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London, United Kingdom

Ameen M.,St Johns Institute Of Dermatology
Tropical Doctor

Chromoblastomycosis is a subcutaneous fungal infection caused by the traumatic inoculation of the skin with pigmented saprophytic moulds. Although infection is rarely fatal, it is characteristically chronic and can be complicated by lymphatic damage and malignant transformation. Despite a variety of treatment modalities, which are often combined and include long courses of antifungals, surgical excision and destructive physical therapies, it remains one of the most difficult deep mycotic infections to eradicate. Source

Fassihi H.,St Johns Institute Of Dermatology
Photochemical and Photobiological Sciences

Xeroderma pigmentosum (XP) is a rare autosomal recessive disorder of DNA repair characterised by photosensitivity, progressive pigmentary change, and an increased incidence of ultraviolet (UV)-induced skin and mucous membrane cancers. Approximately 25% of XP patients also have progressive neurological degeneration. There are eight XP complementation groups (XP-A through to XP-G, and XP variant (XP-V)), corresponding to the affected DNA repair gene. Seven of these genes, XPA to XPG, are involved in nucleotide excision repair, removing UV-induced damage from DNA. The eighth gene, XPV (or POLH), encodes for DNA polymerase η, which is required for the replication of DNA containing unrepaired UV-induced damage. There is wide variability in clinical features both between and within XP complementation groups. The diagnosis is made clinically and confirmed by cellular tests for defective DNA repair. This is followed by identification of the defective gene (complementation analysis) and causative mutation(s). Although there is no cure, sun avoidance and regular follow-up to assess and treat any skin cancers increase life expectancy. The neurological abnormalities are progressive and result in a shortened lifespan. The study of patients with XP has highlighted the importance of nucleotide excision repair in the aetiology of skin cancers and neurological degeneration, and has solidified the link between UV exposure, DNA damage, somatic mutations and skin cancer. This journal is © 2013 The Royal Society of Chemistry and Owner Societies. Source

Luzar B.,University of Ljubljana | Calonje E.,St Johns Institute Of Dermatology
Journal of Cutaneous Pathology

The present manuscript gives emphasis on recognizing different morphological variants of atypical fibroxanthoma (AFX), on validation of immunohistochemical markers and on discussing potential diagnostic pitfalls. Material and methods: Histological features analyzed in 66 AFXs were: ulceration, morphological variants, growth pattern, location in the skin and vascular/perineural invasion. The antibodies used were CK-MNF116, CK-AE1/AE3, S100, smooth muscle actin, desmin, CD31 and EMA. Results: The study included 59 males, 7 females, aged 55-95 years, mean 77 years. All developed on sun damaged skUlceration was present in 50%. Morphological patterns were pleomorphic spindle and epithelioid cells (60.6%), predominantly spindle cells (19.7%), purely spindle-cells (13.6%), and predominantly epithelioid cells (6.1%). Most were localized in the dermis (57.6%). An expansile (36.4%) rather than infiltrative (6.1%) growth into superficial subcutis was also noted. No vascular/perineural invasion was seen. Additional changes were hemorrhagic and pseudoangiomatous areas (24.2%), granular cell change (22.7%), keloid-like areas (9.1%), myxoid change (7.6%), osteoclast-like giant cells (6.1%) and clear cell change (4.6%). AFXs were consistently negative for S100, CK-MNF116, CK-AE1/AE3 and desmFocal positivity for SMA (45.2%), EMA (24.4%) and CD 31 (9.5%) was seen. Conclusions: A diagnosis of AFX is still made by exclusion of other malignant neoplasms with similar morphology. Immunohistochemistry plays a crucial role in this distinction, but can also be misleading. This study expands the spectrum of non-vascular CD31 positive tumors. © 2009 John Wiley & Sons A/S. Source

Robson A.,St Johns Institute Of Dermatology

Robson A (2010) Histopathology 56, 71-90 Immunocytochemistry and the diagnosis of cutaneous lymphoma Cutaneous lymphoid infiltrates may pose some of the most difficult diagnostic problems in dermatopathology. Immunocytochemistry is often employed in an effort to determine whether an infiltrate is neoplastic or, in the case of clearly malignant infiltrates, to provide a specific diagnosis. The rarity of these disorders and the variant immunocytochemical profiles they may present further thwart understanding and sometimes prevent an accurate diagnosis. In this review the common immunocytochemical profiles of various cutaneous lymphomas are presented and potential pitfalls and problems considered. Immunocytochemistry is not a diagnostic test but, as in other areas of histopathology, is a highly valuable tool that requires critical interpretation within a context: so applied, it is an indispensable part of the pathologist's arsenal in evaluating lymphoid infiltrates and defining different lymphomas. © 2010 Blackwell Publishing Limited. Source

Mellerio J.E.,St Johns Institute Of Dermatology
Dermatologic Clinics

In all forms of epidermolysis bullosa (EB), skin fragility may result in bacterial colonization or infection, particularly in the more severe forms where wounds may be multiple and long-standing. A balance exists between a wound's bacterial load and the host defenses, such that there is a spectrum from simple contamination, through colonization, critical colonization, to overt infection. The increased bioburden in critically colonized or infected wounds impairs healing and therefore recognition of these situations, and appropriate measures to promote a healing environment, are fundamental to the care of EB wounds. © 2010 Elsevier Inc. Source

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