The rising incidence of childhood type 1 diabetes in New South Wales, 1990-2002

OBJECTIVES: To determine the incidence of childhood type 1 diabetes mellitus (T1DM) in New South Wales from 1997 to 2002; to compare with previously published rates (1990-1996); and to analyse trends in incidence from 1990 to 2002. DESIGN, SETTING AND PARTICIPANTS: Prospective population-based incidence study. Primary ascertainment of incident cases aged < 15 years was from the Australasian Paediatric Endocrine Group NSW children's diabetes register. Secondary ascertainment was from the National Diabetes Supply Scheme until 1999 and from the Australian Institute of Health and Welfare thereafter. Childhood population data were obtained from the Australian Bureau of Statistics. MAIN OUTCOME MEASURES: Age-standardised incidence; trends in incidence by calendar year, and sex and age at diagnosis. RESULTS: There were 3260 incident cases (1629 boys, 1631 girls) in the 13 years. Case ascertainment was 99.7% complete using the capture-recapture method. Mean age-standardised incidence per 100 000 person-years was 20.9 (95% CI, 19.9 to 21.9) from 1997 to 2002 compared with 17.8 (95% CI, 17.0 to 18.7) from 1990 to 1996; there was a plateau in incidence between 1997 and 2002. Overall, the incidence increased on average by 2.8% per year (95% CI, 1.9% to 3.8%, P < 0.001) and increased with age, being 12.2 (95% CI, 11.3 to 13.1) in 0-4 year olds; 18.9 (95% CI, 17.8 to 20.0) in 5-9 year olds and 26.7 (95% CI, 25.4 to 28.1) in 10-14 year olds. The increase per year in 0-4 year olds (3.9%) was not significantly higher than in older children. The mean incidence of T1DM was 19.8 (95% CI, 18.8 to 20.7) in girls and 18.8 (95% CI, 17.9 to 19.7) in boys (P = 0.02). CONCLUSIONS: The incidence of childhood-onset T1DM has increased significantly in all age groups in NSW since 1990. Resource planning in the management of childhood diabetes in NSW should take these findings into account.     

Type 2 diabetes in young Indigenous Australians in rural and remote areas: diagnosis, screening, management and prevention

The burden of type 2 diabetes mellitus (T2DM) among Indigenous children and adolescents is much greater than in non-Indigenous young people and appears to be rising, although data on epidemiology and complications are limited. Young Indigenous people living in remote areas appear to be at excess risk of T2DM. Most young Indigenous people with T2DM are asymptomatic at diagnosis and typically have a family history of T2DM, are overweight or obese and may have signs of hyperinsulinism such as acanthosis nigricans. Onset is usually during early adolescence. Barriers to addressing T2DM in young Indigenous people living in rural and remote settings relate to health service access, demographics, socioeconomic factors, cultural factors, and limited resources at individual and health service levels. We recommend screening for T2DM for any Aboriginal or Torres Strait Islander person aged > 10 years (or past the onset of puberty) who is overweight or obese, has a positive family history of diabetes, has signs of insulin resistance, has dyslipidaemia, has received psychotropic therapy, or has been exposed to diabetes in utero. Individualised management plans should include identification of risk factors, complications, behavioural factors and treatment targets, and should take into account psychosocial factors which may influence health care interaction, treatment success and clinical outcomes. Preventive strategies, including lifestyle modification, need to play a dominant role in tackling T2DM in young Indigenous people.     

HIV and AIDS in aboriginal and Torres Strait Islander Australians: 1992-1998. The National HIV Surveillance Committee

