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Artykuły w czasopismach na temat „Epidermolysis bullosa”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 9 marca 2023

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1

Almeida Jr, Hiram Larangeira de, Lísia Nudelmann, Nara Moreira Rocha i Luis Antonio Suita de Castro. "Light and transmission electron microscopy of generalized dystrophic epidermolysis bullosa (Pasini's albopapuloid subtype)". Anais Brasileiros de Dermatologia 87, nr 2 (kwiecień 2012): 285–87. http://dx.doi.org/10.1590/s0365-05962012000200014.

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Pasini's albopapuloid epidermolysis bullosa is a very rare subtype of generalized dystrophic dominant epidermolyis bullosa. A 30 year-old white female patient presented since her childhood disseminated small blisters and papules. Light microscopy of a blister showed dermal-epidermal cleavage; moreover, focal areas of dermal-epidermal splitting were also observed. Transmission electron microscopy also identified focal areas of cleavage, which were seen below the lamina densa. It is important to recognize this condition as a variant of epidermolysis bullosa, since the most important cutaneous findings are generalized papules and not blisters and erosions as in other forms of epidermolysis bullosa.

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2

Gardner, Kerry M., i Richard I. Crawford. "Distinguishing Epidermolysis Bullosa Acquisita From Bullous Pemphigoid Without Direct Immunofluorescence". Journal of Cutaneous Medicine and Surgery 22, nr 1 (18.07.2017): 22–24. http://dx.doi.org/10.1177/1203475417722734.

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Background: It has been postulated that periodic acid–Schiff staining of basement membrane can predict direct immunofluorescence patterns seen in epidermolysis bullosa acquisita and bullous pemphigoid. It has also been suggested that the type of inflammatory infiltrate or presence of fraying of basal keratinocytes may differentiate these two conditions. Objective: In this study, we aimed to confirm these observations. Methods: We reviewed 13 cases of direct immunofluorescence-confirmed epidermolysis bullosa acquisita and 19 cases of direct immunofluorescence-confirmed bullous pemphigoid, all with a subepidermal blister in the routinely processed specimen. The gold standard for diagnosis of epidermolysis bullosa acquisita vs bullous pemphigoid was taken to be identification of immune deposits on the dermal side (‘floor’ for epidermolysis bullosa acquisita) or the epidermal side (‘roof’ for bullous pemphigoid) of the salt-split direct immunofluorescence specimen. Our tests to distinguish epidermolysis bullosa acquisita from bullous pemphigoid on the routinely processed biopsy included periodic acid–Schiff basement membrane on the blister roof, neutrophilic infiltrate, lack of eosinophilic infiltrate, and absence of keratinocyte fraying. Results: Sensitivity and specificity for each test were as follows: periodic acid–Schiff staining of roof (sensitivity 25%, specificity 95%), neutrophilic infiltrate (sensitivity 54%, specificity 74%), lack of eosinophilic infiltrate (sensitivity 92%, specificity 68%), and absence of keratinocyte fraying (sensitivity 62%, specificity 58%). Conclusions: Features in the routinely processed biopsy were unable to reliably distinguish between epidermolysis bullosa acquisita and bullous pemphigoid. Direct immunofluorescence on salt-split skin remains the standard for differentiation.

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3

Laamari, Kaoutar, Hanane Baybay, Samia Mrabat, Zakia Douhi, Sara Elloudi i Fatima Zahra Mernissi. "Hereditary Epidermolysis Bullosa: New Description". Dermatology and Dermatitis 5, nr 1 (31.03.2020): 01–02. http://dx.doi.org/10.31579/2578-8949/066.

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Epidermolysis bullosa (EB) is a heterogeneous group of genetically determined, mechano-bullous disorders characterized by blister formation in response to mechanical trauma. The blistering of the skin occurs in the varying degrees of severity and can severely incapacitate the life of the afflicted patient. Epidermolysis Bullosa Simplex (EBS), the most commonly occurring type, is dominantly inherited where treatment still remains a major challenge.

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4

Errante, Paolo Ruggero. "Epidermolysis Bullosa. A Rare Disturbance in Clinical Veterinary of Felines". International Journal of Zoology and Animal Biology 5, nr 3 (2022): 1–6. http://dx.doi.org/10.23880/izab-16000379.

