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The Association Between Primary Biliary Cirrhosis and Coeliac Disease: a Study of Relative Prevalences

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The Association Between Primary Biliary Cirrhosis and Coeliac Disease: a Study of Relative Prevalences 120 Gut 1998;42:120–122 The association between primary biliary cirrhosis and coeliac disease: a study of relative prevalences J G C Kingham, D R Parker Abstract the frequency of each disease relative to the Background—Coexistent primary biliary other nor did they systematically review their cirrhosis (PBC) and coeliac disease has respective patient populations for these dis- been recorded but the association has not eases. There have been several subsequent been systematically studied. reports2–5 of these two diseases coexisting with Aims—To determine relative prevalences over 20 cases described6 but there have been no of PBC and coeliac disease in a defined formal attempts to ascertain relative prevalence population over a 12 year period. rates. Patients and methods—All patients with PBC or coeliac disease in a stable popula- tion of 250 000 in South Wales were identi- Methods fied from a clinical register and laboratory Since 1984 we have kept a register of all records. patients with specifically defined gastroentero- Results—Sixty seven patients with PBC logical and liver diseases from a well circum- and 143 patients with coeliac disease have scribed and stable population in South Wales. been diagnosed and followed over a me- The register has been maintained prospectively dian of 86 (4–135) months; point preva- by coding at the time of diagnosis (discharge lences in 1996 were 20 per 100 000 for PBC summary or letter to referring doctor) all inpa- and 54 per 100 000 for coeliac disease. tients, outpatients, and day cases passing PBC in patients with coeliac disease was through the department of gastroenterology. sought by investigating abnormal liver The population is defined by the Unitary function tests. Ten (7%) had persistent Authority of Swansea as follows: city of Swan- abnormalities and three had PBC. Coeliac sea (postcodes SA1–SA9) population 226 000; disease in patients with PBC was sought part of the surrounding rural area (postcodes by investigating malabsorption, haema- SA14, 15, and 18) population 25 000. This population is 51.9% female, 48.1% male, and tinic deficiency, positive antigliadin anti- is predominantly of European ethnic origin body, or coeliac disease family history. (98.5%). ONS figures for 1990–4 showed a Eleven patients underwent duodenal bi- 0.2% population growth with little migration opsy revealing one further coeliac disease or immigration. case. Four patients (three women) have Swansea is served by two district general both conditions giving a point prevalence hospitals with shared laboratory facilities and for patients with both conditions of 1.6 per case notes giving ready access to records of his- 100 000 (95% confidence limits 0.44 to 4.1 topathology, biochemistry, and serology re- per 100 000). Prevalence of PBC in pa- sults. We used the combined resources of our tients with coeliac disease was 3% and of clinical register and computerised laboratory coeliac disease in patients with PBC was records to identify all cases of coeliac disease 6%. and all of PBC resident in this area. The clini- Conclusion—A 12 year study of a stable cal case notes were obtained after establishing 250 000 population revealed a relative any of the following: prevalence of PBC in 3% of 143 patients Recorded clinical diagnosis of PBC or of with coeliac disease and of coeliac disease coeliac disease. in 6% of 67 patients with PBC. PBC and + Histology record of partial or subtotal coeliac disease are therefore associated. villous atrophy on small intestinal biopsy. Screening for PBC in patients with coeliac + Histology record of typical or probable PBC disease using antimitochondrial antibody on liver biopsy. testing and screening for coeliac disease in + Positive antimitochondrial antibody of titre patients with PBC with antigliadin anti- 1/40 or greater. body testing or duodenal biopsy are After scrutiny of the case notes and subse- recommended. quent re-evaluation and investigation we found (Gut 1998;42:120–122) Department of 143 patients (105 women, 38 men) with coeliac Gastroenterology, Keywords: primary biliary cirrhosis; coeliac disease; disease and 67 patients (57 women, 10 men) Singleton Hospital, prevalence with PBC who had been diagnosed and Swansea SA2 8QA, UK J G C Kingham followed regularly over the period 1984–96. D R Parker The diagnostic criteria for coeliac disease were Logan et al in 19781 reported four patients partial or subtotal villous atrophy, with or with- Correspondence to: from Edinburgh and Dublin with coexistent out evidence of malabsorption, responsive to Dr Kingham. coeliac disease and primary biliary cirrhosis gluten withdrawal. The criteria for PBC were