Helicobacter pylori (HP) is now generally accepted as the main aetiological agent in chronic active gastritis and peptic ulcer. Infection with HP is widespread, but the routes of transmission are still unclear. Several studies have shown increasing prevalence of antibodies against HP with age. In developing countries, age at peak incidence of seroconversion is probably considerably lower than in developed countries. We performed a cross-sectional study to determine the age at maximum incidence of seroconversion to HP in a high-prevalence country (Ethiopia) and in a low-prevalence country (Sweden). Sera from 242 Ethiopian children, aged 2-14 years and from 295 Swedish children aged 1-15 years were analysed using an enzyme linked immunosorbent assay (ELISA) for detecting immunoglobulin G (IgG) antibodies. In Ethiopia, a comparison was made of a local and a reference strain for preparation of the antigen, but there was little difference in outcome. A comparison between antigen prepared from the reference strain and the pooled antigen used in the Swedish study also showed little difference. The sharpest rise in seroprevalence was found in the age range 2-4 years. Among 4-year-olds, some 60% had already seroconverted, and among 12-year-olds almost 100% had done so. In Sweden, the sharpest rise appeared between the ages of 9 and 10 years. Above 10 years of age seroprevalence was around 20%. Infection with HP is acquired in early childhood in Ethiopia, but somewhat later, although still before the teens, in Sweden. To determine properly the risk factors for infection with HP, possible exposure must be assessed around the age of seroconversion, since seropositivity may remain for a long time but environmental factors may have changed since primary infection.
We investigated the influence of different aspects of alcohol consumption on the risk of Type 2 diabetes and autoimmune diabetes in adults.
We used data from the Nord-Trøndelag Health Survey (HUNT) study, in which all adults aged = 20 years from Nord-Trondelag County were invited to participate in three surveys in 1984-1986, 1995-1997 and 2006-2008. Patients with diabetes were identified using self-reports, and participants with onset age = 35 years were classified as having Type 2 diabetes if they were negative for anti-glutamic acid decarboxylase (n = 1841) and as having autoimmune diabetes if they were positive for anti-glutamic acid decarboxylase (n = 140). Hazard ratios of amount and frequency of alcohol use, alcoholic beverage choice, and binge drinking and alcohol use disorders were estimated.
Moderate alcohol consumption (adjusted for confounders) was associated with a reduced risk of Type 2 diabetes in men, but not in women (hazard ratio for men 10-15 g/day 0.48, 95% CI 0.28-0.77; hazard ratio for women = 10 g/day 0.81, 95% CI 0.33-1.96). The reduced risk was primarily linked to consumption of wine [hazard ratio 0.93, 95% CI 0.87-0.99 (per g/day)]. No increased risk was seen in participants reporting binge drinking or in problem drinkers. The results were also compatible with a reduced risk of autoimmune diabetes associated with alcohol consumption [hazard ratio 0.70, 95% CI 0.45-1.08 (frequent consumption) and hazard ratio 0.36, 95% CI 0.13-0.97 (2-7 g/day)].
Moderate alcohol consumption associates with reduced risk of both Type 2 diabetes and autoimmune diabetes. A protective effect of alcohol intake may be limited to men. High alcohol consumption does not seem to carry an increased risk of diabetes.
In a previous report, a large regional variation was reported in total mortality and mortality rate from ischaemic heart disease (IHD) in mid-Sweden. In this report, IHD prevalence and risk factor data are presented. A postal questionnaire was sent out to a random sample of men aged 45-64 years in each of 40 communities. 14,675 men (88%) responded. Based on a validity study, IHD cases were defined as those with a history of myocardial infarction and/or angina pectoris. Age, smoking habits, antihypertensive treatment, body mass index, food habits, stress and physical activity during leisure time were used as risk factors. IHD prevalence showed the same geographical variation as IHD mortality, with a low prevalence in the east and a high prevalence in the west. There was a moderate variation in risk factor levels over the 40 communities. When this variation was taken into account the geographical IHD variation was somewhat smaller but still substantial. Other factors may involve socio-economics, drinking water qualities, mineral soil content or other environmental factors. Which of these cause the largest IHD variation is at present unknown, but is subject to systematic examination in this project.
Recently, several genome-wide association studies (GWAS) have independently found numerous loci at which common single-nucleotide polymorphisms (SNPs) modestly influence the risk of developing colorectal cancer. The aim of this study was to test 11 loci, reported to be associated with an increased or decreased risk of colorectal cancer: 8q23.3 (rs16892766), 8q24.21 (rs6983267), 9p24 (rs719725), 10p14 (rs10795668), 11q23.1 (rs3802842), 14q22.2 (rs4444235), 15q13.3 (rs4779584), 16q22.1 (rs9929218), 18q21.1 (rs4939827), 19q13.1 (rs10411210) and 20p12.3 (rs961253), in a Swedish-based cohort.