OBJECTIVE: To describe the epidemiological pattern of newly diagnosed HIV infection and AIDS among Indigenous Australians. DESIGN AND SETTING: National surveillance for newly diagnosed HIV infection and AIDS in Australia. Information on Indigenous status was sought at HIV/AIDS notification in all State/Territory health jurisdictions, except the Australian Capital Territory, and Victoria before June 1998. MAIN OUTCOME MEASURES: Number of people with newly diagnosed HIV per year and population rate of HIV diagnosis; demographic characteristics of people with HIV and AIDS diagnoses by Indigenous status. RESULTS: From 1992 to 1998, 127 Indigenous Australians were newly diagnosed with HIV infection and 55 were diagnosed with AIDS. The population rate of HIV diagnosis among Indigenous Australians (5.23/100,000 per year) was similar to that among non-Indigenous Australians (5.51/100,000 per year). The annual number of HIV diagnoses among Indigenous people was relatively stable, but among non-Indigenous people it declined steadily over time. A higher proportion of Indigenous people diagnosed with HIV were women (26.8% v 8.9%; P < 0.001). Although male homosexual contact was the predominant source of exposure for both Indigenous (46.7%) and non-Indigenous (75.0%) people with HIV infection, exposure by heterosexual contact (36.7% v 15.3%; P < 0.001) was reported more frequently among Indigenous people. CONCLUSION: Although HIV incidence was similar among Indigenous and non-Indigenous Australians, the lack of a recent decline in incidence and the higher proportion of Indigenous people exposed to HIV by heterosexual contact indicate the need to intensify interventions to prevent HIV transmission among Indigenous people.     

Prevalence of Huntington disease in New South Wales in 1996

OBJECTIVE: To estimate the prevalence of Huntington disease (HD) in New South Wales on Australian Census Day (6 August) 1996. DESIGN: Survey of records of the Huntington Disease Service and major hospitals, and of neurologists, psychiatrists, clinical geneticists and genetic counsellors. SUBJECTS AND SETTING: All patients in NSW who, on Census Day 1996, either had a definite diagnosis of HD (motor signs of chorea or ataxia and family history of HD or positive DNA test result) or would have had signs and later received a definite diagnosis (assessed 1 April 1997 to 1 July 1999). MAIN OUTCOME MEASURES: Prevalence (HD patients per 100,000 population); patient characteristics; year and basis of diagnosis. RESULTS: 380 patients with definite HD were identified, giving a prevalence of HD in NSW in 1996 of 6.29 per 100,000 population (95% CI, 5.68-6.96). A third of HD patients were aged 60 years or older. Diagnosis was confirmed by DNA testing for 171 patients (45%), including 30 (8%) with no recorded family history. Average numbers of new diagnoses per year were 11.8 (1984-1988), 21.8 (1989-1993) and 28.6 (1994-1998). Estimated number of people with a 50% risk of inheriting the HD mutation was 25.2 per 100,000 population. Estimated incidence of HD in 1996 was 0.65 per 100,000 population. CONCLUSIONS: Prevalence of HD in NSW is similar to estimated prevalence in other Australian and Western populations. Increasing numbers of cases are being diagnosed, and the 18 chronic care beds currently designated for HD patients in NSW are unlikely to be sufficient.     

Incidence of autism spectrum disorders in children in two Australian states

AIM: To ascertain the incidence of autism spectrum disorders in Australian children. SETTING: New South Wales (NSW) and Western Australia (WA), July 1999 to December 2000. DESIGN: Data were obtained for WA from a prospective register and for NSW by active surveillance. MAIN OUTCOME MEASURES: Newly recognised cases of autism spectrum disorders (defined as autistic disorder, Asperger disorder and pervasive developmental disorder not otherwise specified [PDD-NOS]) in children aged 0-14 years; incidence was estimated in 5-year age bands (0-4 years, 5-9 years, 10-14 years). RESULTS: In WA, 252 children aged 0-14 years were identified with autism spectrum disorder (169 with autistic disorder and 83 with Asperger disorder or PDD-NOS). Comparable figures in NSW were 532, 400 and 132, respectively. Most children were recognised with autistic disorder before school age (median age, 4 years in WA and 3 years in NSW). Incidence of autistic disorder in the 0-4-years age group was 5.5 per 10,000 in WA (95% CI, 4.5-6.7) and 4.3 per 10,000 in NSW (95% CI, 3.8-4.8). Incidence was lower in older age groups. The ratio of all autism spectrum disorders to autistic disorder alone was 1.5:1 in WA and 1.3:1 in NSW, and rose with age (1.8:1 and 2.9:1 in 10-14-year-olds in WA and NSW, respectively). CONCLUSIONS: These are the first reported incidence rates for autism for a large Australian population and are similar to rates reported from the United Kingdom. Ongoing information gathering in WA and repeat active surveillance in NSW will help to monitor any future changes.     

