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1. |
Epidemiology and prognosis of subungual melanoma in 34 Japanese patients |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 383-387
T. KATO,
T. SUETAKE,
Y. SUGIYAMA,
N. TABATA,
H. TAGAMI,
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摘要:
SummaryThe incidence of malignant melanoma is much lower in the Japanese than in Caucasians. However, amongst the various types of malignant melanoma, the subungual and periungual sites are commonly found in the Japanese. One hundred and fifty‐one cases of cutaneous malignant melanoma were seen over a 25‐year period at our hospital. We found that. In 34 patients (23%). the subungual region was involved, a high frequency for one institution. We have analysed these patients and looked at their treatment. The finger nails were affected in 21 cases (62%) and the toe nails in 1 3 cases (38%). The thumb nails or great toe nails were at tecled in 25 of the 34 patients (73%). In 25 patients, histopathological features of acral lentiginous melanoma were found, with four cases of superficial spreading melanoma and five of nodular amelanotic melanoma. Of the latter group, four mimicked tibrous histiocytic tumour, and one was a desmoplastic malignant melanoma. I he proportion of patients presenting with stage III disease decreased after 1982. with a corresponding increase in patients whose tumour thickness was less than 4 mm (stage II). Concurrently, the prognosis for subungual malignant melanoma improved. The 5‐year survival rate in each of the periods 1969–82 and 1981—93 was 5 3 and 87%. respectively. This is similar to that found in plantar malignant melanoma and is fell to be due to a greater public awareness of the condition and to the introduction of effective chemotherapy (the DTIC‐AC nitro surear vincristine (OAV) regimen). Although the frequency of malignant melanoma is rather low in the Japanese, our data indicate that there is a high incidence of subungual malignant melanoma. Public awareness of the early stage of malignant melanoma seems to have improve
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.19754.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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2. |
CD69 expression and tumour necrosis factor‐α immunoreactivity in the inflammatory cell infiltrate of halo naevi |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 388-393
J. FERNÁNDEZ‐HERRERA,
E. FERNÁNDKZ‐RUIZ,
M. LÓPEZ‐CABRERA,
A. GARCÍA‐DÍEZ,
F. SÁNCHEZ‐MADRID,
R. GONZÁLEZ‐AMARO,
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摘要:
SummaryIt has been suggested that the involution of the pigmented lesions of halo naevus (HN) is mediated by an immune response, with the involvement of specific cytotoxic T lymphocytes. To explore further the pathogenesis of HN. skin biopsies from six patients with this condition were obtained and the characteristics of the infiltrating inflammatory ceils were studied by immunostaining techniques. We found that the cell infiltrate of HN is mainly composed by CD8+T lymphocytes that express the activation molecule CD69. Tumour necrosis factor‐α (TNF‐α) immunoreactivity was detected on the inflammatory cells, a finding that suggests that the infiltrating T cells of HN are actively synthesizing this cytokine. Our results indicate that the infiltrating cells of HN predominantly have an activated cytotoxic phenotype, and suggest that these cells are indeed involved in the regression of the naevomelanocytic naevus
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.20755.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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3. |
Incidence of familial dermatitis herpetiformis |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 394-398
T. REUNALA,
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摘要:
SummaryDermatitis herpetiformis (DH) and coeliac disease (CD) are gluten‐sensitive diseases which have a common immunogenetic background, with the histocompatibility locus antigen (HLA) alleles DQ Al*0501 and Bl*0201 in the short arm of chromosome 6. CD is well known to cluster in families whereas DH has not been generally regarded as a familial disease. To study the familial incidence of DH, a prospective study was started in 1969 at the Department of Dermatology of Helsinki University Hospital and in 1976 at the Department of Dermatology of Tampere University Hospital. A total of 1018 patients with DH were diagnosed and questioned for positive family histories. Of the 999 unrelated DH patients. 105 (10·5%) had one or several affected first‐degree relatives. The disease in the relatives was either DH (4–4%) or CD (6·1%), Analysis of the 105 families showed that 13·6% of parents, 18·7% of siblings and 14·0% of children were affected, a segregation pattern which fits well to a dominant mode of Mendelian inheritance. Gender may also be important because the first‐degree relatives affected with DH were more often females and those affected with CD twice as often females as males. In contrast, there were more males among the 105 propositi with DH and also among the 894 DH patients with no affected relativesThe present study clearly shows that DH is a familial disease in which the first‐degree relatives can be affected both with DH and CD, presumably because of a common genetic background. The environmental factors which could cause the rather high penetrance of DH and CD in the first‐degree relatives of DH patient
