Amy S Paller

Northwestern University, Evanston, Illinois, United States

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Publications (311)1602.11 Total impact

  • Journal of the European Academy of Dermatology and Venereology 09/2015; DOI:10.1111/jdv.13344 · 2.83 Impact Factor
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    ABSTRACT: Background: A subset of atopic dermatitis is associated with increased susceptibility to eczema herpeticum (ADEH+). We previously reported that common single nucleotide polymorphisms (SNPs) in the IFN-γ (IFNG) and IFN-γ receptor 1 (IFNGR1) genes were associated with the ADEH+ phenotype. Objective: We sought to interrogate the role of rare variants in interferon pathway genes for the risk of ADEH+. Methods: We performed targeted sequencing of interferon pathway genes (IFNG, IFNGR1, IFNAR1, and IL12RB1) in 228 European American patients with AD selected according to their eczema herpeticum status, and severity was measured by using the Eczema Area and Severity Index. Replication genotyping was performed in independent samples of 219 European American and 333 African American subjects. Functional investigation of loss-of-function variants was conducted by using site-directed mutagenesis. Results: We identified 494 single nucleotide variants encompassing 105 kb of sequence, including 145 common, 349 (70.6%) rare (minor allele frequency <5%), and 86 (17.4%) novel variants, of which 2.8% were coding synonymous, 93.3% were noncoding (64.6% intronic), and 3.8% were missense. We identified 6 rare IFNGR1 missense variants, including 3 damaging variants (Val14Met [V14M], Val61Ile, and Tyr397Cys [Y397C]) conferring a higher risk for ADEH+ (P = .031). Variants V14M and Y397C were confirmed to be deleterious, leading to partial IFNGR1 deficiency. Seven common IFNGR1 SNPs, along with common protective haplotypes (2-7 SNPs), conferred a reduced risk of ADEH+ (P = .015-.002 and P = .0015-.0004, respectively), and both SNP and haplotype associations were replicated in an independent African American sample (P = .004-.0001 and P = .001-.0001, respectively). Conclusion: Our results provide evidence that both genetic variants in the gene encoding IFNGR1 are implicated in susceptibility to the ADEH+ phenotype.
    The Journal of allergy and clinical immunology 09/2015; DOI:10.1016/j.jaci.2015.06.047 · 11.48 Impact Factor
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    ABSTRACT: Given the recent National Institutes of Health proposal for balanced use of male and female cells and animals in preclinical studies, we explored whether sex bias exists in skin research. We surveyed 802 dermatological research articles from 2012 to 2013. No information about the sex of studied cells or animals was provided in 60% of papers. Among keratinocytes of known sex, 70% were male. Few studies compared male versus female cells or animals. Disclosure of sex and comparative studies contribute to our understanding of the biologic basis of sex differences. Addressing sex-specific differences in preclinical research informs subsequent clinical trial design and promotes individualized therapy.Journal of Investigative Dermatology advance online publication, 20 August 2015; doi:10.1038/jid.2015.298.
    Journal of Investigative Dermatology 08/2015; DOI:10.1038/jid.2015.298 · 7.22 Impact Factor
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    ABSTRACT: Safe and effective therapies are needed for pediatric patients with psoriasis. The purpose of this study was to evaluate ustekinumab in patients age 12 to 17 years who had moderate-to-severe psoriasis. Patients (n = 110) were randomly assigned to ustekinumab standard dosing (SD; 0.75 mg/kg [≤60 kg], 45 mg [>60-≤100 kg], and 90 mg [>100 kg]) or half-standard dosing (HSD; 0.375 mg/kg [≤60 kg], 22.5 mg [>60-≤100 kg], and 45 mg [>100 kg]) at weeks 0 and 4 and every 12 weeks or placebo at weeks 0 and 4 with crossover to ustekinumab SD or HSD at week 12. Clinical assessments included the proportion of patients achieving a Physician's Global Assessment of cleared/minimal (PGA 0/1), at least 75% improvement in Psoriasis Area and Severity Index (PASI 75), and at least 90% in PASI (PASI 90). Adverse events (AEs) were monitored through week 60. At week 12, 67.6% and 69.4% of patients receiving ustekinumab HSD and SD, respectively, achieved PGA 0/1 versus 5.4% for placebo (P < .001). Significantly greater proportions receiving ustekinumab achieved PASI 75 (HSD, 78.4%; SD, 80.6%; placebo, 10.8%) or PASI 90 (HSD, 54.1%; SD, 61.1%; placebo, 5.4%) at week 12 (P < .001). Through week 12, 56.8% of placebo patients, 51.4% of HSD patients, and 44.4% of SD patients reported at least one AE; through week 60, 81.8% reported AEs. The study was small relative to adult trials. In this patient population (12-17 years), the standard ustekinumab dose provided response comparable to that in adults with no unexpected AEs through 1 year. Copyright © 2015 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.
