Cigarette smoking, appendectomy, and tonsillectomy as risk factors for the development of primary sclerosing cholangitis: a case control study.
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BACKGROUND AND AIMS: The strong clinical association between primary sclerosing cholangitis (PSC) and ulcerative colitis (UC) suggests common factors in their pathogenesis. Smoking, previous appendectomy, and tonsillectomy have been associated with a decreased risk of developing UC. In this study, our aim was to examine these risk factors in patients with PSC with and without underlying inflammatory bowel disease (IBD). METHODS: The smoking habits and history of previous appendectomy and/or tonsillectomy of 170 patients with PSC, 41 without underlying IBD, 170 patients with UC but normal liver function tests, and 170 age and sex matched community controls were obtained by questionnaire. RESULTS: A total of 112 PSC patients (66%) had never smoked compared with 66 controls (39%). Only 12 PSC patients (7%) were current smokers versus 43 controls (25%). The resultant odds ratio of having PSC was 0.17 (95% confidence interval (CI) 0.08-0.35) among current smokers and 0.33 (95% CI 0.21-0.52) among ever (former+current) smokers. Among former smokers, the odds of having PSC were also significantly decreased (odds ratio 0.45, 95% CI 0.26-0.73; p<0.05). In the subgroup of PSC patients without IBD, only 5% were current smokers versus 26% of matched controls, and never smokers were overrepresented (68% v 37%). The rate of previous appendectomy was similar in all three study groups (14%, 12%, and 13%) but the frequency of tonsillectomy was reduced in the PSC group (21% v 31%; p=0.05). CONCLUSION: PSC, like UC, is a disease of non-smokers as the odds of having PSC was significantly decreased among current and former smokers. The association between non-smoking and PSC was independent of whether the PSC patient had underlying IBD. Previous tonsillectomy but not appendectomy may also be associated with a decreased risk of PSC but this warrants further study. (+info)
Train-of-four nerve stimulation in the management of prolonged neuromuscular blockade following succinylcholine.
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Four patients, all possessing an atypical form of plasma cholinesterase, developed prolonged paralysis following succinylcholine administration. The clinical management of all four cases was facilitated by monitoring the train-of-four stimulus. All patients showed marked "fade" of the train-of-four ratio, the initial ratios of the fourth to the first twitches being 50 per cent or less, indicating variable degrees of nondepolarizing neuromuscular blockade. Reversal of paralysis with anticholinesterase agents was completely successful in three cases, but only partially effective in the fourth because of the probable presence of a mixture of both depolarizing block and nondepolarizing block. In such a situation, caution in the interpretation of the train-of-four ratio is necessary, since this test measures only the nondepolarizing component of the block. Whether or not reversal with anticholinesterase drugs is attempted, clinical estimates of neuromuscular function, such as head lift, vital capacity, and inspiratory force, must be carefully correlated with train-of-four values. If reversal is attempted, the brief action of edrophonium provides a useful clinical trial. (+info)
Rates of detection of Neisseria meningitidis in tonsils differ in relation to local incidence of invasive disease.
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Nasopharyngeal swabbing substantially underestimates carriage of Neisseria meningitidis. Real-time PCR assays were employed to examine the presence of a broad range of bacteria and of N. meningitidis groups B and C, respectively, in tonsils from 26 individuals from Oxford, England, and 72 individuals from Zurich, Switzerland. The detection limit of each PCR system was DNA from one bacterial cell per reaction mixture. Tonsillar DNA did not inhibit amplification of meningococcal gene sequences, and N. meningitidis was detected in tonsils exposed to the bacterium. Whereas in both sets of patients other bacteria were detected, N. meningitidis group B and group C were only found in tonsils from Oxford where the incidence of invasive meningococcal disease is much higher than in Zurich. These observations suggest that PCR-based methods could be used for the detection of meningococcal carriage and that difference in disease incidence could be explained by different transmission rates in the community rather than host genetics or coexisting infections. (+info)
Pharmacogenetics of codeine metabolism in an urban population of children and its implications for analgesic reliability.