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.21756.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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4. |
Calcitonin gene‐related peptide, endothelin‐1, the cutaneous microvasculature and Raynaud's phenomenon |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 399-406
C. B. BUNKER,
P. C. GOLDSMITH,
T. A. LESLIE,
N. HAYES,
J. C. FOREMAN,
P. M. DOWD,
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摘要:
SummaryIt has been argued that the digital cutaneous microvasculature is the site of the anomaly which causes Raynaud's phenomenon (RP). Both endothelin‐1 (ET‐1), a potent vasoconstrictor peptide present in the digital cutaneous microvasculature. and calcitonin gene‐related peptide (CGRP). a powerful vasodilator present in digital cutaneous perivascular nerves, have been implicated in the pathogenesis of RP. Circulating ET‐1 levels are raised, and there is a diminution of CORP‐containing perivascular nerves in linger skin in RPWe undertook a pharmacological study to investigate the sensitivity of the digital cutaneous microvasculature to intradermal ET‐l and CGRP. Differences were found in RP compared with normal digital skin, supporting the idea that the digital cutaneous microvasculature is actively involved in the pathogenesis of RP. In RP, the erythematous response to ET‐1 was diminished at both 20 and 5°C (a low temperature at which RP classically occurs) providing pharmacological support for the morphological evidence that in RP there is a deficiency of CGRP‐containing nerves in the dis
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.22757.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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5. |
Antineutrophil cytoplasmic autoantibodies in patients with systemic sclerosis |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 407-410
S. AKIMOTO,
O. ISHIKAWA,
T. TAMURA,
Y. MIYACHI,
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摘要:
SummaryPerinuclear type of antineutrophil cytoplasmic antibodies (p‐ANCA) have been found in patients with periarteritis nodosa. Churg‐Strauss arteritis. or pauci‐immune idiopathic crescentic glomerulonephritis. Recently, the association of p‐ANCA and normotensive renal failure, in patients with systemic sclerosis (SSc), was reported. We have studied the incidence of p‐ANCA in patients with SSc and have investigated its relationship to clinical and laboratory findings. Sera from 77 patients with SSc were examined by the indirect immunofluorescence (IIF) test, employing an ethanol‐fixed human neutrophil and enzyme‐linked immunosorbent assay, using purified myeloperoxidase (MPO) as an antigen (MPO‐ELISA). The sera from seven patients (9‐1%) were p‐ANCA positive, by both IIF and MPO‐ELISA. One patient died from systemic necrotizing angiitis but the remaining six patients have shown no symptoms of systemic vasculitis or of renal involvement. There was a tendency for patients positive for p‐ANCA (anti‐MPO antibody) to also be positive for other autoantibodies. such as anti‐Sc1‐70 antibody, anti‐centromere antibody, anti‐microsome antibody, anti‐thyroglobulin antibody and rheumatoid factor. Although the incidence of p‐ANCA (anti‐MPO antibody) is low in patients with SSc, and its clinical significance in SSc needs further investigations, this could be a serolog
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.23758.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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6. |
Plasminogen activator inhibitor type‐2 in the lesional epidermis of lupus erythematosus |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 411-419
M. J. BECHTEL,
B. M. SCHAEFER,
M. D. KRAMER,
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摘要:
