment by maintaining the water balance of the skin.

    Essential fatty acids (EFAs), such as linoleic and linolenic acid, are significant components of the epidermal barrier. In atopic dermatitis, delta-desaturase activity is deficient,5 which leads to decreased linoleic and linolenic acid metabolites. Loss of EFAs results in increased transepidermal water loss and subsequent xerosis (dryness). The EFAs form the substrate of the inflammatory mediators (prostaglandins and leukotrienes), resulting in a secondary deficiency of prostaglandin E1.

    Defects in the epidermal barrier also lead to increased susceptibility to atopens (atopic allergens such as home dust mites, grass, or pollen).

    When such allergens contact atopic skin, they stimulate TH2 lymphocytes to produce cytokines such as IL-4, IL-5, and IL-13, which in turn promote an increase in IgE synthesis.6 Atopic dermatitis patients often own high levels of IgE antibodies due to home dust mites and other allergens. Eliminating these allergens from the environment, an extremely hard undertaking, can improve atopic dermatitis.

    Defective cell-mediated immunity leads to increased susceptibility to numerous bacterial, viral, and fungal infections of the skin.

    Children with atopic dermatitis are particularly susceptible to severe, widespread herpes simplex virus infection (eczema herpeticum)—a systemic and potentially fatal infection that primarily affects areas of athletic atopic eczema. Widespread infections with human papillomavirus (warts) and molluscum contagiosum are also common in children with atopic dermatitis.

    In Dermatology, the microbiome includes resident microorganisms of the skin and plays an significant role in regulating immunity.

    In comparison to patients with normal skin, patients with atopic dermatitis protest an altered microbiome in affected areas. There are even detectable environmental differences in the non-inflamed skin of atopic patients.7 Additionally, unaffected patients carry Staphylococcus epidermidis on their skin that acts to improve any immune defense against microbes. Most patients with atopic dermatitis not only own a compromised skin barrier but are also colonized with Staphylococcus aureus (S aureus). Studies support that this bacterium further worsens the inflammatory response and may be coupled with a decrease in antimicrobial defense.8

    Numerous factors exacerbate or trigger atopic dermatitis, including colonization with S aureus, stress, anxiety, systemic illness, and xerosis.

    The most common trigger is S aureus colonization. More than 90% of patients with atopic dermatitis own S aureus colonization of lesional skin, and more than 75% own colonization of uninvolved skin.9 Staphylococci exacerbate atopic dermatitis by 2 mechanisms: acting as superantigens by stimulating an augmented T cell response—thereby exacerbating the skin disease—and promoting increased production of IgE. IgE has anti–S aureus properties and helps control colonization and infection in normal persons. In atopic dermatitis patients, the elevated IgE levels contribute to immune dysregulation.

    Treatment with topical or oral antistaphylococcal antibiotics (or both) decreases the colonization of the skin and often leads to improvement.

    Family studies support a genetic basis for atopic dermatitis. When both parents are atopic, their offspring own a 70% risk for atopic dermatitis5; the risk of inheritance is higher if the mom is atopic. The mode of inheritance appears to be complicated and likely involves several genes. To date, no specific single gene has been identified as a unique marker for atopic dermatitis or atopy.10

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    Signs and Symptoms

    Atopic dermatitis is a chronic disease with periods of remissions and exacerbations.

    Three age-related stages exist: the infantile stage (up to 2 years old), the childhood stage (from 2 to 12 years), and the adult stage (puberty onward). The manifestations vary with age, even in the same patient. Every stages are characterized by xerosis, fissures, pruritus, and lichenification. The main differentiating factor is the area of involvement.

    The infantile stage is characterized by pruritic, red, eczematous plaques on the cheeks and extensor extremities.

    Secondary impetiginization, with honey-colored crust, is common in infants. Scalp involvement can resemble seborrheic dermatitis. The diaper area is spared.

    The childhood stage is primarily a papular dermatitis affecting the flexural areas, especially the antecubital and popliteal fossa, wrists, ankles, and neck. Thickened, lichenified plaques with excoriation (Figures 2 to 4) are common. In darker-pigmented children, follicular papules may be the only manifestation. Hypopigmentation and hyperpigmentation can happen, which can cause grand anxiety in parents. Pityriasis alba, characterized by hypopigmented, scaly patches on the face, is commonly seen. Keratosis pilaris, or spiny hair follicles, commonly affects the posterior aspects of the upper arms and the anterior thighs.