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Epidermolysis bullosa is an inherited group of rare genetic dermatosis characterized by mucocutaneous fragility and blister formation, inducible by often minimal trauma. Epidermolysis bullosa is described in humans and domestic animals, and this dermatosis in humans is classified in four categories based predominantly on the plane of skin cleavage in simplex epidermolysis bullosa, junctional epidermolysis bullosa, dystrophic epidermolysis bullosa and Kindler epidermolysis bullosa. In veterinary medicine the classification of epidermolysis bullosa is based in the human classification the according with the level of ultrastructural separation of skin. The epidermolysis bullosa in cats is a rare disease with a description of isolated cases involving the forms simplex, junctional and dystrophic. The laboratory diagnosis of cats under suspicion of epidermolysis bullosa should include dermo histopathology, transmission electron microscopy, immunofluorescence for antigen mapping and when possible, mutation analysis. There is no specific treatment for epidermolysis bullosa in cats, and care is palliative. The few case reports of epidermolysis bullosa in cats indicates a short time of survival with few months to years, being the cats sacrificed or dying during the first months of life. Due to these factors, it is essential the deep studies of disease in cats so that they can present an increase in expectancy and quality of life.

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5

Yadav, Randhir Sagar, Amar Jayswal, Shumneva Shrestha, Sanjay Kumar Gupta i Upama Paudel. "Dystrophic Epidermolysis Bullosa". Journal of Nepal Medical Association 56, nr 213 (31.10.2018): 879–82. http://dx.doi.org/10.31729/jnma.3791.

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Epidermolysis bullosa is a rare inherited blistering disease with an incidence of 8-10 per million live births. Dystrophic epidermolysis bullosa is a type of epidermolysis bullosa caused by mutation in type VII collagen, COL7A1. There are 14 subtypes of dystrophic epidermolysis bullosa and 400 mutations of COL7A1. Electron microscopy is the gold standard diagnostic test but expensive. Immunofluorescence study is a suitable diagnostic alternative. Trauma prevention along with supportive care is the mainstay of therapy. Squamous cell carcinoma develops at an early age in epidermolysis bullosa than other patients, particularly in recessive dystrophic epidermolysis bullosa subtypes. Regular follow up is imperative in detecting and preventing complications. Gene therapy, cell therapy and bone marrow transplantation are the emerging novel therapeutic innovations. Preventing possible skin and mucosal injury in patients requiring surgery should be worked on. Here, we present a case of dystrophic epidermolysis bullosa in a 26 year male.

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6

MSALIH, M. A., B. D. LAKE, M. A. HAG i D. J. ATHERTON. "Lethal epidermolytic epidermolysis bullosa: a new autosomal recessive type of epidermolysis bullosa". British Journal of Dermatology 113, nr 2 (sierpień 1985): 135–43. http://dx.doi.org/10.1111/j.1365-2133.1985.tb02055.x.

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7

Mahato, Shyam Kumar, Susana Lama, Nikhil Agarwal i Nagendra Chaudhary. "Inherited Epidermolysis Bullosa: A case report". Journal of Universal College of Medical Sciences 3, nr 3 (31.12.2015): 39–42. http://dx.doi.org/10.3126/jucms.v3i3.24248.

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Epidermolysis bullosa (EB) is a heterogeneous group of genetically determined, mechano-bullous disorders characterized by blister formation in response to mechanical trauma. The blistering of the skin occurs in the varying degrees of severity and can severely incapacitate the life of the afflicted patient. Epidermolysis Bullosa Simplex (EBS), the most commonly occurring type, is dominantly inherited where treatment still remains a major challenge. We report a newborn female with blistering of the skin during the immediate neonatal period.

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8

Prosty, Connor, Justina Guirguis, May Chergui, Waqqas Afif i Elena Netchiporouk. "Epidermolysis bullosa acquisita treated with ustekinumab: A case report". SAGE Open Medical Case Reports 10 (styczeń 2022): 2050313X2210916. http://dx.doi.org/10.1177/2050313x221091600.

