Relevant bibliographies by topics / Keratoderma palmoplantar

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Keratoderma palmoplantar'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "Keratoderma palmoplantar"

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Dessureault, Josee, Yves Poulin, Marc Bourcier, and Eric Gagne. "Olmsted Syndrome—Palmoplantar and Periorificial Keratodermas: Association with Malignant Melanoma." Journal of Cutaneous Medicine and Surgery 7, no. 3 (2003): 236–42. http://dx.doi.org/10.1177/120347540300700309.

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Background: Olmsted syndrome is a rare congenital disorder with mutilating palmoplantar keratoderma, periorificial keratotic plaques, and other variable features. Objective: We describe a 65-year-old woman with Olmsted syndrome complicated by the occurrence of a malignant melanoma inside the plantar keratoderma. To our knowledge, this is the first reported case of such an occurrence in Olmsted syndrome. The published cases of this rare disorder are reviewed. Conclusion: An association between malignant epithelial tumors and Olmsted syndrome has already been reported. The association of malignant melanoma with other types of palmoplantar keratodermas has been reported. This may suggest a predisposition to melanocytic as well as squamous cell malignancies in congenital keratodermas. Oral retinoids appear to be the most promising treatment for Olmsted syndrome and for other symptomatic keratodermas.
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Bhansali, Ashok, Setu Mathur, Gunjan Bhansali, and Anuroopa Kishan. "Palmoplantar Keratoderma with Periodontitis." Journal of Health Sciences & Research 8, no. 2 (2017): 89–92. http://dx.doi.org/10.5005/jp-journals-10042-1057.

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ABSTRACT Palmoplantar keratodermas (PPKs) comprise a heterogeneous group of keratinization disorders with hyperkeratotic thickening of palms and soles. The PPKs are distinguished by their mode of inheritance and by the presence of certain associated clinical features. Periodontitis was reported in association with more than one syndrome characterized by PPK. Knowledge about heterogeneous groups of acquired or hereditary PPK is important, leading to an appropriate diagnosis and corrective therapies in the future. This case report aims at critically reviewing the literature concerned with PPK and its clinical presentation, in addition to other syndromes manifested along with periodontitis. How to cite this article Bhansali A, Kishan A, Mathur S, Bhansali G. Palmoplantar Keratoderma with Periodontitis. J Health Sci Res 2017;8(2):89-92.
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OʼConnor, Elizabeth A., and William W. Dzwierzynski. "Palmoplantar Keratoderma." Annals of Plastic Surgery 67, no. 4 (2011): 439–41. http://dx.doi.org/10.1097/sap.0b013e3182085a8b.

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Lestre, Sara, Eva Lozano, Cláudia Meireles, and Ana Barata Feio. "Autoimmune Thyroiditis Presenting as Palmoplantar Keratoderma." Case Reports in Medicine 2010 (2010): 1–3. http://dx.doi.org/10.1155/2010/604890.

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Palmoplantar keratoderma is a heterogeneous group of hereditary and acquired disorders characterized by abnormal thickening of palms and soles. Hypothyroidism is an unusual cause of palmoplantar keratoderma, rarely reported in the literature. We report a case of a 43-year-old woman presented with a 3-month history of a diffuse palmoplantar hyperkeratosis unresponsive to topical keratolytics and corticosteroids. Her past medical and family histories were unremarkable. She complained of recent asthenia, mood changes and constipation. Laboratory evaluation revealed an autoimmune thyroiditis with hypothyroidism. Other causes of acquired palmoplantar keratoderma were excluded. After hormonal replacement therapy institution, a gradual improvement of skin condition was observed. The diagnosis of underlying causes for acquired palmoplantar keratoderma can be a difficult task; however its recognition is essential for successful treatment results. Although a very rare association, hypothyroidism must be suspected in patients with acquired palmoplantar keratoderma, particularly when it occurs in association with systemic symptoms.
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USUKI, Kazunari. "Aquagenic Palmoplantar Keratoderma." Nishi Nihon Hifuka 65, no. 5 (2003): 443–45. http://dx.doi.org/10.2336/nishinihonhifu.65.443.

