Philip Fleckman

Trinity Washington University, Washington, Washington, D.C., United States

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Publications (103)506.82 Total impact

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    ABSTRACT: The incidence, cost, morbidity, and mortality associated with non-healing of chronic skin wounds are dramatic. With the increasing numbers of people with obesity, chronic medical conditions, and an increasing life expectancy, the healthcare cost of non-healing ulcers has recently been estimated at $25 billion annually in the United States. The role played by bacterial biofilm in chronic wounds has been emphasized in recent years, particularly in the context of the prolongation of the inflammatory phase of repair. Rapid high-throughput genomic approaches have revolutionized the ability to identify and quantify microbial organisms from wounds. Defining bacterial genomes and using genetic approaches to knock out specific bacterial functions, then studying bacterial survival on cutaneous wounds is a promising strategy for understanding which genes are essential for pathogenicity. When an animal sustains a cutaneous wound, understanding mechanisms involved in adaptations by bacteria and adaptations by the host in the struggle for survival is central to development of interventions that favor the host. Characterization of microbiomes of clinically well characterized chronic human wounds is now under way. The use of in vivo models of biofilm-infected cutaneous wounds will permit the study of the mechanisms needed for biofilm formation, persistence, and potential synergistic interactions among bacteria. A more complete understanding of bacterial survival mechanisms and how microbes influence host repair mechanisms are likely to provide targets for chronic wound therapy.
    Advances in wound care. 09/2013; 2(7):389-399.
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    ABSTRACT: This statement, focused on melanonychia and nail plate dermoscopy, is intended to guide medical professionals working with melanonychia and to assist choosing appropriate management for melanonychia patients. The International Study Group on Melanonychia was founded in 2007 and currently has 30 members, including nail experts and dermatopathologists with special expertise in nails. The need for common definitions of nail plate dermoscopy was addressed during the Second Meeting of this Group held in February 2008. Prior to this meeting and to date (2010) there have been no evidence-based guidelines on the use of dermoscopy in the management of nail pigmentation.
    Anais brasileiros de dermatologia 04/2013; 88(2).
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    ABSTRACT: Recent studies of mice with hair defects have resulted in major contributions to the understanding of hair disorders. To use mouse models as a tool to study nail diseases, a basic understanding of the similarities and differences between the human and mouse nail unit is required. In this study we compare the human and mouse nail unit at the macroscopic and microscopic level and use immunohistochemistry to determine the keratin expression patterns in the mouse nail unit. Both species have a proximal nail fold, cuticle, nail matrix, nail bed, nail plate, and hyponychium. Distinguishing features are the shape of the nail and the presence of an extended hyponychium in the mouse. Expression patterns of most keratins are similar. These findings indicate that the mouse nail unit shares major characteristics with the human nail unit and overall represents a very similar structure, useful for the investigation of nail diseases and nail biology. Anat Rec, 296:521-532, 2013. © 2013 Wiley Periodicals, Inc.
    The Anatomical Record Advances in Integrative Anatomy and Evolutionary Biology 03/2013; 296(3):521-32. · 1.34 Impact Factor
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    ABSTRACT: Management of ichthyoses is a complex and continuously dynamic process. Primary treatments of ichthyosis are by means of topical moisturizers and topical medications. Patients and families need to have reasonable and realistic expectations when it comes to topical therapy. Topical medications cannot cure the scaling, but can gradually reduce it and thus improve their condition. No one treatment regimen works for everyone, and the best topical therapy for each patient may be the result of months (or years) of painstaking effort on both the physician's and the patient's behalf. As patients get older and their activities and lifestyles change, so should their topical treatment regimen. Bear in mind that the more complex the skin care regimen and costly the topical treatments, the less likely a patient and their family will be compliant.
