A weli defined cohort of coeliac patients was studied prospectively to assess the prevalence of coexisting thyroid disease and positive thyroid autoantibodies. Comparison with epidemiological data on the prevalence of coeliac disease in a neighbouring area suggested that few adult coeliac patients had been missed. Overall, 140% of the coeliac patients had thyroid disease: 10.3% were hypothyroid and 3.7% hyperthyroid, both significantly more than expected. There were significantly more coeliac disease patients with thyroid autoantibodies than expected -11% had thyroglobulin antibodies and 15% had thyroid microsomal antibodies. This association is clinically important. Three patients are described in whom the coexistence of coeliac disease and hypothyroidism led to diagnostic difficulties and delay of treatment. (Gut 1994; 35: 844-846) Case reports CASE 1 A 27 year old woman presented with constipation and menorrhagia. Investigation showed a normal haemoglobin (12 g/dl); mild iron deficiency, with a serum iron of 10 jimol/ (normal range 11-30 p,mol/l); and autoimmune hypothyroidism: thyroid stimulating hormone (TSH) 109 mU/l (normal range 0-4-5O0 mU/l), thyroxine T4 19 nmolI (normal range 70-155 nmol/1), thyroglobulin antibodies titre 1/640. She was started on thyroxine but despite adequate replacement therapy (TSH 1 2 mU/l) she lost 28 lb in weight and developed diarrhoea. Further investigation showed continued iron deficiency and new folate deficiency. Distal duodenal biopsy specimens showed subtotal villous atrophy and there was a noticeable clinical response to a gluten free diet. Repeat biopsies six months later confirmed significant histological improvement.

SUMMARY In man, the main pancreatic duct is normally derived from ventral and dorsal embryological buds of the pancreas. In a minority of people, failure of fusion of the two buds results in separate drainage of the dorsal and ventral pancreas, so that the accessory duct provides the main drainage for the gland. Patients with this anomaly demonstrated at endoscopic retrograde pancreatography (ERP) have been investigated to assess whether non-fusion of the main pancreatic duct predisposes to the development of pancreatitis. A failure of fusion of the pancreatic ducts was seen in 21 out of 449 (4-7 %) successful pancreatograms; four of these 21 patients had definite clinical evidence of pancreatitis and two patients had possible pancreatic disease, but in the remainder the anomaly was not considered to be clinically relevant. An abnormal pancreatogram suggesting pancreatitis was present in 116 out of the 428 patients (27.1 %) with a normally fused duct system. The anomaly was found as frequently in the whole series as it was seen in patients with pancreatitis. These findings suggest that embryological failure of pancreatic duct fusion does not predispose to the development of pancreatitis. However, the presence of this anomaly may lead to misinterpretation of ultrasonographic and CT scan findings.The pancreas is formed embryologically from distinct ventral and dorsal buds which arise from the duodenal diverticulum after rotation of the ventral bud and have fused by the seventh week of life (Meckel, 1812). Wirsung (1642) first demonstrated the main pancreatic duct in man and Santorini (1775) accurately described the duct system and demonstrated the accessory pancreatic duct.Normally, the main pancreatic duct is derived from both embryological parts of the pancreas; the dorsal pancreas provides the main duct in the tail and body of the gland with the ventral anlage providing the main duct in the head of the gland. The accessory duct (of Santorini) is the remaining portion of the duct in the dorsal pancreas which may drain through an accessory papilla more proximally in the duodenal loop.It is thus not surprising that anomalies of the pancreatic duct system occur and their frequency has been documented in large systematic necropsy studies by Baldwin

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