14^thInternational Conference on Clinical and Experimental Dermatology June 19-20, 2017 Philadelphia ,USA

Lauren Bonomo, BA graduated with honors from Yale University and is now a Medical student at the Icahn School of Medicine at Mount Sinai. She is currently on a scholarly year, pursuing research in Icahn’s Department of Dermatology. She is particularly interested in inflammatory and autoimmune skin disease, including atopic dermatitis, psoriasis, vitiligo, and alopecia areata.

Introduction: Drugs are responsible for 0.1-2.0% of acute pancreatitis occurrence in the United States. Medications implicated in drug-induced acute pancreatitis (DIAP) are classified based on strength of evidence, TNF-a inhibitors are Class III drugs (see Table 1). To our knowledge, we contribute the first documented case of TNF-α inhibitor class induced-pancreatitis. Case Study: We present a case of a 27-year-old female with severe psoriatic arthritis (PsA) that presented to the emergency department (ED) with severe epigastric abdominal pain radiating to the back. The patient denied alcohol or drug consumption, sick contacts, insect bites or trauma. The patient was only taking weekly methotrexate for her psoriasis treatment. However, that morning she had received her second infusion of Infliximab 5mg/kg as part of a new regimen. Physical exam was unremarkable except for psoriatic plaques in her back, right elbow and bilateral knees. Further work-up revealed a lipase of 5,000U/L and an abdominal ultrasound without evidence of cholelithiasis. Abdominal computerized tomography (CT) evidenced an edematous pancreas and the patient was diagnosed with acute pancreatitis. Given the history and timing of acute pancreatitis after Infliximab infusion, drug-induced acute pancreatitis (DIAP) was strongly suspected and patient had the biological agent discontinued. Six months later, given refractory PsA, Adalimumab was added to her methotrexate regimen. After the second injection of Adalimumab 40mg, she developed new abdominal pain radiating to the back. The patient presented again to our ED and was readmitted with a diagnosis of acute pancreatitis based on clinical findings and a lipase level of 1,500U/L. Blood chemistries, ethanol levels and abdominal ultrasound were again within normal limits. After 2 days, the patient had complete resolution of the pancreatitis. Conclusion: Despite 10 possible cases have been reported to the Food and Drug Administration (FDA), no formally documented cases were available in the literature to date. We thoroughly excluded other causes of pancreatitis. Given the tim-ing of acute pancreatitis after infusion of Infliximab and positive re-challenge to Adalimumab, we strongly believe that this is a case of Tumor Necrosis Factor-α inhibitor class-induced acute pancreatitis. In current studies, Infliximab has proved to be beneficial for treatment of acute pancreatitis in rat models but human studies are pending. Our case raises concern for the use of TNF-α inhibitors for acute pancreatitis in humans, although further formal documented reports are necessary to strengthen this association.

Lauren Bonomo graduated with honors from Yale University and is now a medical student at the Icahn School of Medicine at Mount Sinai. She is currently on a scholarly year, pursuing research in Icahn’s Department of Dermatology. She is particularly interested in inflammatory and autoimmune skin disease, including atopic dermatitis, psoriasis, vitiligo, and alopecia areata

Background: Treatment of moderate to severe psoriasis or psoriatic arthritis often poses a challenge to the physician. Patients with moderate to severe disease frequently do not respond to initial, non-systemic therapies such as topical medications or phototherapy. The next step in treatment for these patients is initiation of a single-agent systemic therapy. However, systemic monotherapy is often insufficient in attaining the desired level of control, and increasing the dose of many of the first-line medications may pose a safety risk to the patient. As such, combination therapies are frequently used in these difficult cases. There is a paucity of literature related to combination therapies involving newer agents, such as biologic drugs. Initial investigations suggest that biologics in combination with cyclosporine, methotrexate, acitretin, or even another biologic are promising options for recalcitrant plaque psoriasis. Methods: In this retrospective chart review, all patients billed with the ICD-10 code L40.0 (psoriasis vulgaris) at a single U.S. tertiary referral center in the past two years were identified. Anonymized data that were collected included sex, year of birth, age at diagnosis, psoriasis type, presence of psoriatic arthritis, comorbidities, previous therapies, clinical severity before and after combination treatment, and adverse events experienced. Results: Of the 523 patients billed for a diagnosis code of psoriasis in the past two years, there were 47 patients who met inclusion criteria. They represented 60 distinct treatment combinations. The combinations we evaluated were, for the most part, one biologic drug with one traditional oral therapy (Table 1). Despite the severity and history of prior treatment failure in our cohort, 65% of combination regimens elicited at least a 50% response. Only 6% of combinations resulted in no clinical response (defined as less than 25% improvement). While there were no statistically significant differences among the unique combinations, methotrexate in combination with a biologic was the regimen that appeared to produce the best response (p=0.115). Conclusion: We conclude that combination therapy should be considered in patients with recalcitrant psoriasis who have failed multiple single-agent regimens. Our results suggest methotrexate may be particularly effective in combination with a biologic agent.