    Dermatologic Therapy 01/2013; 26(1):16-25. · 1.96 Impact Factor
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    Journal of Investigative Dermatology 09/2012; · 6.19 Impact Factor
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    Philip Fleckman
    Journal of Investigative Dermatology 07/2012; 132(7):1745. · 6.19 Impact Factor
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    ABSTRACT: Pityriasis rubra pilaris (PRP) is a papulosquamous disorder phenotypically related to psoriasis. The disease has been occasionally shown to be inherited in an autosomal-dominant fashion. To identify the genetic cause of familial PRP, we ascertained four unrelated families affected by autosomal-dominant PRP. We initially mapped PRP to 17q25.3, a region overlapping with psoriasis susceptibility locus 2 (PSORS2 [MIM 602723]). Using a combination of linkage analysis followed by targeted whole-exome sequencing and candidate-gene screening, we identified three different heterozygous mutations in CARD14, which encodes caspase recruitment domain family, member 14. CARD14 was found to be specifically expressed in the skin. CARD14 is a known activator of nuclear factor kappa B signaling, which has been implicated in inflammatory disorders. Accordingly, CARD14 levels were increased, and p65 was found to be activated in the skin of PRP-affected individuals. The present data demonstrate that autosomal-dominant PRP is allelic to familial psoriasis, which was recently shown to also be caused by mutations in CARD14.
    The American Journal of Human Genetics 06/2012; 91(1):163-70. · 11.20 Impact Factor
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    ABSTRACT: Bacterial biofilm has been shown to play a role in delaying wound healing of chronic wounds, a major medical problem that results in significant health care burden. A reproducible animal model could be very valuable for studying the mechanism and management of chronic wounds. Our previous work showed that Pseudomonas aeruginosa (PAO1) biofilm challenge on wounds in diabetic (db/db) mice significantly delayed wound healing. In this wound time course study, we further characterize the bacterial burden, delayed wound healing, and certain aspects of the host inflammatory response in the PAO1 biofilm-challenged db/db mouse model. PAO1 biofilms were transferred onto 2-day-old wounds created on the dorsal surface of db/db mice. Control wounds without biofilm challenge healed by 4 weeks, consistent with previous studies; none of the biofilm-challenged wounds healed by 4 weeks. Of the biofilm-challenged wounds, 64% healed by 6 weeks, and all of the biofilm-challenged wounds healed by 8 weeks. During the wound-healing process, P. aeruginosa was gradually cleared from the wounds while the presence of Staphylococcus aureus (part of the normal mouse skin flora) increased. Scabs from all unhealed wounds contained 10(7) P. aeruginosa, which was 100-fold higher than the counts isolated from wound beds (i.e., 99% of the P. aeruginosa was in the scab). Histology and genetic analysis showed proliferative epidermis, deficient vascularization, and increased inflammatory cytokines. Hypoxia inducible factor expression increased threefold in 4-week wounds. In summary, our study shows that biofilm-challenged wounds typically heal in approximately 6 weeks, at least 2 weeks longer than nonbiofilm-challenged normal wounds. These data suggest that this delayed wound healing model enables the in vivo study of bacterial biofilm responses to host defenses and the effects of biofilms on host wound healing pathways. It may also be used to test antibiofilm strategies for treating chronic wounds.
    Wound Repair and Regeneration 05/2012; 20(3):342-52. · 2.76 Impact Factor
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    ABSTRACT: This study investigates mouse cutaneous responses to long-term percutaneously implanted rods surrounded by sphere-templated porous biomaterials engineered to mimic medical devices surrounded by a porous cuff. We hypothesized that keratinocytes would migrate through the pores and stop, permigrate, or marsupialize along the porous/solid interface. Porous/solid-core poly(2-hydroxyethyl methacrylate) [poly(HEMA)] and silicone rods were implanted in mice for 14 days, and for 1, 3, and 6 months. Implants with surrounding tissue were analyzed (immuno)histochemically by light microscopy. Poly(HEMA)/skin implants yielded better morphologic data than silicone implants. Keratinocytes at the poly(HEMA) interface migrated in two different directions. "Ventral" keratinocytes contiguous with the dermal-epidermal junction migrated into the outermost pores, forming an integrated collar surrounding the rods. "Dorsal" keratinocytes appearing to emanate from the differentiated epithelial layer, extended upward along and into the exterior portion of the rod, forming an integrated sheath. Leukocytes persisted in poly(HEMA) and silicone pores for the duration of the study. Vascular and collagen networks within the poly(HEMA) pores matured as a function of time up to 3-months implantation. Nerves were not observed within the pores. Poly(HEMA) underwent morphological changes by 6 months of implantation. Marsupialization, foreign body encapsulation, and infection were not observed in any implants.