SummaryUnder certain pathophysiological conditions epidermal keratinocytes produce urokinase‐type plasminogen activator (LIPA) or tissue‐type PA (tPA). These PAs are subject to regulation by PA inhibitors (PAI). including PAl type‐2 (PAI‐2). In the normal epidermis. PAI‐2 is present in the differentiating suprabasal layers, albeit in the apparent absence of PAs. It has, therefore, been suggested that PAI‐2 plays a role in epidermal differentiation not linked to its ability lo inhibit PAs. In line with this hypothesis, we have studied, by immunohistochemistry. the distribution of PAI‐2. uPA and tPA in the normal and in the lesional epidermis of patients with lupus erythematosus (LE). a disease in which epidermal differentiation is disturbed. The PAI‐2 antigen was detectable in the normal epidermis and in the lesional epidermis of LE. In the normal epidermis, the PAI‐2 antigen was most pronounced in the granular layer. In the hyperkeratotic epidermal lesions of LE. the PAI‐2 antigen was increased. In normal and lesional skin. PAI‐2 was distributed along the cell periphery. Indicating its association with the cornified envelope. Neither uPA nor tPA was detectable in normal or lesional epidermis. Our findings show that PAI‐2 is a major type of PAI in normal epidermis and in the lesional epidermis of LE, and that increased epidermal PAI‐2 is observed in a disease which is not associated with an increase in epidermal PAs. The data support the hypothesis that epidermal PAI‐2 may have other functions than th
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.24759.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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7. |
The relevance and effect of amalgam replacement in subjects with oral lichenoid reactions |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 420-423
S. H. IBBOTSON,
E. L. SPEIGHT,
R. I. MACLEOD,
E. R. SMART,
C. M. LAWRENCE,
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摘要:
SummaryIn this study we examined the prevalence of mercury hypersensitivity in patients with oral lichenoid reactions (OLR) and the effect of amalgam replacement in subjects with amalgams adjacent to OLR irrespective of their mercury sensitivity status. One hundred and ninety‐seven patients with oral problems were examined: 109 with OLR. 22 with oral and generalized lichen planus. and 66 with other oral diagnoses, including aphthous ulcers and orofacial granulomatosis. Nineteen per cent of patients with OLR reacted to mercury on patch testing, significantly more than in those with generalized lichen planus (0%) and in those with other oral diagnoses (3%). Twenty‐two patients with OLR and adjacent amalgams had amalgam replacement and. in 16 of 17 mercury‐positive subjects and three of four mercury‐negative subjects, the OLR resolved after amalgam removal. In conclusion, we found a significantly increased prevalence of mercury hypersensitivity in patients with localized OLR in comparison to subjects with other oral problems. Amalgam replacement resulted in resolution of OLR in the majority of patients with amalgams adjacent to OLR irrespective of their mercury sensitivity
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.25760.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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8. |
Differential irritant skin responses to topical retinoic acid and sodium lauryl sulphate: alone and in crossover design |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 424-430
I. EFFENDY,
S. WELTFRIEND,
S. PATIL,
H. I. MAIBACH,
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摘要:
SummaryTopically applied all‐trans retinoic acid (RA) is often associated with skin irritation. A detailed quantification of RA‐induced functional changes in stratum corneum is. however, still limited. U sing noti‐invasive bioengineering techniques of measurements of transepidermal water loss (TEWL), stratum corneum hydration and cutaneous blood flow (CBF). we quantified the irritant effects of 0·05% and 0·1% RA in ethanol on normal skin compared with 1% sodium lauryl sulphate (SLS) in water as a model irritant in a 24‐h occlusive patch‐test assay. Additionally, in order to document data possibly related to the mechanism of action, skin responses to both compounds applied in tandem was also investigated over 18 daysThe extent of the irritant response to 0·05 and 0·1% RA, respectively, were similar, implying analogous irritation potency. While RA caused more intense scaling than SLS. other skin responses to RA were significantly weaker than those due to SLS. An increase in TEWL. on day 7. in RA‐exposed sites indicates a secondary delayed impairment of the stratum corneum (SC) barrier. In a tandem‐design assay, pretreatment with RA appeared to reduce the irritant effects of SLS on SC hydration and CBF. In contrast, pre‐exposure to SLS showed a synergestic response in erythema, scaling and TEWLOur results demonstrate that RA, like SLS. is capable of impairing SC water barrier function, which may be responsible, in part, for the irritation associated with its topical use. However, the distinctive biological responses to these compounds suggest a different mode of action of RA and SLS. In addition, the precise reason for the unique results observed in the tandem‐desig
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.26761.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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9. |
