C.-C. E. Lan

FK506 promotes melanocyte and melanoblast growth and creates a favourable milieu for cell migration via keratinocytes: possible mechanisms of how tacrolimus ointment induces repigmentation in patients with vitiligo

Backgroundu2002 Vitiligo is an acquired pigmentary disorder characterized by depigmentation of skin and hair. As the pathogenesis of this disease is still obscure, the treatment of vitiligo has generally been unsatisfactory and often disappointing. Topical tacrolimus (FK506) ointment has recently been added to the armamentarium against this pigmentary disorder. Despite its clinical efficacy, the underlying mechanisms of how topical tacrolimus induces repigmentation in vitiligo have rarely been investigated. As tacrolimus ointment is applied directly to the skin, its impact on keratinocytes (KCs) requires thorough investigation.

CXC chemokine receptor CXCR4 expression enhances tumorigenesis and angiogenesis of basal cell carcinoma

Backgroundu2002 Chemokines and their receptors, well known for their ability to attract leucocytes, also play important roles for tumour progression.

Cutaneous metastases from different internal malignancies: a clinical and prognostic appraisal.

Backgroundu2002 Cutaneous metastases are perceived as a sign of advanced disease and are regarded as a grave prognostic indicator. In addition, few reports have focused on the cutaneous metastasis profiles of Asian patients.

Effects of psoralen plus ultraviolet A irradiation on cultured epidermal cells in vitro and patients with vitiligo in vivo

Backgroundu2002 Both psoralen plus ultraviolet (UV) A (PUVA) and narrowband UVB (NB‐UVB) irradiation are effective treatments for vitiligo vulgaris. However, the mechanisms of PUVA and NB‐UVB in repigmentation are not thoroughly clarified. Our previous results showed that NB‐UVB irradiation directly promotes melanocyte (MC) migration and stimulates MC proliferation via keratinocytes (KCs).

Distinct SPINK5 and IL‐31 polymorphisms are associated with atopic eczema and non‐atopic hand dermatitis in Taiwanese nursing population

Abstract:u2002 The term ‘hand dermatitis’ describes inflammatory skin condition localized to the hands. Nurses working at hospital settings are prone to develop hand dermatitis. The current study aimed to evaluate whether certain genetic polymorphisms were associated with the development of atopic eczema or non‐atopic hand dermatitis in Taiwanese population. Nurses of Kaohsiung Medical University Hospital were recruited. Atopic eczema, non‐atopic hand dermatitis and normal control groups were identified. The serine protease inhibitor Kazal type 5 (SPINK5), filaggrin and interleukin‐31 (IL‐31) gene variants were compared between the diseased and control groups. Our results showed that rs2303070 T allele of SPINK5 (assuming recessive model; ORu2003=u20033.58, 95% CI 1.63–7.84; Pu2003=u20030.0014) and rs7977932u2003G allele of IL‐31 (assuming recessive model; ORu2003=u200318.25, 95% CIu2003=u20033.27–101.94; Pu2003=u20030.0009) were associated with increased risks of developing atopic eczema, while rs6892205u2003G allele of SPINK5 (assuming dominant model; ORu2003=u20033.79, 95% CI 1.55–9.28; Pu2003=u20030.0036) was associated with the development of non‐atopic hand dermatitis. In summary, our results showed that distinct SPINK5 and IL‐31 gene variants were associated with the development of atopic eczema and non‐atopic hand dermatitis. The barrier function, particularly those regulated by SPINK5, may play an important role in the development of both atopic eczema and non‐atopic hand dermatitis.

Hand dermatitis among university hospital nursing staff with or without atopic eczema: assessment of risk factors.

Background. Nurses are prone to develop hand dermatitis. Although an atopic constitution has been identified as a genetic risk factor, the behavioural risk factors associated with hand dermatitis in wet work conditions have not been fully explored.

Pigmented eccrine poroma with enhanced endothelin-1 expression: implications for mechanism of hyperpigmentation