    The adult stage is unpredictable. Affected patients may own had only a few outbreaks since infancy or they may own had a chronic, relapsing course.

    What does atopic allergy mean

    Hand dermatitis is common and may be the only manifestation of adult atopic dermatitis, which can lead to significant disability. Love affected children, adults also commonly own lichenification of the flexures and facial dermatitis.

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    Treatment

    Atopic dermatitis tends to be a chronic relapsing disease. The goals of therapy should be to reduce the number and severity of flares and to increase the number of disease-free periods. The mainstay of treatment for atopic dermatitis is hydrating the skin with the regular use of emollients and suppressing cutaneous inflammation with topical corticosteroids.

    Topical calcineurin inhibitors own become an significant adjunctive therapy. For severe disease, especially during acute flares, systemic corticosteroids may be necessary. Secondary infections require treatment with topical or oral antibiotics, or both. Oral antihistamines can assist decrease pruritus. In severe, recalcitrant cases, phototherapy or systemic immunosuppressive medications may be necessary.

    Most patients with atopic dermatitis require hydration though the liberal use of bland emollients, which serve to hydrate the stratum corneum and maintain the lipid barrier.

    Sufficient emollients applied liberally several times a day may be enough to significantly reduce the disease activity of atopic dermatitis. Parents of infants and toddlers should apply a bland emollient to the entire body with each diaper change. Older children should apply bland emollients in the morning, after school, and at bedtime. Bathing should be limited to brief, cool showers once daily. Soap, which dries and irritates the skin, should be avoided, but tender lipid-free cleansers are beneficial.

    Corticosteroids suppress lymphocyte activity in the skin, thereby decreasing inflammation.

    Patients can use a low-potency topical steroid (hydrocortisone or desonide) for day-to-day control of mild disease and a medium-potency steroid (triamcinolone acetonide, fluticasone, or fluocinolone) for more severe flares. Low-potency topical steroids are suitable for infants and for intertriginous and sensitive areas (face, genitals); more potent steroids should be avoided on these sites. Severe, widespread disease can require systemic corticosteroids. Because of the well-known side effects of systemic corticosteroids (e.g., adrenal suppression, osteoporosis, hypertension, diabetes, obesity, striae), their use should be limited to patients with severe disease.

    Topical calcineurin inhibitors (tacrolimus, pimecrolimus) are effective alternatives to the chronic use of topical corticosteroids.

    Topical calcineurin inhibitors bind calcineurin and block the activation of T cells by cytokines, thus halting the inflammatory cascade that leads to atopic dermatitis. Topical calcineurin inhibitors are especially suitable for more delicate areas such as the face and genitals because they do not carry the risks of atrophy, telangiectasias, and striae associated with the chronic use of steroids. Reports own surfaced suggesting a possible risk of lymphoma associated with high-dose oral pimecrolimus in animal studies,12 prompting the US Food and Drug istration to put out a black box warning advising against the use of topical calcineurin inhibitors in children younger than 2 years.

    However, there are no data to support an increased risk of lymphoma with topical treatment in humans.12 Topical calcineurin inhibitors should be used for a limited time and only on affected skin. They should not be used as a daily moisturizer, first-line therapy, or preventive therapy.

    The pruritus associated with atopic dermatitis can be severe and often interferes with school, work, and sleep. Despite a lack of objective data to support their use, antihistamines are commonly used to break the itch-scratch-itch cycle.13 Nonsedating antihistamines such as fexofenadine, cetirizine, loratadine, and desloratadine can assist offset daytime itching without somnolence.

    Sedating antihistamines such as diphenhydramine or hydroxyzine are often helpful for nighttime pruritus.

    Patients with atopy own an abnormal tolerance to S aureus colonization of the skin, which can exacerbate the dermatitis. Affected patients should use lipid-free antibacterial cleansers. For open wounds, a topical antibiotic such as mupirocin can assist to prevent secondary impetiginization (Figures 5 and 6). An oral antibiotic with S aureus coverage and excellent skin penetration, such as amoxicillin-clavulanic acid, cephalexin, or azithromycin, is necessary for extensive excoriations and impetigo.

