J.M. Marks
Royal Victoria Infirmary
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Featured researches published by J.M. Marks.
The Lancet | 1985
P.M. Farr; J.M. Marks; L.B. Krause; Sam Shuster
A randomised double-blind placebo-controlled study showed improvement of scalp psoriasis with oral ketoconazole, although the study had to be stopped before completion because of the possibility of drug toxicity. The common appearance of psoriasis in the scalp and certain other sites may be due to pityrosporal colonisation that also causes seborrhoeic dermatitis and dandruff.
British Journal of Dermatology | 1989
E.M. Higgins; C.S. Munro; J.M. Marks; P.S. Friedmann; Sam Shuster
Seventeen patients with chronic psoriasis were given cyclosporin A (CsA) 5 mg/kg per day. Twelve patients cleared within 3 months and their relapse rate, 41% at 6 months, was not significantly different from that previously reported with dithranol or PUVA. This pilot study also suggests that continuing CsA for up to 4 weeks after clinical clearance confers no advantage with regard to relapse. Significant adverse effects on renal function and blood pressure did not occur.
British Journal of Dermatology | 1986
J.M. Marks
MADAM, We were interested to read the report by Drs Meyrick-Thomas and Kennedy {British Journal of Dermatology, 1986,114,377) describing the development of perineal lichen sclerosus et atrophicus in a pair of monozygotic female twins. We have recently seen the same disorder in a pair of non-identical female twins, who developed lesions at the age of 2 years and 27 years respectively. Both girls are otherwise well; their sister (aged 5 years) is unaffected, and there is no family history of autoimmune disease. Their mother had had granuloma annulare several years previously. The striking feature of these twins, like those described by Meyrick-Thomas and Kennedy, was the development of lesions in both twins within a 6-month period. This supports the feeling that there may be a genetic aspect in some cases of lichen sclerosus et atrophicus.
Clinical and Experimental Dermatology | 1993
C. S. Munro; N. H. Cox; J.M. Marks; S. Natarajan
Four patients with lichen nitidus who presented with palmoplantar or nail lesions arc reported. In three cases palmoplantar hyperkeratosis was marked; these cases also had nail‐plate lesions, but in all four, lesions of lichen nitidus at other sites were absent, sparse or asymptomatic.
Clinical and Experimental Dermatology | 1993
S.M. Bhate; G.R. Sharpe; J.M. Marks; Sam Shuster; W.M. Ross
The prevalence of skin and internal malignancies was estimated from the general practitioners’notes of 2247 patients with psoriasis and 4494 age‐ and sex‐matched controls. The prevalence of skin cancer in the psoriatics was 155% that of controls, but this was not significant at the 5% level. Subgroup analysis showed an increase in skin cancers in women (P > 0.05). There was no difference in the age of onset of skin cancers between psoriatics and controls and there was no evidence of a cumulative therapeutic risk. There was no difference in the prevalence of non‐skin cancers between psoriatics and controls.
British Journal of Dermatology | 1993
David J. Gawkrodger; J.P. Vestey; S. O'mahony; J.M. Marks
Fifteen (5.3%) of 282 patients with dermatitis herpetiformis (DH) were diagnosed as suffering from coeliac disease before the onset of their DH. This group showed a female preponderance, and a later than usual onset of DH. The mean age at which DH developed was 40.0 years, and there was a mean interval of 132.2 years between the two diagnoses. Seven patients had stopped their gluten‐free diet, and a further four were poor compliers. Persistent gluten ingestion in coeliacs with a specific genetic predisposition may result in the development of DH.
British Journal of Dermatology | 1978
I.J. Karlsson; M.G.C. Dahl; J.M. Marks
Skin biopsies from 17 patients with coeliac disease, but without dermatitis herpetiformis, were examined by direct immunofluorescence. In none of them was IgA detectable. In contrast, IgA was present in dermal papillae and/or in relation to the dermo‐epidermal junction in 80 out of 83 patients with dermatitis herpetiformis. These findings confirm that cutaneous deposition of IgA at these sites is a very characteristic feature of dermatitis herpetiformis and is unrelated to coeliac disease itself.
British Journal of Dermatology | 1981
H. Moseley; B.L. Diffey; J.M. Marks; Rona M. Mackie
Patients undergoing oral psoralen photochemotherapy (PUVA) for psoriasis receive a known amount of UV‐A in the treatment cubicle and an unknown amount of UV‐A from sunlight. In order to measure the solar UV‐A dose, fifty‐six patients received a UV‐sensitive film badge to be worn from the time they took their psoralen tablet throughout the course of the day, except during treatment. The UV‐A doses measured in this way varied from less than 0.2 J cm‐2 to 7 J cm‐2, with a median of around 1 J cm‐2. These results show that the solar UV‐A received by patients who have been photosensitized by 8‐MOP may not be insignificant in relation to the treatment dose.
Clinical and Experimental Dermatology | 1991
J. McLelland; S. Young; J.M. Marks; C.M. Lawrence
Granuloma annulare may be recurrent and various precipitating factors have been described1 but seasonal cases have not been previously reported.
Drug Investigation | 1990
C. S. Munro; E. M. Higgins; B. Ramsay; J. McLelland; J.M. Marks; P. S. Friedmann; P. M. Farr; R. Dover; J. Rees; S. Young; C. M. Lawrence; F. Humphreys; Sam Shuster
SummaryTo try to explain the wide therapeutic range of cyclosporin A, we examined its effects on physiological functions of skin and responses to immunological and inflammatory stimuli during and before or after administration of 5 mg/kg/day of cyclosporin A in the treatment of various skin diseases.Pilocarpine-stimulated, sweat rate (10 patients), sebum excretion rate (10), scalp hair growth rate (8) and epidermal proliferation in response to tape-stripping (7) were not affected by cyclosporin A; nail growth rate was unaltered in patients without psoriasis (12), but was significantly slowed by treatment in patients with psoriasis (7) who had abnormally rapid growth before treatment.Induction of cell-mediated sensitisation to 2,4-dinitrochlorobenzene (DNCB) was inhibited by cyclosporin A treatment (22 patients), but 7 patients sensitised to DNCB before cyclosporin treatment reacted normally to DNCB challenge during treatment. The immediate hypersensitivity response to intradermal house dust mite antigen was increased during treatment in 8 patients with atopy.Weal responses to histamine (9 patients) and compound 48/80 (12), the 24 hour erythemal response to ultraviolet B (UVB) irradiation (10) and the inflammatory response to topical leukotriene B4 (16) were not affected, but cyclosporin A produced a striking inhibition of anthralin inflammation (21).Since the methods we used will have detected all but minor changes, we conclude that cyclosporin A has no gross physiological effects on the skin and is not cytostatic; hypertrichosis must be due to a prolonged hair cycle. Secondly, cyclosporin A (a) impairs induction of cell-mediated sensitisation in doses which permit some continued expression, but (b) increases immediate hypersensitivity. Thirdly, cyclosporin A has no general anti-inflammatory effect, but we have found a novel and specific inhibitory effect on anthralin inflammation, the mechanism of which may underlie some of its therapeutic effects. The therapeutic effect of cyclosporin A may not be due solely to its immune effects, and other activities such as the anti-inflammatory effect we found need further exploration.