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Biomedical subjects

A D Burden

Publications and source records attributed to A D Burden.

At least 37 records · Page 2Linked to original sources
PubMed2000

Accuracy of questions related to allergic contact dermatitis.

BACKGROUND: The ability of a physician to select individuals likely to benefit from patch testing depends on his or her ability to interpret responses to enquiries related to contact allergy. The significance of such responses to questions of nickel, fragrance and colophon allergy is unclear. OBJECTIVE: The specificity, sensitivity and predictive value of questions relating to nickel, fragrance and colophony allergy were determined. METHOD: A total of 258 patients attending for routine patch testing were questioned about skin reactions to nickel, fragrances and Elastoplast (Smith and Nephew Healthcare, Hull, England). All subjects were then patch tested to nickel, fragrance mix, and colophony. Responses to questions were compared with patch test results. RESULTS: The sensitivity of questions relating to nickel, fragrance, and colophony was 82%, 49%, and 71%, respectively. The specificity of the same questions was 77%, 79%, and 90%; the positive predictive value was 54%, 46% and 29%, respectively. After adjustment to include clinical relevance, the sensitivity of nickel questions rose to 100%. CONCLUSION: These data permit greater understanding of the role of patient history in selection of patients for patch testing.

Allergens↗
PubMed1999

Genetic and environmental influences in the development of multiple primary melanoma.

OBJECTIVES: To identify risk factors and the prognosis associated with the development of multiple primary melanoma (MPM). DESIGN: Case-comparison studies of subjects with MPM and single primary melanoma. Sequencing of CDKN2A in germline DNA. SETTING: Population-based study of patients with invasive melanoma in Scotland between 1979 and 1996. PATIENTS: For mortality studies, 108 patients with MPM and 216 single melanoma controls matched for age, sex, site, and tumor thickness. For risk factor studies, 48 patients with MPM and 48 single melanoma controls matched as above. For CDKN2A analysis, a sample of 23 subjects with MPM. RESULTS: The development of MPM was found not to be an independent prognostic factor. The risk of MPM was greatest in those with a family history of melanoma, with large numbers of benign nevi, and the presence of clinically or histologically atypical nevi. Germline mutations of CDKN2A were present in 6 of 23 patients with MPM and in 5 cases consisted of the base pair substitution Met53Ile. CONCLUSIONS: The importance of MPM should be addressed in melanoma follow-up protocols. Those patients at greatest risk can be identified by a family history of melanoma and their mole pattern. Germline mutations in CDKN2A occur in both familial and sporadic MPM and further studies are required to determine the value of analysis of this gene in melanoma surveillance. Patients should be informed that the development of MPM does not adversely affect their prognosis.

Disease Susceptibility↗
PubMed1999

Management of psoriasis in childhood.

It is not unusual for psoriasis to start in childhood although a mild or atypical presentation sometimes makes it difficult to establish a confident diagnosis at this age. All adult forms occur but flexural psoriasis and guttate psoriasis are particularly common. Management involves education of the child and parents concerning the nature of psoriasis and the effects of treatment. Genetic counselling may be provided if needed based on population data. Environmental triggers of psoriasis should be sought particularly infection. Psoriasis can usually be treated effectively in children with topical agents including emollients, coal tar, corticosteroids, dithranol and calcipotriol according to age and the sites affected. In those who do not respond, consideration should be given first to day care or in-patient treatment which may be combined with UVB phototherapy. Systemic therapy should be used only under extreme circumstances such as resistant erythrodermic, pustular or arthropathic psoriasis. There are no controlled trials in this age group but the most experience has been with retinoids which are probably the second-line drug of choice for children. Methotrexate and cyclosporin appear to be effective in children but more efficacy and safety data are required.

Administration, Topical↗
PubMed1999

Upregulation of connexin 26 is a feature of keratinocyte differentiation in hyperproliferative epidermis, vaginal epithelium, and buccal epithelium.