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KAWAI, Kazuhiro, Tomoko FUKUSHIGE, Masanao SAKANOUE, and Takuro KANEKURA. "Striate palmoplantar keratoderma." Journal of Dermatology 37, no. 9 (2010): 854–56. http://dx.doi.org/10.1111/j.1346-8138.2010.00874.x.

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Yan, Albert C., Sumaira Z. Aasi, William J. Alms, et al. "Aquagenic palmoplantar keratoderma." Journal of the American Academy of Dermatology 44, no. 4 (2001): 696–99. http://dx.doi.org/10.1067/mjd.2001.113479.

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Patel, Shaily, Matthew Zirwas, and Joseph C. English. "Acquired Palmoplantar Keratoderma." American Journal of Clinical Dermatology 8, no. 1 (2007): 1–11. http://dx.doi.org/10.2165/00128071-200708010-00001.

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Imbernón-Moya, A., A. Aguilar-Martínez, and E. Vargas-Laguna. "Linear Palmoplantar Keratoderma." Actas Dermo-Sifiliográficas (English Edition) 109, no. 3 (2018): 269. http://dx.doi.org/10.1016/j.adengl.2018.02.014.

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Bukhari, Rahaf, Waseem Alhawsawi, Aisha Ahmad Radin, Hawazin D. Jan, Khalid Al Hawsawi, and Marwan Al Ahmadi. "Punctate Palmoplantar Keratoderma: A Case Report of Type 1 (Buschke-Fischer-Brauer Disease)." Case Reports in Dermatology 11, no. 3 (2019): 292–96. http://dx.doi.org/10.1159/000503337.

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Punctate palmoplantar keratoderma is a rare hereditary palmoplantar keratoderma. Herein we report a 59-year-old male, otherwise healthy, who presented with a 25-year history of asymptomatic persistent slowly progressing skin lesions on both hands. The parents are non-consanguineous and none of his family members had similar lesions. Skin examination revealed multiple tiny keratotic pits on both palms. Punch skin biopsy from the palmar lesion revealed epidermal depression with an overlying column of compact orthokeratosis. Based on the above clinicopathological findings, a diagnosis of punctate palmoplantar keratoderma type 1 was made. The patient was started on 40% urea and 20% salicylic acid ointment for months but with little improvement.
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Dissertations / Theses on the topic "Keratoderma palmoplantar"

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Ratnavel, Ravi C. "The molecular basis of inherited palmoplantar keratoderma." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361890.

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Armstrong, Dermot Keith Brown. "A clinical and molecular genetic study of hereditary striate palmoplantar keratoderma and vohwinkel's keratoderma." Thesis, Queen's University Belfast, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287204.

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Preus, Hans R. "Actinobacillus actinomycetemcomitans in rapidly destructive periodontitis of Papillon-Lèfevre syndrome." Oslo, Norway : Dept. of Periodontology and Microbiology, Dental Faculty, University of Oslo, 1989. http://books.google.com/books?id=LwJqAAAAMAAJ.

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Gedicke, Malenka Mona. "Loricrin-Keratoderma." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2006. http://dx.doi.org/10.18452/15442.

