Evening primrose oil and atopic eczema

Evening primrose oil and atopic eczema

Jones KM, Seeger JF, Yoshiro MT. Ipsilateral 2 motor deficit resulting from a subdural hematoma and a Kernohan notch. AJNR Am J Neuroradiol 1991; 12...

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Jones KM, Seeger JF, Yoshiro MT. Ipsilateral

2

motor deficit resulting from a subdural hematoma and a Kernohan notch. AJNR Am J Neuroradiol 1991; 12: 1238-39. Wender SS. Operation on the wrong side, an avoidable adverse event. J Fla Med Assoc 1990; 77: 585-86.

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does who

the unethical basis of these pictures. Doctors government employees or contractors should uphold professional ethical standards.’ In our opinion, the immediate withdrawal of these pictures by the National Institutes of Health is morally necessary. *G

Eschewing

the

predictable

Robyn Norton

Department of Community Paediatric Research, McGill University-Montreal Children’s Hospital Research Institute, Montreal, Québec, Canada H3H 1P3, and Department of Community Medicine, University of Auckland, New Zealand 1

Roberts I, Norton R, Jackson R, Dunn R, Hassall I. Effect of environmental factors on risk of injury of child pedestrians by vehicles: a case-control study. BMJ 1995; 310: 91-94.

Ethics of executed person SiR-We Dec 10,

on

motor

Internet

find Internet (see McConnell, anatomic slides and corresponding pictures of medical imaging of an executed murderer who donated his body to the US government for science and teaching. The belief that anyone in medicine might benefit from the knowledge gained by these pictures is absurd. The death penalty itself and all medical participation before, during, and after an execution is unethical under all conditions.’ The scientific world agrees without question that publishing data that are obtained under the slightest suspicion of unethical circumstances is clearly and necessarily unethical, irrespective of their scientific or teaching merit.2 Informed consent by the executed person 260

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upset

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presenting

1 2

3

dispel

are

M Roeggla Emergency Medicine, University of Vienna, A-1090 Vienna, Austria

Roeggla, U Landesmann,

Department

SIR-In his Nov 5 commentary McCormick describes as "banal" a study that we conducted on the determinants of childhood pedestrian injury. However, his comments were made without understanding of the local context in which the study was undertaken (and the report in question published) and without knowledge of the broader objectives. In New Zealand, Maori and Pacific Island children are 2-3 times more likely than their Pakeha/European counterparts to be injured as pedestrians. This excess risk is not infrequently ascribed by arguably racist lay observers to the so-called irresponsibility of Maori and Pacific Island parents and care-givers. Such accusations undoubtedly compound the distress caused to families by the loss or serious injury of a child. However, rarely has the notion of increased pedestrian exposure to risk by Maori and Pacific Island children (as a result of the poor families generally not having cars) been proposed as an alternative explanation. Our clear demonstration of the importance of exposure and the subsequent publicity it has received in New Zealand has hopefully served to remove some of the guilt felt by Maori and Pacific Island families of injured children. Banal, perhaps, but in our view worthwhile. Nevertheless, the causes of childhood pedestrian injury are diverse and in our large case-control study from which the exposure data were obtained we investigated the role of various factors, some of which are modifiable. Reports from the study on other risk factors are now in press.’ McCormick did not ask us whether or not we had looked beyond the question of exposure in studying the causes of child pedestrian injury. His assumption that we have not is wrong. Finally, our project was used by McCormick as an example of general practice research. The research was done from the Department of Community Health at the University of Auckland and this was clearly reported in our paper. Rather than eschewing the so-called predictable as suggested by McCormick, the Lancet readers would be well advised to eschew such superficial commentaries. *Ian Roberts,

not

of

W, Curran W. Doctors, the death penalty and lethal injections. N Engl J Med 1982; 307: 1532-33. Angell M. The Nazi hypothermia experiments and unethical research today. N Engl J Med 1990; 322: 1462-64. Editorial. US physicians and the death penalty. Lancet 1994; 343: 743.