In epidermis, it has been suggested, intercellular communication through gap junctions is important in coordinating cell behavior. The connexins, may facilitate selective assembly or permeability of gap junctions, influencing the distribution of metabolites between cells. Using immunohistochemistry, we have compared the distribution of connexins 26 and 43 with that of proliferating cells (Ki67 labeling) in normal epidermis, hyperplastic epidermis (tape-stripped epidermis, psoriatic lesions, and viral warts), and vaginal and buccal epithelia. Connexin 43 was abundant in spinous layers of all epidermal specimens and in vaginal and buccal epithelia. Connexin 26 was absent from the interfollicular and interductal epidermis of normal hair-bearing skin, and nonlesional psoriatic epidermis but present at very low levels in plantar epidermis. Connexin 26 was prominent in lesional psoriatic epidermis and viral warts and in vaginal and buccal epithelia. In three independent experiments connexin 26 appeared in a patchy intercellular distribution in the basal epidermis within 24 h of tape stripping, proceeding to more extensive distribution in basal and suprabasal layers by 48 h. The increase in connexin 26 preceded that in cell proliferation. In vaginal epithelium, buccal epithelium, and viral warts connexin 26 was restricted mainly to suprabasal, nonproliferating cells. In psoriatic lesional epidermis connexin 26 was also located mainly in suprabasal, nonproliferating cells. Connexin 26 was present in a patchy distribution in the basal layer of psoriatic lesional epidermis, but double labeling for connexin 26 and Ki67 showed that many connexin 26 positive basal cells were nonproliferative, suggesting that connexin 26 may be related to differentiation rather than to proliferation. These observations would be consistent with a role for connexin 26 containing gap junctions during both early and later stages of keratinocyte differentiation in hyperplastic epidermis and in vaginal and buccal epithelia.

Cell Differentiation↗
PubMed1999

The genetics of allergic contact hypersensitivity to nickel.

We have examined evidence for familial disposition to nickel allergic contact dermatitis (Ni ACD). 258 patients attending for routine patch testing were recruited prospectively. 39 patients were diagnosed with Ni ACD. 31 of 209 1st-degree relatives (15%) of probands had a history of nickel hypersensitivity. 84 patients with no history of nickel hypersensitivity and negative patch tests to nickel were used as controls. 24 of 458 1st degree relatives of controls (5.2%) had a history of Ni ACD. The risk ratio for 1st degree relatives of a patient with Ni ACD is 2.83 (95% confidence intervals are 2.45, 3.27). This is the 1st study to present a statistic to represent risk to relatives of developing ACD. Relatives of patients with Ni ACD have an increased risk of developing the condition, but the genetic basis for this is not yet known. With currently available techniques, this value of relative risk makes a positional cloning approach to gene identification impractical.

Dermatitis, Allergic Contact↗
PubMed1998

Lichen sclerosus and lichen planus: a spectrum of disease? Report of two cases and review of the literature.

There has long been controversy concerning the relationship between lichen planus and lichen sclerosus. Whilst these two conditions are now considered distinct, there are shared clinical and pathological features. We now describe two patients with the cutaneous involvement of both lichen planus and lichen sclerosus, presenting a review of similar reported cases and discussing the implications for pathogenesis of these two diseases. Neither lichen planus (LP) nor lichen sclerosus (LS) are uncommon yet they have only infrequently been reported as coexisting. In his original description of LS, however, Hallopeau considered it to be a variant of LP and Gougerot has also commented on a possible common pathogenesis for the two conditions. Features which tend to support such as association include the distribution of the cutaneous lesions, histopathological features such as hydropic basal cell degeneration and a band-like lymphohistiocytic infiltrate in the dermis, and the reported association with autoimmune disease. We now report two patients in whom coexistent cutaneous LS and LP was confirmed histologically.

Adult↗
PubMed1998

Genetics of psoriasis: paternal inheritance and a locus on chromosome 6p.

