Food allergy or intolerance in severe recurrent aphthous ulceration of the mouth.

Wright, A; Ryan, F P; Willingham, S E; Holt, Shaun; Page, Andrew C.; Hindle, M.O.; Franklin, C.D.

doi:10.1136/bmj.292.6530.1237

Cited by 42 publications

(16 citation statements)

References 7 publications

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“…Poor sulphoxidation is common in subjects with food reactions [30]. As oral aphthous ulceration has been linked to dietary factors [31], a further study would be required to investigate a potential relationship between OGU and sulphoxidation.…”

Section: Discussionmentioning

confidence: 99%

Thalidomide-induced neuropathy and genetic differences in drug metabolism

Harland

Steventon

Marsden

1995

Eur J Clin Pharmacol

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A pharmacogenetic predisposition to thalidomide-induced neuropathy has been investigated. Differences of drug metabolism were examined in 16 patients with severe orogenital ulceration, who were treated with thalidomide (< or = 200 mg/day) for 0.3-5.0 years. Eight had evidence of early peripheral neuropathy according to nerve conduction studies. Rates of C-hydroxylation, N-acetylation, and conjugation reactions with sulphate, glucuronide and glycine, were tested with the probe compounds debrisoquine, sulphadimidine, paracetamol and aspirin, respectively. Urinary drug metabolites were analysed by high pressure liquid chromatography. Results were compared with 16 healthy age- and sex-matched volunteers. Of the patients 6.25% and 13.3% of the controls had a poor Debrisoquine Hydroxylator Ratio (DMR); none of the patients with neuropathy had a poor DMR as compared to 12.5% without neuropathy. Of the patients 40.0% and 35.7% of the controls were slow acetylators; 28.6% with neuropathy were slow acetylators as opposed to 50% without neuropathy. Similarly, there were no significant differences in rates of conjugation between groups. All unaffected patients were active smokers, whereas only two of those with neuropathy smoked. Cumulative dose or duration of therapy were unrelated to risk of neuropathy. In conclusion, changes of nerve conductivity are a frequent and unpredictable adverse effect of thalidomide (< or = 200 mg/day), although smoking may have a protective action against their development. Nerve conduction studies are required before and during treatment, irrespective of the prescribed dose.

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Section: Discussionmentioning

confidence: 99%

Thalidomide-induced neuropathy and genetic differences in drug metabolism

Harland

Steventon

Marsden

1995

Eur J Clin Pharmacol

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“…The haplotype of HLA-DRw1O and DQwl may predispose patients with GSE to RAS (Majorana et al, 1992;Meini et al, 1993). There may also be occasional patients who have RAS with no detectable clinical or histological evidence of celiac disease on jejunal biopsy, yet who may respond to dietary withdrawal of gluten (Wray, 1981;Wright et al, 1986). However, the withdrawal of gluten does not often result in significant benefit (Hunter et al, 1993) (Tuft and Ettleson, 1956), while others have failed to find any significant correlation (Spouge and Diamond, 1963;Wray et al, 1982;Eversole et al, 1983;Hay and Reade, 1984).…”

Section: Clinical Featuresmentioning

confidence: 99%

Recurrent Aphthous Stomatitis

Porter

Scully

Pedersen

1998

Critical Reviews in Oral Biology & Medicine

252

143

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“…In a similar way, there seems to be an association with alopecia areata (1,2). In some patients, RAS and sensitization to specific foods are described to correlate (5,7,8,11); in other patients, epidemiological researchers assume, but do not actually demonstrate, a possible association between RAS and FA/FI (4,6,9). Therefore, since (a) it is well known that atopy manifestations are frequently associated with FA/FI (1, 12, 13), (b) it has been shown in both clinical and epidemiological studies that aphthae are sometimes correlated with FI/FA, and (c) it is known that patients with aphthae can be atopic, it is conceivable that some patients affected by RAS could also have clinical or latent atopy.…”

Section: Discussionmentioning

confidence: 95%