Casscells

Evening primrose oil and atopic

eczema

SiR-Epogam evening primrose oil (EPO) provides gamolenic acid (GLA) for the management of atopic eczema. EPO is the only drug treatment for atopic eczema that has a rational basis: in eczema there is evidence that the conversion of dietary linoleic acid to GLA is impaired, leading to deficits of dihomogammalinolenic acid (DGLA) and arachidonic acid (AA) which are required for normal skin structure and function.,,2 This concept receives powerful support from a prospective study which showed that at birth those children who later develop eczema have raised levels of linoleic acid and severely reduced concentrations of DGLA and AA.3 EPO is therefore a rational and exceptionally safe treatment for the long-term management of atopic eczema since all it is doing is reversing a demonstrable biochemical deficit. EPO is the only treatment that has been shown in controlled trials to relieve itch/ the symptom that a recent British Association of Dermatologists’ working party emphasised as of central importance in atopic eczema.s In the light of these developments it is appropriate to revisit the report from Leicester published in The Lancet on June 19, 1993, which purported to show that Epogam was ineffective in the management of atopic eczema. In that report important data were omitted, including the findings using the main validated and established assessment system for eczema. Contrary to the authors’ claims, the study provides substantial evidence for the beneficial effects of Epogam. When the Leicester study is added to the other studies on Epogam in a meta-analysis, the significance of the beneficial effect of Epogam increases rather than diminishes. The study was specifically set up to investigate whether Epogam or placebo would have an additional beneficial effect in patients with moderate to severe eczema who continued to take moderately potent or potent steroids. This is a very severe test, for addition of another potent steroid would not be expected to exert a beneficial effect. The authors failed to emphasise this point and misrepresented the study as a simple comparison between Epogam and placebo. The trial was planned as part of a multicentre study in patients taking steroids but, because one of the Leicester authors wished to use it as part of a thesis project, that group decided to do their own study. Among the secondary aims of the trial were: (a) a comparison of the newly devised Leicester scoring system for eczema, which rates the whole body, including non-affected areas, with the validated Costa system, which appropriately rates the worst affected areas; and (b) an investigation of what happens on stopping treatment with Epogam. Since Epogam is likely to produce long-lasting changes in cell membrane composition, its effects should persist whereas those of placebo should decline rapidly. The Leicester group recruited 83 patients into the trial comparing Epogam and placebo: 70 completed the

phase of 16 weeks and 67 the 8-week follow-up to weeks. 24 They estimated that the SD of change from baseline would be 30% and that 37 patients per group would be required for a study with 80% power to detect a difference of 20% between active and placebo treatment

Acute

treatment

on the Costa scores. The authors failed that the SD for the Leicester scoring was 37%, point considerably higher than the 30% they had estimated. Moreover, because it includes all the unaffected areas of the body, the Leicester 0-3 point system is insensitive to change. A part of the body that is normal cannot improve, and on the Leicester 3-point system 71% of the baseline scores were either 0 or 1, giving little scope for demonstration of an effect. By contrast, on the Costa 7-point system, 54% of baseline scores were 4 or more and only 23% were 0 or 1. The SD for change from baseline on the Costa system was 31%. The Costa system shuuld have sufficient power with around 40 patients in active and placebo groups, whereas the Leicester system would require at least 60 per group. (2) To do a proper analysis of the Costa system results. By repeated measures of variance at 16 and 24 weeks, oedema (p<0-008), excoriation (p
with to