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Epidermolysis bullosa acquisita is a rare autoimmune disease involving cutaneous blistering and scarring associated with collagen VII autoantibodies. Similarly, collagen VII autoantibodies are present in the majority of Crohn’s disease patients and approximately a quarter of epidermolysis bullosa acquisita patients have coexisting Crohn’s disease. Treatment options for epidermolysis bullosa acquisita are limited and are largely ineffective. Here, we describe a 36-year-old female with a history of Crohn’s disease presenting with a 7-year history of severe blistering and scarring of acral surfaces. Diagnostic workup revealed subepidermal cleavage on skin biopsy and elevated serum collagen VII autoantibodies, indicative of epidermolysis bullosa acquisita. She was given ustekinumab for her coexisting Crohn’s disease and, afterwards, her epidermolysis bullosa acquisita resolved as evidenced by a lack of new blisters or scarring. Further studies are required to evaluate the effects of ustekinumab on epidermolysis bullosa acquisita.

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9

KENNA, MARGARET A., SYLVAN E. STOOL i SUSAN B. MALLORY. "Junctional Epidermolysis Bullosa of the Larynx". Pediatrics 78, nr 1 (1.07.1986): 172–74. http://dx.doi.org/10.1542/peds.78.1.172.

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Epidermolysis bullosa is a rare genetically determined, dermatologic disease in which minor trauma causes blister formation.1 A new variant of hereditary epidermolysis bullosa, generalized atrophic benign epidermolysis bullosa, junctional form, has been recently reported.2 Airway involvement has not been a notable feature of this disease. We report the first case of an infant having benign junctional epidermolysis bullosa with laryngeal involvement. CASE REPORT An 11-month-old white boy with known junctional epidermolysis bullosa and mild stridor since birth was referred by his dermatologist for increasing stridor of 24 hours duration. He was initially thought to have croup; however, conservative treatment with mist and racemic epinephrine did not improve his symptoms.

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10

Hughes, Amy P., i Jeffrey P. Callen. "Epidermolysis Bullosa Acquisita Responsive to Dapsone Therapy". Journal of Cutaneous Medicine and Surgery 5, nr 5 (wrzesień 2001): 397–99. http://dx.doi.org/10.1177/120347540100500505.

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Background: Epidermolysis bullosa acquisita (EBA) is a chronic subepidermal blistering disease that is frequently resistant to therapy. Objective: A 58-year-old man who had a one-year history of a bullous eruption involving the hands, forearms, trunk, scalp, and oral mucosa. Histopathology revealed a subepidermal bulla, and direct and indirect immunofluorescence studies were consistent with EBA. The patient failed respond to niacinamide and tetracycline and oral prednisone 40 mg per day. Methods: Complete control of his blistering was achieved within two months of initiating oral dapsone, 150 mg per day. Conclusion: Dapsone may be an effective agent for some patients with EBA.

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11

Chikin, V. V., L. F. Znamenskaya, M. A. Nefedova i V. A. Charikov. "Epidermolysis bullosa acquisita". Vestnik dermatologii i venerologii 91, nr 3 (24.06.2015): 109–18. http://dx.doi.org/10.25208/0042-4609-2015-91-3-109-118.

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The article describes present-day information on the pathogenesis, clinical picture, treatment and differential diagnostics of epidermolysis bullosa acquisita, an autoimmune skin disease caused by the production of anti-Type VII collagen autoantibodies and manifested mainly by subepidermal blisters and erosions. The authors present the results of a case study of a rare form of epidermolysis bullosa - epidermolysis bullosa acquisita in a male patient aged 53. A combined therapy with peroral prednisolone and subcutaneous injections of methotrexate had a positive effect in the form of epithelialization of most of the erosions.

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12

Pai, Shan, i M. Peter Marinkovich. "Epidermolysis Bullosa". American Journal of Clinical Dermatology 3, nr 6 (2002): 371–80. http://dx.doi.org/10.2165/00128071-200203060-00001.

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13

MacKinnon, Petrina. "Epidermolysis bullosa". Nursing Standard 6, nr 5 (23.10.1991): 29–32. http://dx.doi.org/10.7748/ns.6.5.29.s34.

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14

Price-Douglas, Webra, i Beth Diehl-Svrjcek. "Epidermolysis Bullosa". Advances in Neonatal Care 7, nr 6 (grudzień 2007): 289–94. http://dx.doi.org/10.1097/01.anc.0000304967.46708.ea.