which excluded systemic disease. As there were no remnants of lesion, radiotherapy was not performed. Mycophenolate mofetil and tacrolimus ANH were reduced to half the previous dosage. There was no recurrence at 12-month follow-up. Cutaneous CD30+ ALTCL is characterized by the expression of CD30 (an activation marker for B or T cells) in more than 75% of cells, and can be subdivided mainly into a primary cutaneous form, defined by skin-only involvement at presentation, or a systemic form, with secondary skin involvement from a node-based lymphoma, or following transformation of mycosis fungoides. The localization of PTLs in the skin, as well as the CD30+ ALTCL type, are very uncommon. To our knowledge, only five cases of CD30+ PT ALTCL have been reported to date: three in kidney recipients, one in a heart transplant and the other in a combined liver and heart transplantation recipient. Whereas classical primary cutaneous CD30+ ALTCL usually carries a good prognosis, CD30+ PT ALTCLs seem to pursue an aggressive course: the previously reported cases were characterized by multiple lesions at presentation and ⁄or a rapid appearance of new nodules within a few months. In our patient, there was a unique tumour at presentation, and no further lesions appeared within 12 months, although we think that a longer follow-up is necessary to evaluate the clinical behaviour more thoroughly. We think that the small size of the lesion was the most favourable prognostic factor in our case, as it allowed for a complete excision of tumour. We also found strong positivity for MUM1 ⁄ IRF4, which is thought to be crucial for lymphoid development and has been found to be strongly expressed in various types of leukaemia, Band T-cell lymphomas, including ALTCL. MUM1 ⁄ IRF4 expression is thought to be helpful for diagnostic purposes, whereas its prognostic role is controversial, probably depending on the type of leukaemia ⁄ lymphoma considered. MUM1 ⁄ IRF4 was not investigated in the previously reported cases of CD30+ PT ALTCLs; it could be worthwhile to study its expression on a larger series of PTLs. The unusual clinical behaviour and histotype and the immunophenotype of our case may add knowledge to the spectrum of PTLs.

A huge verrucous carcinoma of the lower lip treated with intra-arterial infusion of methotrexate.

9700 thermal cycler (Applied Biosystems). The amplification conditions were: 95 C for 5 min, followed by 38 cycles of 95 C for 45 s, 60 C for 45 s and 72 C for 45 s. Aliquots (5 lL) of the PCR products were analysed by 2Æ5% agarose gel electrophoresis. PCR products were then purified using QIAquick PCR Purification Kit (Qiagen, Crawley, U.K.) and sequenced directly in an ABI 310 genetic analyser (Applied Biosystems). Direct sequencing revealed a homozygous frameshift mutation, 507delT, in exon 6 (Fig. 2). This leads to a premature stop codon 23 bp downstream and is predicted to ablate all three isoforms of ECM1. Interestingly, this particular mutation has been documented previously, in two Thai brothers and an Iranian family with lipoid proteinosis. Moreover, haplotype analysis (based on intragenic polymorphisms) in these and our Indian patient has demonstrated that the mutation 507delT in ECM1 has been inherited on different genetic backgrounds. Thus, this particular mutation represents a recurrent mutation, the only one to be described so far in ECM1 in patients with lipoid proteinosis. This nucleotide deletion occurs in part of the gene surrounded by palindromic runs of multiple C or G nucleotide repeats and may therefore have arisen through slipped mispairing during DNA replication. From a practical perspective, screening for the mutation 507delT can easily be accomplished by restriction endonuclease digestion of the exon 6 PCR products with HpaII (New England BioLabs, Hitchin, Herts, U.K.). As this is now the most common mutation reported, we recommend initial screening for this sequence variant in new cases of lipoid proteinosis. If 507delT is not detected, direct sequencing of exons 6 and 7 of ECM1 should then follow, as over 60% of the other mutations detected have occurred in these two exons.

Erosive pustular dermatosis of the scalp after gefitinib and radiotherapy for brain metastases secondary to lung cancer.

stippled appearance due to the deposition of tiny amounts of the fake tan in the uneven contours on the surface (Fig. 1a). The dermatoscopic appearances are even more striking, and do not conform to any of the recognized findings in melanocytic or nonmelanocytic lesions (Figs 1b and 2a,b). We would suggest that these features are not specific to seborrhoeic keratoses as suggested by Orpin et al., but can be found in any skin lesions with textural irregularity or hyperkeratosis e.g. compound naevi or seborrhoeic keratoses. Similarly, fake tan has also been found incidentally to aid in the diagnosis of porokeratosis, where it stained and highlighted the outer rim of lesions. We agree that it is important that dermatologists are aware of the fact that fake tan can alter the appearance of a skin lesion, and enquiries should be made about previous or current use of such a product when taking a history. The dermatoscope is a useful diagnostic tool in confirming such cases and could prevent unnecessary excision of benign lesions. A. G. Affleck and W. Perkins Department of Dermatology, Queen’s Medical Centre, Nottingham University Hospitals NHS Trust, Nottingham, NG7 2UH, UK E-mail: andyaffleck@doctors.org.uk Conflict of interest: none declared. Accepted for publication 27 May 2007

Onychomycosis caused by Fusarium solani in a woman with diabetes

A case of untreated fusarial onychomycosis leading to serious consequences is reported. Fusarium solani is a widespread fungus and an occasional human pathogen. It usually invades rapidly in immunocompromised hosts, and often results in a poor outcome despite treatment. We report a woman with diabetes mellitus who had untreated fusarial infection of the nails, which developed into subcutaneous fusariosis, superinfected by bacteria, and then evolved into osteomyelitis that subsequently resulted in septic shock. Early management of mycotic nails in immunocompromised hosts is crucial to prevent life‐threatening disease.