a

cursory report out

between vaccination and infection we cannot be certain if the patient showed no response to initial vaccination or if infection was secondary to a decline in antibody. Ballinger and Clark favour the latter possibility and contend that "100% of healthy men seroconvert after vaccination", which is not correct as the reference they cite in support shows.’ Laukamm-Josten and colleagues’ reported that 98% (53/54) of their healthy male heterosexual cohort, 92% (46/50) of their homosexual cohort, and 98% (42/43) of the HIVnegative subjects in their homosexual cohort seroconverted. (The details of the Laukamm-Josten paper are cited incorrectly by Ballinger and Clark and are reproduced correctly here.) Non-responders (ie, those that never produce 10 mIU/L or more of anti-HBs) typically make up 3% of large cohorts of healthy vaccinees.2 Long-term followup of vaccinees showed that non-responders were at the same risk as unvaccinated individuals of HBV infection and of consequent carrier status.3 The same workers identified no carriers among responders, despite the finding that the antibody concentrations of 42% of vaccinees dropped below 10 mIU/L. They concluded that protection against clinically significant disease outlasts meaningful antibody levels. Ballinger and Clark’s report, however, highlights the uncertainty that surrounds follow-up of vaccinees. Briefly, there are three main options. The first is vaccination with no follow-up blood tests. This may be the only option in universal childhood immunisation campaigns in some countries, but the difficulty of non-responders makes it inappropriate in the context of the UK programme of selected vaccination of high-risk groups. The second option is vaccination followed by blood tests 1-3 months postvaccination and, for those with an adequate response, boosters at predetermined intervals (without further blood tests). The third possibility is regular follow-up blood tests for all vaccinees to facilitate the timing of booster doses aimed at maintenance of anti-HBs concentrations at 10 mIU/L or higher. Ballinger and Clark have not clearly shown a need for the last option and its attendant extra cost. What is needed is a powerful cost-benefit analysis comparing options two and three above. Paul G

Microbiology and Public Health Laboratory, Addenbrooke’s Hospital, Cambridge CB2 2QW, UK

1

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Manku MS, Horrobin DF, Morse NL, et al. Essential fatty acids in the of patients with atopic eczema. Br J Dermatol

1984; 110: 643-48. 2

3

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Strannegard I-L, Svennerholm L, Strannegard O. Essential fatty acids in serum lecithin of children with atopic dermatitis and in umbilical cord serum of infants with high or low IgE levels. Int Arch Allergy Appl Immunol 1987; 82: 422-23. Galli E, Picardo M, Chine L, et al. Analysis of polyunsaturated fatty acids in newborn sera: a screening tool for atopic disease? Br J Dermatol 1994; 130: 752-56. Morse PF, Horrobin DF, Manku MS, et al. Meta-analysis of placebocontrolled studies of the efficacy of gamma-linolenic acid in the treatment of atopic eczema. Br J Dermatol 1989; 121: 75-90. Working Party Report. The UK Working Party’s diagnostic criteria for atopic dermatitis. Br J Dermatol 1994; 131: 383-96.

Laukamm-Josten U, von Laer G, Feldmeier H, et al. Active immunisation against hepatitis B: immunogenicity of a recombinant DNA vaccine in

*David F Horrobin, P F Morse

plasma phospholipids

McIntyre

Clinical

Scotia Pharmaceuticals Ltd, Guildford, Surrey GU1 1BA, UK

1

B infection after vaccination

SiR-Ballinger and Clark (Nov 5, p 1292) report an interesting case of clinically obvious acute hepatitis B virus (HBV) infection in a man previously vaccinated (with three doses of Engerix-B, SmithKline Beecham). Since the patient did not return for antibody (anti-HBs) testing in the 2 years

responses.

Curiously, the Leicester paper failed in three respects. (1) To present and compare the results of the two scoring systems. Only the Leicester scores were presented in detail,

hepatitis

3

females, heterosexual and homosexual males.

Postgrad Med J 1987; 63 (suppl 2): 143-46. Szmuness W, Stevens CE, Harley EJ, et al. The immune response of healthy adults to a reduced dose of hepatitis B vaccine. J Med Virol 1981; 8: 123—29. Hadler SC, Francis DP, Maynard JE, et al. Long-term immunogenicity and efficacy of hepatitis B vaccine in homosexual men. N Engl J Med 1986; 315: 209-14.

SIR-Ballinger and Clark’s report is surprising sinceassumptions were made and virological examination was incomplete. All studies of the antibody response to licensed hepatitis B vaccines have shown that between 5% and 10% or more of normal healthy subjects do not mount an anti-HBs response or that they respond poorly (eg, ref 1). The exact proportion 261