    Journal of Biomedical Materials Research Part A 02/2012; 100(5):1256-68. · 2.83 Impact Factor
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    ABSTRACT: Staphylococcus aureus biofilms are associated with chronic skin infections and are orders of magnitude more resistant to antimicrobials and host responses. S. aureus contains conserved nonribosomal peptide synthetases that produce the cyclic dipeptides tyrvalin and phevalin (aureusimine A and B, respectively). The biological function of these compounds has been speculated to be involved in virulence factor gene expression in S. aureus, protease inhibition in eukaryotic cells, and interspecies bacterial communication. However, the exact biological role of these compounds is unknown. Here, we report that S. aureus biofilms produce greater amounts of phevalin than their planktonic counterparts. Phevalin had no obvious impact on the extracellular metabolome of S. aureus as measured by high-performance liquid chromatography-mass spectrometry and nuclear magnetic resonance. When administered to human keratinocytes, phevalin had a modest effect on gene expression. However, conditioned medium from S. aureus spiked with phevalin amplified differences in keratinocyte gene expression compared to conditioned medium alone. Phevalin may be exploited as potential biomarker and/or therapeutic target for chronic, S. aureus biofilm-based infections.
    PLoS ONE 01/2012; 7(7):e40973. · 3.53 Impact Factor
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    ABSTRACT: Bacteria colonizing chronic wounds often exist as biofilms, yet their role in chronic wound pathogenesis remains unclear. Staphylococcus aureus biofilms induce apoptosis in dermal keratinocytes, and given that chronic wound biofilms also colonize dermal tissue, it is important to investigate the effects of bacterial biofilms on dermal fibroblasts. The effects of a predominant wound pathogen, methicillin-resistant S. aureus, on normal, human, dermal fibroblasts were examined in vitro. Cell-culture medium was conditioned with equivalent numbers of either planktonic or biofilm methicillin-resistant S. aureus and then fed to fibroblast cultures. Fibroblast response was evaluated using scratch, viability, and apoptosis assays. The results suggested that fibroblasts experience the same fate when exposed to the soluble products of either planktonic or biofilm methicillin-resistant S. aureus, namely limited migration followed by death. Enzyme-linked immunosorbent assays demonstrated that fibroblast production of cytokines, growth factors, and proteases were differentially affected by planktonic and biofilm-conditioned medium. Planktonic-conditioned medium induced more interleukin-6, interleukin-8, vascular endothelial growth factor, transforming growth factor-β1, heparin-bound epidermal growth factor, matrix metalloproteinase-1, and metalloproteinase-3 production in fibroblasts than the biofilm-conditioned medium. Biofilm-conditioned medium induced more tumor necrosis factor-α production in fibroblasts compared with planktonic-conditioned medium, and suppressed metalloproteinase-3 production compared with controls.
    Wound Repair and Regeneration 01/2012; 20(2):253-61. · 2.76 Impact Factor
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    ABSTRACT: [This corrects the article on p. e40973 in vol. 7.].
    PLoS ONE 01/2012; 7(10). · 3.53 Impact Factor
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    ABSTRACT: Recently a new polyomavirus was identified in a patient with trichodysplasia spinulosa (TS), a rare follicular skin disease of immunocompromised patients characterized by facial spines and overgrowth of inner root sheath cells. Seroepidemiological studies indicate that TSPyV is ubiquitous and latently infects 70% of the healthy individuals. To corroborate the relationship between active TSPyV infection and TS disease by analyzing the presence, load, and precise localization of TSPyV infection in TS patients and in controls. TS lesional and non-lesional skin samples were retrieved from TS patients through a PubMed search. Samples were analyzed for the presence and load of TSPyV DNA with quantitative PCR, and for expression and localization of viral protein with immunofluorescence. Findings obtained in TS patients (n=11) were compared to those obtained in healthy controls (n=249). TSPyV DNA detection was significantly associated with disease (P<0.001), with 100% positivity of the lesional and 2% of the control samples. Quantification revealed high TSPyV DNA loads in the lesional samples (∼10(6)copies/cell), and low viral loads in the occasionally TSPyV-positive non-lesional and control samples (<10(2)copies/cell). TSPyV VP1 protein expression was detected only in lesional TS samples, restricted to the nuclei of inner root sheath cells over-expressing trichohyalin. The high prevalence and load of TSPyV DNA only in TS lesions, and the abundant expression of TSPyV protein in the affected hair follicle cells demonstrate a tight relation between TSPyV infection and TS disease, and indicate involvement of active TSPyV infection in TS pathogenesis.