    In severe, recalcitrant cases, ultraviolet (UV) light treatments (UVB or psoralen plus UVA [PUVA]) and immunosuppressive medications (e.g., methotrexate, cyclosporine, azathioprine, mycophenolate mofetil) may be helpful.13 These should be used extremely cautiously and with shut monitoring and should be reserved for the most severe cases.

    Allergic contact dermatitis from topical medications, cosmetics, or metals should be considered in patients with recalcitrant disease. Evaluation by an environmental dermatologist and an allergist, including patch, pinprick, and serum radioallergosorbent testing, may be warranted.

    Topical medications that are known sensitizers, such as lidocaine, doxepin cream, and diphenhydramine cream, as well as topical antibiotics such as neomycin, should be strictly avoided. Allergic contact dermatitis to topical steroids should be considered in any patient who fails to improve or worsens with the use of topical steroids.

    A multitude of new treatments are currently available or under investigation for atopic dermatitis. These range from oral to topical agents and each has an significant inflammatory target.

    Key components of this TH2-mediated disease include cytokines such as IL-4, IL-5, IL-13, and IL-31. Dupilumab binds a subunit of the IL-4 receptor and therefore blocks IL-4 and IL-13. This medication is approved for the treatment of moderate-to-severe atopic dermatitis and there are ongoing long-term studies.14

    Similarly, lebrikizumab is an IL-13 antibody in trial that has demonstrated efficacy in atopic patients who were still using topical corticosteroids; continued studies are needed.15

    IL-31 seems to frolic a role in atopic dermatitis and itch development.

    Nemolizumab (CIM331) targets the IL-31 receptor A and has been shown to decrease itch sensation among affected patients in early reports.16

    A related approach includes targeting Janus kinase (JAK) signaling, which plays an significant role in immune function and is involved in inflammatory skin conditions including chronic itch. While further investigation remains necessary, early data show JAK inhibitors (jakinibs) to be a promising therapy option.17 JAK assists in the function and effect of various TH2 cytokines discussed above.

    Baricitinib, an inhibitor of JAK1 and JAK2, has been shown to reduce atopic dermatitis and itch in patients who continued to use topical corticosteroids.18 Additional JAK1 inhibitors currently under study include PF-04965842 and ABT-494 (upadacitinib).17

    While the JAK pathway was first targeted with oral tofacitinib citrate (a JAK1 and JAK3 inhibitor)19, topical preparations are in trial including topical tofacitinib.20 In addition, the efficacy and safety of a topical JAK inhibitor called JTE-052—which notably inhibits JAK1, JAK2, JAK3, and tyrosine kinase 2—has been reported with promising results.21 Topical ruxolitinib studies are underway as well.17

    Lastly, crisaborole, a topical phosphodiesterase 4 inhibitor, is approved for patients with mild-to-moderate atopic dermatitis and has demonstrated efficacy.22 Targeting this pro-inflammatory molecule has led to the development of other phosphodiesterase 4 inhibitors.23

    With novel therapies emerging, it is necessary to continue investigation into the efficacy and safety of these various systemic and topical treatments.

    Furthermore, studies are overall lacking in the pediatric population. Nonetheless, the future for the treatment of atopic dermatitis is encouraging and rapidly expanding.

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    What Else Should I Know?

    If you live with eczema, tune in to what triggers it and how to manage it. For example, if you discover that some types of makeup irritate your skin, enquire a dermatologist to recommend brands that are less likely to do so.

    Your self-esteem doesn’t own to suffer because you own eczema, and neither does your social life! Getting involved in your school and extracurricular activities can be a grand way to get your mind off the itch.

    Don’t forget to exercise.

    It’s a grand way to blow off stress — attempt walking, bike riding, swimming, or another sport that keeps your skin cool and dry while you work out.