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BACKGROUND: Codeine analgesia is wholly or mostly due to its metabolism to morphine by the cytochrome P450 enzyme CYP2D6, which shows significant genetic variation in activity. The aims of this study were to investigate genotype, phenotype and morphine production from codeine in children undergoing adenotonsillectomy, and to compare analgesia from codeine or morphine combined with diclofenac. METHODS: Ninety-six children received either codeine 1.5 mg kg(-1) or morphine 0.15 mg kg(-1) in a randomized, double-blind design. Genetic analysis was performed and plasma morphine concentrations at 1 h were determined. Postoperative analgesia and side-effects were recorded. RESULTS: Forty-seven per cent of children had genotypes associated with reduced enzyme activity. Mean (SD) morphine concentrations were significantly lower (P<0.001) after codeine [4.5 (0.3) ng ml(-1)] than after morphine [24.7 (1.5) ng ml(-1)], and morphine and its metabolites were not detected in 36% of children given codeine. There was a significant relationship between phenotype and plasma morphine (P=0.02). More children required rescue analgesia after codeine at both 2 (P<0.05) and 4 h after administration (P<0.01). Fifty-six per cent of children vomited after morphine and 29% after codeine (P<0.01). Neither phenotype nor morphine concentration was correlated with either pain score or the need for rescue analgesia (r=-0.21, 95% confidence interval -0.4, -0.01). CONCLUSIONS: Reduced ability for codeine metabolism may be more common than previously reported. Plasma morphine concentration 1 h after codeine is very low, and related to phenotype. Codeine analgesia is less reliable than morphine, but was not well correlated with either phenotype or plasma morphine in this study. (+info)
Evidence for infectious component of Hodgkin's disease and related considerations.
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The four epidemiological approaches used to evaluate the hypothesis that Hodgkin's disease might have an infectious component are reviewed. The limitations of each approach are summarized and some related questions are raised. The emerging picture for Hodgkin's disease is that a variety of factors, both environmental and genetic, might be important in the etiology of this disorder. (+info)
Delayed infection, late tonsillectomy or adenoidectomy and adult leukaemia: a case-control study.
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In a population-based case-control study among adults in Italy, of 261 lymphoid and 313 myeloid leukaemias and 1718 controls, a later age at adenoidectomy and tonsillectomy (after age 10 years) increased considerably the risk of lymphocytic (but not myeloid) leukaemia (odds ratio 4.2, 95% confidence interval 1.1-16.2). We propose that late infection is a proliferative stimulus for B-cells. (+info)
Propofol 1% versus propofol 2% in children undergoing minor ENT surgery.
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BACKGROUND: The induction characteristics of propofol 1% and 2% were compared in children undergoing ENT surgery, in a prospective, randomized, double-blind study. METHODS: One hundred and eight children received propofol 1% (n=55) or 2% (n=53) for induction and maintenance of anaesthesia. For induction, propofol 4 mg kg(-1) was injected at a constant rate (1200 ml h(-1)), supplemented with alfentanil. Intubating conditions without the use of a neuromuscular blocking agent were scored. RESULTS: Pain on injection occurred in 9% and 21% of patients after propofol 1% and 2%, respectively (P=0.09). Loss of consciousness was more rapid with propofol 2% compared with propofol 1% (47 s vs 54 s; P=0.02). Spontaneous movements during induction occurred in 22% and 34% (P=0.18), and intubating conditions were satisfactory in 87% and 96% (P=0.19) of children receiving propofol 1% or 2%, respectively. There were no differences between the two groups in respect of haemodynamic changes or adverse events. CONCLUSIONS: For the end-points tested, propofol 1% and propofol 2% are similar for induction of anaesthesia in children undergoing minor ENT surgery. (+info)
Tonsillar IgA1 as a possible source of hypoglycosylated IgA1 in the serum of IgA nephropathy patients.
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BACKGROUND: There are many reports of incompletely glycosylated O-linked oligosaccharides on the IgA1 hinge region in certain IgA nephropathy patients. In addition, other reports have noted a relationship between tonsillectomy and IgA nephropathy. METHODS: Immunoglobulins from extracts of tonsillectomized tissue and other sources were analysed by isoelectric focusing (IEF) and by enzyme-linked immunosorbent assay (ELISA). RESULTS: The IEF profile of tonsillar IgA differed from that of serum IgA and it was enriched in cationic IgA. However, extracts from tonsillitis controls and IgA nephropathy patients exhibited profiles that were very similar. Enzymatic removal of sialic acid induced a shift of the peaks to the cathode side. The profiles of IgA from treated tonsillar extract and treated serum were closely overlapped. In addition, asialo Galbeta1,3GalNAc was clearly present in cationic IgA from tonsillar extract and in aberrant IgA1 from serum following enzymatic transfer of sialic acid to IgA1. Serum IgA also contained partly sialylated IgA1. Quantitative analysis of IgA and IgG in the extracts indicated that IgA was significantly higher, whereas IgG was significantly lower in IgA nephropathy patients. CONCLUSIONS: We found that the IgA1 produced in tonsillar tissue differed from serum IgA1. Furthermore, an overproduction of asialo IgA1 resulted from the disordered balance between IgA- and IgG-producing cells in the tonsils from the IgA nephropathy patient. Although it is unclear how such asialo IgA1 molecules are transferred from tonsil tissue to serum, a tonsillar source may produce a few micrograms of aberrant IgA1 that then appears in serum. (+info)