Patterns of drowning in Australia, 1992-1997

OBJECTIVE: To determine patterns of victims, circumstances and locations of drownings in Australia in 1992-1997, inclusive. METHODS: Population figures and available details of all drownings were obtained from the Australian Bureau of Statistics. Accidental non-boating drownings (ICD E910), boating incidents (E830-832), homicide (E964), suicide (E954), and other deaths without a drowning E code but "flagged" because drowning was involved (although not the primary cause of death) were included. RESULTS: The overall accidental non-boating drowning rate was 1.44/100,000 population/year. The commonest sites for non-boating drowning were ocean or estuary (22%), private swimming pools (17%), non-tidal lakes and lagoons (17%), surfing beach (10%) and bathtub (7%). 22% of victims were aged under 5 years; this group had a drowning rate of 4.6/100,000 population/year. Very few young children drowned in the ocean or in boating incidents. The rate of boating drownings was 0.29/100,000 population/year. Overseas tourists comprised 4.7% of all non-boating drownings, 18% of surf and ocean drownings, and 25% of all scuba drownings. Indigenous people had a much higher drowning rate than the general population. CONCLUSIONS: Drownings in children aged less than 5 years continue to be the greatest challenge for water safety organisations and legislators. Drownings in the Indigenous community and among tourists requires more detailed study and action. To assist in developing preventive strategies, the National Water Safety Council will need to clarify the categories described as "ocean/estuary" and "lake, lagoon, dam and waterhole".     

Hospitalisation for head injury due to assault among Indigenous and non-Indigenous Australians, July 1999--June 2005

OBJECTIVE: To describe rates of hospitalisation for head injury due to assault among Indigenous and non-Indigenous Australians. DESIGN, SETTING AND PARTICIPANTS: Secondary analysis of routinely collected hospital morbidity data for 42,874 inpatients at public and private hospitals in Queensland, Western Australia, South Australia and the Northern Territory for the 6-year period 1 July 1999--30 June 2005. MAIN OUTCOME MEASURES: Rates per 100,000 population of head injury due to assault by Indigenous status, age, sex and location of residence. RESULTS: The overall rate of head injury due to assault was 60.4 per 100,000 population (95% CI, 59.8-60.9). The rate among the Indigenous population was 854.8 per 100,000 (95% CI, 841.0-868.9), 21 times that among the non-Indigenous population (40.7 per 100,000; 95% CI, 40.2-41.2). Most Indigenous (88%) and non-Indigenous (83%) victims of head injury due to assault were aged between 15 and 44 years. The peak incidence among the Indigenous population was in the 30-34-year age group, whereas that among the non-Indigenous population was in the 20-24-year age group. Indigenous females experienced 69 times the injury rate experienced by non-Indigenous females. CONCLUSIONS: Indigenous people, particularly women, were disproportionately represented among those hospitalised for head injury due to assault. Head injury imposes a substantial burden of care on individuals and communities. Along with the costs of treating head injury, these are good reasons to strengthen efforts to prevent head injury generally, with special attention to high-risk population segments.     

Invasive pneumococcal disease in Indigenous people in north Queensland, 1999-2004