    Journal of clinical virology: the official publication of the Pan American Society for Clinical Virology 12/2011; 53(3):225-30. · 3.12 Impact Factor
  • Iwei Yeh, Evan George, Philip Fleckman
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    ABSTRACT: We present a case of hidradenitis occurring in a patient after chemotherapy for acute myeloid leukemia (AML) in the setting of profound neutropenia. Neutrophilic eccrine hidradenitis (NEH) presents as tender erythematous papules and plaques and is often associated with chemotherapy for AML. NEH is postulated to be due to toxic injury to the sweat glands followed by neutrophilic inflammation. Alternatively, some hypothesize that NEH represents a primary neutrophilic process. Our patient's clinical presentation was similar to previously reported cases of NEH; however, degenerative changes of the sweat ducts were noted on microscopy without neutrophilic inflammation. She had fewer than 0.01 thousand neutrophils per microliter for 4 days preceding the biopsy. At the same time, a separate area of superficial skin infection developed because of Staphylococcus epidermidis and also lacked neutrophilic inflammation. The similar clinical course and shared histopathologic features between our case and NEH argue that neutrophils are a secondary response to a toxic effect rather than the primary effector in NEH. Neutrophil-poor variants of hidradenitis, both infectious and due to drug toxicity, should be considered diagnostically in neutropenic patients.
    Journal of Cutaneous Pathology 11/2011; 38(11):905-10. · 1.77 Impact Factor
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    ABSTRACT: Many chronic diseases, such as non-healing wounds are characterized by prolonged inflammation and respond poorly to conventional treatment. Bacterial biofilms are a major impediment to wound healing. Persistent infection of the skin allows the formation of complex bacterial communities termed biofilm. Bacteria living in biofilms are phenotypically distinct from their planktonic counterparts and are orders of magnitude more resistant to antibiotics, host immune response, and environmental stress. Staphylococcus aureus is prevalent in cutaneous infections such as chronic wounds and is an important human pathogen. The impact of S. aureus soluble products in biofilm-conditioned medium (BCM) or in planktonic-conditioned medium (PCM) on human keratinocytes was investigated. Proteomic analysis of BCM and PCM revealed differential protein compositions with PCM containing several enzymes involved in glycolysis. Global gene expression of keratinocytes exposed to biofilm and planktonic S. aureus was analyzed after four hours of exposure. Gene ontology terms associated with responses to bacteria, inflammation, apoptosis, chemotaxis, and signal transduction were enriched in BCM treated keratinocytes. Several transcripts encoding cytokines were also upregulated by BCM after four hours. ELISA analysis of cytokines confirmed microarray results at four hours and revealed that after 24 hours of exposure, S. aureus biofilm induced sustained low level cytokine production compared to near exponential increases of cytokines in planktonic treated keratinocytes. The reduction in cytokines produced by keratinocytes exposed to biofilm was accompanied by suppressed phosphorylation of MAPKs. Chemical inhibition of MAPKs did not drastically reduce cytokine production in BCM-treated keratinocytes suggesting that the majority of cytokine production is mediated through MAPK-independent mechanisms. Collectively the results indicate that S. aureus biofilms induce a distinct inflammatory response compared to their planktonic counterparts. The differential gene expression and production of inflammatory cytokines by biofilm and planktonic cultures in keratinocytes could have implications for the formation and persistence of chronic wounds. The formation of a biofilm should be considered in any study investigating host response to bacteria.
