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Biomedical subjects

J E Sansom

Publications and source records attributed to J E Sansom.

At least 19 recordsLinked to original sources
PubMed1999

Colophony allergy: a review.

Colophony is a complex mixture of over 100 compounds derived from pine trees. It has countless applications at home and at work and exposure to colophony and modified-colophony is universal. It is the oxidation products of unmodified and modified colophony and some of the new resin acids synthesized during modification that are the principle allergens in colophony. The neutral fraction may account for a small % of positive reactions. When screening for allergy using unmodified gum rosin, allergy to modified rosin will not be revealed. When patients react to both materials, it is probably due to unmodified colophony present in both, rather than a cross-reaction. Relevant positive reactions may be missed if only colophony 20% pet is relied upon as the screening material.

Allergens↗
PubMed1997

Urinary leukotriene E4 levels in patients with atopic dermatitis.

Leukotriene synthesis may be increased in a variety of inflammatory diseases. Urinary leukotriene E4 is a stable metabolite of leukotrienes C4 and D4 which has previously been found to be increased in exacerbations of severe asthma and after antigen inhalation. Levels of urinary LTE4 in seven patients during and after a severe flare of atopic dermatitis were measured by high-performance liquid chromatography (HPLC) and radioimmunoassay (RIA). Mean urinary LTE4 levels (+/- SEM) were not increased during (16.7 +/- 3.7 pg/mumol) or after (16.9 +/- 4.8 mumol) the acute exacerbation of atopic dermatitis when compared with the normal range (mean = 23.8 [95% confidence interval 19.9-28.2] pg/mumol creatinine). These findings do not provide evidence of cysteine leukotriene involvement in the pathogenesis of atopic dermatitis.

Acute Disease↗
PubMed1997

Susceptibility of Malassezia furfur subgroups to terbinafine.

Malassezia furfur, the fungus causing pityriasis versicolor, has been reported to be sensitive to terbinafine in vitro but although topical therapy is effective in the treatment of pityriasis versicolor, oral therapy is not. This phenomenon was investigated by determining the susceptibility to terbinafine of different M. furfur subgroups in vivo (during topical or oral application) and in vitro. All M. furfur subgroups were suppressed (approximately 10-fold) by topical terbinafine. Oral treatment resulted in no significant suppression of cutaneous M. furfur populations with the exception of a single subgroup (A), which was reduced to undetectable levels on the skin of eight of 10 patients receiving oral terbinafine. Isolates of subgroup A were also markedly more susceptible to terbinafine in laboratory tests. The importance of the recognition of distinct subgroups within the cutaneous lipophilic yeasts when evaluating their antifungal susceptibility and their role in disease is discussed.

Administration, Cutaneous↗
PubMed1996

Effects of H1- and H2-antihistamines on platelet-activating factor and bradykinin-induced inflammatory responses in human skin.

Previous studies show that oral antihistamines affect the weal and flare response to intradermal injections of the inflammatory mediators platelet-activating factor (PAF) and bradykinin (BK). The aim of this study was to compare the effects of terfenadine (an H1-antagonist) and cimetidine (an H2-antagonist) on weal and flare responses to PAF and BK in healthy non-atopic human volunteers. The effects of doxepin on PAF responses were investigated, as there is evidence that doxepin may have direct anti-PAF effects in addition to its known antihistaminic actions. Terfenadine significantly reduced weal and flare responses to PAF (mean reduction 53 and 73%, respectively) and flare responses to BK (mean reduction 78%) but had no effect on weal responses to BK. Doxepin significantly reduced both weal and flare responses to PAF (mean reduction 43 and 68%, respectively, at higher doses of PAF). Cimetidine had no effect on weal or flare responses to PAF or BK. These findings suggest that the flare response to intradermal BK is mediated via histamine release while the weal response is not. The effects of the various antagonists of PAF-induced responses suggest that its effects too may be mediated via histamine, the similarity of the effects of terfenadine and doxepin on these responses indicating that the effects of doxepin may be due to its known antihistamine activity rather than to any specific PAF-antagonistic properties. Platelet-activating factor (PAF) is a phospholipid which is released from a wide range of cell types and also from vascular endothelium. PAF is formed by the conversion of ether-linked phospholipids initially to the biologically inactive lyso-PAF and then by acetylation to PAF. Intradermal injection of PAF in human skin causes vasodilatation and increased vascular permeability, producing a weal and flare response with accompanying pruritus. Bradykinin (BK) is a vasoactive polypeptide formed by the action of enzymes known as kallikreins on inactive precursors called kininogens. Its effects include an increase in blood flow and vascular permeability and stimulation of the release of prostaglandins and histamine. On intradermal injection in human skin it causes a weal and flare response with associated pain rather than pruritus. Previous studies have suggested that the weal and flare response to PAF may be mediated in part by histamine release. Given that BK is known to cause histamine release it appears possible that the responses to both compounds may be modified by conventional antihistamines. Experiments based on this premise have found that antihistamines have a pronounced effect on the flare response to PAF but a less marked effect on weal responses. The weal response to BK was unaffected by systemic antihistamines but studies have produced conflicting results with regard to effects on the flare response. The aim of this study was to compare the effects of terfenadine (an H1-antagonist) and cimetidine (an H2-antagonist) on PAF- and BK-induced weal and flare responses in healthy, non-atopic human volunteers. Based on the treatment of cold urticaria it has been suggested that doxepin, which has known H1- and H2-antagonistic effects, may in addition show specific anti-PAF activity. We compared the effects of doxepin on PAF-induced intradermal responses with those of terfenadine and cimetidine in this study.

Administration, Oral↗
PubMed1994

A fatal case of scleredema of Buschke.

Scleredema of Buschke is a rare disorder characterized by the development of areas of skin induration which usually resolve spontaneously. It is occasionally associated with a benign gammopathy, and rarely with myelomatosis. We describe a 60-year-old woman with extensive skin changes, who developed IgA myeloma. Unusually, her skin disease did not respond to conventional myeloma therapy. Death occurred as a consequence of the progressive skin disease.

Esophagus↗