A.V. Thilliainayagam A.S. Arvind E.S. Cook Diagnostic efficiency of an ultra-rapid endoscopy room test for Helicobacter pylori Gut 31 1991 467 469

Abstract

ENDOSCOPY AROUND THE WORLD Editor for Abstracts, James Barthel, MD Diagnostic efficiency of an ultra-rapid endoscopy room test for Helicobacter pylori THILLIAINAYAGAM AV, ARVIND AS, COOK ES, ET AL. Gut 1991;31:467-9 Thilliainayagam et al. describe a modified rapid urease test (RUT) for detection of Helicobacter pylori capable of providing an immediate result, thereby allowing treatment decisions to be made before the patient leaves the physician's office. In their study, antral biopsy specimens were endoscopically obtained from 220 patients and comparative analyses for the presence of H. pylori were performed by using culture, gram stain, Christensen's 2% urea broth, and finally, the authors' modified ultra-rapid urease test. Their test consisted of a 10% urea solution that, unlike Christensen's urea broth, was unbuffered, permitting more rapid changes in pH and, consequently, detectable color change. A positive test required a color change within the first minute. Using culture as gold standard, the authors demonstrated that their method yielded an accuracy of 96%, a sensitivity of 89%, a specificity of 100%, and positive and negative predictive values of 100 and 94%, respectively. These results were superior to those obtained from the gram stain and Christensen's urea broth. More importantly, the result of the ultra-rapid urease test was available in 1 min, whereas gram stain took 1 to 3 hours, Christensen's urea broth took up to 24 hours, and culture took up to 4 to 7 days. The authors concluded that their RUT was highly accurate in diagnosing H. pylori infection and that the immediacy of a result makes it attractive for routine clinical practice. Since the discovery of H. pylori in gastric biopsies of patients with histologic gastritis by Warrin et al. (Lancet 1983;1:12735) and its subsequent etiologic role in various dyspeptic conditions, there has followed a number of diagnostic methods to detect the presence of the organism. They include culture, histology, serology, urea breath testing, and finally, the RUT, which relies on detection of the enzyme characteristically anomaly (with the exception of Nagorney et al. ). McWhorter first described the association between congenital dilation of the bile duct and pancreas divisum, possibly an incomplete one, based on postmortem study prior to the ERCP era. Radiologists and endoscopists alike, unaware of this association, might be taxed by the composite radiographic appearances with multiple overlapping ducts. The complexity of the ductal anatomy is compounded by being obscured by the grossly dilated bile duct and also by irregular dilation of the pancreatic duct in some instances. Not surprisingly, therefore, the association has been labeled categorically and/ or erroneously as complex union,12 choledochocystopancreatic fistula (personal communication),12 bizarre arrangements ofpancreaticobiliary ductal system, 8 or bifid common bile duct. Delineation of the exact anatomy mandates examination of films taken in various projections, in conjunction with an awareness of the aforementioned association. To date, we have been ambivalent about the clinical meaning of IPD. In none of the 14 cases of Sugawa et alY and 7 cases of Moreira et al.1 did IPD manifest itself as pancreatitis. In contrast, patients with IPD associated with AJPBDS predominantly presented with pancreatitis, which is most probably related to ill-effects of the long common channel rather than IPD per se. J. W. D. Ng, MD M. K. Wong, MD J. Huang, MD Y. T. Chan, MD