Biomedical subjects

Seamus O'Mahony

Publications and source records attributed to Seamus O'Mahony.

4 recordsLinked to original sources

PubMed2006

Comparison of three stool antigen assays with the 13C- urea breath test for the primary diagnosis of Helicobacter pylori infection and monitoring treatment outcome.

BACKGROUND: The urea breath test (UBT) is the gold-standard non-invasive test for the detection of Helicobacter pylori infection, however, the lack of availability of the UBT due to the high cost of the test, and in particular the need for expensive analytical instrumentation, limits the usefulness of this method. Stool antigen assays may offer an alternative non-invasive method for the diagnosis of infection. OBJECTIVE: To compare the accuracy of three stool antigen assays (HpSA, IDEIA HpStAR, and ImmunoCard STAT) against the UBT for the primary diagnosis of H. pylori infection and for monitoring treatment outcome. METHODS: A total of 102 patients attending two gastroenterology day-case clinics for the investigation of dyspepsia were included. Each patient provided breath and stool samples for analysis. Patients who tested positive for H. pylori by the validated UBT were prescribed triple therapy and invited to return for repeat breath and stool sample analysis 6 weeks post-treatment. RESULTS: Of the 102 patients tested, 48 were diagnosed with H. pylori infection by the UBT. The HpSA assay interpreted 38 of these as positive (79% sensitive). Of the 54 UBT-negative patients the HpSA assay interpreted all 54 as negative (100% specific). The IDEIA HpStAR assay correctly identified 44 patients as positive (92% sensitive) and 50 as negative (92.5% specific). The ImmunoCard STAT assay interpreted 38 patients as positive (79% sensitive) and 52 as negative (96.3% specific). CONCLUSION: The findings indicate that the IDEIA HpStAR stool antigen kit is the most accurate assay of the three assays evaluated, and possibly represents a viable alternative to the UBT for the primary diagnosis of H. pylori infection and for monitoring treatment outcome.

Adult↗

PubMed2005

Advanced hepatocellular carcinoma associated with cystic fibrosis.

Advances in the treatment of the respiratory complications of cystic fibrosis, including the availability of lung transplantation have led to a greater awareness of the manifestations of liver disease in up to 40% of patients with Cystic Fibrosis (CF). We report the case of an 18 year old female with CF who presented with advanced hepatocellular carcinoma and no prior clinical evidence of chronic liver disease. Hepatocellular carcinoma is usually the most severe manifestation of advanced cirrhosis although its development in non-cirrhotic cases of chronic liver disease has been reported. With the increasing life expectancy of CF patients it is likely that more unusual hepatic complications of this disease may be identified. Greater awareness may perhaps lead to earlier diagnosis in those at risk.

Adolescent↗

PubMed2005

Tetomilast.

Otsuka is developing a once-daily oral formulation of the phosphodiesterase-4 inhibitor tetomilast for the potential treatment of ulcerative colitis (phase III) and chronic obstructive pulmonary disease (phase II).

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed2002

Coagulation factor XIII and markers of thrombin generation and fibrinolysis in patients with inflammatory bowel disease.

OBJECTIVE: To relate factor XIII levels and other prothrombotic markers to inflammatory bowel disease and investigate the frequency of valine34leucine and its effect on factor XIII cross-linking activity in patients with inflammatory bowel disease. DESIGN: Fifty patients with active inflammatory bowel disease but no venous thromboembolism (32 with ulcerative colitis, 18 with Crohn's disease), 50 patients with inactive inflammatory bowel disease but no venous thromboembolism (32 with ulcerative colitis, 18 with Crohn's disease), two age- and gender-matched healthy control groups of 100 subjects each were recruited. To further explore the relationship between valine34leucine and inflammatory bowel disease, 21 patients with the disease (13 with ulcerative colitis and eight with Crohn's disease) and venous thromoembolism (male to female ratio = 7 : 14, median age 59.5 years (range, 19-80 years)) were recruited. Two hundred and fifteen control subjects (M : F = 121 : 94, median age 62 years (28-74 years)), with venous thromboembolism (119 with deep venous thrombosis, and 96 with pulmonary embolism) were drawn from the same geographical area as the patients. METHODS: Factor XIII A, B-subunit antigen and A2B2 tetramer levels were measured using an in-house sandwich enzyme-linked immunoassay method. RESULTS: Factor XIII A2B2 tetramer and the A-subunit were significantly decreased in patients with active inflammatory bowel disease compared with controls (59% vs 95%, P < 0.0001 and 75% vs 102%, P < 0.0001, respectively), but not between the inactive inflammatory bowel disease group and controls. The D-dimer and prothrombin 1+2 fragment levels in patients with active inflammatory bowel disease were raised compared with controls (178 (152) vs 109 (84), P = 0.0007 and 82 (43) vs 55 (28), P = 0.0001, respectively). The factor XIII B-subunit and factor XIII cross-linking activity were not significantly different between patients with active or inactive inflammatory bowel disease and controls. There was no significant difference in genotype distribution in inflammatory bowel disease patients with or without venous thromboembolism and respective control subjects. Levels of tissue plasminogen activator antigen were significantly increased in patients with active inflammatory bowel disease when compared to inactive inflammatory bowel disease and controls (8.9 (3.7) vs 6.7 (3.4) vs 6.9 (3.4), P < 0.001). CONCLUSIONS: Active inflammatory bowel disease is associated with activation of coagulation. Factor XIII A and A2B2 tetramer levels were markedly decreased in active inflammatory bowel disease. Variations in the level of factor XIII in patients with inflammatory bowel disease could be multifactorial and in part may result from the increased formation of microthrombi and accelerated turnover of the factor XIII. We found no evidence of association of factor XIII valine34leucine polymorphism and inflammatory bowel disease.

Case-Control Studies↗