Accepted for publication (PBC), questioning whether this was a signifi- positive antimitochondrial antibody, cholestatic 16 July 1997 cant association. They did not attempt to assess biochemistry, and liver biopsy consistent with Primary biliary cirrhosis and coeliac disease 121 Table 1 Liver function abnormalities in 35/143 patients with coeliac disease coeliac disease was 54 per 100 000 and of PBC was 20 per 100 000. (The corresponding Pattern of liver function No abnormal No persistently transaminases at any time abnormal Diagnosis figures for women for 1996 are 77 per 100 000 for coeliac disease and 34 per 100 000 for Bilirubin↑, AST↑,AP↑,ã-GT↑ 2 2 PBC PBC PBC.) AST↑,AP↑,ã-GT↑ 12 4 PBC Four patients were identified on clinical, his- PBC tological, biochemical, and serological grounds NSRH MC as suVering from both conditions with a point AST↑ 8 2 FNH prevalence of 1.6 per 100 000 (95% confi- Fatty liver dence limits 0.44 to 4.1 per 100 000). In AP↑, ã-GT↑ 10 2 Secondary adenocarcinoma patients with coeliac disease evidence of PBC Secondary was sought by identifying abnormal liver func- lymphoma ã-GT↑ 30 tion tests. Twenty four per cent (35/143) had an abnormality of at least one liver function test AST, aspartate aminotransferase; AP, alkaline phosphatase; ã-GT, ã-glutamyltransferase; PBC, at some point (table 1). Of these, most were primary biliary cirrhosis; NSRH, non-specific reactive hepatitis; MC, macronodular cirrhosis; FNH, focal nodular hyperplasia. transient and not specifically cholestatic. Ten patients had persistent abnormalities of liver PBC. Sixty seven were classified as having defi- function tests and were fully evaluated. Four nite (56 patients) or probable (11 patients) had PBC, one macronodular cirrhosis, one PBC.7 Confidence intervals were calculated 8 focal nodular hyperplasia, one non-specific using a Poisson distribution. reactive hepatitis, one fatty liver, and two secondary cancer. Results Of the 67 patients with PBC, one was simul- The catchment population from which these taneously diagnosed as having coeliac disease; patients were drawn is approximately 250 000. in two the diagnosis of coeliac disease was In 1995, 136/143 patients with coeliac disease made first. In the remaining 64 patients with and 51/67 patients with PBC were alive. In that PBC evidence of possible coeliac disease was year all four patients with both conditions were sought by features suggestive of malabsorption still living, though in one coeliac disease had (in seven), a family history of coeliac disease (in yet to be diagnosed; this came to light after one), the presence of antireticulin antibody (in investigation in 1996. Thus the point preva- one), or the finding of otherwise unexplained lence in this population in 1995 and 1996 of haematinic deficiency anaemia (in six). Eleven Table 2 Case histories of the four patients with both PBC and coeliac disease Age Sex Symptoms and signs Initial investigations Subsequent investigations and outcome 51 F Diarrhoea, pruritus, weight Hb11.3g/dl;MCV76fl;ferritin<5ng/l; folate 1.6 ng/ml; AP Gluten exclusion led to rapid resolution of loss, pigmentation, 1813 U/l; bilirubin 18 µmol/l; AST 89 U/l; ã-GT 582 U/l; albumin diarrhoea and weight gain, repeat duodenal steatorrhoea 35 g/l; AMA 1/1000; ANF 1/40; liver biopsy: PBC, grade 4 biopsy at 9/12: minimal partial villous cirrhosis; duodenal biopsies: subtotal villous atrophy atrophy, liver disease progressed: liver transplant at three years after initial presentation, currently well 57 F Diarrhoea, abdominal pain, Hb 8.8 g/dl; MCV 76 fl; vitamin B12 130 ng/l; folate 2.3 ng/ml; Well for nine years then developed CRST weight loss, ferritin 6 ng/l; faecal fat 30 g/day; AP 36.5 KA units; AST 164 U/l; syndrome and hyperslenism, repeat hepatosplenomegaly AMA 1/2560; liver biopsy: PBC, grade 3 cirrhosis; duodenal duodenal biopsies: partial villous atrophy, biopsies: subtotal villous atrophy repeat LFTs: AP 540 U/l; AST 47 U/l; albumin 31 g/l, multiple transfusions required for hypersplenism, died of pneumonia 15 years after initial presentation 32 F Pruritus, anorexia, weight Hb 8 g/dl; MCV 66 fl; AP 794 U/l; AST 85 U/l; bilirubin 17 Gluten exclusion and haematinic loss µmol/l; albumin 34 g/l; duodenal biopsy: subtotal villous atrophy; supplements resulted in weight gain, liver biopsy: non-specific inflammation pruritus persisted; LFTs remained abnormal, started oral contraceptive: developed jaundice; resolved on stopping, LFTs remained abnormal; repeat duodenal biopsy: good response to gluten exclusion, AMA 1/1024, review of previous liver biopsy: PBC, four years after initial presentation: xanthelasmata, spider naevi, jaundice, hepatospenomegaly, started on ursodeoxycholic acid: LFTs improved, currently asymptomatic 51 M Osteoporosis AP 1131 U/l; AST 77 U/l; ã-GT 904 U/l; liver biopsy: minimal No diagnosis at first, over next 10 years portal tract inflammation only developed
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