Lauren Bonomo graduated with honors from Yale University and is now a medical student at the Icahn School of Medicine at Mount Sinai. She is currently on a scholarly year, pursuing research in Icahn’s Department of Dermatology. She is particularly interested in inflammatory and autoimmune skin disease, including atopic dermatitis, psoriasis, vitiligo, and alopecia areata.

Background: Atopic dermatitis (AD) is known to be associated with other allergic diseases. These conditions include asthma, food allergy, and allergic rhinoconjunctivitis. AD typically occurs in early childhood with allergic comorbidities developing later in life in a serial fashion. This progression is termed the “atopic march” and is considered the classical presentation of atopic disease. However, recent evidence suggests that this paradigm may not hold true for a significant portion of patients with these conditions. Not only is the timing of development likely more complex than previously believed, the comorbidities associated with AD are possibly more numerous and varied. Methods: We conducted a systematic search of the literature on AD and associated extracutaneous disease. The two-step search involved a targeted search of PubMed and EMBASE and a hand search of all abstracts published in 5 key journals. The final yield was 65 articles, which consisted of 41 case-control studies (63.1%), 19 cohort studies (29.2%) and 5 meta-analyses (7.7%). Results: The results of this systematic review support the notion that atopic dermatitis is strongly associated with other atopic diseases, including asthma, hay fever, and allergic rhinoconjunctivitis. However, it also suggests that the classical paradigm of the “atopic march” does not apply to all patients with atopic dermatitis. There is likely a diversity of phenotypes for patters of allergic disease. We found a major association between AD and neuro-psychiatric disorders, particularly autism spectrum and attention deficit hyperactivity disorders. We found evidence that patients with AD may have an increased risk of developing lymphoma, squamous cell carcinoma (SCC) and basal cell carcinoma (BCC). There was also a small body of evidence suggesting an increased risk for myocardial infarction, stroke and cardiovascular death. The evidence on autoimmune comorbidities was mixed, with the only significant association being a reduced risk of type 1 diabetes mellitus. Conclusion: Our analysis supports a significant association between AD and neuro-psychiatric, cardiovascular and infectious disorders as well as increased risk for malig-nancies. Surprisingly, patients with AD had a decreased risk of developing type1 dia-betes mellitus.

Alvaro J. Ramos, MD, is currently a medicine resident physician at the Icahn School of Medicine at Mount Sinai West. He is the author of the recently published textbook Dermatology for the USMLE. Dr. Ramos has dedicated a major part of his medical career to teaching and helping students prepare for the USMLE, including teaching review courses. His interest in dermatology include DRESS syndrome, toxic erythema of chemotherapy, atopic dermatitis, psoriasis and infectious skin disorders.

Background: Toxic erythema of chemotherapy (TEC) is a relatively new term used to describe a spectrum of clinical cutaneous entities that occur after initia-tion of cytotoxic chemotherapeutic agents such as antimetabolites (i.e. cytara-bine) and anthracyclines (i.e. doxorubicin). Typically, it presents as a severe skin reaction manifesting as acral erythema, edema and dysesthesias of the hands and feet. The goal of this study is to more clearly define the various clin-ical and histological presentations of TEC and identify the most common caus-ative agents. Methods: We retrospectively reviewed the charts of 500 patients who had un-dergone allogeneic or peripheral stem cell transplant from January 2010 to December 2015 and were receiving chemotherapy. Out of 500 patients, only 39 had cutaneous manifestations consistent with TEC. Each patient’s skin bi-opsy was reviewed with a dermatopathologist to confirm features of TEC. Data extracted included age, gender, distribution and morphology of rash, chemo-therapy used, timing and resolution of drug reaction, underlying malignancy and histopathological features. Results: The incidence of TEC in our cohort was 7.8% with the majority of cases occurring in patient with acute myeloid leukemia (41%). Out of the 39 cases, 24 were males (61%) and 15 were females (39%); the mean age of the patients was 44.1 years. Mean time to onset of the rash from administration of offending chemotherapeutic agent was 13.3 days. Mean time to resolution was 29.0 days. The most common implicated drug was cytarabine, followed by clofarabine (see Table 1). The most common clinical presentation was bilateral erythema, edema and pain in the palm and soles with varied intertriginous involvement. Other significant coexisting variations included dermatomyositis-like features, hyperpigmentation, bullous and violaceous erythema with lichenoid papules. The most common histological finding was vacuolar interface dermatitis and dysmaturation of keratinocytes. Conclusion: We conclude that rather than having an exponential number of terms to describe toxic reactions to cytotoxic chemotherapy agents, consolidat-ing the clinical and histological features into a singular term as TEC. We believe this will aid in timely recognition, diagnosis and referral onto dermatology specialists for subsequent management

