Alopecia areata update

Madani, Shabnam; Shapiro, Jerry

doi:10.1016/s0190-9622(00)90164-6

Cited by 235 publications

(351 citation statements)

References 129 publications

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“…Although there are no reports of cytokine profiles in mouse alopecia, human studies have demonstrated that alopecia is an autoimmune disease with predominantly T H 1 cytokines. 44,45 About one third of sensitized mice had the eczematous eruption and alopecia, whereas the incidence of spontaneous alopecia areata in female C3H/HeJ mice is reportedly 0.25%. Recently, spontaneous alopecia in aging mice was shown to be an autoimmune disorder.…”

Section: Discussionmentioning

confidence: 99%

Murine model of atopic dermatitis associated with food hypersensitivity

Kleiner²,

Huang³

et al. 2001

Journal of Allergy and Clinical Immunology

110

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Background: Atopic dermatitis (AD) is an eczematous skin eruption that generally begins in early infancy and affects up to 12% of the population. The cause of this disorder is not fully understood, although it is frequently the first sign of atopic disease and is characterized by an elevated serum IgE level, eosinophilia, and histologic tissue changes characterized early by spongiosis and a CD4 + T H 2 cellular infiltrate. Hypersensitivity to foods has been implicated as one causative factor in up to 40% of children with moderate-to-severe AD. Objective: The purpose of this study was to establish a murine model of food-induced AD. Methods: Female C3H/HeJ mice were sensitized orally to cow's milk or peanut with a cholera toxin adjuvant and then subjected to low-grade allergen exposure. Histologic examination of skin lesions, allergen-specific serum Ig levels, and allergen-induced T-cell proliferation and cytokine production were examined. Atopic dermatitis (AD) is a form of eczema that generally begins in early infancy and is characterized by extreme pruritus, chronically relapsing course, and distinctive distribution. AD is often the first sign seen in a child who is prone to atopic disease, with 50% of all AD developing in the first year of life and 80% developing by 5 years of age. 1 In chronic skin lesions the epidermis has moderate-to-marked hyperplasia, with elongation of the rete ridges and prominent hyperkeratosis. Spongiosis is variable, and the numbers of mast cells and Langerhans cells are significantly increased. 2,3 Eosinophils are sparse, although eosinophil products (major basic protein) are prominent. 4 Although the pathogenic role of allergy in AD has been debated for over a century, clinical studies over the past 2 decades have supported the pathogenic role of food allergy in a subset of patients with AD. 5-7 A recent study found that approximately 40% of children with moderate-to-severe AD attending a university dermatology clinic had food hypersensitivity. 7 Other studies delineating the role of IgE-bearing antigen-presenting cells in establishing T H 2 lymphocytic responses 8 and demonstrating the predominant T H 2-lymphocytic infiltrate in acute eczematous lesions 9 have provided further support for the pathogenic role of allergy in AD.Animal models provide powerful tools for dissecting pathogenic mechanisms responsible for various disorders. A number of murine models of asthma have been developed in the past several years that have contributed greatly to our understanding of the immunopathogenesis of allergen-induced asthma. 10-12 Models of antigenassociated AD have been reported in cats and dogs, but because of difficulties with consistent induction of ADlike eruptions and high expense, they have not been widely studied. 13,14 A mouse strain, NC/Nga, has been reported that spontaneously has an AD-like skin lesion and IgE hyperproduction, presumably triggered by environmental factors. 15 More recently, a murine model of AD was described in which BALB/c mice were sensitized to ovalbumin (OVA...

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Section: Discussionmentioning

confidence: 99%

Murine model of atopic dermatitis associated with food hypersensitivity

Kleiner²,

Huang³

et al. 2001

Journal of Allergy and Clinical Immunology

110

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“…Although the cause of AA is unknown, it is widely believed to be an autoimmune disease (McDonagh and Messenger, 1994;Sahn, 1995;Schwartz and Janniger, 1997;McElwee et al, 1999;Madani and Shapiro, 2000;Yano et al, 2002). Treatment of AA consists of various therapies, through which limited success has been achieved.…”

Section: Discussionmentioning

confidence: 99%

“…It can affect men, women or children (Madani and Shapiro, 2000). Although other causes have been suggested, it is widely believed that AA is an autoimmune disease (Sahn, 1995;McElwee et al, 1999;Madani and Shapiro, 2000;Yano et al, 2002) because of the likely presence of antimicrosomal antibody (Ab), antithyroglobulin Ab, antigastric parietal cell Ab and adrenal cell Ab (Paus et al, 1993;McDonagh and Messenger, 1994;Schwartz and Janniger, 1997). There is no conclusive diagnostic test for AA.…”