OBJECTIVE: To describe the epidemiology of invasive pneumococcal disease (IPD), and the impact of pneumococcal vaccines on IPD, in Indigenous people in north Queensland. SETTING: North Queensland, 1999-2004; there are about 53 750 Indigenous people in the region, including nearly 6900 children < 5 years and nearly 5650 adults > or = 50 years. MAIN OUTCOME MEASURES: Incidences of IPD in Indigenous children and in Indigenous adults compared between the 3 years before and after the introduction of a 7-valent pneumococcal conjugate vaccine (7vPCV) (1999-2001 versus 2002-2004). RESULTS: Estimated annual incidence of IPD in Indigenous children < 5 years of age declined from 170 to 78 cases per 100 000 in the 3 years following the introduction of 7vPCV in 2001. The annual incidence of vaccine-preventable IPD in Indigenous adults had declined by 86% since a 23-valent pneumococcal polysaccharide vaccine (23vPPV) was introduced to the region in 1996, to 15 cases per 100 000 (95% CI, 8-25) in 2002-2004. CONCLUSION: Although there was a rapid decline in IPD in young Indigenous children, it is unlikely that the incidence will fall much further with the current 7-valent vaccine. There was a suggestion that vaccinating Indigenous children indirectly protected those aged 5-14 years and Indigenous adults > or =15 years of age. Incidence of IPD in Indigenous adults in 2002-2004 was the lowest on record in the region.     

Prevalence and reasons of increased type 2 diabetes in Gulf Cooperation Council Countries

Arab Gulf Cooperation Council countries are considered as one of the most regions exhibiting a high prevalence of diabetes including the kingdom of Saudi Arabia, Bahrain, Qatar, Oman, Kuwait, and United Arab of Emirates, which have similar population characteristics (for example, religion, language, lifestyle, diet, and income). The frequency rate of diabetes in these countries ranged from 8 to 22% according to the last International Diabetes Federation (IDF) report. Many factors impact the prevalence in this region including obesity, unhealthy lifestyle, increased life expectancy, increased healthcare expenditures, increased the incidence of type 2 diabetic mellitus (T2DM) among children and young persons, and genetic susceptibility. This study aims to review the published papers on the incidence of T2DM and explore the most reasons behind elevated incidence of T2DM in these countries.     

Metformin and lactic acidosis in an Australian community setting: the Fremantle Diabetes Study

OBJECTIVE: To determine the incidence of lactic acidosis in community-based patients with type 2 diabetes, with special reference to metformin therapy. DESIGN: Substudy within a longitudinal observational study, the Fremantle Diabetes Study (FDS). PARTICIPANTS AND SETTING: 1279 patients from a postcode-defined population of 120 097 people in Western Australia. MAIN OUTCOME MEASURES: Confirmed hospitalisation with lactic acidosis identified through the WA Data Linkage System during two periods: (1) from study entry, between 1993 and 1996, and study close in November 2001; and (2) from study entry to 30 June 2006. RESULTS: At entry, 33.3% of patients were metformin-treated, and 23.1% of these had one or more contraindications to metformin (55.1% and 38.0%, respectively, after 5 years' follow-up). Five confirmed cases of lactic acidosis were identified during 12 466 patient-years of observation; all had at least one other potential cause, such as cardiogenic shock or renal failure. From study entry to close, the incidence was 0/100,000 patient-years in both metformin-treated and non-metformin-treated patients. Between study entry and 30 June 2006, incidence was 57/100,000 patient-years (95% CI, 12-168) in metformin-treated patients and 28/100,000 patient-years (95% CI, 3-100) in the non-metformin-treated group, an incidence rate difference of -30 (-105 to 46) (P=0.4). CONCLUSION: The incidence of lactic acidosis in patients with type 2 diabetes is low but increases with age and duration of diabetes, as cardiovascular and renal causes become more prevalent. Metformin does not increase the risk of lactic acidosis, even when other recognised precipitants are present.     

A nine-year prospective study on the incidence of childhood type 1 diabetes mellitus in China

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Invasive pneumococcal disease in Indigenous people in north Queensland: an update, 2005-2007