    BMC Microbiology 06/2011; 11:143. · 3.10 Impact Factor
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    ABSTRACT: The sinus between skin and a percutaneous medical device is often a portal for infection. Epidermal integration into an optimized porous biomaterial could seal this sinus. In this study, we measured epithelial ingrowth into rods of sphere-templated porous poly(2-hydroxyethyl methacrylate) implanted percutaneously in mice. The rods contained spherical 20-, 40-, or 60-μm pores with and without surface modification. Epithelial migration was measured 3, 7, and 14 days post-implantation utilizing immunohistochemistry for pankeratins and image analysis. Our global results showed average keratinocyte migration distances of 81 ± 16.85 μm (SD). Migration was shorter through 20-μm pores (69.32 ± 21.73) compared with 40 and 60 μm (87.04 ± 13.38 μm and 86.63 ± 8.31 μm, respectively). Migration was unaffected by 1,1' carbonyldiimidazole surface modification without considering factors of pore size and healing duration. Epithelial integration occurred quickly showing an average migration distance of 74.13 ± 12.54 μm after 3 days without significant progression over time. These data show that the epidermis closes the sinus within 3 days, migrates into the biomaterial (an average of 11% of total rod diameter), and stops. This process forms an integrated epithelial collar without evidence of marsupialization or permigration.
    Journal of Biomedical Materials Research Part A 06/2011; 98(4):499-508. · 2.83 Impact Factor
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    ABSTRACT: Although it is widely accepted that filaggrin (FLG) deficiency contributes to an abnormal barrier function in ichthyosis vulgaris and atopic dermatitis, the pathomechanism of how FLG deficiency provokes a barrier abnormality in humans is unknown. We report here that the presence of FLG mutations in Caucasians predicts dose-dependent alterations in epidermal permeability barrier function. Although FLG is an intracellular protein, the barrier abnormality occurred solely via a paracellular route in affected stratum corneum. Abnormal barrier function correlated with alterations in keratin filament organization (perinuclear retraction), impaired loading of lamellar body contents, followed by nonuniform extracellular distribution of secreted organelle contents, and abnormalities in lamellar bilayer architecture. In addition, we observed reductions in corneodesmosome density and tight junction protein expression. Thus, FLG deficiency provokes alterations in keratinocyte architecture that influence epidermal functions localizing to the extracellular matrix. These results clarify how FLG mutations impair epidermal permeability barrier function.
    American Journal Of Pathology 05/2011; 178(5):2252-63. · 4.60 Impact Factor
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    ABSTRACT: To assess the clinical outcomes of 45 cases of harlequin ichthyosis and review the underlying ABCA12 gene mutations in these patients. Multicenter, retrospective, questionnaire-based survey. Dermatology research institute. Patients with harlequin ichthyosis for whom we had performed ABCA12 mutation analysis. Referring physicians were asked to complete a questionnaire using the patients' notes, detailing the clinical outcome of the affected child. In each case, the causative ABCA12 mutation was identified using standard polymerase chain reaction and sequencing techniques. Of the 45 cases, the ages of the survivors ranged from 10 months to 25 years, with an overall survival rate of 56%. Death usually occurred in the first 3 months and was attributed to sepsis and/or respiratory failure in 75% of cases. The early introduction of oral retinoids may improve survival, since 83% of those treated survived, whereas 76% who were not given retinoids died. Recurrent skin infections in infancy affected one-third of patients. Problems maintaining weight affected 44%. Three children developed an inflammatory arthritis, and developmental delay was reported in 32%. Mutation analysis revealed that 52% of survivors had compound heterozygous mutations, whereas all deaths were associated with homozygous mutations. Harlequin ichthyosis should be regarded as a severe chronic disease that is not invariably fatal. With improved neonatal care and probably the early introduction of oral retinoids, the number of survivors is increasing. Compound heterozygotes appear to have a survival advantage.