    8.00 Skin Disorders

    A. What skin disorders do we assess with these listings?

    We use these listings to assess skin disorders that may result from hereditary, congenital, or acquired pathological processes. The kinds of impairments covered by these listings are: Ichthyosis, bullous diseases, chronic infections of the skin or mucous membranes, dermatitis, hidradenitis suppurativa, genetic photosensitivity disorders, and burns.

    B. What documentation do we need?

    When we assess the existence and severity of your skin disorder, we generally need information about the onset, duration, frequency of flare-ups, and prognosis of your skin disorder; the location, size, and appearance of lesions; and, when applicable, history of exposure to toxins, allergens, or irritants, familial incidence, seasonal variation, stress factors, and your ability to function exterior of a highly protective environment. To confirm the diagnosis, we may need laboratory findings (for example, results of a biopsy obtained independently of Social Security disability evaluation or blood tests) or evidence from other medically acceptable methods consistent with the prevailing state of medical knowledge and clinical practice.

    C.

    How do we assess the severity of your skin disorder(s)?

    We generally base our assessment of severity on the extent of your skin lesions, the frequency of flare-ups of your skin lesions, how your symptoms (including pain) limit you, the extent of your treatment, and how your treatment affects you.

    1. Extensive skin lesions.

    Extensive skin lesions are those that involve multiple body sites or critical body areas, and result in a extremely serious limitation. Examples of extensive skin lesions that result in a extremely serious limitation include but are not limited to:

    a. Skin lesions that interfere with the motion of your joints and that extremely seriously limit your use of more than one extremity; that is, two upper extremities, two lower extremities, or one upper and one lower extremity.

    b. Skin lesions on the palms of both hands that extremely seriously limit your ability to do fine and gross motor movements.

    c. Skin lesions on the soles of both feet, the perineum, or both inguinal areas that extremely seriously limit your ability to ambulate.

    2. Frequency of flare-ups.

    If you own skin lesions, but they do not meet the requirements of any of the listings in this body system, you may still own an impairment that prevents you from doing any gainful activity when we consider your condition over time, especially if your flare-ups result in extensive skin lesions, as defined in C1 of this section.

    Therefore, if you own frequent flare-ups, we may discover that your impairment(s) is medically equal to one of these listings even though you own some periods during which your condition is in remission. We will consider how frequent and serious your flare-ups are, how quickly they resolve, and how you function between flare-ups to determine whether you own been unable to do any gainful activity for a continuous period of at least 12 months or can be expected to be unable to do any gainful activity for a continuous period of at least 12 months. We will also consider the frequency of your flare-ups when we determine whether you own a severe impairment and when we need to assess your residual functional capacity.

    3. Symptoms (including pain).

    Symptoms (including pain) may be significant factors contributing to the severity of your skin disorder(s). We assess the impact of symptoms as explained in §§ 404.1521, 404.1529, 416.921, and 416.929 of this chapter.

    4. Treatment.

    We assess the effects of medication, therapy, surgery, and any other form of treatment you get when we determine the severity and duration of your impairment(s). Skin disorders frequently reply to treatment; however, response to treatment can vary widely, with some impairments becoming resistant to treatment.

    Some treatments can own side effects that can in themselves result in limitations.

    a. We assess the effects of continuing treatment as prescribed by determining if there is improvement in the symptoms, signs, and laboratory findings of your disorder, and if you experience side effects that result in functional limitations. To assess the effects of your treatment, we may need information about:

    i. The treatment you own been prescribed (for example, the type, dosage, method, and frequency of istration of medication or therapy);

    ii. Your response to the treatment;

    iii. Any adverse effects of the treatment; and

    iv. The expected duration of the treatment.

    b.

    Because treatment itself or the effects of treatment may be temporary, in most cases sufficient time must elapse to permit us to assess the impact and expected duration of treatment and its side effects. Except under 8.07 and 8.08, you must follow continuing treatment as prescribed for at least 3 months before your impairment can be sure to meet the requirements of a skin disorder listing. (See 8.00H if you are not undergoing treatment or did not own treatment for 3 months.) We consider your specific response to treatment when we assess the overall severity of your impairment.

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    D. How do we assess impairments that may affect the skin and other body systems?

    When your impairment affects your skin and has effects in other body systems, we first assess the predominant feature of your impairment under the appropriate body system. Examples include, but are not limited to the following.

