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EDITOR - Feighery described in a clinical review the association of celiac sprue with various autoimmune diseases including autoimmune thyroid disease, Sjögren's syndrome and primary biliary cirrhosis.1

We report a case of a 24 year old woman from Kosovo with celiac sprue(CS) who developed Takayasu arteritis(TA). To our knowledge this is the first report that describes the association of TA and CS. The young woman has been known for CS for two years. She showed clinical improvement after institution of gluten free diet but was readmitted to our hospital because of recurrence of weight loss, malaise, night sweats, fever, diffuse myalgias and bilateral mandibular pain. Clinical examination revealed a decreased left radialis artery pulse, a loud bruit over the left subclavian artery and a 15 mmHg difference in systolic blood pressure between the arms. Laboratory tests showed microcytic anemia, thrombocytosis, hypergammaglobulinemia, an erythrocyte sedimentation rate of 110 mm/h and c-reactive protein of 91 mg/l(nThe diagnosis of CS was confirmed by jejunal biopsy and positive IgA and IgG antigliadin antibodies. Further examinations excluded an intestinal lymphoma, a colitis or an infectious disease. The arteriography showed a narrowing of both subclavian, renal and vertebral arteries and a longdistance narrowing of the descending aorta. The diagnosis of TA was supported by the presence of 5 of the 6 criteria for the classification of TA.2

TA is an inflammatory and obliterative disease of the large and medium- sized arteries with striking predilection for aorta and its major branches. There seems to be a genetic predisposition for these diseases as evidenced by an association with various HLA-phenotypes mainly A2, A11, A24, B7, B35, B39, B40-42, B50, B52, B62.3 Similarly CS is associated with DR3, DR4, DR7, DR52, DQ2.

While the association of TA with inflammatory bowel disease like ulcerative colitis and Crohn's disease is well documented the involvement of other organ systems including skin, kidney, heart, lungs and the gastrointestinal tract has been reported only rarely.4 The HLA-genotypes A2, A11, B6, B35, B50, DR 12(5), DR7, DR52, DQ2, DQ7 present in our patient are overrepresented in patients with TA and CS respectively. Therefore we propose that the simultaneous occurence of both diseases represents a true association and not pure coincidence.

Christine Eich, MD
Martin Krause, MD
Division of Internal Medicin, Kantonsspital Münsterlingen, Switzerland

1 Feighery C : Coeliac disease, clinical review BMJ 1999;319:236-239

2 Arend WP, Michel BA, Bloch DA et al: The American College of Rheumatology: 1990 Criteria for the classification of Takayasu arteritis. Arthritis and Rheumatisme, Vol.33, No 8 (1990)

3 Numano F, Kobayashi Y, Maruyama al: Takayasu arteritis: Clinical characteristics and the role of genetic factors in ist pathogenesis. Vascular Medizin 1996; 1: 227-233

4 Sharma BK, Jain S, Sagar S: Systemic manifestations of Takayasu arteritis: The expanding spectrum. International Journal of cardiology 54 suppl. (1996) S 149-S154

Editorial note
The patient has given her consent to publication.

Competing interests: None declared

Christine Eich

Martin Krause

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While coeliac disease is underdiagnosed as a cause of osteoporosis, the suggestion that "all patients with osteoporosis should be screened for coeliac disease by measurement of endomysial antibodies" seems an unreal expectation. Has any other group replicated the results of Lindh (reference 1, who found 12% of their osteoporotic subjects had elevated IgA antibodies to gliadin? Is there any published cost benefit analysis to support screening for coeliac disease in osteoporotic patients? If there is, it would have widespread implications which should be publicised. If not,it would be helpful to have some guidelines as to which osteoporotic patients should have their endomysial antibody level measured. How much does such a test cost?


1;Lindh E, Ljunghall S, Larsson K, Lavo B. Screening for antibodies against gliadin in patients with osteoporosis. J Intern Med 1992;234:403-6.

Competing interests: None declared

Richard FitzGerald, Consultant Radiologist

New Cross Hospital, Wolverhampton WV10 0QP

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In his review of coeliac disease Feighery rightly comments on the high incidence of osteoporosis in coeliac patients and that this may be a presenting feature. However he goes further to recommend that all patients with osteoporosis should be screened for coeliac disease by measurement of endomysial antibodies.(1) The vast majority of patients with osteoporosis do not have coeliac disease and it is our experience that it is unusual for such patients to present without some other feature of coeliac disease. In his survey of 92 patients with osteoporosis, Lindh comments that none of those patients found to have coeliac disease had intestinal symptoms but no mention was made of anaemia.(2) Such a proposal would have considerable resource implications both in the cost of the assays and also the substantial number of patients that would require referral to the gastroenterologists for intestinal biopsy. It is our suggestion that screening for coeliac disease be reserved for when unexplained osteoporosis presents in association with anaemia, low serum calcium, “tired all the time”, pre-menopausal women, men <60 years, family history of coeliac disease or any gastrointestinal symptoms.