    Journal of the American Academy of Dermatology 08/2015; 73(4). DOI:10.1016/j.jaad.2015.07.002 · 4.45 Impact Factor
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    ABSTRACT: Atopic dermatitis affects a substantial number of children, many of whom seek initial treatment from their pediatrician or other primary care provider. Approximately two-thirds of these patients have mild disease and can be adequately managed at the primary care level. However, recent treatment guidelines are written primarily for use by specialists and lack certain elements that would make them more useful to primary care providers. This article evaluates these recent treatment guidelines in terms of evaluation criteria, treatment recommendations, usability, accessibility, and applicability to nonspecialists and integrates them with clinical evidence to present a streamlined severity-based treatment model for the management of a majority of atopic dermatitis cases. Because each patient's situation is unique, individualization of treatment plans is critical as is efficient communication and implementation of the plan with patients and caregivers. Specifically, practical suggestions for individualizing, optimizing, implementing, and communicating treatment plans such as choosing a moisturizer formulation, avoiding common triggers, educating patients/caregivers, providing written treatment plans, and scheduling physician follow-up are provided along with a discussion of available resources for patients/caregivers and providers. Copyright © 2015 by the American Academy of Pediatrics.
    PEDIATRICS 08/2015; DOI:10.1542/peds.2014-3678 · 5.47 Impact Factor
  • Women s Health 08/2015; 11(4):1-4. DOI:10.2217/WHE.15.28
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    ABSTRACT: Identifying differences and similarities between cutaneous lymphocyte antigen (CLA)(+) polarized T-cell subsets in children versus adults with atopic dermatitis (AD) is critical for directing new treatments toward children. We sought to compare activation markers and frequencies of skin-homing (CLA(+)) versus systemic (CLA(-)) "polar" CD4 and CD8 T-cell subsets in patients with early pediatric AD, adults with AD, and control subjects. Flow cytometry was used to measure CD69/inducible costimulator/HLA-DR frequency in memory cell subsets, as well as IFN-γ, IL-13, IL-9, IL-17, and IL-22 cytokines, defining TH1/cytotoxic T (TC) 1, TH2/TC2, TH9/TC9, TH17/TC17, and TH22/TC22 populations in CD4 and CD8 cells, respectively. We compared peripheral blood from 19 children less than 5 years old and 42 adults with well-characterized moderate-to-severe AD, as well as age-matched control subjects (17 children and 25 adults). Selective inducible costimulator activation (P < .001) was seen in children. CLA(+) TH2 T cells were markedly expanded in both children and adults with AD compared with those in control subjects, but decreases in CLA(+) TH1 T-cell numbers were greater in children with AD (17% vs 7.4%, P = .007). Unlike in adults, no imbalances were detected in CLA(-) T cells from pediatric patients with AD nor were there altered frequencies of TH22 T cells within the CLA(+) or CLA(-) compartments. Adults with AD had increased frequencies of IL-22-producing CD4 and CD8 T cells within the skin-homing population, compared with controls (9.5% vs 4.5% and 8.6% vs 2.4%, respectively; P < .001), as well as increased HLA-DR activation (P < .01). These data suggest that TH2 activation within skin-homing T cells might drive AD in children and that reduced counterregulation by TH1 T cells might contribute to excess TH2 activation. TH22 "spreading" of AD is not seen in young children and might be influenced by immune development, disease chronicity, or recurrent skin infections. Copyright © 2015 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
    Journal of Allergy and Clinical Immunology 07/2015; DOI:10.1016/j.jaci.2015.05.049 · 11.48 Impact Factor
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    ABSTRACT: Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature (CANDLE) syndrome is a newly characterized autoinflammatory disorder, caused by mutations in PSMB8. It is characterized by early-onset fevers, accompanied by a widespread, violaceous, and often annular cutaneous eruption. Although the exact pathogenesis of this syndrome is still obscure, it is postulated that the inflammatory disease manifestations stem from excess secretion of interferons. Based on preliminary blood cytokine and gene expression studies, the signature seems to come mostly from type I interferons, which are proposed to lead to the recruitment of immature myeloid cells into the dermis and subcutis. In this study, we systematically analyzed skin biopsies from 6 patients with CANDLE syndrome by routine histopathology and immunohistochemistry methods. Skin lesions showed the presence of extensive mixed dermal and subcutaneous inflammatory infiltrate, composed of mononuclear cells, atypical myeloid cells, neutrophils, eosinophils, and some mature lymphocytes. Positive LEDER and myeloperoxidase staining supported the presence of myeloid cells. Positive CD68/PMG1 and CD163 staining confirmed the existence of histiocytes and monocytic macrophages in the inflammatory infiltrate. CD123 staining was positive, demonstrating the presence of plasmacytoid dendritic cells. Uncovering the unique histopathological and immunohistochemical features of CANDLE syndrome provides tools for rapid and specific diagnosis of this disorder and further insight into the pathogenesis of this severe life-threatening condition.