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15

Lin, A. N., i D. M. Carter. "Epidermolysis Bullosa". Annual Review of Medicine 44, nr 1 (luty 1993): 189–99. http://dx.doi.org/10.1146/annurev.me.44.020193.001201.

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16

Schober-Flores, Carol. "Epidermolysis Bullosa". Journal of the Dermatology Nurses’ Association 6, nr 4 (2014): 199–205. http://dx.doi.org/10.1097/jdn.0000000000000060.

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17

Bodán, Rebecca Cross. "Epidermolysis Bullosa". Journal of the Dermatology Nurses’ Association 8, nr 1 (2016): 46–56. http://dx.doi.org/10.1097/jdn.0000000000000188.

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Schober-Flores, Carol. "Epidermolysis Bullosa". Journal of the Dermatology Nurses' Association 1, nr 1 (styczeń 2009): 21–28. http://dx.doi.org/10.1097/jdn.0b013e3181977521.

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&NA;. "Epidermolysis Bullosa". Journal of the Dermatology Nurses' Association 1, nr 1 (styczeń 2009): 29–30. http://dx.doi.org/10.1097/jdn.0b013e318199f167.

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20

Lin, James, i Jose N. Fayad. "Epidermolysis Bullosa". Ear, Nose & Throat Journal 86, nr 4 (kwiecień 2007): 192. http://dx.doi.org/10.1177/014556130708600404.

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21

Haber, Richard M., Colin A. Ramsay i Lionel B. H. Boxall. "Epidermolysis Bullosa:." International Journal of Dermatology 24, nr 1 (styczeń 1985): 324–28. http://dx.doi.org/10.1111/j.1365-4362.1985.tb05489.x.

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22

Haber, Richard M., Colin A. Ramsy i Lionel B. H. Boxall. "Epidermolysis Bullosa." International Journal of Dermatology 24, nr 5 (czerwiec 1985): 324–28. http://dx.doi.org/10.1111/j.1365-4362.1985.tb05796.x.

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23

Fine, Jo-David. "Epidermolysis Bullosa." International Journal of Dermatology 25, nr 3 (kwiecień 1986): 143–57. http://dx.doi.org/10.1111/j.1365-4362.1986.tb02206.x.

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24

Kero, Matti, i Kirsti-Maria Niemi. "Epidermolysis Bullosa". International Journal of Dermatology 25, nr 2 (marzec 1986): 75–82. http://dx.doi.org/10.1111/j.1365-4362.1986.tb04542.x.

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25

Sedano, Heddie O., i Robert J. Gorlin. "Epidermolysis bullosa". Oral Surgery, Oral Medicine, Oral Pathology 67, nr 5 (maj 1989): 555–63. http://dx.doi.org/10.1016/0030-4220(89)90272-7.

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Schumann, H. "Epidermolysis bullosa". Der Hautarzt 60, nr 8 (28.06.2009): 614–21. http://dx.doi.org/10.1007/s00105-008-1677-x.

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27

Has, C., i L. Bruckner-Tuderman. "Epidermolysis bullosa". Der Hautarzt 62, nr 2 (27.01.2011): 82–90. http://dx.doi.org/10.1007/s00105-010-2049-x.

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Broster, T., R. Placek i G. W. N. Eggers. "Epidermolysis Bullosa". Obstetric Anesthesia Digest 7, nr 3 (październik 1987): 128. http://dx.doi.org/10.1097/00132582-198710000-00043.

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29

McGrath, John A., i Jemima E. Mellerio. "Epidermolysis bullosa". British Journal of Hospital Medicine 67, nr 4 (kwiecień 2006): 188–91. http://dx.doi.org/10.12968/hmed.2006.67.4.20864.

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Broster, Thomas, Richard Placek i G. W. N. Eggers. "Epidermolysis Bullosa". Anesthesia & Analgesia 66, nr 4 (kwiecień 1987): 341???343. http://dx.doi.org/10.1213/00000539-198704000-00010.

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31

Hochberg, Mark S., Ivan A. Vazquez-Santiago i Martin Sher. "Epidermolysis bullosa". Oral Surgery, Oral Medicine, Oral Pathology 75, nr 1 (styczeń 1993): 54–57. http://dx.doi.org/10.1016/0030-4220(93)90406-t.