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Thema dieser Arbeit war die klinische sowie molekulargenetische Analyse einer Familie mit der Verdachtsdiagnose autosomal dominante lamelläre Ichthyose (ADLI). Mit direkter Sequenzierung des Loricrin-Gens (LOR) wurde die Mutation 730insG identifiziert und die Diagnose Loricrin-Keratoderma gestellt. Durch Analyse weiterer Patienten wurde gezeigt, dass ADLI keine Loricrin-Keratoderma darstellt. Nach eingehender klinischer Untersuchung und Literaturanalyse konnten für die hier beschriebene Entität folgende Merkmale definiert werden: Als Hauptmerkmale eine honigwabenförmige Palmoplantarkeratose sowie eine leichte Ichthyose, als Nebenmerkmale Pseudoainhums, Autoamputationen, Kollodiumbaby, prominente Fingerknöchel sowie Hyperkeratosen an Knien und Ellenbögen. Die genetisch als Loricrin-Keratoderma charakterisierte Verhornungsstörung in der beschriebenen Familie sollte nunmehr klinisch als honigwabenförmige Palmoplantarkeratose mit Ichthyose bezeichnet werden. Zur Standarddiagnostik von Loricrin-Keratoderma wurde die direkte Sequenzierung von LOR auf DNA-Basis etabliert. Die Mutation 730insG resultiert in einer neuen argininreichen Domäne und einer Verlängerung des Proteins um 22 Aminosäuren. Eine Expressionsanalyse mittels Pyrosequenzierung zeigte eine gleichwertige Expression des mutierten und des Wildtyp-Allels. Dies unterstützt die „gain-of-function“-Theorie für das veränderte Loricrin und stützt die Aussage des für Loricrin-Keratoderma existierenden transgenen Mausmodells.<br>The main focus of this thesis was the clinical and genetic analysis of a family referred to us with the diagnosis of autosomal dominant lamellar ichthyosis (ADLI). Through direct sequencing of the loricrin gene (LOR) the mutation 730insG was identified and the family was diagnosed as having loricrin keratoderma. By sequencing further patients it was shown that ADLI is not a loricrin keratoderma. Based on refined clinical examination and analysis of the literature the following criteria could be defined for the entity seen: Compulsory features are honeycomb-like palmoplantar keratoderma and ichthyosis, optional features are pseudoainhums, autoamputations, collodion baby, prominent knuckle pads as well as hyperkeratotic lesions on knees and elbows. Therefore the disorder of keratinisation of the family described here genetically characterised as loricrin keratoderma should be clinically termed “honeycomb-like palmoplantar keradoderma with ichthyosis”. To molecularly diagnose loricrin keratoderma direct sequencing of LOR with DNA samples was established. The mutation 730insG results in a new arginine rich domain and an elongation of the protein by 22 residues. Expression analysis showed an equal expression of mutant and wild-type allele. This underlined the “gain-of-function” theory of the modified loricrin and supported the findings in the transgenic mouse model for loricrin keratoderma.
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Kobayashi, Setsu. "Keratin9 point mutation in the pedigree of epidermolytic hereditary palmoplantar keratoderma perturbs keratin intermediate filament network formation." Kyoto University, 1998. http://hdl.handle.net/2433/182271.

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Dedeić, Zinaida. "Investigating the role of iASPP in cutaneous disorders." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:9d393f2d-1e85-46fe-a751-427a0faa23f4.

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Desmosomes are intercellular junctions that anchor intermediate filaments to the sites of intercellular contacts. They are critical for maintaining the integrity of tissues that experience constant mechanical and structural stresses, like the skin and heart. Perturbation of desmosomal adhesion can lead to devastating epidermal and myocardial diseases. However, little is known about the regulators of desmosomes and the role of desmosomes in cell signalling events. Recent work has suggested that iASPP, an inhibitor of the p53 family of proteins, localises at the intercalated discs where desmosomes reside. However, its role at the desmosomes has remained elusive. Thus, in this thesis, it was investigated whether iASPP is a dual function protein that links desmosome adhesion to gene expression and if desmosome-related diseases develop in the absence of iASPP. iASPP was found to be a novel regulator of desmosomes, co-localising with them by physically interacting with the desmosomal components desmoplakin and K5 intermediate filaments. Loss of iASPP resulted in increased phosphorylation and solubilisation of desmoplakin, leading to the formation of K5 aggregates. This culminated in disrupted intercellular adhesion and enhanced cellular migration. Consistent with the role of iASPP in the maintenance of desmosomal adhesion integrity, focal palmoplantar keratoderma was observed in iASPP-deficient mice — a disorder often associated with desmosome dysfunction. This was accompanied by disrupted intracellular signalling, as exemplified by the disrupted expression of differentiation markers; an increase in the thickness of cell layers expressing differentiation marker K1 was noted, and K5 and K6 cells were ectopically expressed throughout the diseased palmoplantar epidermis. Impaired intercellular adhesion and migration had consequences for wound healing, as iASPP-deficient mice exhibited delayed wound closure. Furthermore, defects in eyelid closure in iASPP-deficient mice were found to be due to increased apoptosis. The localisation of apoptotic cells at the leading edge of the eyelid epidermis implied that apoptosis might have occurred due to a loss of cell-matrix or cell-cell contact, i.e. anoikis. Taken together, these results suggest that iASPP is involved in pathological (palmoplantar keratoderma), physiological (wound healing) and developmental processes (embryonic eyelid closure) through its regulation of desmosomes and their dynamics. Therefore, iASPP represents a new candidate gene in cutaneous disorders and could be implicated in a variety of epidermal and myocardial diseases.
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SEGAULT, LAGARDE DOMINIQUE. "Pheochromocytome et keratodermie palmo-plantaire." Saint-Etienne, 1991. http://www.theses.fr/1991STET6412.