    The American Journal of dermatopathology 07/2015; 37(7):517-522. DOI:10.1097/DAD.0000000000000340 · 1.39 Impact Factor
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    ABSTRACT: Spherical or nucleic acid (SNA) gold nanoparticle conjugates (13-nm-diameter gold cores functionalized with densely packed and highly oriented nucleic acids) dispersed in Aquaphor have been shown to penetrate the epidermal barrier of both intact mouse and human skin, enter keratinocytes, and efficiently down-regulate gene targets. ganglioside-monosialic acid 3 synthase (GM3S) is a known target that is overexpressed in diabetic mice and responsible for causing insulin resistance and impeding wound healing. GM3S SNAs increase keratinocyte migration and proliferation as well as insulin and insulin-like growth factor-1 (IGF1) receptor activation under both normo- and hyperglycemic conditions. The topical application of GM3S SNAs (50 nM) to splinted 6-mm-diameter full-thickness wounds in diet-induced obese diabetic mice decreases local GM3S expression by >80% at the wound edge through an siRNA pathway and fully heals wounds clinically and histologically within 12 d, whereas control-treated wounds are only 50% closed. Granulation tissue area, vascularity, and IGF1 and EGF receptor phosphorylation are increased in GM3S SNA-treated wounds. These data capitalize on the unique ability of SNAs to naturally penetrate the skin and enter keratinocytes without the need for transfection agents. Moreover, the data further validate GM3 as a mediator of the delayed wound healing in type 2 diabetes and support regional GM3 depletion as a promising therapeutic direction.
    Proceedings of the National Academy of Sciences 05/2015; 112(18):201505951. DOI:10.1073/pnas.1505951112 · 9.67 Impact Factor
  • Mark A. Seeger · Amy S. Paller
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    ABSTRACT: Significance: The re-epithelialization of wounded skin requires the rapid and coordinated migration of keratinocytes (KC) into the wound bed. Almost immediately after wounding, cells present at or attracted to the wound site begin to secrete a complex milieu of growth factors. These growth factors exert mitogenic and motogenic effects on KCs, inducing the rapid proliferation and migration of KCs at the wound edge. Recent Advances: New roles for growth factors in KC biology are currently being discovered and investigated. This review will highlight the growth factors, particularly transforming growth factor-α (TGF-α), heparin-binding epidermal growth factor (HB-EGF), insulin-like growth factor 1 (IGF-1), fibroblast growth factor 7 (FGF-7), FGF-10, and hepatocyte growth factor (HGF), which have conclusively been shown to be the most motogenic for KCs. Critical Issues: The cellular and molecular heterogeneity of wounded tissue makes establishing direct relationships between specific growth factors and KC migration difficult in situ. The absence of this complexity in simplified in vitro experimental models of migration makes the clinical relevance of the results obtained from these in vitro studies ambiguous. Future Directions: Deciphering the relationship between growth factors and KC migration is critical for understanding the process of wound healing in normal and disease states. Insights into the basic science of the effects of growth factors on KC migration will hopefully lead to the development of new therapies to treat acute and chronic wounds.