The pathogenesis of psoriasis is not fully understood, but population and twin studies suggest a large heritable component to the etiology. Several large population studies have also suggested a parental sex effect. Since 1994, three main genetic loci (on chromosomes 17q, 4q, and 6p) have been reported in genome scans. With a view to elucidating the genetic basis of psoriasis, we have carried out linkage analysis in a large number of families with well-characterized psoriasis. From a cohort of 1250 probands with psoriasis, 395 individuals (301 affected, 94 unaffected) in 103 families were recruited. Each subject was carefully examined by an experienced dermatologist and stringent diagnostic criteria applied. Genotypes were generated at 11 polymorphic loci on chromosomes 17q, 4q, and 6p and the results were analyzed parametrically and nonparametrically. In the population from which the probands were drawn, there was evidence of a parental sex effect, more probands having an affected father than an affected mother. Genetic anticipation was also apparent and most marked if the disease was inherited from the father. The loci on chromosomes 17 and 4 were not replicated but there was strong evidence for linkage to chromosome 6p (maximum two point LOD score 4.63 at D6S291). The evidence for linkage in sibling pair analysis was greatest when the allele was of paternal origin and was most significant in those families without psoriatic arthritis. These studies confirm the presence of a susceptibility gene on chromosome 6p. The available evidence suggests that a different genetic susceptibility may underlie psoriasis and psoriatic arthritis.

Age of Onset↗
PubMed1996

IgA class anticardiolipin antibodies in cutaneous leukocytoclastic vasculitis.

BACKGROUND: Autoantibodies may be detected in the serum of some patients with cutaneous leukocytoclastic vasculitis. We have previously reported the presence of IgA anticardiolipin antibodies (ACAs) in one patient with leukocytoclastic vasculitis associated with IgA nephropathy. OBJECTIVE: Our purpose was to determine the prevalence of IgA ACAs in unselected groups of patients with cutaneous vasculitis, IgA nephropathy, and Henoch-Schönlein purpura. METHODS: Thirty patients (10 each with cutaneous vasculitis, IgA nephropathy, and Henoch-Schönlein purpura) and 31 healthy control subjects were studied. ACA titers were measured by a standardized enzyme-linked immunosorbent assay. RESULTS: ACAs restricted to the IgA isotype were present in 6 of 10 patients with cutaneous leukocytoclastic vasculitis. IgA ACA levels were significantly higher in these patients than in the control subjects. The presence of IgA ACAs did not correlate with disease severity or involvement of other organs and persisted after resolution of the vasculitis in most patients. In five of the six patients with IgA ACAs, drugs were implicated in the pathogenesis of the vasculitis. By contrast, ACAs were present in only a minority of children with Henoch-Schönlein purpura and adults with IgA nephropathy and were not restricted to the IgA isotype. CONCLUSION: We have demonstrated a clear association between IgA ACAs and cutaneous leukocytoclastic vasculitis. The absence of IgA ACAs in Henoch-Schönlein purpura argues against their being an epiphenomenon in vasculitis.

Adult↗
PubMed1996

Mdm-2 is not induced by p53 in human keratinocytes in vivo.

Normal p53 protein protects the genome after DNA damage by delaying replication and allowing DNA repair. mdm-2 is a recently discovered protein that controls p53 activity by binding to and inactivating p53 protein. A negative feedback loop has been suggested in which p53 induces mdm-2 expression. We have shown that doses of ultraviolet B radiation that cause mild sunburn clinically, produce thymine dimers in keratinocytes detectable by immunocytochemistry. This causes an elevation of p53 protein without a concomitant p53-mediated induction of mdm-2.

DNA Damage↗
PubMed1996

The spectrum of nail involvement in palmoplantar pustulosis.

Abnormalities of the nail are not a well recognized feature of palmoplantar pustulosis (PPP). However, in a group of 50 patients with PPP, we found nail dystrophy in 15 (30%). The most frequent pattern was subungual pustulation, present in 10 patients, and progressing to nail destruction in two. Onycholysis and pitting of the nail were present in a few patients. In contrast to psoriasis vulgaris, the rate of linear nail growth in PPP was no greater than in matched normal controls. This is another clinical feature of PPP that separates it from psoriasis vulgaris.

Adult↗
PubMed1994

IgA anticardiolipin antibodies associated with Henoch-Schönlein purpura.

Henoch-Schönlein purpura is associated with the deposition of immune complexes containing IgA. The nature of the antigen in these immune complexes is uncertain but in some reported cases has included autoantigens such as IgA rheumatoid factor and IgA antineutrophil cytoplasmic antibody. We report the finding of an IgA class anticardiolipin antibody in a 51-year-old patient with Henoch-Schönlein purpura. A potential role for IgA autoantibodies in Henoch-Schönlein purpura needs to be further explored.

Antibodies, Anticardiolipin↗