Journal of Neurology Neurosurgery and Psychiatry 2002;72:259-261
© 2002 Journal of Neurology Neurosurgery and Psychiatry
Dermatitis herpetiformis and neurological dysfunction
A J Wills1, B Turner1, R J Lock2, S L Johnston2, D J Unsworth2 and L Fry3
1 Department of Neurology, Queen’s Medical Centre, Nottingham, UK
2 Department of Immunology, Southmead Hospital, Bristol, UK
3 Department of Dermatology, Imperial College School of Medicine, London, UK
Dr Adrian J Wills;
Received 20 December 2000
In final revised form 18 July 2001
Accepted 23 October 2001
Dermatitis herpetiformis and coeliac disease are gluten sensitive diseases, which have common immunopathological and genetic mechanisms. Neuropsychiatric complications have been reported in up to 26% of patients with coeliac disease. This is probably an overestimate, because of the chance associations with some common neurological conditions such as epilepsy. The pathogenesis is speculative but it has been postulated that gluten is neurotoxic possibly via immune mechanisms. The frequency of neurological dysfunction in patients with dermatitis herpetiformis has not been characterised. Patients with dermatitis herpetiformis might be expected to be particularly susceptible to neuronal damage as some continue to consume gluten when their dermatological symptoms are controlled by dapsone. Thirty five patients were recruited with dermatitis herpetiformis from dermatology clinics at St Mary’s Hospital, London and Queen’s Medical Centre, Nottingham and investigated for evidence of neurological abnormality. All patients underwent a full neurological examination and were asked about their neurological and general medical history by means of a structured questionnaire. Serum samples were taken and screened for the presence of anti-neuronal antibodies (anti-Hu and Yo) as well as anti-gliadin (IgA and G) anti-endomysial (IgA), and anti-tissue transglutaminase (IgA) antibodies. Neurophysiological tests were carried out where appropriate. Only two patients were identified with unexplained neurological abnormalities (one essential tremor, and one chorea). Two other patients had a history of migraine. The patient with chorea also had borderline/equivocally positive anti-Hu antibodies by immunofluorescence assay. All other samples were negative for anti-neuronal antibodies. Fifteen patients were positive for anti-gliadin antibodies (IgA and/or IgG), four for anti-endomysial antibodies (monkey oesophagus or umbilical cord), and six for anti-tissue transglutaminase antibodies. The presence of these antibodies did not correlate with the presence of neurological abnormalities. No cases of “gluten ataxia” were identified.
In conclusion, there was no convincing evidence for immune mediated neurological damage in this pilot study of dermatitis herpetiformis.
- Reunala T. Dermatitis herpetiformis: coeliac disease of the skin. Ann Med 1998;30:416–8.[Medline]
- Egan CA, O’Loughlin S, Gormally S, et al. Dermatitis herpetiformis: a review of fifty-four patients. Ir J Med Sci 1997;166:241–4.[Medline]
- Jepsen LV, Ullman S. Dermatitis herpetiformis and gluten-sensitive enteropathy in monozygotic twins. Acta Derm Venereol 1980;60:353–5.[Medline]
- Reunala T. Incidence of familial dermatitis herpetiformis. Br J Dermatol 1996;134:394–8.[Medline]
- Reunala T, Hallstrom O. Similar high frequency of IgA antireticulin and antiendomysial antibodies in dermatitis herpetiformis. J Am Acad Dermatol 1990;23(6 Pt 1):1188–9.[Medline]
- Finelli PF, McEntee WJ, Ambler M, et al. Adult coeliac disease presenting as cerebellar syndrome. Neurology 1990;30:245–9.[Abstract/Free Full Text]
- Vascotto M, Fois A. Frequency of epilepsy in coeliac disease and vice versa: a collaborative study. In: Gobbi G, Andermann F, Naccarato S, et al, eds. Epilepsy and other neurological disorders in coeliac disease. London: John Libbey, 1997:105–110.