    04/2015; 4(4):213-224. DOI:10.1089/wound.2014.0540
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    ABSTRACT: Atopic dermatitis (AD) primarily affects infants and young children. Although topical corticosteroids (TCSs) are often prescribed, noncorticosteroid treatments are needed because compliance with TCSs is poor due to concerns about their side effects. In this longest and largest intervention study ever conducted in infants with mild-to-moderate AD, pimecrolimus 1% cream (PIM) was compared with TCSs. A total of 2418 infants were enrolled in this 5-year open-label study. Infants were randomized to PIM (n = 1205; with short-term TCSs for disease flares) or TCSs (n = 1213). The primary objective was to compare safety; the secondary objective was to document PIM's long-term efficacy. Treatment success was defined as an Investigator's Global Assessment score of 0 (clear) or 1 (almost clear). Both PIM and TCSs had a rapid onset of action with >50% of patients achieving treatment success by week 3. After 5 years, >85% and 95% of patients in each group achieved overall and facial treatment success, respectively. The PIM group required substantially fewer steroid days than the TCS group (7 vs 178). The profile and frequency of adverse events was similar in the 2 groups; in both groups, there was no evidence for impairment of humoral or cellular immunity. Long-term management of mild-to-moderate AD in infants with PIM or TCSs was safe without any effect on the immune system. PIM was steroid-sparing. The data suggest PIM had similar efficacy to TCS and support the use of PIM as a first-line treatment of mild-to-moderate AD in infants and children. Copyright © 2015 by the American Academy of Pediatrics.
    PEDIATRICS 03/2015; 135(4). DOI:10.1542/peds.2014-1990 · 5.47 Impact Factor
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    ABSTRACT: Widespread reversion of genetic disease is rare; however, such events are particularly evident in some skin disorders in which normal clones develop on a background of affected skin. We previously demonstrated that mutations in keratin 10 (KRT10) cause ichthyosis with confetti (IWC), a severe dominant disorder that is characterized by progressive development of hundreds of normal skin spots via revertant mosaicism. Here, we report on a clinical and histological IWC subtype in which affected subjects have red, scaly skin at birth, experience worsening palmoplantar keratoderma in childhood, and develop hundreds of normal skin spots, beginning at around 20 years of age, that increase in size and number over time. We identified a causal de novo mutation in keratin 1 (KRT1). Similar to IWC-causing KRT10 mutations, this mutation in KRT1 resulted in a C-terminal frameshift, replacing 22 C-terminal amino acids with an alternate 30-residue peptide. Mutant KRT1 caused partial collapse of the cytoplasmic intermediate filament network and mislocalized to the nucleus. As with KRT10 mutations causing IWC, reversion of KRT1 mutations occurred via mitotic recombination. Because reversion is not observed with other disease-causing keratin mutations, the results of this study implicate KRT1 and KRT10 C-terminal frameshift mutations in the high frequency of revertant mosaicism in IWC.
    Journal of Clinical Investigation 03/2015; 125(4). DOI:10.1172/JCI64415 · 13.22 Impact Factor
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    Journal of Allergy and Clinical Immunology 02/2015; 135(2):AB391. DOI:10.1016/j.jaci.2014.12.1903 · 11.48 Impact Factor
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    ABSTRACT: Pediatric discoid lupus erythematosus (DLE) is rare. The risk of progression to systemic lupus erythematosus (SLE) is uncertain. We sought to determine the risk of progression of pediatric DLE to SLE and to characterize its phenotype. This was a retrospective review of 40 patients with DLE. Six (15%) of 40 patients presented with DLE as a manifestation of concurrent SLE. Of the remaining 34, 9 (26%) eventually met SLE criteria and 15 (44%) developed laboratory abnormalities without meeting SLE criteria. Only 10 (29%) maintained skin-limited disease. The average age at progression to SLE was 11 years, with greatest risk in the first year after DLE diagnosis. Most (89%) patients with SLE met diagnostic criteria with mucocutaneous disease (discoid lesions, malar rash, oral and nasal ulcers, photosensitivity), positive antibodies, and/or cytopenia without developing end-organ damage over 5 years of median follow-up. The study was retrospective. In pediatric patients, DLE carries a significant risk of progression to SLE but may predict a milder phenotype of systemic disease. All patients require careful monitoring for SLE, particularly within the first year of diagnosis. Copyright © 2014 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.
