scholarly journals Epidermolytic Hyperkeratosis

2020 ◽  
Author(s):  
Keyword(s):  
Epidermolytic Hyperkeratosis

Localized epidermolytic hyperkeratosis. A form of keratoderma of the palms and soles

1970 ◽  
Vol 101 (3) ◽  
pp. 272-275 ◽  
Author(s):  
S. Klaus
Keyword(s):  
Epidermolytic Hyperkeratosis

Familial Congenital Epidermolytic Hyperkeratosis Confined to the Palms and Soles

1974 ◽  
Vol 67 (9) ◽  
pp. 1126-1131 ◽  
Author(s):  
MAJ DETLEF K. GOETTE
Keyword(s):  
Epidermolytic Hyperkeratosis

Congenital epidermolytic hyperkeratosis associated with multiple malignancies

1989 ◽  
Vol 120 (1) ◽  
pp. 141-144 ◽  
Author(s):  
J.M. Edwards ◽  
M.A.C.S. Cooper ◽  
S. Bannerjee
Keyword(s):  
Multiple Malignancies ◽  
Epidermolytic Hyperkeratosis

scholarly journals Epidermolytic hyperkeratosis: clinical update

2019 ◽  
Vol Volume 12 ◽  
pp. 333-344 ◽  
Author(s):  
Denice Peter Rout ◽  
Anushka Nair ◽  
Anand Gupta ◽  
Piyush Kumar
Keyword(s):  
Epidermolytic Hyperkeratosis

scholarly journals Epidermolytic Hyperkeratosis: Ultrastructure and Biochemistry of Skin and Amniotic Fluid Cells from Two Affected Fetuses and a Newborn Infant

1983 ◽  
Vol 80 (4) ◽  
pp. 222-227 ◽  
Author(s):  
Karen A. Holbrook ◽  
Beverly A. Dale ◽  
Virginia P. Sybert ◽  
Richard W. Sagebiel
Keyword(s):  
Amniotic Fluid ◽  
Newborn Infant ◽  
Epidermolytic Hyperkeratosis ◽  
Amniotic Fluid Cells

Epidermolytic Hyperkeratosis Associated With Melanocytic Nevi

2002 ◽  
Vol 24 (1) ◽  
pp. 23-25 ◽  
Author(s):  
Phillip A. Conlin ◽  
Ronald P. Rapini
Keyword(s):  
Melanocytic Nevi ◽  
Epidermolytic Hyperkeratosis

scholarly journals Ichthyosis (concept, pathohistology, clinical picture, treatment)

2021 ◽  
Vol 97 (3) ◽  
pp. 6-13
Author(s):  
Tatyana Gennadyevna Takhtarova ◽  
Zarema Rimovna Khismatullina ◽  
Lyudmila Dmitrievna Panova ◽  
Anastasia Nikolaevna Panova
Keyword(s):  
Clinical Picture ◽  
Specific Treatment ◽  
Electron Microscopic Examination ◽  
Allergic Diseases ◽  
Electron Microscopic ◽  
Lamellar Ichthyosis ◽  
Congenital Ichthyosis ◽  
Age Related ◽  
Epidermolytic Hyperkeratosis ◽  
Definition Of

Ichthyosis is a skin disease that is hereditary, has pronounced symptoms in the form of a violation of the skin, and the presence of formations resembling fish scales. It is possible to distinguish different approaches to the definition of ichthyosis, based on the modern study of this issue. Ichthyosis is classified by type: congenital and acquired. Congenital ichthyosis has its own classification depending on the manifestation of changes in the skin, the course of the disease, concomitant pathologies. Congenital ichthyosis is divided into ordinary (vulgar autosomal dominant, simple) ichthyosis, lamellar ichthyosis (dry ichthyosiform erythroderma, "collodion child", lamellar ichthyosis), X-linked ichthyosis (ichthyosis associated with the X chromosome, blackening ichthyosis), congenital bullous ichthyosiform erythroderma (erythroderma Broca's disease, ichthyosiform epidermolytic hyperkeratosis), fetal ichthyosis (intrauterine ichthyosis, universal hyperkeratosis, "Harlequin fetus", congenital keratosis), other congenital ichthyosis. Ichthyosiform conditions (the so-called acquired ichthyosis) are divided into symptomatic, age-related (senile), discoid ichthyosis. The causes of acquired ichthyosis can be various diseases, taking medications, improper skin care, unbalanced nutrition. Each form of ichthyosis differs by the type of inheritance, prevalence in the population, clinical picture, verified by histological examination of skin biopsies and electron microscopic examination of the skin. It may be accompanied by seasonality of exacerbation of the clinical picture, association with other diseases (allergic, diseases of the gastrointestinal tract, congenital malformations). There is no specific treatment for ichthyosis. In systemic therapy, derivatives of vitamin A are used, keratolytics, as well as moisturizing and emollient agents are used for external treatment. The use of therapeutic baths, general ultraviolet irradiation is effective.

Epidermolytic hyperkeratosis (bullous ichthyosis)

2000 ◽  
Vol 14 (4) ◽  
pp. 324-325 ◽  
Author(s):  
Ml Khatri ◽  
M Shafi ◽  
M Ben-Ghazeil
Keyword(s):  
Epidermolytic Hyperkeratosis

Epidermolytic hyperkeratosis

2004 ◽  
pp. 214-214
Keyword(s):  
Epidermolytic Hyperkeratosis

Mutations in the non-helical linker segment L1-2 of keratin 5 in patients with Weber-Cockayne epidermolysis bullosa simplex

1994 ◽  
Vol 107 (4) ◽  
pp. 765-774
Author(s):  
Y.M. Chan ◽  
Q.C. Yu ◽  
J. LeBlanc-Straceski ◽  
A. Christiano ◽  
L. Pulkkinen ◽  
...  
Keyword(s):  
Epidermolysis Bullosa ◽  
Intermediate Filament ◽  
Point Mutations ◽  
Epidermolysis Bullosa Simplex ◽  
Keratin Gene ◽  
Filament Assembly ◽  
Keratin Polypeptides ◽  
Epidermolytic Hyperkeratosis ◽  
Hands And Feet ◽  
Linker Segment

Keratins are the major structural proteins of the epidermis. Analyzing keratin gene sequences, appreciating the switch in keratin gene expression that takes place as epidermal cells commit to terminally differentiate, and elucidating how keratins assemble into 10 nm filaments, have provided the foundation that has led to the discoveries of the genetic bases of two major classes of human skin diseases, epidermolysis bullosa simplex (EBS) and epidermolytic hyperkeratosis (EH). These diseases involve point mutations in either the basal epidermal keratin pair, K5 and K14 (EBS), or the suprabasal pair, K1 and K10 (EH). In severe cases of EBS and EH, mutations are found in the highly conserved ends of the alpha-helical rod domain, regions that, by random mutagenesis, had already been found to be important for 10 nm filament assembly. In order to identify regions of the keratin polypeptides that might be more subtly involved in 10 nm filament assembly and to explore the diversity in mutations within milder cases of these diseases, we have focused on Weber-Cockayne EBS, where mild blistering occurs primarily on the hands and feet in response to mechanical stress. In this report, we show that affected members of two different W-C EBS families have point mutations within 1 residue of each other in the non-helical linker segment of the K5 polypeptide. Genetic linkage analyses, the absence of this mutation in > 150 wild-type alleles and filament assembly studies suggest that these mutations are responsible for the W-C EBS phenotype. These findings provide the best evidence to date that the non-helical linker region in the middle of the keratin polypeptides plays a subtle but significant role in intermediate filament structure and/or intermediate filament cytoskeletal architecture.

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