Alvaro J. Ramos is currently a medicine resident physician at the Icahn School of Medicine at Mount Sinai West. He is the author of the recently published textbook Dermatology for the USMLE. Dr. Ramos has dedicated a major part of his medical career to teaching and helping students prepare for the USMLE, including teaching review courses. His interest in dermatology include DRESS syndrome, toxic erythema of chemotherapy, atopic dermatitis, psoriasis and infectious skin disorders.

Background: Drug reaction with eosinophilia and systemic symptoms (DRESS) is a type-IV hypersensitivity drug reaction with multi-organ involvement. It carries up to a 10% mortality risk; therefore, early recognition and discontinuation of the offending agent are key to managing this potentially life-threatening condition. Diagnosis is based on clinical criteria, which include rash, fever, lymphadenopathy, eosinophilia, atypical lymphocytes, and involvement of internal organs. We present a rare case of DRESS syndrome induced by self-medicated over-the-counter guaifenesin for nasal congestion. The purpose of our study is to create awareness of possible lethal reactions that may occur even when using some of the least (presumed) harmful drugs in clinical practice. Case Report: A 32-year-old male with no past medical history presented to the Emergency Department (ED) with 2 weeks of weakness and a generalized pruritic maculopapular rash (Image 1). Patient reported no history of sick contacts, exposure to animals, insects, wild plants, or new hygiene products. He denied taking any medications except for over-the-counter guaifenesin for nasal congestion 3 weeks prior to ED visit. Initial physical exam was unremarkable except for a diffuse maculopapular rash with follicular accentuation sparing palms, soles, and mucous membranes (Image 2). Laboratories were significant for a white blood cell count of 21,900 cells/uL and eosinophils of 3,500 cells/uL. Other labs including comprehensive metabolic panel, hepatitis panel, Mycoplasma, EBV, HIV, and Herpesvirus were negative. During the course of hospitalization, the patient developed acute kidney injury (AKI) along with prominent submandibular and submental lymphadenopathy and desquamation of his rash. Atypical lymphocytes were found on peripheral smear. Skin biopsy showed spongiosis and a superficial mixed inflammatory infiltrate with eosinophils, consistent with DRESS. Based on RegiSCAR criteria, patient was diagnosed with DRESS and treatment was initiated with 20-day prednisone taper. Patient had complete resolution of his skin eruption in 2 weeks. Conclusion: This case reminds us that there can be unexpected side effects and reactions from drugs that we use in our everyday clinical practice. In this case, the skin rash was the initial sign of more serious internal organ involvement. We conclude that over-the-counter guaifenesin was the culprit drug and should be suspected as a cause of DRESS syndrome in the right clinical context

Alvaro J. Ramos is currently a medicine resident physician at the Icahn School of Medicine at Mount Sinai West. He is the author of the recently published textbook Dermatology for the USMLE. Dr. Ramos has dedicated a major part of his medical career to teaching and helping students prepare for the USMLE, including teaching review courses. His interest in dermatology include DRESS syndrome, toxic erythema of chemotherapy, atopic dermatitis, psoriasis and infectious skin disorders.