OBJECTIVE: To examine trends in invasive pneumococcal disease (IPD) in Indigenous people in north Queensland following the introduction of the 7-valent pneumococcal conjugate vaccine (7vPCV). DESIGN: Trends in IPD were compared over three 3-year periods: before the introduction of 7vPCV for Indigenous children (1999-2001), and two consecutive periods after its introduction (2002-2004 and 2005-2007). MAIN OUTCOME MEASURES: Incidences of IPD in Indigenous children and adults in 1999-2001 and 2005-2007; trends in IPD caused by 7vPCV and non-7vPCV serotypes; and trends in indirect protective effects and emergence of non-7vPCV serotype IPD. RESULTS: From 1999-2001 to 2005-2007, there was a 60% decline in IPD, with the virtual elimination of 7vPCV serotype IPD in young (< 5 years) Indigenous children. There is no evidence yet of an increase in non-7vPCV serotype IPD in these children. Although the annual incidence of IPD in Indigenous adults remained virtually unchanged, there was a 75% decline in 7vPCV serotype IPD in these adults (chi2(trend) = 11.65, P < 0.001). However, the incidence of IPD caused by non-7vPCV serotypes more than tripled in adults (chi2(trend) = 7.58, P = 0.006). Serotype 1 IPD has been prominent over the 9 years, but there is no evidence of a recent increase in serotype 19A IPD. CONCLUSIONS: Vaccinating Indigenous children with 7vPCV has protected Indigenous adults in north Queensland through an indirect "herd immunity" effect. However, this benefit has been offset by a recent increase in non-7vPCV IPD in Indigenous adults. Newer pneumococcal conjugate vaccines could prevent, both directly and indirectly, a considerable amount of the persisting IPD in Indigenous people in the region.     

The Ability of Baseline Triglycerides and Total Cholesterol Concentrations to Predict Incidence of Type 2 Diabetes Mellitus in Chinese Men and Women: A Longitudinal Study in Qingdao,China

ObjectivesThe purpose of this study was to assess the association between triglycerides (TG), total cholesterol (TC) at baseline, and type 2 diabetes mellitus (T2DM) incidence in a general Chinese population. Further, it aimed to evaluate the ability of TG and TC to predict T2DM incidence.MethodsQingdao Diabetes Prevention Program participants recruited between 2006 and 2009 were followed up in 2012–2015. TG, TC, and T2DM status were measured. Cox proportional hazards models were used to estimate the association between TG, TC, and T2DM incidence. The receiver operating characteristic (ROC) curve was used to evaluate the ability of TG and TC to identify T2DM participants.ResultsThe incidence of T2DM significantly increased with TG in women and TC in both men and women (P_trend < 0.05). Univariate Cox regression indicated that higher TG {borderline high TG [hazards ratio (HR): 2.05; 95% confidence interval (CI): 1.40, 3.00] and hypertriglyceridemia [HR: 2.64; 95% CI: 1.68, 4.15]} and TC [hypercholesterolemia (HR: 2.05; 95% CI: 1.43, 2.95)] were significantly associated with increased risk of T2DM incidence in women but not in men. Multivariate Cox regression showed that hypertriglyceridemia in women (HR: 1.78, 95% CI: 1.07, 2.97), borderline high TC in men (HR: 1.61, 95% CI: 1.04, 2.48), and hypercholesterolemia in women (HR: 1.68, 95% CI: 1.81, 2.61) had a higher significant risk of T2DM incidence. The optimal cutoff values of TG were > 1.15 and > 1.23 mmol/L in men and women, respectively. For TC, they were > 5.17 and > 5.77 mmol/L in men and women, respectively. The area under the ROCs of TG and TC were 0.54 (0.51–0.57) and 0.55 (0.52–0.58), respectively, in men, and 0.60 (0.58–0.62) and 0.59 (0.56–0.61), respectively, in women.ConclusionElevated TG and TC were risk factors for T2DM incidence. However, no predictive capacity was found for both factors to identify T2DM incidence in Chinese men and women. Hence, TG and TC levels in both Chinese men and women might be used for decreasing the incidence of T2DM but no clinical predictive capacity for T2DM.     