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Stevens, Howard Peter. "Clinical, genetic and cellular studies in the palmoplantar keratodermas, monilethrix and sensorineural deafness." Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300177.

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Zamiri, Mozheh. "Towards a comprehensive resource for elucidating the pathogenesis of inherited keratodermas." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4829.

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Keratoderma – pathological hyperkeratosis of palms and soles - is a cause of disability in many clinical situations, including the rare and heterogeneous group of inherited palmoplantar keratodermas (PPKs). The aim of this study was to work towards better understanding of molecular mechanisms active in the pathogenesis of PPK by the creation of a cell and tissue culture resource and its initial application to laboratory studies. My study was based on a diverse group of autosomal dominant disorders, previously ascertained in families from Scotland, in whom the precise genetic aetiology was known. I established a tissue and cell culture resource of inherited keratodermas of known single-gene aetiology from patients with proven keratin 1, 9, 17, loricrin and mitochondrial mutations. An additional pedigree with striate keratoderma with an unknown mutation was recruited, and the causative mutation identified as a novel heterozygous A-to-T transversion in exon 5 (c.430A>T) of the desmoglein 1 gene, converting an arginine residue to a premature termination codon (p. Arg144stop). The keratinocyte culture resource was established from patients with keratin 1, 9, 17 and loricrin mutations, as well as controls. Due to the pain associated with direct infiltration of plantar skin, biopsies were obtained using peripheral nerve block for plantar biopsy. The effectiveness of this approach, which may be useful for future administration of treatment, was made the subject of an open clinical trial. Histological and immunocytochemical studies were carried out on affected plantar skin obtained from PPK patients and compared to control tissue, in an attempt to identify common and distinct pathways resulting in hyperkeratosis. Histological changes, e.g. hypergranulosis, extent of hyperkeratosis, acanthosis or acantholysis, were not uniform across different subtypes of inherited PPK and varied even between individuals within subtypes. Prominent eosin staining of spinous cells was a common feature in inherited PPK due to underlying K1 and K17 mutations. Electron microscopy showed abnormal keratin filaments in PPK with underlying keratin mutations only but was not a uniform finding within subtypes, and other electron microscopic features also varied between individuals. Immunocytochemical study did not demonstrate significant differences in expression of a selection of markers of differentiation (keratins 1, 9, 14 and 17), and cornified envelope protein filaggrin. Abnormal involucrin expression was observed, with premature expression in basal and lower spinous layers in all PPK subtypes raising the possibility of a common underlying mechanism in the development of hyperkeratosis. Prominent loricrin staining was noted in areas of acantholysis in K1 and K9 subtypes, but was uniform across other subtypes. Markers of proliferation and apoptosis demonstrated no overt change in epidermal turnover, although it is possible that only small changes in proliferative index are required to produce plantar hyperkeratosis. Overall, using morphological criteria, plantar hyperkeratosis was not readily distinguishable between inherited PPK of different underlying genetic causes. This raises the possibility that many of the reported structural features of inherited PPK are secondary phenomena as opposed to critical steps in the pathogenesis of hyperkeratosis. Initial attempts at RNA extraction using laser and manual microdissection have to date been unsuccessful in generating RNA of the quality and concentration to run a pilot microarray experiment, using standard RNA extraction kits. Plans for future projects include the further development of a possible microarray experiment in the Pachyonychia Congenita type 2 pedigree with the McLean laboratory in Dundee. The tissue resource has been made available for collaborative study via the GENESKIN project, as well as through the McLean and Lane laboratories, Dundee for both functional studies and immortalisation of cell lines.
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PETRISSANS, MARIE-THERESE. "Place du traitement chirurgical dans la keratodermie mutilante de vohwinkel." Toulouse 3, 1992. http://www.theses.fr/1992TOU31120.