Dr.W.E. Fickling
Research Registrar
Royal United Hospital, Combe Park, Bath BA1 3NG

Dr.A.K. Bhalla
Consultant Rheumatologist
Royal National Hospital for Rheumatic Diseases, Upper Borough Walls, Bath BA1 1RL


1. Feighery C Fortnightly review: Coeliac Disease BMJ 1999;319:236- 239 (24 July)

2. Lindh E, Ljunghall S, Larsson K, Lavo B Screening for antibodies against gliadin in patients with osteoporosis J Intern Med 1992 Apr; 231(4):403-6

Competing interests: None declared

W E Fickling

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The Editor, Childhood Coeliac Disease.

The clinical review of Coeliac disease (CD) by Feighery(1) was thorough and raises the profile of this common, yet underdiagnosed disease. He included information on the well established rising incidence of CD in adulthood and most paediatricians would also agree with him that the classical presentation of CD in infants under two is now uncommon. We would however dispute his claim that "Although CD is strongly linked with childhood, it is now well recognised that CD in childhood has become increasingly uncommon." He quotes 2 papers from the 1998 Proceedings of the 7th International symposium on CD to support this claim. The variation in change of frequency in the diagnosis of childhood CD has however been inconsistent throughout Europe. In Sweden it has both risen and fallen over the last 24 years(2), whilst in the Netherlands(3) it has risen steadily over the last 20 years. There are however few data existing on the prevalence of childhood CD in the UK; it was thought to be declining in the mid 1980s(4), although we reported studies in South Wales Children over a similar time period showing no decrease(5). This year we have also reported a dramatic threefold rise in childhood CD over the last 5 years, probably due to the facilitating of diagnosis by serological screening(6).

Our studies in a well defined geographical area suggest that the true incidence of childhood CD in the UK is thus more common than previously thought. This is in keeping with other recent studies on childhood CD suggesting that it is frequently underdiagnosed; recent screening studies from around the world have reported prevalence rates in childhood of between 1:85(7) to 1:230(8).

Thus the incidence of childhood CD is still changing and indeed in the UK it appears to be increasing. Reports of it's death have been greatly exaggerated!

Yours sincerely

Dr D Tuthill Lecturer in Child Health

Dr HR Jenkins Paediatric Gastroenterologist


1 Feighery C. Coeliac Disease. BMJ 1999;319:236-9.

2 Ivarrson A, Persson LA, Hernell O. The rise and fall in incidence of coeliac disease in Swedish children-an effect not only of dietary changes? (Abstract) J Pediatr Gastr Nutr 1999, 28;559.

3 Csizmadia CGDS et al. Childhood coeliac disease: an iceberg in the Netherlands. (Abstract) J Pediatr Gastr Nutr 1999, 28;552.

4 Challacombe D, Mecrow IK, Elliott K, Clarke FJ, Wheeler EE. Changing infant feeding practices and declining incidence of coeliac disease in West Somerset. Arch Dis Child 1997;77:206-9.

5 Jenkins HR, Hawkes N, Swift GL. Incidence of coeliac disease [letter]. Arch Dis Child 1998;79:198-9.

6 Tuthill DP, Hawkes N, Jenkins HR. The rise of Childhood Coeliac Disease Following the introduction of Serological Testing. (Abstract) Arch Dis Child 1999;80:A22

7 Korponay-Szabo IR, Kovacs JB, Czinner A, Goracz G, Vamos A, Szabo T. High prevalence of silent celiac disease in preschool children screened with IgA/IgG antiendomysium antibodies. J Pediatr Gastr Nutr 1999;28:26-30.

8 Catassi C, Ratsch IM, Fabiani E, Ricci S, Bordicchia F, Pierdomenico R, Giorgi PL. University Department of Paediatrics, Ancona, Italy. High prevalence of undiagnosed coeliac disease in 5280 Italian students screened by antigliadin antibodies. Acta Paediatrica. 1995; 84:672-6.

Competing interests: None declared

David Tuthill, Lecturer in Child Health.

University of Wales College of Medicine.

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