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Frank, Jorge. "Epidermolysis bullosa". hautnah dermatologie 39, S1 (luty 2023): 38–43. http://dx.doi.org/10.1007/s15012-023-7668-x.

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Lee, Myn Wee, George Varigos, Peter Foley i Gayle Ross. "Photodynamic Therapy for Basal Cell Carcinoma in Recessive Dystrophic Epidermolysis Bullosa". ISRN Dermatology 2011 (27.04.2011): 1–4. http://dx.doi.org/10.5402/2011/346754.

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A 22-year-old male with recessive dystrophic epidermolysis bullosa with a large superficial and nodular basal cell carcinoma on his right forehead was treated with photodynamic therapy. The treatment was well tolerated, and the site healed well. Patients with epidermolysis bullosa are at increased risk of developing skin cancers, particularly squamous cell carcinomas. However, basal cell carcinomas are rare in recessive dystrophic epidermolysis bullosa. As patients with epidermolysis bullosa have recurrent blistering and poor wound healing, surgery may not be the optimal choice in treating skin cancers. We present this case to highlight that photodynamic therapy may be a helpful and safe technique in the treatment of superficial skin cancers in patients with epidermolysis bullosa, as an alternative to more radical methods.

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Hayashi, Ryota, Ken Natsuga, Mika Watanabe, Hiroaki Iwata, Satoru Shinkuma, Akiko Ito, Yukiko Masui, Masaaki Ito i Yutaka Shimomura. "Epidermolysis Bullosa Acquisita Develops in Dominant Dystrophic Epidermolysis Bullosa". Journal of Investigative Dermatology 136, nr 1 (styczeń 2016): 320–23. http://dx.doi.org/10.1038/jid.2015.370.

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Laimer, Martin, Gabriela Pohla-Gubo, Anja Diem, Christine Prodinger, Johann W. Bauer i Helmut Hintner. "Epidermolysis bullosa House Austria and Epidermolysis bullosa clinical network". Wiener klinische Wochenschrift 129, nr 1-2 (1.12.2016): 1–7. http://dx.doi.org/10.1007/s00508-016-1133-3.

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Salas-Alanis, Julio Cesar, Cesar Eduardo Rosales-Mendoza i Jorge Ocampo-Candiani. "Bullous Mastocytosis Mimicking Congenital Epidermolysis Bullosa". Case Reports in Dermatology 6, nr 2 (8.05.2014): 129–33. http://dx.doi.org/10.1159/000362755.

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De Jong, Marcelus C. J. M. "Bullous Pemphigoid and Epidermolysis Bullosa Acquisita". Archives of Dermatology 132, nr 2 (1.02.1996): 151. http://dx.doi.org/10.1001/archderm.1996.03890260053008.

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Kumar, Sneh. "An Unusual Case Report of Dystrophica Epidermolysis Bullosa in a Child". Journal of Evolution of Medical and Dental Sciences 10, nr 37 (13.09.2021): 3314–16. http://dx.doi.org/10.14260/jemds/2021/672.

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Epidermolysis bullosa (EB) is a genetically inherited severe skin disease involving dermal-epidermal junction. Based on the appearance and involvement, it is grouped into simplex, junctional & dystrophic forms. These disorders represent heterogeneous phenotypes and are correlated with a variable range of complications, from localized skin fragility to neonatal death. Genetic testing had made a precise diagnosis and it requires only supportive and symptomatic therapy. Here we report an atypical case of dystrophica epidermolysis bullosa in a 6-year-old male child. Epidermolysis bullosa (EB) is a general term used for heterogeneous group of congenital, genetic blistering disorders. It has a wide spectrum of clinical presentations. 1 It is characterized by induction of blisters by trauma, exacerbation of blistering in warm weather and healing with scarring. EB can be categorized under three major groups - epidermolysis bullosa simplex (EBS), junctional epidermolysis bullosa (JEB) and dystrophic epidermolysis bullosa (DEB). EB simplex has an incidence and a prevalence rate of 10.75 and 4.65, 2.04 and 0.44 of junctional EBs and 2.86 and 0.99 of dystrophic EBs and recessive dystrophic EB 2.04 and 0.92 respectively.2 The dystrophic forms are characterized by deformities of the skin including coalescence of the fingers, nail changes and milia formation.3 This case report highlights the rare presentation of recurrent episodes of blisters and limb deformities in 6 - year - old male children.