Background: A reaction to the treatment of syphilis was noted as early as the 15th century when arsenic was utilized as therapy. This classical reaction is known as the Jarisch-Herxheimer reaction (JHR) and is thought to occur secondary to antigen release and immune-complex formation after treponemal death. It is characterized by development of fever, tachycardia, hypotension and exacerbation of underlying cutaneous lesions within hours of antimicrobial administration. We present a rare case of a classical Jarisch-Herxheimer reaction revealing the unexpected diagnosis of advanced syphilis. Clinical Case: A 30-year-old African-American male was brought to the emergency room with generalized weakness, unsteady gait and watery diarrhea for one month. Past medical history was unremarkable. On examination, he was ill-appearing and cachectic. Skin exam showed mildly noticeable 1x1cm hyperpigmented macules on the trunk and palms. The rest of the exam was within normal limits except for generalized weakness and mild nuchal tenderness. Routine laboratories were unremarkable except for a positive rapid HIV test. Later in the hospitalization, the CD4 count resulted as 1cell/ml and the patient was started on highly active antiretroviral therapy (HAART) regimen and azithromycin for possible disseminated Mycobacterium avium complex (MAC). Six hours after the administration of azithromycin, the patient developed severe hyperpyrexia (42.7ï‚°C), and tachycardia, and his skin lesions became accentuated (Image 1). Given the timing of the hyperpyrexia and worsening skin eruption after antimicrobial administration, a Jarisch-Herxheimer reaction (JHR) was strongly suspected. Treponema pallidum IgG was 8.4; he was thus diagnosed with JHR and secondary syphilis. The patient was adequately treated with weekly doses of intramuscular penicillin for three weeks with excellent clinical improvement. Conclusion: Approximately 25% of patients with AIDS have syphilis. Given the wide spectrum of clinical presentations, syphilis often poses a diagnostic challenge to physicians. This case highlights how an unexpected Jarisch-Herxheimer reaction in a patient with AIDS uncovered the diagnosis of secondary syphilis and prompted the rapid initiation of adequate life-saving treatment. Skin rash accentuation in relation to antimicrobial administration was paramount. We conclude that physicians should have a strong suspicion for syphilis in all patients with AIDS and a skin rash.

Christopher Mancuso has experience in research as an undergraduate and graduate student at Johns Hopkins University. His interests conducting benchwork and working on clinical studies have been in the fields of neurosurgery and dermatology. Currently, he is a third year medical student at Nova Southeastern University College of Osteopathic Medicine and hopes to pursue a career as a dermatologist and Mohs surgeon.

Keloid scarring is a chronic disfiguring condition that is characterized as overproduction of collagen caused by excessive fibroblast proliferation in response to dermal injury [1, 2]. Diagnosis of keloids is based on the clinical presentation and history. The treatment options include one or a combination of the following: intralesional injections of corticosteroids or 5-fluorouracil, topical Imiquimod or silicone gel sheets, pressure therapy, cryotherapy, surgical excision, radiation therapy, and laser therapy [1]. It has been proposed that a combination of intralesional corticosteroid injections with surgical excision be considered as a first-line therapy for earlobe keloids [3]. While there is a large body of research on keloids and the treatments have been well established, the recurrence rates remain high and variable and there are currently no available guidelines or algorithms for the number of injections of corticosteroids that should precede surgical excision. The goal of this case report is to demonstrate the use of xenografts in the reconstruction of keloid excisions on the ear.

Dr. Kwan-Kyu Park, M.D., Ph.D., now is a professor of pathology, a chief of the pathology laboratory in college of medicine, Catholic University of Daegu, based in Daegu, Republic of Korea. Prof. Park has published over 300 papers about various inflammatory disease and pathology. He is an expert in kidney and liver pathology and his main research interest is inflammatory diseases including dermatitis. He is also interested in therapeutic effects of bee venom and its component on various diseases. The papers he published about bee venom are over 30. Further, he has been studied about gene therapy using oligodeoxynucleotide decoy and siRNA. Currently, Dr. Park Kwan-Kyu leads 8 members of the pathology laboratory, and works as a specialist for Daegu Catholic University Medical Center.