Topical retinoic acid changes the epidermal cell surface glycosylation pattern towards that of a mucosal epithelium |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 431-436
C. E. M. GRIFFITHS,
E. DABELSTEEN,
J. J. VOORHEES,
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摘要:
SummaryTopical all‐trims retinoic acid (RA) produces a number of epidermal changes which are indistinguishable from those observed following treatment with a local irritant, namely sodium lauryl sulphate (SI. S). This observation has led to criticism that the efficacy of RA in disorders such as photoageing. Is merely a result of irritancy. In stratified epithelia, the cellular differentiation process is characterized by a stepwise synthesis of cell surface carbohydrates, and each type of stratified epithelium has its own specific pattern of carbohydrate expression. Glycosyltransferases, which are responsible for carbohydrate synthesis, are influenced by retinoids. Thus, we investigated whether epidermal cell surface glycosylation is altered in skin treated with topical RA, and contrasted it with changes induced by topical SLSSkin biopsies were obtained from seven normal volunteers who had been treated, on three separate areas of buttock skin, with single applications of 0·1% RA. 2% SLS, or vehicle creams, followed by 4‐day occlusion. Biopsies were assessed immunohistologically using highly specific monoclonal antibodies to cell surface carbohydrates (types 1, 2 and 3 chain structures), previously demonstrated in the epidermis and in oral mucosal epithelium. Although type 1 chain structures were not demonstrated in any of the samples, the distribution of type 2 and 3 chain structures in RA‐treated epidermis was altered towards that seen in a mucosal epithelium. T antigen, a mucin‐type cell surface carbohydrate structure normally expressed throughout the epidermis, was only observed in the granular layer of RA‐treated epidermis‐a feature of mucosal epithelia. Ley, normally only seen in non‐keratinized buccal epithelium, was strongly expressed in RA‐treated epidermis. In contrast, the glycosylation pattern of the SLS‐treated epidermis was not significantly different from that observed after vehicle treatment. Thus, RA treatment converts normal stratified epithelium towards the phenotype of mucosal epithelium with a decrease in T antigen and a concomitant increase in Ley. These changes the not observed following treatment with SLS and identify an important difference between RA eff
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.27762.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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10. |
A comparison of the culture and growth of dermal papilla cells from hair follicles from non‐balding and balding (androgenetic alopecia) scalp |
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British Journal of Dermatology,
Volume 134,
Issue 3,
1996,
Page 437-444
V. A. RANDALL,
N. A. HIBBERTS,
K. HAMADA,
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摘要:
SummaryMale pattern baldness is a common, androgen‐dependent skin problem in adult men which is not well understood, although androgens are believed to act on the hair follicle via the mesenchyme‐derived dermal papilla situated in the middle of the hair follicle bulb. Since dermal papilla cells retain specific characteristics in culture, such as hair‐growth promoting ability and appropriate features of the mechanism of androgen action, dermal papilla cells from follicles undergoing androgen‐stimulated miniaturization may provide a useful in vitro model system. Therefore, dermal papilla cells have been derived from intermediate follicles from balding and nearly clinically normal sites of men with androgenetic alopecia. Balding dermal papillae were much smaller than non‐balding ones and grew much less well under normal growth conditions. Supplementing the medium with human serum, rather than fetal calf serum, increased both the yield of established cultures and the number and health of the dermal papilla cells produced. Non‐balding cells also grew faster in human serum. Balding cells retained the normal fibroblastic shape and aggregative behaviour of dermal papilla cells, but always grew less well than non‐balding cells. Nearly clinically normal dermal papillae were similar, or slightly smaller, in size to non‐balding ones, but their growth resembled balding cells. Since balding dermal papilla cells can be cultured, though with much greater difficulty than non‐balding ones, and exhibit differing growth characteristics to non‐balding cells, they merit further investigation which may Increase our understanding of. and ability to control, an
ISSN:0007-0963
DOI:10.1046/j.1365-2133.1996.28763.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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