1224

in which

they are produced are subjected by inspectors from the Department of Health (and now, the Medicines Control Agency). Although homoeopathic products are not included in the European Community directive on proprietary medicinal products, specifically covering this area is at an advanced stage of Current UK law is strong and comprehensive and new era drafting. tissue salts are not exempt-for example, claims are controlled under the Medicines (Labelling and Advertising to the Public)

a

directive

Regulations 1978. Regulations and orders under the Medicines Act 1968 and the Food Act 1984 restrict the promotion of unlicensed food products. For example, medicine legislation prohibits the promotion of unlicensed foods for treating or diagnosing disease. It allows unlicensed foods to be offered for preventive medicinal purposes provided they do not contain more than prescribed levels of vitamins A, D, B,2, and folic acid or unless the advertisement is to be sent or delivered to a doctor or dentist. The legislation is in the Medicines Act and the Medicines Exempt from Licences (Foods and Cosmetics) orders. The preventive medicinal claims allowed to be made to the public for unlicensed foods are limited to those considered suitable for self-medication. Food legislation prohibits claims that a food can prevent or treat disease unless it is licensed under the Medicines Act (Food Labelling Regulations 1984). This removes the freedom to offer foods for preventive purposes that exists under medicine legislation. The prohibition on medicinal claims is removed when useful information or recommendations intended exclusively for those qualified in dentistry, medicine, nutrition, dietetics, or pharmacy is being disseminated (Food Labelling Regulations 1984). Hence, whilst medicines legislation allows preventive medicinal claims for unlicensed foods, food legislation removes this freedom except when the claim is addressed to a qualified person. The Health Food Manufacturers’ Association cooperates with Government departments concerned with food and health in maintaining a strong legislative framework, which your editorialist has clearly not examined. Lately there has been a spate of advertising for products such as royal jelly making, in my opinion, clearly medicinal claims. This was brought to the attention of the Medicines Control Agency last September but the advertisement was still appearing in March, despite requests from us to have it

stopped. There is no reason to think that responsible supplement and health product manufacturers are in any way involved in the promotion of "pseudonutrition". Your editorial is misdirected: it should be addressed to the enforcement agencies. I would caution your readers to be wary of indiscriminate "quack-busting" even though there are a few real abuses (and your editorial mentioned some) that all agree should be cleared up by due process of law.

MAURICE HANSSEN, 63 Hampton Court Way, Thames Ditton, Surrey KT7 OLT, UK

President, Health Food Manufacturers’ Association

Salmonella lipopolysaccharide in synovial cells from patients with reactive arthritis SIR,-Dr Granfors and colleagues (March 24, p 685) have detected salmonella lipopolysaccharide (LPS) in synovial cells and synovial tissue from patients with salmonella-triggered reactive arthritis. I agree that bacterial LPS is an important factor in the pathogenesis of reactive arthritis. Granfors et al had previously suggested that unusually strong opsonisation of bacteria in patients with reactive arthritis contributes to an overactive interplay between cells and the polymorphonuclear microorganism.’1 cells of HLA-B27 individuals react Polymorphonuclear positive strongly to extrinsic stimuli.2 I suspect that it is cytokines such as interleukins and tumour necrosis factor, produced with the processed LPS by mononuclear cells, that give rise to inflammation, at least in part by stimulating polymorphonuclear cells.3 To confirm a contribution of salmonella LPS to the pathogenesis of salmonella-triggered reactive arthritis we need to know if the LPS stimulates synovial lymphocytes, as measured by 3Hthymidine uptake; such stimulation has been reported in the sexually acquired Reiter’s syndrome stimulated with chlamydial or

ureaplasmal antigen, a disease which correlates with the preceding infection.4 In Japan, where the prevalence of HLA-B27 is low (08% vs 7-5% in whites)reactive arthritis is so rare that physicians often misdiagnose or overlook the disorder. We need a simple assay which can detect the specific LPS of every offending bacterium in synovial cells and so diagnose reactive arthritis correctly. I also hope that the term "salmonella-triggered reactive arthritis" will be scrapped and replaced by "salmonella arthritis". Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160, Japan