    Journal of the American Academy of Dermatology 01/2015; 72(4). DOI:10.1016/j.jaad.2014.12.028 · 4.45 Impact Factor
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    ABSTRACT: The National Eczema Association has received increasing numbers of patient inquiries regarding "steroid addiction syndrome," coinciding with the growing presence of social media dedicated to this topic. Although many of the side effects of topical corticosteroids (TCS) are addressed in guidelines, TCS addiction is not. We sought to assess the current evidence regarding addiction/withdrawal. We performed a systematic review of the current literature. Our initial search yielded 294 results with 34 studies meeting inclusion criteria. TCS withdrawal was reported mostly on the face and genital area (99.3%) of women (81.0%) primarily in the setting of long-term inappropriate use of potent TCS. Burning and stinging were the most frequently reported symptoms (65.5%) with erythema being the most common sign (92.3%). TCS withdrawal syndrome can be divided into papulopustular and erythematoedematous subtypes, with the latter presenting with more burning and edema. Low quality of evidence, variability in the extent of data, and the lack of studies with rigorous steroid addiction methodology are limitations. TCS withdrawal is likely a distinct clinical adverse effect of TCS misuse. Patients and providers should be aware of its clinical presentation and risk factors. Copyright © 2014 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.
    Journal of the American Academy of Dermatology 01/2015; 72(3). DOI:10.1016/j.jaad.2014.11.024 · 4.45 Impact Factor
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    ABSTRACT: Atopic dermatitis (AD) is a distressing dermatological disease which is highly prevalent during infancy, can persist into later life and requires long-term management with anti-inflammatory compounds. The introduction of the topical calcineurin inhibitors (TCIs), tacrolimus and pimecrolimus, more than 10 years ago was a major breakthrough for the topical anti-inflammatory treatment of AD. Pimecrolimus 1% is approved for second-line use in children (≥2 years old) and adults with mild-to-moderate AD. The age restriction was emphasised in a boxed warning added by the FDA in January 2006, which also highlights the lack of long-term safety data and the theoretical risk of skin malignancy and lymphoma. Since then, pimecrolimus has been extensively investigated in short- and long-term studies including over 4000 infants (<2 years old). These studies showed that pimecrolimus effectively treats AD in infants, with sustained improvement with long-term intermittent use. Unlike topical corticosteroids, long-term TCI use does not carry the risks of skin atrophy, impaired epidermal barrier function or enhanced percutaneous absorption, and so is suitable for AD treatment especially in sensitive skin areas. Most importantly, the studies of pimecrolimus in infants provided no evidence for systemic immunosuppression, and a comprehensive body of evidence from clinical studies, post-marketing surveillance and epidemiological investigations does not support potential safety concerns. In conclusion, the authors consider that the labelling restrictions regarding the use of pimecrolimus in infants are no longer justified and recommend that the validity of the boxed warning for TCIs should be reconsidered.This article is protected by copyright. All rights reserved.
    Pediatric Allergy and Immunology 01/2015; 26(4). DOI:10.1111/pai.12331 · 3.40 Impact Factor
  • Pediatric Rheumatology 01/2015; 13(Suppl 1):P154. DOI:10.1186/1546-0096-13-S1-P154 · 1.61 Impact Factor
  • Katherine M Mercy · Kenneth B Gordon · Amy S Paller
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    ABSTRACT: JAMA DERMATOLOGY Undertreatment, Treatment Trends, and Treatment Dissatisfaction Among Patients With Psoriasis and Psoriatic Arthritis in the United States: Findings From the National Psoriasis Foundation Surveys, 2003-2011 April W. Armstrong, MD, MPH; Andrew D. Robertson, PhD; Julie Wu, BS; Clayton Schupp, PhD; Mark G. Lebwohl, MD IMPORTANCE Psoriasis and psoriatic arthritis inflict significant morbidity. Data on undertreatment, treatment use, and treatment satisfaction are paramount to identify priority areas for advocacy, education, and research to improve patient outcomes. OBJECTIVES To determine the extent of nontreatment and undertreatment of psoriatic diseases, trends in treatment use, treatment satisfaction, and reasons for medication discontinuation among patients with psoriasis and psoriatic arthritis. DESIGN, SETTING, AND PARTICIPANTS We used the national