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Books on the topic "Keratoderma palmoplantar"

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Sybert, Virginia P. Disorders of The Epidermis: Differentiation and Kinetics. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780195397666.003.0002.

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Ichthyoses – Bullous Congenital Ichthyosiform Erythroderma – Continual Peeling Skin – Harlequin Fetus – Ichthyosis Bullosa of Siemens – Ichthyosis Hystrix – Ichthyosis Vulgaris – Lamellar Exfoliation of the Newborn – Lamellar Ichthyosis/Nonbullous Congenital Ichthyosiform Erythroderma – Netherton Syndrome – Restrictive Dermopathy – X-linked Recessive Ichthyosis – Erythrokeratodermas – Erythrokeratodermia Variabilis – Pityriasis Rubra Pilaris – Progressive Symmetric Erythrokeratoderma – Acrokeratoderma – Acrokeratoelastoidosis – Acrokeratosis Verruciformis (HOPF) – Hereditary Palmoplantar Keratodermas – Hereditary Palmoplantar Keratoderma with Deafness – Hereditary Palmoplantar Keratoderma Epidermolytic Hyperkeratosis – Hereditary Palmoplantar Keratoderma Howel-Evans – Hereditary Palmoplantar Keratoderma Olmsted – Hereditary Palmoplantar Keratoderma Punctate – Hereditary Palmoplantar Keratoderma Striata – Hereditary Palmoplantar Keratoderma Unna-Thost – Hereditary Palmoplantar Keratoderma Vohwinkel – Keratolytic Winter Erythema – Mal de Meleda – Papillon-Lefèvre – Scleroatrophic and Keratotic Dermatosis of the Limbs – Porokeratoses – Porokeratosis of Mibelli – Other Disorders of the Epidermis – Absence of Dermatoglyphics – Acanthosis Nigricans – Darier-White Disease – Hereditary Painful Callosities – Keratosis Follicularis Spinulosa Decalvans – Knuckle Pads – Kyrle/Flegel Disease – Ulerythema Ophryogenes – Syndromic Disorders – CHILD Syndrome – Chondrodysplasia Punctata – Ichthyosis with Hypogonadism – KID Syndrome – Neu-Laxova Syndrome – Neutral Lipid Storage Disease with Ichthyosis – Refsum Disease – Richner-Hanhart Syndrome – Sjögren-Larsson Syndrome – Cohesion – Epidermolysis Bullosa – Epidermolysis Bullosa Simplex Dowling-Meara – Epidermolysis Bullosa Simplex Generalized – Epidermolysis Bullosa Simplex Localized – Epidermolysis Bullosa Junctional Generalized – Epidermolysis Bullosa Junctional Generalized Atrophic Benign – Epidermolysis Bullosa Dystrophica Cockayne-Touraine – Epidermolysis Bullosa Dystrophica, Hallopeau-Siemens – Epidermolysis Bullosa Dystrophica Pretibial – Transient Bullous Dermolysis of the Newborn – Hailey-Hailey Disease
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Sybert, Virginia P. Disorders of the Epidermis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190276478.003.0002.