HIDETO AKAMA

1. Tertti R, Granfors K, Lahesmaa-Rantala R, Toivanen A. Serum opsonic capacity against Yersima enterocolitica 0:3 in yersiniosis patients with or without reactive arthritis. Clin Exp Immunol 1989; 76: 227-32 2. Repo H, Leinsalo-Repo M, Koivuranta-Vaara P. Exaggerated inflammatory responsiveness plays a part in the pathogenesis of HLA-B27 linked diseases: hypothesis. Ann Clin Res 1984, 16: 47-50. 3. Akama H, Ichikawa Y, Matsushita Y, Shinozawa T, Homma M. Mononuclear cells enhance prostaglandin E2 production of polymorphonuclear leukocytes via tumor necrosis factor. Biochem Biophys Res Commun (in press). 4. Ford DK, de Roza DM, Shah P, Wenman WM. Cell-mediated immune responses of synovial mononuclear cells in Reiter’s syndrome against ureaplasmal and chlamydial antigens. J Rheumatol 1980; 7: 751-55. 5. Tiwan JL, Terasaki PI. The HLA complex. In: HLA and disease associations. New York: Springer-Verlag, 1985: 4-17.

Paralytic ileus associated with ipratropium SIR,-Dr Mulherin and Dr Fitzgerald (March 3,

p 552) report meconium ileus by ipratropium bromide. I have seen a case of paralytic ileus following nebulised ipratropium bromide. A 28-year-old man was admitted with an acute asthmatic attack. He had been born prematurely and spastic diplegia developed, with reasonable power (Medical Research Council grade 4) in his legs but striking spasticity. He had had pyloric stenosis operated on as a child. On admission he was in respiratory distress with a paradox of 20 mm Hg and a peak flow of 120 1/min. He was treated with intravenous hydrocortisone (then oral prednisolone), nebulised terbutaline, and nebulised ipratropium bromide initially at a dose of 500 ag 3 hourly. There was no evidence of chest infection and a chest radiograph showed only hyperexpanded lung fields. His peak flow rate improved to 300 1/min. However, on day five he had abdominal pain and distension and abdominal radiographs showed dilated loops of large bowel, with fluid levels on the erect X-ray film. The subsequent day he vomited and repeat radiographs also showed additional small bowel dilatation. A barium enema showed free flow of barium to the caecum. Potassium and amylase were normal. Paralytic ileus was diagnosed. Ipratropium bromide was stopped; all other drugs were continued. Two doses of neostigmine 2-5 mg were given intravenously with uncertain benefit. He remained unchanged until day 8, after which he gradually improved. At follow-up he was well on a terbutaline puffer alone, with no gastrointestinal symptoms. Paralytic ileus has been reported in association with several systemic disorders but not, as far as I am aware, with acute asthma. It has rarely been associated with severe pneumonia, but this patient showed no evidence of this. However, there are several reports associating it with the use of drugs with anticholinergic activity including atropine, antipsychotics, and tricyclics.1,2 When nebulised ipratropium bromide is given some is known to be swallowed, and may act on cholinergic receptors in the gastrointestinal tract, depressing motility.3 This action may have precipated paralytic ileus in this patient. Why it did so is uncertain but the high initial dose used may have been a factor. In addition, as Mulherin and Fitzgerald suggest, other factors producing immobility (in this case both the spastic diplegia and the severe asthma attack) may have been predisposing factors.

possible precipitation of

Department of Neurology, Middlesex Hospital, London W1 N 1RP, UK 1. Beatson N.

H. S. MARKUS

Atropine and paralytic ileus. Postgrad Med J 1982; 58:

451-53

2. Wade LC, Ellenor GL. Combination mesondazine and benztropine mesylate induced

paralytic ileus. Drug Intell Clin Pharm 1980, 14: 17-22. NJ. Ipratropium bromide. N Engl J Med 1988, 319:

3. Gross

486-94.

Paralytic ileus associated with ipratropium.

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