Atopic dermatitis (AD) is a multifactorial skin disease, with complex interactions of innate and adaptive immune responses based on a genetic, pharmacological and psychological predisposition. Purified bee venom (BV) and its major component melittin (Mel) has been widely used as a traditional medicine for various diseases. It has multiple effects including antibacterial, antiviral, and anti-inflammatory activities in various cell types. However, the precise mechanism of BV and Mel in ameliorating the AD is not fully understood. This study investigated the pharmacological effects of BV and Mel on AD symptoms by using tumor necrosis factor (TNF)-α-/interferon (IFN)-γ-activated human keratinocyte. The human keratinocyte HaCaT cells were pretreated with BV (1, 10 and 100 ng/ml), and Mel (0.1, 0.5 and 1 µg/ml) for 30 min and then stimulated with recombinant human TNF-α/IFN-γ (10 ng/ml) for 9 h. In order to determine whether BV and Mel inhibit thymus-and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22), this study analyzed these chemokines with real-time PCR in mRNA HaCaT cells. BV and Mel inhibited the mRNA expression of TARC/CCL17 and MDC/CCL2 in TNF-α-/IFN-γ-stimulated HaCaT cells. In addition, BV and Mel treatment suppressed the expression of pro-inflammatory cytokines such as IL-1 β, IL-6, and IFN-γ in protein level of TNF-α-/IFN-γ-stimulated HaCaT cells. And also, BV and Mel effectively inhibited NF-κB signaling pathway and JAK2-mediated distal signaling phospho-STAT1 and phospho-STAT3 in TNF-α/IFN-γ-stimulated HaCaT cells. In conclusion, this study provides novel insights into the pharmacological actions of BV and Mel as a potential agent for use in the treatment of AD-like skin lesions.

Dr. Kwan Kyu Park, M.D., Ph.D., now is a professor of pathology, a chief of the pathology laboratory in college of medicine, Catholic University of Daegu, based in Daegu, Republic of Korea. Prof. Park has published over 300 papers about various inflammatory disease and pathology. He is an expert in kidney and liver pathology and his main research interest is inflammatory diseases including dermatitis. He is also interested in therapeutic effects of bee venom and its components on various diseases. The papers he published about bee venom are over 30. Further, he has been studied about gene therapy using oligodeoxynucleotide decoy and siRNA. Currently, Dr. Park Kwan-Kyu leads 8 members of the pathology laboratory, and works as a specialist for Daegu Catholic University Medical Center. Email: kkpark@cu.ac.kr

Background: Atopic dermatitis (AD) is one of inflammatory skin diseases that is characterized by intense pruritus and relapsable eczematous lesions. The hallmarks of AD are defects of epidermal barrier and immunoglobulin E (IgE)-mediated sensitization to several environmental allergens, and immune disorder mediated by an imbalance towards T-helper-2 (Th2) response. Melittin (Mel), a major component of Bee venom, has been studied in various inflammatory diseases including liver cirrhosis, atherosclerosis, and acne. However, beneficial effects of Mel on AD-like animal have not been explored. Therefore, we investigated the anti-atopic effects of Mel. Methods: AD was induced on shaved back of BALB/c by using ovalbumin (OVA) patch. Mel was treated epicutaneously or intraperitoneally. After agent treatment, skin lesions and sera were extracted from sacrificed mice. Skin tissues were divided and used for H&E staining, Quantitative real-time PCR, and Western blot. Cytokines and IgE in the sera were determined by ELISA. Results: OVA-induced skin thickening and inflammatory infiltration were decreased in Mel-treated group. Mel prevented OVA-induced filaggrin deficiency. Furthermore, Mel ameliorated OVA-induced imbalanced inflammatory mediators. Conclusions: This study has shown that Mel inhibits OVA-induced AD-like symptoms in mice. The OVA can contribute crucially to the AD-like cutaneous symptoms, such as skin thickening, mast cells infiltration, filaggrin deficiency, exaggerated serum-IgE, and increased inflammatory mediators. However, Mel ameliorated the OVA-induced AD-like cutaneous symptoms and inflammatory mediators leading to the progression of AD. Furthermore, this study may be the first evidence that Mel can use for anti-inflammatory effects on OVA-induced AD. Therefore, it is suggested that Mel is regarded as an alternative therapeutic agent for AD.

Young Kyoung Seo is currently the Leader of Clinical Evaluation Department in DERMAPRO Ltd. She has been working for 13 years after studying Chemistry and Physiology. She has worked in the cosmetic field and functional food for skin condition. She has been focusing on the aging of skin and odor.