新疆哈萨克族超重2型糖尿病患者血脂、血尿酸与胰岛素抵抗的关系

目的:分析新疆哈萨克族超重2型糖尿病(T2DM)患者血脂、血尿酸与胰岛素抵抗(IR)的关系。方法:选取245例T2DM患者,其中哈萨克族121例(超重组63例、非超重组58例),汉族124例(超重组65例、非超重组59例),另选同期体检正常者129例为对照组,其中哈萨克族65例,汉族64例。比较各组一般资料以及两民族T2DM患者使用降糖药情况,分析两民族T2DM患者稳态模型胰岛素抵抗指数(HOMA-IR)与各指标的相关性。结果:两民族超重组TC、TG显著高于其对照组;哈萨克族超重组HDL-C水平与对照组比较无明显差异(P>0.05),而显著高于汉族超重组和汉族非超重组,LDL-C水平显著高于其对照组、低于汉族超重组;哈萨克族超重组血尿酸水平显著高于其余各组,且HOMA-IR明显大于其对照组和汉族各组(P<0.05或P<0.01)。两民族T2DM患者降糖药使用情况比较无显著差异(P>0.05)。相关性分析表明,两民族T2DM患者HOMA-IR均与血尿酸水平均呈明显正相关(P<0.05)。结论:哈萨克族超重T2DM患者IR和高尿酸血症更为突出,而汉族超重者HDL-C降低及LDL-C升高更为突出。     

Long-term trends in Indigenous deaths from chronic diseases in the Northern Territory: a foot on the brake, a foot on the accelerator

OBJECTIVE: To examine trends in Northern Territory Indigenous mortality from chronic diseases other than cancer. DESIGN: A comparison of trends in rates of mortality from six chronic diseases (ischaemic heart disease [IHD], chronic obstructive pulmonary disease [COPD], cerebrovascular disease [CVD], diabetes mellitus [DM], renal failure [RF] and rheumatic heart disease [RHD]) in the NT Indigenous population with those of the total Australian population. PARTICIPANTS: NT Indigenous and total Australian populations, 1977-2001. MAIN OUTCOME MEASURES: Estimated average annual change in chronic disease mortality rates and in mortality rate ratios. RESULTS: Death rates from IHD and DM among NT Indigenous peoples increased between 1977 and 2001, but this increase slowed after 1990. Death rates from COPD rose before 1990, but fell thereafter. There were non-significant declines in death rates from CVD and RHD. Mortality rates from RF rose in those aged > or = 50 years. The ratios of mortality rates for NT Indigenous to total Australian populations from these chronic diseases increased throughout the period. CONCLUSIONS: Mortality rates from IHD and DM in the NT Indigenous population have been increasing since 1977, but there is evidence of a slower rise (or even a fall) in death rates in the 1990s. These early small changes give reason to hope that some improvements (possibly in medical care) have been putting the brakes on chronic disease mortality among Aboriginal and Torres Strait Islander peoples.     

Long-term trends in cancer mortality for Indigenous Australians in the Northern Territory

OBJECTIVE: To examine long-term trends in cancer mortality in the Indigenous people of the Northern Territory (NT) of Australia. DESIGN: Comparison of cancer mortality rates of the NT Indigenous population with those of the total Australian population for 1991-2000, and examination of time trends in cancer mortality rates in the NT Indigenous population, 1977-2000. PARTICIPANTS: NT Indigenous and total Australian populations, 1977-2000. MAIN OUTCOME MEASURES: Cancer mortality rate ratios and percentage change in annual mortality rates. RESULTS: The NT Indigenous cancer mortality rate was higher than the total Australian rate for cancers of the liver, lungs, uterus, cervix and thyroid, and, in younger people only, for cancers of the oropharynx, oesophagus and pancreas. NT Indigenous mortality rates were lower than the total Australian rates for renal cancers and melanoma and, in older people only, for cancers of the prostate and bowel. Differences between Indigenous and total Australian cancer mortality rates were more pronounced among those aged under 64 years for most cancers. NT Indigenous cancer mortality rates increased over the 24-year period for cancers of the oropharynx, pancreas and lung, all of which are smoking-related cancers. CONCLUSIONS: Cancer is an important and increasing health problem for Indigenous Australians. Cancers that affect Indigenous Australians to a greater extent than other Australians are largely preventable (eg, through smoking cessation, Pap smear programs and hepatitis B vaccination).     

