Multiple biliary hamartomas (von Meyenberg complexes) are an uncommon benign biliary neoplasm detected incidentally on imaging. To our knowledge the appearances of multiple biliary hamartomas on microbubble contrast-enhanced ultrasound have not been previously described. We report a case using Coherent Contrast Imaging® and Agent Detection Imaging® techniques with the contrast agents Sonovue®and Levovist®. While both methodologies failed to differentiate these focal liver lesions from malignant neoplasms, they enhanced the conspicuity of the hamartomas. Radiologically-guided biopsy and histological analysis remain the reference standard in the diagnosis of multiple biliary hamartomas.
SUMMARY Mucosal cell proliferation in the first part of the duodenum was studied in 24 patients using a tissue culture technique in which endoscopic biopsies were subjected to autoradiography after exposure to tritiated thymidine. Eight patients had a normal duodenum, eight had duodenal ulcer, and eight had symptomatic chronic non-specific duodenitis. The mean crypt labelling index (LI) in normal duodenum was 8.8 ±0.4 % (SEM). Increased labelling indices of 15.6± 1-7 % were found near the edge of duodenal ulcers and 17.8 ±1.8 % in duodenitis. Treatment with cimetidine reduced both the severity of duodenitis and the mean crypt LI. The LI of histologically normal duodenal mucosa distal to ulcer or duodenitis was similar to that of the control subjects' mucosa. The increased mucosal cell proliferation seen in severe duodenitis, either alone or associated with duodenal ulceration, suggested that erosions and ulcers arose when the crypts passed into 'high output failure' and were unable to compensate for further epithelial cell loss. There was no evidence in our study for a generalised failure of mucosal cell proliferation in duodenal ulcer or duodenitis.Interest in the pathophysiology of duodenal ulceration has centred on gastric acid and possible abnormalities in the regulation of acid secretion.12 Less is known of the mucosal changes that result in the discrete ulcer34 or whether there is a generalised defect in mucosal repair in ulcer patients.6 The relationship between non-specific duodenitis and ulcer disease remains controversial.6-8 This study was undertaken to provide information on the simple question posed by Eastwoodg of whether or not there is a failure of epithelial renewal in duodenal disease. Methods PATIENTSEndoscopically and histologically normal duodenal mucosa was biopsied in eight control subjects, four men, mean age 51.8 years (range 43-57 years) whose diagnoses proved to be pelviureteric obstruction, myocardial ischaemia, gall stones, and anxiety state, and four women, mean age 56.8 years (range 48-71 years), three having hiatus hernia and one gallstones.The duodenal ulcer patients were six men, mean age 41.5 years (range 32-75 years) and two women Received for publication 10 November 1980 of 68 and 40 years. Mucosa from patients with symptomatic duodenitis in the absence of an ulcer was biopsied in seven men, mean age 42-9 years (range 34-58 years) and a woman of 39 years.Ten patients (two controls with hiatus hernia, three ulcer and five duodenitis) were rebiopsied after a four week course of cimetidine 1 g/day. PROCEDURESAfter anaesthetising the oropharynx, the patients were sedated with diazepam and given atropine or hyoscine as required. Four biopsies were taken with the Olympus GIF K endoscope from the normal bulb, ulcer edge, or area of duodenitis; additional biopsies were taken from the distal first part of duodenum away from obviously pathological mucosa. Biopsies were placed in iced Hanks solution and transferred to 5 ml of Medium 199 with Hanks salts and Hepes buffer (Gibco Bio-Cu...
Epithelial cell proliferation in the duodenum was investigated in 50 patients by incubating mucosal biopsy samples with tritiated thymidine, followed by autoradiography. Fifteen patients had a normal duodenum, 15 duodenal ulcer undergoing elective surgery, 10 perforated duodenal ulcer, and 5 severe non-ulcer-associated duodenitis. The mean crypt cell labelling index in the duodenal bulb of controls was 8.8 +/- 0.4% (mean +/- SEM), at the edge of perforated ulcers 19.1 +/- 2.0%, at the edge of elective ulcers 18.6 +/- 1.4%, and in biopsy specimens from non-ulcer-associated duodenitis 14.0 +/- 1.2%. The mean labelling index in the distal first part of duodenum of control patients was 9.1 +/- 0.8 similar to the values found in histologically normal specimens distal to ulcer or duodenitis. The results indicate active epithelial cell proliferation in both duodenal ulcer and duodenitis. There was no evidence of impairment of epithelial cell proliferation in duodenal ulcer patients.
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