    What does atopic allergy mean

    1. Tuberous sclerosis primarily affects the brain. The predominant features are seizures, which we assess under the neurological listings in 11.00, and developmental delays or other mental disorders, which we assess under the mental disorders listings in 12.00.

    2. Malignant tumors of the skin (for example, malignant melanomas) are cancers, or neoplastic diseases, which we assess under the listings in 13.00.

    3. Autoimmune disorders and other immune system disorders (for example, systemic lupus erythematosus (SLE), scleroderma, human immunodeficiency virus (HIV) infection, and Sjögren’s syndrome) often involve more than one body system. We first assess these disorders under the immune system disorders listings in 14.00. We assess SLE under 14.02, scleroderma under 14.04, Sjögren’s syndrome under 14.10, and HIV infection under 14.11.

    4. Disfigurement or deformity resulting from skin lesions may result in loss of sight, hearing, lecture, and the ability to chew (mastication). We assess these impairments and their effects under the special senses and lecture listings in 2.00 and the digestive system listings in 5.00.

    Facial disfigurement or other physical deformities may also own effects we assess under the mental disorders listings in 12.00, such as when they affect mood or social functioning.

    E. How do we assess genetic photosensitivity disorders?

    1. Xeroderma pigmentosum (XP). When you own XP, your impairment meets the requirements of 8.07A if you own clinical and laboratory findings showing that you own the disorder. (See 8.00E3.) People who own XP own a lifelong hypersensitivity to every forms of ultraviolet light and generally lead extremely restricted lives in highly protective environments in order to prevent skin cancers from developing. Some people with XP also experience problems with their eyes, neurological problems, mental disorders, and problems in other body systems.

    2. Other genetic photosensitivity disorders.

    Other genetic photosensitivity disorders may vary in their effects on diverse people, and may not result in an inability to engage in any gainful activity for a continuous period of at least 12 months. Therefore, if you own a genetic photosensitivity disorder other than XP (established by clinical and laboratory findings as described in 8.00E3), you must show that you own either extensive skin lesions or an inability to function exterior of a highly protective environment to meet the requirements of 8.07B.

    You must also show that your impairment meets the duration requirement. By inability to function exterior of a highly protective environment we mean that you must avoid exposure to ultraviolet light (including sunlight passing through windows and light from unshielded fluorescent bulbs), wear protective clothing and eyeglasses, and use opaque wide spectrum sunscreens in order to avoid skin cancer or other serious effects. Some genetic photosensitivity disorders can own extremely serious effects in other body systems, especially special senses and lecture (2.00), neurological (11.00), mental (12.00), and neoplastic (13.00). We will assess the predominant feature of your impairment under the appropriate body system, as explained in 8.00D.

    3. Clinical and laboratory findings.

    a. General. We need documentation from an acceptable medical source to establish that you own a medically determinable impairment.

    What does atopic allergy mean

    In general, we must own evidence of appropriate laboratory testing showing that you own XP or another genetic photosensitivity disorder. We will discover that you own XP or another genetic photosensitivity disorder based on a report from an acceptable medical source indicating that you own the impairment, supported by definitive genetic laboratory studies documenting appropriate chromosomal changes, including abnormal DNA repair or another DNA or genetic abnormality specific to your type of photosensitivity disorder.

    b. What we will accept as medical evidence instead of the actual laboratory report. When we do not own the actual laboratory report, we need evidence from an acceptable medical source that includes appropriate clinical findings for your impairment and that is persuasive that a positive diagnosis has been confirmed by appropriate laboratory testing at some time prior to our evaluation.

    To be persuasive, the report must state that the appropriate definitive genetic laboratory study was conducted and that the results confirmed the diagnosis. The report must be consistent with other evidence in your case record.

    F. How do we assess burns?

    Electrical, chemical, or thermal burns frequently affect other body systems; for example, musculoskeletal, special senses and lecture, respiratory, cardiovascular, renal, neurological, or mental.

