Pernicious Anaemia with Gastric Carcinoids.

We report the case of a 42 year male with history of chronic anaemia who was found to have pernicious anaemia with beta thalassemia trait and had on esophago-gastric-duodenoscopy, gastric carcinoids with gastric atrophy. Pernicious anaemia and gastric carcinoids occurring simultaneously in a single individual is rare. Our case emphasises the need for esophago-gastric-duodenoscopy in cases of pernicious anaemia.

Laboratory diagnosis of clostridium difficile infection. An evaluation of tests for faecal toxin, glutamate dehydrogenase, lactoferrin and toxigenic culture in the diagnostic laboratory.

Faecal samples from 1007 patients suspected of having diarrhoea caused by Clostridium difficile infection are investigated for the presence of toxins A and B and for the presence of C. difficile-specific glutamate dehydrogenase (GDH). Toxigenic culture is performed on all samples and is used as the 'gold standard' for the purpose of the study. A marker for intestinal inflammation, faecal lactoferrin, is used on any samples that give a positive result in any of the above tests. Part of the study also involves an assessment of six commercial toxin kits to detect the presence of C. difficile toxins in faecal samples. This study revealed that the commercial toxin detection kits used can give rise to false-positive and false-negative results and that all demonstrated poor sensitivity when compared to the gold standard of toxigenic culture. Testing of faecal samples for GDH can be useful as a negative screening method as the results of this test show high correlation with culture. Faecal toxin testing can then be performed on all GDH-positive samples (GDH positivity is independent of toxigenicity in strains of C. difficile). The combined use of GDH and toxin testing, coupled with toxigenic culture, revealed that some patients with diarrhoea who harboured toxigenic strains of C. difficile were faecal toxin-negative. Lactoferrin appears to be a useful marker for the presence of inflammatory diarrhoea.

Detection of Clostridium difficile infection: a suggested laboratory diagnostic algorithm.

Currently, the diagnosis of Clostridium difficile infection (CDI) relies on the detection of toxins A and B in faeces but the sensitivity of these tests has been questioned, particularly in advanced disease. In this context, additional methods to enhance the diagnosis of C. difficile have been investigated. In this study, 1007 faecal samples are tested using toxigenic culture, an immunoassay for toxins AB and the C. difficile-specific glutamate dehydrogenase (GDH) test. Samples positive by any of the above tests are evaluated for the presence of faecal lactoferrin as an indicator of intestinal inflammation. Patients with evidence of inflammation but with negative toxin AB tests are followed up to assess clinical outcome. The toxin AB test was positive in 35 samples (3.4%), while 121 (12%) samples were culture-positive, 87 (8.6%) of which were toxigenic. Glutamate dehydrogenase proved to be a sensitive and specific marker of C. difficile with a negative predictive value of 99.3% (95% CI: 0.98-1.00). Faecal lactoferrin was positive in 52/129 (40.3%) samples tested. A cohort of 15 patients with a negative faecal toxin AB and a positive lactoferrin test was C. difficile culture-positive with a toxigenic isolate; clinically, all had advanced CDI. All demonstrated faecal toxin between five and 41 days later on repeat testing. It is suggested that a two-step algorithm be used to include screening faecal samples for GDH, with positive samples tested for faecal toxin AB and lactoferrin. Patients who present with a negative faecal toxin AB test and a positive lactoferrin test were serially tested for faecal toxin AB every five to seven days until a diagnosis was established. More sensitive tests than enzyme-linked immunosorbent assay (ELISA) for the detection of faecal toxin, or the use of a rapid specific test for the presence of a toxigenic strain, must be considered in such patients.

Bone remodelling around a cemented polyethylene cup. A longitudinal densitometry study.

The aims of this study were to examine the repeatability of measurements of bone mineral density (BMD) around a cemented polyethylene Charnley acetabular component using dual-energy x-ray absorptiometry and to determine the longitudinal pattern of change in BMD during the first 24 months after surgery. The precision of measurements of BMD in 19 subjects ranged from 7.7% to 10.8% between regions, using a four-region-of-interest model. A longitudinal study of 27 patients demonstrated a transient decrease in net pelvic BMD during the first 12 months, which recovered to baseline at 24 months. The BMD in the region medial to the dome of the component reduced by between 7% and 10% during the first three months, but recovered to approximately baseline values by two years. Changes in BMD in the pelvis around cemented acetabular components may be measured using dual-energy x-ray absorptiometry. Bone loss after insertion of a cemented Charnley acetabular component is small, transient and occurs mainly at the medial wall of the acetabulum. After two years, bone mass returns to baseline values, with a pattern suggesting a uniform transmission of load to the acetabulum.

Primary hydatid disease of the spine: an unusual cause of progressive paraplegia. Case report and review of the literature.

Although rare, spinal hydatid disease is a manifestation of hydatid infestation. The authors present the report of a patient who presented with primary spinal hydatid disease. This disease is often misdiagnosed as tuberculous spondylitis, and thus patients may subsequently receive inappropriate treatment. The patient in this case presented, with an increasing weakness in the lower limbs, to a different clinic from an area in India where hydatid infections are endemic. The infection was misdiagnosed as tuberculous spondolytis based on evaluation of plain x-ray films, and the patient underwent antituberculous chemotherapy and a posterior surgical decompressive procedure. The patient presented to the authors' clinic with increasing paraparesis 1.5 years later. Radiographs and a magnetic resonance image of the spine were obtained, which strongly suggested hydatid disease. Examination of serum levels confirmed the diagnosis. The patient underwent a decompressive procedure of the spine in which stabilization was performed. Postoperatively her paraparesis resolved, and good control over the disease was achieved by chemotherapy. The authors conclude that primary spinal hydatid disease of the spine, although a rare manifestation, should be considered in the differential diagnosis in patients with infectious and destructive lesions of the spine in regions in which the disease is endemic. Advanced imaging studies should be performed to diagnose the disease. Early decompressive surgery with stabilization of the spine, in addition to adjuvant chemotherapy, is the treatment of choice for these patients.