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Chapter 2 covers Ichthyoses (Bullous Congenital Ichthyosiform Erythroderma, Harlequin Ichthyosis, Ichthyosis Bullosa of Siemens, Ichthyosis Hystrix, Ichthyosis Vulgaris, Lamellar Exfoliation of the Newborn, Lamellar Ichthyosis/Nonbullous Congenital Ichthyosiform Erythroderma, Netherton Syndrome, Peeling Skin Syndrome, Restrictive Dermopathy, and X-linked Recessive Ichthyosis), Erythrokeratodermas (Erythrokeratodermia Variabilis ET PROGESSIVA, and Pityriasis Rubra Pilaris), Acrokeratoderma (Acrokeratoelastoidosis, Acrokeratosis Verruciformis (HOPF)), Hereditary Palmoplantar Keratodermas (Hereditary Palmoplantar Keratoderma with Deafness, Hereditary Palmoplantar Keratoderma Epidermolytic Hyperkeratosis, Hereditary Palmoplantar Keratoderma Howel-Evans, Hereditary Palmoplantar Keratoderma Olmsted, Hereditary Palmoplantar Keratoderma Punctate, Hereditary Palmoplantar Keratoderma Striata, Hereditary Palmoplantar Keratoderma Unna-Thost, Hereditary Palmoplantar Keratoderma Vohwinkel, Keratolytic Winter Erythema, Mal de Meleda, Papillon-Lefèvre, Scleroatrophic and Keratotic Dermatosis of the Limbs), Porokeratoses (Porokeratosis of Mibelli), Other Disorders of the Epidermis (Absence of Dermatoglyphics, Acanthosis Nigricans, Darier-White Disease, Hereditary Painful Callosities, Keratosis Follicularis Spinulosa Decalvans, Knuckle Pads, Kyrle/Flegel Disease, Ulerythema Ophryogenes), Syndromic Disorders (CHILD Syndrome, Chondrodysplasia Punctata, Ichthyosis with Hypogonadism, KID Syndrome, Neu-Laxova Syndrome, Neutral Lipid Storage Disease with Ichthyosis, Refsum Disease, Richner-Hanhart Syndrome, Sjögren-Larsson Syndrome), Cohesion (Epidermolysis Bullosa, Epidermolysis Bullosa Simplex Dowling-Meara, Epidermolysis Bullosa Simplex Generalized, Epidermolysis Bullosa Simplex Localized, Epidermolysis Bullosa Junctional Generalized, Epidermolysis Bullosa Junctional Generalized Atrophic Benign, Epidermolysis Bullosa Dystrophica Cockayne-Touraine, Epidermolysis Bullosa Dystrophica, Hallopeau-Siemens, Epidermolysis Bullosa Dystrophica Pretibial, Transient Bullous Dermolysis of the Newborn, Hailey-Hailey Disease). Each condition is discussed in detail, including dermatologic features, associated anomalies, histopathology, basic defect, treatment, mode of inheritance, prenatal diagnosis, and differential diagnosis.
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Book chapters on the topic "Keratoderma palmoplantar"

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, et al. "Palmoplantar Keratoderma." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9300.

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Shwayder, Tor, Samantha L. Schneider, Devika Icecreamwala, and Marla N. Jahnke. "Palmoplantar Keratoderma." In Longitudinal Observation of Pediatric Dermatology Patients. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98101-7_8.

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Inai, Kei, Alexander K. C. Leung, Jouni Uitto, et al. "Epidermolytic Palmoplantar Keratoderma." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6522.

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Chen, Harold. "Epidermolytic Palmoplantar Keratoderma." In Atlas of Genetic Diagnosis and Counseling. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-2401-1_82.

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Chen, Harold. "Epidermolytic Palmoplantar Keratoderma." In Atlas of Genetic Diagnosis and Counseling. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6430-3_82-2.

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, et al. "Palmoplantar Keratoderma Vörner-Unna-Thost." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1358.

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Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, et al. "Hypotrichosis-Osteolysis-Peridontitis-Palmoplantar Keratoderma Syndrome." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_913.

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El-Darouti, Mohammad Ali. "Guttate Hypopigmentation and Punctate Palmoplantar Keratoderma." In Challenging Cases in Dermatology. Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-4249-2_78.

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Lipsker, Dan. "Palmoplantar Keratodermas." In Clinical Examination and Differential Diagnosis of Skin Lesions. Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0411-8_38.

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Silverberg, Nanette B., and Nanette B. Silverberg. "Icthyoses and Palmoplantar Keratodermas." In Atlas of Pediatric Cutaneous Biodiversity. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3564-8_7.

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