The cohort was composed of 1786 cases and 1749 controls that were genotyped and analysed statistically. Genotype-phenotype analysis, for all 11 SNPs and sex, age of onset, family history of CRC and tumour location, was performed.
Of eleven loci, 5 showed statistically significant odds ratios similar to previously published findings: 8q23.3, 8q24.21, 10p14, 15q13.3 and 18q21.1. The remaining loci 11q23.1, 16q22.1, 19q13.1 and 20p12.3 showed weak trends but somehow similar to what was previously published. The loci 9p24 and 14q22.2 could not be confirmed. We show a higher number of risk alleles in affected individuals compared to controls. Four statistically significant genotype-phenotype associations were found; the G allele of rs6983267 was associated to older age, the G allele of rs1075668 was associated with a younger age and sporadic cases, and the T allele of rs10411210 was associated with younger age.
Our study, using a Swedish population, supports most genetic variants published in GWAS. More studies are needed to validate the genotype-phenotype correlations.
Cites: Cancer Epidemiol Biomarkers Prev. 2009 Nov;18(11):3062-719843678
Cites: Cancer Epidemiol Biomarkers Prev. 2009 Feb;18(2):616-2119155440
With the aid of a computer-based anaesthetic record-keeping system, all cardiac arrests during anaesthesia at the Karolinska Hospital between July 1967 and December 1984 were retrieved. There were a total of 170 cardiac arrests and 250,543 anaesthetics in the data file, which gives an incidence of 6.8 cardiac arrests per 10,000 anaesthetics. Sixty patients died, constituting a mortality of 2.4 per 10,000 anaesthetics: 42 were considered as inevitable deaths (rupture of aortic or cerebral aneurysm, multitrauma, etc.); 13 cases of cardiac arrest were considered as non-anaesthetic, i.e. complications due to surgery and other procedures. Nine of these patients died. 115 cases of cardiac arrest were considered as caused by the anaesthetic and nine of these patients died. Thus mortality caused by anaesthesia was 0.3 per 10,000 anaesthetics. The most common cause of cardiac arrest due to anaesthesia was hypoxia because of ventilatory problems (27 patients), postsuccinylcholine asystole (23 patients) and post-induction hypotension (14 patients). The highest mortality was seen when spinal or epidural anaesthetics were given to patients with impaired physical status including hypovolaemia. The incidence of cardiac arrest has declined considerably during the period studied, and this coincides with an increasing number of qualified anaesthetists employed in the department during the same period.
The computerized anaesthetic record-keeping system at the Karolinska hospital at present (1980) contains anaesthetic records from approximately 200,000 cases. In order to evaluate the importance of circulatory disturbances during routine anaesthetic work, all records from 1967-1977 were searched for notes concerning complications. 5,996 anaesthetics were thus retrieved, having a total of 7,296 complications. This corresponds to an overall frequency of slightly more than 4 p. cent. Circulatory disturbances amounted to approximately 10 p. cent of all complications. Arrhythmias were common. Serious troubles i. e. circulatory arrests were very rare and these cases were studied individually. Differences in the frequency of complications as correlated to the preanaesthetic status of the patient including the risk group and diagnosis could be demonstrated. It is concluded that circulatory complications during anaesthesia exhibit patterns that can be analyzed from data collected during routine anaesthetic work provided a computerized anaesthetic record-keeping system is used.
The incidence of and possible factors influencing ECG abnormalities were analysed in one patient group with subarachnoid haemorrhages (n = 406) and another with intracranial tumours (n = 400). The highest incidence of each ECG abnormality was always found in the patients with subarachnoid haemorrhages. In this group an ECG pattern, possibly attributable to the cerebral disease and comprising abnormalities of the T and U waves and prolongation of the Q-Tc interval, was frequently identified.
BACKGROUND: The absence of all Kell blood group antigens (K(0) phenotype) is very rare. K(0) persons, however, can produce clinically significant anti-Ku (K5) after transfusion and/or pregnancy and require K(0) blood for transfusion. Ten alleles giving rise to the K(0) phenotype have been reported: different populations were studied although none from Scandinavia. STUDY DESIGN AND METHODS: Three K(0) samples were identified by blood banks in Sweden (Uppsala, Umeå, and Linköping) during a 20-year period. Kell antigen typing was performed with standard serologic techniques by the respective blood banks and K(0) status was confirmed by the International Blood Group Reference Laboratory in Bristol, England. Polymerase chain reaction and DNA sequencing of the KEL coding region (exons 1-19) was performed on genomic DNA. RESULTS: The Uppsala K(0) was homozygous for a 1540C>T substitution in exon 13, leading to an immediate stop codon. The Umeå K(0) was homozygous for 1023delG in exon 8 that results in a frameshift and a premature stop codon in exon 9. In the Linköping K(0), a previously reported mutation g>a at +1 of intron 3 was found. CONCLUSION: Two novel and one previously reported null alleles at the KEL locus are described. The identified nonsense mutations abolish expression of the Kell glycoprotein and are thus responsible for the K(0) phenotype in these Swedish families.