    Consequently, we assess burns the way we assess other disorders that can affect the skin and other body systems, using the listing for the predominant feature of your impairment. For example, if your soft tissue injuries are under continuing surgical management (as defined in 1.00M), we will assess your impairment under 1.08. However, if your burns do not meet the requirements of 1.08 and you own extensive skin lesions that result in a extremely serious limitation (as defined in 8.00C1) that has lasted or can be expected to final for a continuous period of at least 12 months, we will assess them under 8.08.

    G. How do we determine if your skin disorder(s) will continue at a disabling level of severity in order to meet the duration requirement?

    For every of these skin disorder listings except 8.07 and 8.08, we will discover that your impairment meets the duration requirement if your skin disorder results in extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed. By persist, we mean that the longitudinal clinical record shows that, with few exceptions, your lesions own been at the level of severity specified in the listing. For 8.07A, we will presume that you meet the duration requirement. For 8.07B and 8.08, we will consider every of the relevant medical and other information in your case record to determine whether your skin disorder meets the duration requirement.

    H. How do we assess your skin disorder(s) if your impairment does not meet the requirements of one of these listings?

    1. These listings are only examples of common skin disorders that we consider severe enough to prevent you from engaging in any gainful activity. For most of these listings, if you do not own continuing treatment as prescribed, if your treatment has not lasted for at least 3 months, or if you do not own extensive skin lesions that own persisted for at least 3 months, your impairment cannot meet the requirements of these skin disorder listings.

    (This provision does not apply to 8.07 and 8.08.) However, we may still discover that you are disabled because your impairment(s) meets the requirements of a listing in another body system or medically equals the severity of a listing. (See §§ 404.1526 and 416.926 of this chapter.) We may also discover you disabled at the final step of the sequential evaluation process.

    2. If you own not received ongoing treatment or do not own an ongoing relationship with the medical community despite the existence of a severe impairment(s), or if your skin lesions own not persisted for at least 3 months but you are undergoing continuing treatment as prescribed, you may still own an impairment(s) that meets a listing in another body system or that medically equals a listing.

    If you do not own an impairment(s) that meets or medically equals a listing, we will assess your residual functional capacity and proceed to the fourth and, if necessary, the fifth step of the sequential evaluation process in §§ 404.1520 and 416.920 of this chapter. When we decide whether you continue to be disabled, we use the rules in §§ 404.1594 and 416.994 of this chapter.

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    8.01 Category of Impairments, Skin Disorders

    8.02 Ichthyosis, with extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

    What does atopic allergy mean

    8.03 Bullous disease (for example, pemphigus, erythema multiforme bullosum, epidermolysis bullosa, bullous pemphigoid, dermatitis herpetiformis), with extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed. .

    8.04 Chronic infections of the skin or mucous membranes, with extensive fungating or extensive ulcerating skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

    8.05 Dermatitis (for example, psoriasis, dyshidrosis, atopic dermatitis, exfoliative dermatitis, allergic contact dermatitis), with extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

    8.06 Hidradenitis suppurativa, with extensive skin lesions involving both axillae, both inguinal areas or the perineum that persist for at least 3 months despite continuing treatment as prescribed.

    8.07 Genetic photosensitivity disorders, established as described in 8.00E.

    A. Xeroderma pigmentosum. Consider the individual disabled from birth.

    B. Other genetic photosensitivity disorders, with:

    1. Extensive skin lesions that own lasted or can be expected to final for a continuous period of at least 12 months,

    OR

    2. Inability to function exterior of a highly protective environment for a continuous period of at least 12 months (see 8.00E2).

    8.08Burns, with extensive skin lesions that own lasted or can be expected to final for a continuous period of at least 12 months (see 8.00F).

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    What is allergy?

    Allergy is an immunological hypersensitivity mediated by immunoglobulin E antibody (IgE). It is not a disease itself, but a mechanism leading to diseases such as rhinoconjunctivitis, urticaria, asthma and anaphylaxis. A normally harmless substance — love pollen, food or cat saliva — will cause the immune system to defend the body against it.

    In an allergic reaction the mast cells release a chemical called histamine, which is the primary cause for the allergic symptoms.

    Allergies can be seen in numerous organs, but most commonly they affect the skin and mucous membranes, as these are the barriers between the body and the exterior environment. Pollen allergy causes itching in the eyes and a runny nose. Contact allergies can induce a rash. Food allergies cause itching in the mouth as well as abdominal pain and vomiting. The most severe allergic reaction is anaphylaxis.