    Archives of dermatology 02/2011; 147(6):681-6. · 4.76 Impact Factor
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    ABSTRACT: In normal mammalian epidermis, cell division occurs primarily in the basal layer where cells are attached to the basement membrane. Upon release from the basement membrane, these basal cells stop dividing and begin to differentiate and stratify producing cornified cells expressing differentiation markers, including the keratin bundling protein filaggrin, and cornified envelope proteins. Little is understood about the regulatory mechanisms of these processes. A rat epidermal keratinocyte cell line synthesizing and processing profilaggrin at confluence in a synchronous manner for 4-5 days provides a useful culture model for epidermal differentiation. Profilaggrin expression in this cell line however decreases with passaging, and its processing involves extensive nonspecific proteolysis. Our objective was to identify culture conditions that effect the decrease in profilaggrin expression with passaging and nonspecific proteolysis of profilaggrin in order to study epidermal differentiation more closely. The large amount of nonspecific proteolysis suggested autophagocytosis. To test this, cells were cultured in the presence of 3-methyladenine (3-MA). Two known gradients in epidermis are decreasing serum components and increasing calcium concentrations in the upper cell layers. To determine whether these gradients effected processing, cells were cultured in serum/DMEM or in serum-free KGM and under varying external calcium concentrations. Cells were also cultured in presence of aminoguanidine in an attempt to maintain profilaggrin expression with passaging. Profilaggrin expression was enhanced in the presence of 3-MA, with optimum around 6mM. In the absence of aminoguanidine, profilaggrin expression decreased as a function of increasing passage number; in its presence, profilaggrin expression remained high in some, but not in all of the independently maintained cell lines. Thus, culturing in aminoguanidine was necessary, but not sufficient, for sustained ability to express profilaggrin at confluence. Production of filaggrin from profilaggrin was maximized in a serum-free medium with [Ca(2+)] at 5mM. Filaggrin associates with phospholipid vesicles in vitro forming aggregates similar to those seen in vivo, suggesting that filaggrin release induces vesicular aggregation and autophagocytosis. We have used a keratinocyte cell line that synthesizes and processes profilaggrin after confluence as a culture model to study epidermal differentiation. In this system profilaggrin processing must be preceded by inhibition of autophagosome formation and/or modulation of vesicular trafficking, and these processes are regulated by epidermal calcium and serum factor gradients.
    Journal of dermatological science 01/2011; 61(1):51-9. · 3.71 Impact Factor
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    ABSTRACT: Inherited ichthyoses belong to a large, clinically and etiologically heterogeneous group of mendelian disorders of cornification, typically involving the entire integument. Over the recent years, much progress has been made defining their molecular causes. However, there is no internationally accepted classification and terminology. We sought to establish a consensus for the nomenclature and classification of inherited ichthyoses. The classification project started at the First World Conference on Ichthyosis in 2007. A large international network of expert clinicians, skin pathologists, and geneticists entertained an interactive dialogue over 2 years, eventually leading to the First Ichthyosis Consensus Conference held in Sorèze, France, on January 23 and 24, 2009, where subcommittees on different issues proposed terminology that was debated until consensus was reached. It was agreed that currently the nosology should remain clinically based. "Syndromic" versus "nonsyndromic" forms provide a useful major subdivision. Several clinical terms and controversial disease names have been redefined: eg, the group caused by keratin mutations is referred to by the umbrella term, "keratinopathic ichthyosis"-under which are included epidermolytic ichthyosis, superficial epidermolytic ichthyosis, and ichthyosis Curth-Macklin. "Autosomal recessive congenital ichthyosis" is proposed as an umbrella term for the harlequin ichthyosis, lamellar ichthyosis, and the congenital ichthyosiform erythroderma group. As more becomes known about these diseases in the future, modifications will be needed. We have achieved an international consensus for the classification of inherited ichthyosis that should be useful for all clinicians and can serve as reference point for future research.
    Journal of the American Academy of Dermatology 10/2010; 63(4):607-41. · 4.91 Impact Factor

Publication Stats

4k Citations
506.82 Total Impact Points

Institutions

  • 2013
    • Trinity Washington University
      Washington, Washington, D.C., United States
  • 1984–2013
    • University of Washington Seattle
      • • Division of Dermatology
      • • Department of Biochemistry
      Seattle, Washington, United States
  • 2009–2012
    • Montana State University
      • Center for Biofilm Engineering
      Bozeman, MT, United States
    • Trinity College Dublin
      • Institute of Molecular Medicine
      Dublin, L, Ireland
  • 2011
    • University of California, San Francisco
      • Department of Dermatology
      San Francisco, CA, United States
    • University of Colorado at Boulder
      • Department of Chemistry and Biochemistry
      Boulder, CO, United States
  • 2006
    • University of Dundee
      Dundee, Scotland, United Kingdom
  • 2005
    • Seattle University
      Seattle, Washington, United States
    • Radboud University Nijmegen
      • Department of Dermatology
      Nijmegen, Provincie Gelderland, Netherlands
  • 1997
    • Wayne State University
      Detroit, Michigan, United States
  • 1988–1990
    • University of Utah
      • Department of Internal Medicine
      Salt Lake City, UT, United States