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Paracetamol is the most commonly used substance in self poisoning (about 70 000 cases annually in Britain[1]) and is the most frequent subject of inquiries to the National Poisons Information [...]

There are an estimated nine million new outpatient referrals each year.[1] Between 60% and 80% of these referrals originate from general practitioners.[2] Additional referrals arise predominantly from hospital departments. A [...]

Background. Increased levels of collagen types I, III and V are found in strictures of patients with Crohn's disease (CD) compared with normal gut tissue. Type IV collagen is present in the basement membranes, basal lamina, retina and cornea. Elevated levels of antibody to Klebsiella pneumoniae are found in both active CD and active ankylosing spondylitis (AS) patients compared with healthy controls.Methods. Reactivities for immunoglobulin class‐specific antibodies (IgM, IgG and IgA) against collagen types I, III, IV, V and whole K. pneumoniae were measured by ELISA in nine patients with early CD and 10 with late CD from King's College Hospital and 12 late CD patients and 36 HLA‐B27‐positive AS patients from Middlesex Hospital and was compared with values for 26 healthy controls from the Blood Transfusion Service in London.Results. Levels of class‐specific IgM, IgG and IgA antibodies to collagen types I, III, IV, V and K. pneumoniae were significantly elevated in early and late CD patients compared with healthy controls (P<0.001). Levels of IgM, IgG antibody to the four collagen types and K. pneumoniae were also significantly elevated (P<0.001) in AS patients compared with healthy controls. In addition, the level of IgA antibody to K. pneumoniae was elevated in AS patients (P<0.001). Furthermore, a positive correlation between antibody levels to collagen types I, III, IV and K. pneumoniae was demonstrated in both early and late CD patients and in those with AS, whilst a positive correlation to type V was found in early CD.Conclusion. The role of K. pneumoniae and anti‐collagen antibodies in the aetiopathogenesis of CD and AS requires further study.

Background and aimsAssessing the presence and degree of intestinal inflammation objectively, simply, and reliably is a significant problem in gastroenterology. We assessed faecal excretion of calprotectin, a stable neutrophil specific marker, as an index of intestinal inflammation and its potential use as a screening test to discriminate between patients with Crohn's disease and those with irritable bowel syndrome.MethodsThe validity of faecal calprotectin as a marker of intestinal inflammation was assessed in 22 patients with Crohn's disease (35 studies) by comparing faecal excretions and concentrations using four day faecal excretion of ¹¹¹indium white cells. A cross sectional study assessed the sensitivity of faecal calprotectin concentration for the detection of established Crohn's disease (n=116). A prospective study assessed the value of faecal calprotectin in discriminating between patients with Crohn's disease and irritable bowel syndrome in 220 patients referred to a gastroenterology clinic.ResultsFour day faecal excretion of ¹¹¹indium (median 8.7%; 95% confidence interval (CI) 7-17%; normal &lt;1.0%) correlated significantly (p&lt;0.0001) with daily (median ranged from 39 to 47 mg; normal &lt;3 mg; r=0.76-0.82) and four day faecal calprotectin excretion (median 101 mg; 95% CI 45-168 mg; normal &lt;11 mg; r=0.80) and single stool calprotectin concentrations (median 118 mg/l; 95% CI 36-175 mg/l; normal &lt;10 mg/l; r=0.70) in patients with Crohn's disease. The cross sectional study showed a sensitivity of 96% for calprotectin in discriminating between normal subjects (2 mg/l; 95% CI 2-3 mg/l) and those with Crohn's disease (91 mg/l; 95% CI 59-105 mg/l). With a cut off point of 30 mg/l faecal calprotectin has 100% sensitivity and 97% specificity in discriminating between active Crohn's disease and irritable bowel syndrome.ConclusionThe calprotectin method may be a useful adjuvant for discriminating between patients with Crohn's disease and irritable bowel syndrome.

Background & Aims: Inflammatory bowel disease (IBD) is a complex disorder of unknown etiology. Epidemiological investigations suggest a genetic basis for IBD. Recent genetic studies have identified several IBD linkages. The significance of these linkages will be determined by studies in large patient collections. The aim of this study was to replicate IBD linkages on chromosomes 12 and 16 in a large European cohort. Methods: Three hundred fifty-nine affected sibling pairs from 274 kindreds were genotyped using microsatellite markers spanning chromosomes 12 and 16. Affection status of the sibling pairs was defined as Crohn's disease (CD) or ulcerative colitis (UC). Results: Nonparametric statistical analyses showed linkage for both chromosomes. Two-point results for chromosome 12 peaked at D12S303 (logarithm of odds [LOD], 2.15; P = 0.003) for CD and at D12S75 (LOD, 0.92; P = 0.03) for UC. Multipoint analyses produced a peak LOD of 1.8 for CD. Chromosome 16 showed linkage for CD at marker D16S415 (LOD, 1.52; P = 0.007). Multi-point support peaked above markers D16S409 and D16S411 (LOD, 1.7). Conclusions: These data are consistent with linkage of IBD to chromosomes 12 and 16. The replication of genetic risk loci in a large independent family collection indicates important and common susceptibility genes in these regions and will facilitate identification of genes involved in IBD. GASTROENTEROLOGY 1998;115:1066-1071

Abstract: Epidemiological and genome-wide linkage analyses have provided firm evidence for a genetic component in the pathogenesis of inflammatory bowel disease. The linkage regions on chromosomes 12 and 16 have been replicated in several independent samples. These represent the best positional evidence in the search for inflammatory bowel disease susceptibility genes. While systematic association and physical mapping studies in these regions are under way, the direct analysis of immunologically relevant genes as positional and functional candidates may provide a shortcut in this process. The interferon-γ gene resides in the chromosome 12 linkage region near the marker D12S83. Interferon-γ is an important proinflammatory cytokine in the interleukin-12 cascade and has been implicated in the pathogenesis of mucosal inflammation. We tested this gene for evidence of linkage and association in 133 German multiplex families and 506 single patients with their parents. An intragenic, highly informative CA-repeat marker in intron 1 of the gene was typed using fluorescence-labeled polymerase chain reaction and analysis on an automated sequencer. In the nonparametric linkage analysis using GENEHUNTER, a nonsignificant maximum LOD score of 0.67 was obtained. The transmission disequilibrium test for association was negative (P≥0.22) for Crohn's disease, ulcerative colitis, and the combined inflammatory bowel disease phenotype. In summary, the findings make interferon-γ a very unlikely candidate for the major susceptibility gene in the chromosome 12 linkage interval. Future efforts can concentrate on other transcripts in the region.

The causes of blindness in Sierra Leone were studied in 7286 new patients attending the eye clinic in the year 1981. Blindness, defined as an inability to count fingers at 3 meters with the better eye (WHO, 1973), was present in 762 persons, due to cataract (39%), ocular onchocerciasis (30%), primary glaucoma (8%), measles keratitis (3%), trachoma (3%) and other causes. The prevalence of blindness was estimated from simple field surveys covering 41 villages with an estimated population of 10,559. The average prevalence of blindness was found to be 1.3% of the total population.