survey data collected by the National Psoriasis Foundation via biannual surveys conducted from January 1, 2003, through December 31, 2011, in the United States. Survey data were collected from randomly sampled patients with psoriasis and psoriatic arthritis in the US population from a database of more than 76 000 patients with psoriatic diseases. MAIN OUTCOMES AND MEASURES Nontreatment, undertreatment, and treatment trends determined by the use of prescription medication (topical, phototherapeutic, oral systemic, and biologic), as well as treatment satisfaction and reasons for medication discontinuation. RESULTS A total of 5604 patients with psoriasis or psoriatic arthritis completed the survey. From 2003 through 2011, patients who were untreated ranged from 36.6% to 49.2% of patients with mild psoriasis, 23.6% to 35.5% of patients with moderate psoriasis, and 9.4% to 29.7% of patients with severe psoriasis. Among those receiving treatment, 29.5% of patients with moderate psoriasis and 21.5% of patients with severe psoriasis were treated with topical agents alone. The most frequently used phototherapy modality is UV-B, whereas methotrexate is the most commonly used oral agent. Although adverse effects and a lack of effectiveness were primary reasons for discontinuing biological agents, the inability to obtain adequate insurance coverage was among the top reasons for discontinuation. Overall, 52.3% of patients with psoriasis and 45.5% of patients with psoriatic arthritis were dissatisfied with their treatment. CONCLUSIONS AND RELEVANCE Nontreatment and undertreatment of patients with psoriasis and psoriatic arthritis remain a significant problem in the United States. While various treatment modalities are available for psoriasis and psoriatic arthritis, widespread treatment dissatisfaction exists. Efforts in advocacy and education are necessary to ensure that effective treatments are accessible to this patient population. JAMA Dermatol. 2013; 149(10): 1180-1185. doi: 10.1001/jamadermatol.2013.5264.
    JAMA The Journal of the American Medical Association 12/2014; 312(24):2676-7. DOI:10.1001/jama.2014.12494 · 35.29 Impact Factor

Publication Stats

7k Citations
1,602.11 Total Impact Points


  • 1990–2015
    • Northwestern University
      • • Department of Pediatrics
      • • Division of Dermatology
      • • Department of Cell and Molecular Biology
      • • Division of Hospital Medicine
      • • Feinberg School of Medicine
      • • Division of Pediatric Dermatology
      Evanston, Illinois, United States
  • 1989–2015
    • University of Illinois at Chicago
      • • Department of Dermatology (Chicago)
      • • Department of Pediatrics (Peoria)
      Chicago, Illinois, United States
    • Pennsylvania State University
      • Fusarium Research Center
      University Park, Maryland, United States
  • 2012
    • Ann & Robert H. Lurie Children's Hospital of Chicago
      Chicago, Illinois, United States
    • Oregon Health and Science University
      Portland, Oregon, United States
  • 1985–2011
    • Children's Memorial Hospital
      Chicago, Illinois, United States
  • 2010
    • University of Minnesota Duluth
      Duluth, Minnesota, United States
  • 2009
    • Henry Ford Hospital
      Detroit, Michigan, United States
  • 2007
    • National Research Center (CO, USA)
      Boulder, Colorado, United States
    • University of Texas Medical School
      Houston, Texas, United States
  • 2003–2006
    • University of California, San Diego
      • Department of Pediatrics
      San Diego, California, United States
    • Columbia University
      • Department of Dermatology
      New York, New York, United States
  • 1990–2006
    • Northwestern Memorial Hospital
      • Northwestern Medicine
      Chicago, Illinois, United States
  • 2002
    • The University of Chicago Medical Center
      Chicago, Illinois, United States
    • Our Ladys Childrens Hospital, Crumlin
      Dublin, Leinster, Ireland
    • University of Alabama at Birmingham
      • Department of Dermatology
      Birmingham, AL, United States
  • 1996–2002
    • Case Western Reserve University School of Medicine
      • Department of Pediatrics
      Cleveland, Ohio, United States
  • 2001
    • Osaka City University
      Ōsaka, Ōsaka, Japan
  • 1999
    • Medical College of Wisconsin
      • Department of Dermatology
      Milwaukee, WI, United States
  • 1997
    • Alpert Medical School - Brown University
      Providence, Rhode Island, United States
  • 1992
    • University of Toronto
      • Hospital for Sick Children
      Toronto, Ontario, Canada
  • 1986
    • Concordia University–Ann Arbor
      Ann Arbor, Michigan, United States