    It can rapidly lead to a life-threatening condition where blood pressure drops and breathing may be obstructed because of throat swelling.

    Allergy often starts at an early age. In most cases it persists through the life, but the symptoms may decrease, and some people outgrow their allergy entirely.

    Sometimes other reactions are incorrectly referred to as allergy. For example, irritating or toxic substances can cause symptoms in the skin or abdomen that resemble an allergic reaction. Occasionally, sensitivity to certain foods, such as lactose intolerance, is also being called allergy.

    However, only the immune-mediated hypersensitivity is true allergy.

    Allergy starts with a sensitization phase that doesn’t yet cause allergic symptoms, but wires the immune system to recognize the allergen. The actual allergic reaction is launched upon the next encounter of the allergen and every time after that.

    Canine atopic dermatitis is love a trickster in a fairy tale-always causing chaos. But let's talk about a more practical helpful of magic. After every, you don't need to be Houdini to get pet owners to cheer for your successful treatment of their itchy pets.

    It is true that an estimated 10% to 15% of dogs suffer from atopic dermatitis; and the actual number is probably considerably higher. Atopic dermatitis typically manifests as pruritus and erythema, but some dogs develop recurrent pyoderma or otitis externa instead. Here's how to take the intrigue out of canine atopic dermatitis-no secret key or sleight of hand required.

    We're talking about a long-term relationship here!

    In his CVC presentation, Dr.

    Darin Dell explained the importance of a supportive relationship with owners of atopic dogs and of asking what they can handle-you're in it for the endless haul! Hear it here:

    No magic pill

    No single therapy is 100% effective at treating atopic dermatitis. Most patients need a core therapy and one or two supportive therapies. Four core allergy therapies that are safe for long-term use are 1) immunotherapy, 2) cyclosporine, 3) oclacitinib and 4) canine atopic dermatitis immunotherapeutic (CADI).

    Immunotherapy

    Immunotherapy, the gold standard of allergy therapy, is the only treatment that changes the immune system's response to allergies rather than suppressing the immune system or dulling the clinical signs.

    Immunotherapy can prevent new allergies from developing. It is also the only therapy that could potentially cure a patient. However, the cure rate is low, and most dogs require immunotherapy for life.1

    Onset of action: Six to 12 months for significant benefit

    Side effects: No major side effects (anaphylaxis can happen but is rare)

    Tips

    Both istration routes (subcutaneous injections and sublingual drops) are effective. The best choice is the one that the owner will comply with.

    Because of the slow onset of action, numerous patients need an additional core therapy when beginning immunotherapy.

    Dogs should get immunotherapy for a year before you and the owner discuss whether it is worth continuing.

    Cyclosporine

    Cyclosporine (Atopica-Elanco) treats allergy signs by suppressing IL-2, T helper cells, and T suppressor cells.2

    Onset of action: Four to six weeks for full effect

    Side effects: Mild vomiting and diarrhea are the most common.

    Hypertrichosis, gingival hyperplasia or immunosuppression is possible.

    Tips

    To assist prevent vomiting, owners can freeze capsules, give the medication with a little meal, divide the dose throughout the day, or start with a low dose and ramp up to the target dose over two weeks.

    Since cyclosporine does not provide immediate relief. I combine it with a corticosteroid during the first two or three weeks of treatment.3

    Do not taper cyclosporine until the desired response has been reached. It is best to taper slowly by eliminating one dose a week until every-other-day dosage is achieved or clinical signs relapse.

    If a relapse occurs, the client should return to the previously effective dosing regimen. An inability to taper does not indicate treatment failure; some dogs require daily therapy endless term.

    Oclacitinib

    Oclacitinib (Apoquel-Zoetis) treats allergy signs by blocking IL-31-the cytokine linked to the feeling of itch-and suppressing IL-2, IL-4, IL-6 and IL-13.

    Onset of action: One or two days, but some dogs improve within 30 minutes. I own had a few patients not reply for five to seven days.

    Side effects: Decreased hematopoiesis and immune suppression are potential side effects, especially at higher dosages and in dogs less than 12 months of age.