Body odor is caused by degraded skin components accumulating on the skin surface as well as secretions from the sweat and sebaceous glands and could be affected by aging. Human aging has been focused on the skin than body odor, so most studies have been studied about the skin change with aging. Only a few studies are known about the age-dependent changes of body odor. The aim of this study was to establish a new method for the evaluation of body odor and to investigate the anti-odor effect of body wash product on randomization, double-blind and cross over study. 22 subjects aged between 51 and 61 years (average age: 55.68±2.69 y), participated in this study. Four odor judges evaluated the efficacy of both products, quantitative analysis of 2-nonenal and isovaleric acid as the cause of body odor by gas chromatography, EEG measurement. Additionally, bactericidal and fungicidal activities were investigated with in vitro microbiologic test. We examined for significant differences between test group and placebo and the correlation of each evaluate parameters. This study has shown decrement effect of Natural Antimicrobial Complex on body odor and the application of EEG method for evaluation of odor test showed the stress rate increased when odor score are high. This methodology is suggested to establish on objective evaluation method in the characterization of facial features in skin care and evaluations of fragrance. Also, this new method could be useful in sensory evaluation field.

Dr. Matsuura has been working on signal transduction studies for most of his career. His current research interests include transforming growth factor-b (TGF-b) and Interleukin-31 (IL-31) signalings in diseases. The former signaling pathways are involved in cancer development and metastasis, while the latter in an itchy skin disease called primary cutaneous amyloidosis (PCA) that is relatively common in Taiwan.

Primary cutaneous amyloidosis (PCA) is an itchy skin disorder that is relatively common in South America and Southeast Asia. The disease is not life threatening, but chronic itch and unsightly appearance of the skin affect patients’ quality of life. There are multiple forms: macular, lichen and nodular amyloidosis, but amyloid deposition in the papillary dermis is the cardinal feature of the disease. The amyloid deposition is thought to be caused by cellular debris from apoptosed keratinocytes. Most of PCA cases are sporadic, but autosomal dominant inheritance has also been identified (familial PCA, FPCA). The mechanism being unknown, there is no radical cure of the disease. Genetic analyses of FPCA patients have revealed a link between the disease and the missense mutations in the interleukin-31 (IL-31) receptor subunits. We previously reported the same mutations from FPCA patients in sporadic cases, suggesting the significant contribution of these mutations in the skin disease. The IL-31 receptor consists of two subunits, OSMR and IL-31RA. All the mutations found in FPCA localize in the membrane proximal fibronectin III (FNIII) domain of either subunit. Several mutations have been identified in the OSMR subunit that is also engaged with other IL-6-type cytokine receptors, while only one mutation has been reported in IL31RA that is specific to the IL-31 receptor. We have previously shown that the FPLCA-derived mutation S521F in the IL-31RA subunit of the receptor impacts monocyte chemotactic protein-1 (MCP-1) production from HaCaT, a human keratinocyte cell line. In the current study we introduced FPCA-derived mutations in OSMR in HaCaT by CRISPR/Cas9-based gene editing. We observed impaired production of MCP-1 from the cells harboring all the mutations tested. This result demonstrated that the impaired MCP-1 production is a common consequence with the mutated receptor subunit of the IL-31 receptor in PCA. Since MCP-1 plays a key role in attracting innate immune cells to keratinocytes to clear cellular debris, the impaired MCP-1 production by the IL-31 receptor mutations may be an important part of the pathogenesis of the skin disease.

Background: Atopic dermatitis is one of common dermatological disease particularity infants and children. however it is reported in all age groups.different diagnostics guidelines have been proposed in this regard. the hanifin- rajka major and minor criteria seem to have got a better acceptance. Objectives: This study aimed at evaluating the clinical pattern of atopic dermatitis based on Hanifin-Rajka criteria in dermatology clinic of tabriz Sina hospital. Material and methods: In an analytical- descriptive cross sectional study 60 patients with atopic dermatitis were recruited in one year in Tabriz. Sina hospital.the patients were selected in three 20 groups. minor and major criteria for atopic dermatitis were evaluated in each group. Results: The major criteria were pruritus 81.7%. characteristic distribution and morphology66.7%. flexural lichenification in adults 25 %. facial and ex-tensor involvement in infants and children 53.3%. chronic and relapsing dermatitis 50%. and personal or family history of atopia/asthma, allergic rhinitis. and allergic dermatitis 46.7%. accordingly the major criteria were positive in 80%. the most common minor criteria were exeroderma 87.3%. eczema perifollicular exacerbation 35%. accentuation of the palralines 31.7%. recurred conjunctivitis 30%. hyper igE 21.7 %. and cheilitis 21.7%. accordingly the minor criteria were present in 83.3%. Conclusions: As there is not any similar reports in Iranian community. the current investigation is the only one reporting fereqncic of major and minor criteria for atopic dermatitis