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Dabelsteen, E. "Molecular Biological Aspects of Acquired Bullous Diseases". Critical Reviews in Oral Biology & Medicine 9, nr 2 (kwiecień 1998): 162–78. http://dx.doi.org/10.1177/10454411980090020201.

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Bullous diseases of the oral mucosa and skin were originally classified on the basis of clinical and histological criteria. The discovery of autoantibodies in some of these patients and the introduction of molecular biology have resulted in a new understanding of the pathological mechanisms of many of the bullous lesions. In this article, updated topics of the immune-mediated bullous lesions which involve oral mucosa and skin are reviewed. Pemphigus antigens, which are desmosomal-associated proteins and belong to the cadherin superfamily of cell adhesion proteins, have been isolated, and their genes have been cloned. The antigens which react with autoantibodies from patients with bullous pemphigoid, cicatricial pemphigoid, acquired epidermolysis bullosa, and linear IgA disease are all proteins of the hemidesmosome basement membrane complex. Interestingly, most of the antigens also appear to be the target for mutations seen in patients with the inherited type of epidermolysis bullosa in which bullous lesions are a prominent clinical feature.

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Tešanović Perković, Deša, Zrinka Bukvić Mokos i Branka Marinović. "Epidermolysis Bullosa Acquisita—Current and Emerging Treatments". Journal of Clinical Medicine 12, nr 3 (1.02.2023): 1139. http://dx.doi.org/10.3390/jcm12031139.

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Epidermolysis bullosa acquisita (EBA) is a rare chronic autoimmune subepidermal blistering disease of the skin and mucous membranes, usually beginning in adulthood. EBA is induced by autoantibodies to type VII collagen, a major component of anchoring fibrils in the dermal–epidermal junction (DEJ). The binding of autoantibodies to type-VII collagen subsequently leads to the detachment of the epidermis and the formation of mucocutaneous blisters. EBA has two major clinical subtypes: the mechanobullous and inflammatory variants. The classic mechanobullous variant presentation consists of skin fragility, bullae with minimal clinical or histological inflammation, erosions in acral distribution that heal with scarring, and milia formation. The inflammatory variant is challenging to differentiate from other autoimmune bullous diseases, most commonly bullous pemphigoid (BP) but also mucous membrane pemphigoid (MMP), Brunsting–Perry pemphigoid, and linear IgA dermatosis. Due to its recalcitrance conventional treatment of epidermolysis bullosa acquisita is shown to be demanding. Here we discuss novel therapeutic strategies that have emerged and which could potentially improve the quality of life in patients with EBA.

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GONZALEZ, ANA, LAWRENCE SCHACHNER i MADELINE MILLER. "Junctional Epidermolysis Bullosa of the Larynx". Pediatrics 79, nr 6 (1.06.1987): 1051–52. http://dx.doi.org/10.1542/peds.79.6.1051.

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To the Editor.— The article by Kenna et al (Pediatrics 1986;78:172-174) points out the complication of respiratory compromise secondary to laryngeal involvement in junctional epidermolysis bullosa. Junctional epidermolysis bullosa, a mechanobullous disorder with autosomal recessive inheritance, has been associated with not only skin lesions but gastrointestinal, respiratory tract, and genitourinary tract abnormalities as well.1 The figure that was presented in the article incorrectly showed a split in the upper layers of the epidermis inconsistent with junctional epidermolysis bullosa.

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FINE, J. D., L. B. JOHNSON, M. WEINER, A. STEIN, S. CASH, J. DELEOZ, D. T. DEVRIES i C. SUCHINDRAN. "Pseudosyndactyly and Musculoskeletal Contractures in Inherited Epidermolysis Bullosa: Experience of the National Epidermolysis Bullosa Registry, 1986–2002". Journal of Hand Surgery 30, nr 1 (luty 2005): 14–22. http://dx.doi.org/10.1016/j.jhsb.2004.07.006.