- Kaplan JG, Pack D, Horoupian D, et al. Distal axonopathy associated with chronic gluten enteropathy: a treatable disorder. Neurology 1988;38:642–5.[Abstract/Free Full Text]
- Pellecchia MT, Scala R, Perretti A, et al. Cerebellar ataxia associated with subclinical celiac disease responding to gluten-free diet. Neurology 1999;53:1606–8.[Free Full Text]
- Cooke WT, Smith WT. Neurological disorders associated with adult coeliac disease. Brain 1966;89:683–722.[Free Full Text]
- Collin P, Pirttila T, Nurmikko T, et al. Celiac disease, brain atrophy, and dementia. Neurology 1991;41:372–5.[Medline]
- Bhatia KP, Brown P, Gregory R, et al. Progressive myoclonic ataxia associated with coeliac disease. The myoclonus is of cortical origin, but the pathology is in the cerebellum. Brain 1995;118:1087–93.[Abstract/Free Full Text]
- Hadjivassiliou M, Grunewald RA, Chattopadhyay AK, et al. Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia. Lancet 1998;352:1582–5.[Medline]
- Hadjivassiliou M, Gibson A, Davies-Jones GA, et al. Does cryptic gluten sensitivity play a part in neurological illness? Lancet 1996;347:369–71.[Medline]
- Pellecchia MT, Scala R, Filla A, et al. Idiopathic cerebellar ataxia associated with celiac disease: lack of distinctive neurological features. J Neurol Neurosurg Psychiatry 1999;66:32–5.[Abstract/Free Full Text]
- Unsworth DJ, Brown DL. Serological screening suggests that adult coeliac disease is underdiagnosed in the UK and increases the incidence by up to 12%. Gut 1994;35:61–4.[Abstract]
- Lock RJ, Pitcher MC, Unsworth DJ. IgA anti-tissue transglutaminase as a diagnostic marker of gluten sensitive enteropathy. J Clin Pathol 1999;52:274–7.[Abstract]
- Unsworth DJ. ACP Broadsheet No 149: September 1996. Serological diagnosis of gluten sensitive enteropathy. J Clin Pathol 1996;49:704–11.[Medline]
- Louis ED, Ottman R, Hauser WA. How common is the most common adult movement disorder? estimates of the prevalence of essential tremor throughout the world. Mov Disord 1998;13:5–10.[Medline]
- Launer LJ, Terwindt GM, Ferrari MD. The prevalence and characteristics of migraine in a population-based cohort: the GEM study. Neurology 1999;53:537–42.[Abstract/Free Full Text]
- Nausieda PA, Koller WC, Klawans HL, et al. Phenytoin and choreic movements. N Engl J Med 1978;298:1093–4.[Medline]
- Schlesinger I, Hering R. Antigliadin antibody in migraine patients. Cephalalgia 1997;17:712.[Medline]
- Reunala T, Collin P, Lewis HM, et al. Associated diseases and malignancy in dermatitis herpetiformis. In: Maki M, Collin P, Visakapi JK, eds. Coeliac disease. Tampere: Coeliac Disease Study Group, 1997:75–80.
- Chapman RW, Laidlow JM, Colin-Jones D, et al. Increased prevalence of epilepsy in coeliac disease. BMJ 1978;ii:250–1.
- Holmes GKT. Neurological and psychiatric complications in coeliac disease. In: Gobbi G, Andermann F, Naccarato S, et al, eds. Epilepsy and other neurological disorders in coeliac disease. London: John Libbey, 1997:251–64.
- Norlund MA, Lee JM, Zainelli GM, et al. Elevated transglutaminase-induced bonds in PHF tau in Alzheimer’s disease. Brain Res 1999;851:154–63.[Medline]
- Chinnery PF, Reading PJ, Milne D, et al. CSF antigliadin antibodies and the Ramsay Hunt syndrome. Neurology 1997;49:1131–3.[Abstract]
children’s ALLERGY Center JL TAMAN BENDUNGAN ASAHAN 5 JAKARTA PUSAT, JAKARTA INDONESIA 10210
PHONE : (021) 70081995 – 5703646
Clinical and Editor in Chief :
email : firstname.lastname@example.org,
Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.
Copyright © 2010, Children Allergy Center Information Education Network. All rights reserved