    Published safety studies own thus far found minimal changes on hematologic tests at maintenance dosing. Vomiting and diarrhea were the most common side effects in clinical studies. 4,5 However, I own had a couple patients develop vomiting severe enough to stop the medication.

    Tips

    A twice-a-day dosage is recommended for the first two weeks and then once daily thereafter. I own had some patients whose skin worsened when the frequency was reduced to daily, but eventually, these dogs did get back to the desired level of relief with the daily dosage.

    Calculate the low and high finish of the dose range using 0.4 to 0.6 mg/kg instead of using the dosing chart provided.

    Editor's note: Apoquel has been in the news-but despite shortage issues in the past, Zoetis announced it's now in fully supply.

    Discover more coverage here.

    CADI

    CADI (Zoetis) is a once-a-month injection of a monoclonal antibody that targets IL-31. It is available through most veterinary dermatologists and some general practitioners.

    Onset of action: One or two days, but some dogs feel itch relief as soon as 30 minutes.

    Side effects: None

    Tips

    It is safe for puppies and dogs with other health problems.

    CADI is beneficial for dogs with owners who may not see well enough to give a pill or may forget to give it every day.

    We do not know what clinical effect CADI will own on allergic otitis, recurrent pyoderma or allergy-related erythema since it only targets the cytokine linked to itch.

    A magical(ish) treatment strategy

    Every allergen patient is different-different allergies, primary signs, and secondary problems-so every treatment needs to be diverse, too.

    Nevertheless, your treatment strategy should be consistent.

    Step 1. Provide adequate flea control. Any allergy (e.g. flea, food, seasonal) can cause other allergies to get worse-it can kick start inflammation. So ensure that fleas are a nonissue by making certain these dogs are receiving appropriate flea control.

    Step 2. Eliminate infections. Eliminating infections reduces pruritus and inflammation while also improving the patient's odor and appearance. Dogs with allergies may be slower to reply to antibiotics than dogs without allergies are, so check progress after three weeks of antibiotic therapy but treat until infections are gone.

    Step 3.

    Rebuild the epidermal barrier with ceramides. When the epidermal barrier is intact, there is less allergen exposure, less risk of infection and less pruritus. You can discover ceramides in shampoos, sprays, conditioners and spot-on products.

    Step 4. Conscientiously select a core treatment. First and foremost, the best treatment is the one that the owner will actually ister correctly. Beyond that, consider the patient's underlying medical conditions, the severity of the allergy, and the primary signs.

    Step 5. Add supportive therapy as needed. These therapies include antibacterial and antipruritic shampoos, wipes and sprays as well as oral antihistamines, oral essential fatty acids and topical ceramides.

    Reevaluate your supportive therapy after a month and then on an on-going basis, as the patient's needs will likely change over time.

    Editor's note: It may not be as obvious as the ancient rabbit out the cap, but successful treatment of atopic dermatitis can be magic for the human-animal bond. For more ideas, tools and tips, check out the dvm360 dermatology toolkit.

    References

    1. Dell L. Darin, Griffin CE, Thompson LA, et al. Owner assessment of therapeutic interventions for canine atopic dermatitis: a long-term retrospective analysis. Vet Dermatol 2012;23:228.

    2.

    Guaguere E, Steffan J, Olivry T. Cyclosporin A: a new drug in the field of canine dermatology. Vet Dermatol 2004;15:61-74.

    3. Dip R, Carmichael J, Letellier I, et al. Concurrent short-term use of prednisolone with cyclosporine A accelerates pruritus reduction and improvement in clinical scoring in dogs with atopic dermatitis. BMC Vet Res 2013;9:173.

    4. Cosgrove SB, Wren JA, Cleaver DM, et al. A blinded, randomized, placebo-controlled trial of the efficacy and safety of the Janus kinase inhibitor oclacitinib (Apoquel) in client-owned dogs with atopic dermatitis.

    Vet Dermatol 2013;24,587-597.

    5. Zoetis, Apoquel package insert, February 2013.

    Darin Dell, DVM, DACVD

    Animal Dermatology Clinic

    3901 East 82nd St.

    Indianapolis, IN 46240


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