高频超声检测2型糖尿病颈总动脉内中膜与体质量指数的关系

目的:探讨2型糖尿病(T2DM)体质量指数(BMI)与颈总动脉内中膜(IMT)及发生斑块的关系。方法:对90例35~79岁T2DM病人测量身高、体质量并计算BMI,按BMI值将研究对象分为正常体质量组、超质量组及肥胖组,对3组颈动脉进行检测,分析3组间BMI与颈总动脉IMT及斑块数量的关系。结果:T2DM病人IMT厚度随BMI增加而增加,两者呈中度正相关(r=0.49,P<0.05)。正常体质量组、超质量组及肥胖组3组间IMT及斑块数量有显著性差异,以肥胖组最高(P<0.05);颈总动脉IMT厚度及斑块数量随BMI增加而增加;3组间有显著性差异,肥胖组最高(P<0.05)。结论:T2DM病人BMI与IMT呈中度正相关,随BMI的增加,颈动脉粥样硬化及斑块的发生增加,BMI是T2DM患者发生动脉粥样硬化的独立危险因素。     

Invasive Haemophilus influenzae type b disease in Sydney children 1985-1987: a population-based study

OBJECTIVE: To determine the incidence and age distribution of invasive Haemophilus influenzae type b (Hib) disease in children (0-14 years) in the Sydney Statistical Division (SSD). DESIGN: Retrospective ascertainment from a defined population, 1985-1987. Eligible cases had Hib isolated from a normally sterile site or endoscopically proven epiglottitis. SETTING: Sydney Statistical Division, which had a population of children aged 0-4 years of 229 165 in 1986. PATIENTS: Cases were identified from all potential sources of relevant recorded information. MAIN OUTCOMES: There were 292 eligible cases. Among 284 previously well children, those under 18 months of age contributed 81 of 143 cases (57%) of meningitis and 22 of 71 (71%) of cellulitis/arthritis but only 8 of 91 (11%) of epiglottitis and 4 of 18 (22%) of infection in other foci. Overall, 9% of cases had occurred by 6 months of age, 42% by 18 months and 55% by 24 months. The annual incidence of invasive Hib disease was 38.5 per 100,000 children aged 0-4 years. In areas with the lowest proportion of young children (less than 5.5%), the incidence of Hib disease in the first 12 months of life was significantly lower than in the remainder of Sydney, although there were no differences in overall disease incidence in the age group 0-4 years. CONCLUSIONS: This study indicates that approximately 1 in 500 urban Australian children develop invasive Hib disease by their fifth birthday. Vaccination of children in Sydney with a conjugate Hib vaccine at 18 months of age would result in a greater potential reduction in Hib disease than in the United States, where universal vaccination at this age is current policy.     

Sudden death due to ischaemic heart disease in young aboriginal sportsmen in the Northern Territory, 1982-1996.

OBJECTIVE: To estimate the incidence of sport-related sudden cardiac death due to ischaemic heart disease (IHD) in competitive young Aboriginal sportsmen. SETTING: Northern Territory (NT), 1982-1996. DESIGN: Retrospective case series with cases identified from Australian Bureau of Statistics cause-of-death listings and NT coronial autopsy records. MAIN OUTCOME MEASURES: Circumstances and incidence of sport-related sudden cardiac deaths due to IHD; autopsy findings. RESULTS: Between 1982 and 1996, there were eight sudden cardiac deaths due to IHD and related to sporting activity among Aboriginal sportsmen aged 15-37 years in the NT. Six were associated with games of Australian (rules) football. All occurred in the Top End of the NT in the wet season, and all occurred after the first half, or within an hour of, a game. Four of the players had macrosopic myocardial abnormalities (hypertrophy or previous infarcts) on autopsy. The estimated incidence of IHD-related sudden cardiac death among Aboriginal Australian football players in the NT was 19-24 per 100,000 player-years, compared with 0.54 per 100,000 player-years among Australian rules footballers of similar ages in Victoria. CONCLUSIONS: Incidence of sudden cardiac death attributable to underlying IHD was extremely high among young NT Aboriginal Australian footballers. Prevention will best be achieved by funding culturally appropriate long-term strategies to reduce the incidence of IHD. However, in the short-term, community-controlled programs with education of athletes, heat-stress reduction strategies, and cardiovascular screening should reduce the incidence of sudden cardiac death in sport.