Section: Introductionmentioning

confidence: 99%

Pseudo Alopecia Areata Caused by Skull‐caps with Metal Pin Fasteners used by Orthodox Jews in Israel

Yosefy

Ronnen

Edelstein³

2003

Journal of Immunology Research

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Background: Alopecia Areata (AA) is a disease characterized by hair loss that is widely believed to be autoimmune in origin. Thus treatment is generally aimed in this direction using immune inhibitors such as steroids and PUVA.Objective: To describe a variant of AA, Pseudo Alopecia Areata, caused by a particular cupola pin holder (tic-tac) and to offer a non-pharmacological treatment option (NPT).Methods: A prospective open label study in 37 Jewish religious patients (34 males, 3 females, mean 35^2 years), previously diagnosed and treated for scalp AA were randomly referred to one of the three NPT intervention methods: small cupola held by two pins, large cupola held by one pin and similar cupola held by a different pin.Results: Three of the ten patients (33.3%) from the first group developed secondary AA from the additional pin. No changes were seen in the second group. Ten of the seventeen patients (58.8%) from the third group achieved immediate improvement subsequent to replacing the original pin with a new one on a larger cupola.Conclusions: Conservative pharmacological treatment failed to repair the lesions. The addition of a second pin caused an additional lesion. In contrast, replacing the cupola with a larger one and the original pin-fastener with a different type, successfully reduced the lesions.

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“…AA'nın patogenezi tam olarak bilinmemekle birlikte, AA'ya birçok otoimmün hastalık ve otoantikorun eşlik etmesi, otoimmün hipotezi güçlendirmektedir (1,2).…”

Section: Introductionunclassified

Presence of Autoimmune Diseases in Alopecia Areata Patients and Their Families and Its Effect on Prognosis

Duman¹,

Köse²,

İşsever³

2016

tdd

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Amaç: Alopesi areatada (AA), etyopatogenezde otoimmünitenin rolünü ve eşlik eden otoimmün hastalıkların prognoz üzerindeki etkilerini araştırmayı amaçladık. Yöntemler: Deri ve zührevi hastalıklar polikliniğine başvurmuş 134 hasta, ailesinde otoimmün hastalık öyküsü ve AA'ya eşlik eden otoimmün hastalık varlığı açısından retrospektif olarak incelendi. Bulgular: Çalışmaya alınan 134 olgunun 79'u erkek (%59), 55'i kadın (%41) idi. Araştırmada %16,4 oranında otoimmün hastalık saptandı. Otoimmün hastalık, kadınlarda (p=0,034) ve ailede otoimmün hastalık öyküsü olanlarda (p=0,011) yüksek bulundu. Otoimmün hastalık birlikteliği ile hastalık süresi, hastalık tipi, hastalık şiddeti, hastalık başlangıç yaşı, tırnak tutulumu, atopi, nevüs flammeus varlığı ve ailede AA öyküsü arasındaki ilişki anlamsızdı. AA'lı ailelerde otoimmün hastalık öyküsü %16,4 idi. Sonuç: AA'lı hem hasta hem de hasta ailelerinde otoimmün hastalık oranının yüksek saptanması, otoimmün hastalığın kadınlarda belirgin yüksekliği, AA'nın bir otoimmün hastalık olabileceği tezini desteklemektedir. Ayrıca otoimmün hastalığın varlığı AA'da kötü prognoza yol açmamaktadır. Objective: We aimed to investigate the role of autoimmunity in the etiopathogenesis of alopecia areata (AA) and the effects of the coexisting autoimmune diseases on the prognosis of AA. Methods: The records of 134 AA patients diagnosed in the dermatology and venereology outpatient clinic were retrospectively analyzed for the history of concomitant autoimmune disease and the family history for autoimmune diseases.

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Alopecia areata update

Cited by 235 publications

References 129 publications

Murine model of atopic dermatitis associated with food hypersensitivity

Murine model of atopic dermatitis associated with food hypersensitivity

Pseudo Alopecia Areata Caused by Skull‐caps with Metal Pin Fasteners used by Orthodox Jews in Israel

Presence of Autoimmune Diseases in Alopecia Areata Patients and Their Families and Its Effect on Prognosis

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