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Mitten deformities of the hands and feet occur in nearly every patient with the most severe subtype (Hallopeau-Siemens) of recessive dystrophic epidermolysis bullosa, and in at least 40–50% of all other recessive dystrophic epidermolysis bullosa patients. Smaller numbers of patients with dominant dystrophic, junctional, and simplex types of epidermolysis bullosa are also at risk of this complication. Surgical intervention is commonly performed to correct these deformities, but recurrence and the need for repeated surgery are common. Higher numbers of epidermolysis bullosa patients also develop musculoskeletal contractures in other anatomic sites, further impairing overall function. Lifetable analyses not only better project the cumulative risk of mitten deformities and other contractures but also emphasize the need for early surveillance and intervention, since both of these musculoskeletal complications may occur within the first year of life.

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Kornev, V. I., O. N. Startseva, A. S. Pleshkov i M. V. Nikiforov. "Endothelial dysfunction in patients with various forms of congenital epidermolysis bullosa". Scientific Notes of the Pavlov University 29, nr 3 (6.07.2022): 101–5. http://dx.doi.org/10.24884/1607-4181-2022-29-3-101-105.

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Introduction. The endothelial system is an important component of vascular-platelet hemostasis, capable of actively responding to mechanical and inflammatory agents. Patients with congenital epidermolysis bullosa are prone to mechanical damage to the skin and the development of a chronic inflammatory syndrome with a high probability of endothelial dysfunction.The study objective was to assess the state of the endothelial system and to reveal the dependence of endothelial dysfunction on the form of epidermolysis bullosa.Methods and materials. The study used venous blood of 57 patients (27 men and 30 women) with congenital epidermolysis bullosa. In patients with simple and dystrophic forms of epidermolysis bullosa, the platelet count, P-selectin, fibrinogen, albumin, C-reactive protein, von Willebrand factor antigen concentration, and factor VIII activity were determined.Results. Comparative results of endothelial dysfunction depending on the form of epidermolysis bullosa were represented and endothelial dysfunction’s dependence on the concentration of albumin, C-reactive protein, and platelet count was determined.Conclusions. In patients with a dystrophic form of epidermolysis bullosa, endothelial dysfunction is accompanied by an increase in the expression of P-selectin, factor VIII activity, and the concentration of von Willebrand factor antigen. Chronic inflammation and impaired nutritional status with a decrease in albumin contribute to the development of endothelial dysfunction.

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SASAI, YOICHIRO. "Epidermolysis bullosa. 1986." Nishi Nihon Hifuka 49, nr 1 (1987): 5–16. http://dx.doi.org/10.2336/nishinihonhifu.49.5.

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Das, JayantaKr, Sujata Sengupta i AsokKr Gangopadhyay. "Epidermolysis bullosa acquisita". Indian Journal of Dermatology, Venereology and Leprology 72, nr 1 (2006): 86. http://dx.doi.org/10.4103/0378-6323.19736.

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Sadighi, Tammy, i Cheryl Swayne. "Epidermolysis Bullosa Simplex". Journal of the Dermatology Nurses' Association 14, nr 1 (styczeń 2022): 16–19. http://dx.doi.org/10.1097/jdn.0000000000000660.

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Cambiaghi, S., A. Brusasco, L. Restano, R. Cavalli i G. Tadini. "Epidermolysis Bullosa Pruriginosa". Dermatology 195, nr 1 (1997): 65–68. http://dx.doi.org/10.1159/000245691.

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ARWILL, TORE, AXEL BERGENHOLTZ i HOLGER THILANDER. "EPIDERMOLYSIS BULLOSA HEREDITARIA". Acta Pathologica Microbiologica Scandinavica 74, nr 3 (17.08.2009): 311–24. http://dx.doi.org/10.1111/j.1699-0463.1968.tb03484.x.

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Cash, Sarah H., Patrice M. Hyde i Jason B. Lee. "Epidermolysis Bullosa Nevus". American Journal of Dermatopathology 27, nr 6 (grudzień 2005): 532. http://dx.doi.org/10.1097/01.dad.0000197729.72168.eb.

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Kim, Whan B., Afsaneh Alavi, Elena Pope i Scott Walsh. "Epidermolysis Bullosa Pruriginosa". International Journal of Lower Extremity Wounds 14, nr 2 (17.02.2015): 196–99. http://dx.doi.org/10.1177/1534734615572469.

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