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Träfflista för sökning "WFRF:(Li Xinjun) srt2:(2010-2014)"

Search: WFRF:(Li Xinjun) > (2010-2014)

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11.
  • Hemminki, Kari, et al. (author)
  • Incidence and survival in non-hereditary amyloidosis in Sweden
  • 2012
  • In: BMC Public Health. - : Springer Science and Business Media LLC. - 1471-2458. ; 12:974
  • Journal article (peer-reviewed)abstract
    • Background: Amyloidosis is a heterogeneous disease caused by deposition of amyloid fibrils in organs and thereby interfering with physiological functions. Hardly any incidence data are available and most survival data are limited to specialist clinics. Methods: Amyloidosis patients were identified from the Swedish Hospital Discharge and Outpatients Registers from years 2001 through 2008. Results: The incidence of non-hereditary amyloidosis in 949 patients was 8.29 per million person-years and the diagnostic age with the highest incidence was over 65 years. Secondary systemic amyloidosis showed an incidence of 1 per million and a female excess and the largest number of subsequent rheumatoid arthritis deaths; the median survival was 4 years. However, as rheumatoid arthritis deaths also occurred in other diagnostic subtypes, the incidence of secondary systemic amyloidosis was likely to be about 2.0 per million. The median survival of patients with organ-limited amyloidosis was 6 years. Most myeloma deaths occurred in patients diagnosed with unspecified or 'other' amyloidosis. These subtypes probably accounted for most of immunoglobulin light chain (AL) amyloidosis cases; the median survival time was 3 years. Conclusions: The present diagnostic categorization cannot single out AL amyloidosis in the Swedish discharge data but, by extrapolation from myeloma cases, an incidence of 3.2 per million could be ascribed to AL amyloidosis. Similarly, based on rheumatoid arthritis death rates, an incidence of 2.0 could be ascribed to secondary systemic amyloidosis.
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12.
  • Hemminki, Kari, et al. (author)
  • Incidence of hereditary amyloidosis and autoinflammatory diseases in Sweden: endemic and imported diseases
  • 2013
  • In: BMC Medical Genetics. - : Springer Science and Business Media LLC. - 1471-2350. ; 14
  • Journal article (peer-reviewed)abstract
    • Background: Amyloidoses are a heterogeneous group of progressive diseases caused by tissue deposition of misfolded proteins. According to the International Classification of Diseases, hereditary amyloidosis is divided into neuropathic and non-neuropathic forms. In Sweden, neuropathic heredofamilial amyloidosis has been identified as familial amyloidotic polyneuropathy (FAP), a fatal disease that is treated by liver transplantation. The non-neuropathic form includes familial autoinflammatory diseases. As no incidence data on these hereditary diseases are available and as even diagnostic data on non-neuropathic forms are lacking we determined the incidence of these diseases and characterized non-neuropathic conditions. Methods: Patients were identified using data from the Swedish Hospital Discharge Register and from the Outpatient Register for 2001 through 2008. All patients discharged with hereditary amyloidosis diagnoses were included and standardized incidence rates were calculated. Results: Non-neuropathic disease was diagnosed in 210 patients, with an incidence of 2.83 per million. FAP was diagnosed in 221 patients, with an incidence of 2.02 per million. Two northern provinces that are home to 5% of the Swedish population accounted for 77% of FAP cases; the incidence in one of them, West Bothnia, was 100 times that in the rest of Sweden. Approximately 98% of non-neuropathic disease patients were immigrants, most of whom were from the Eastern Mediterranean area. Young Syrian descendants had the highest incidence rate, which was over 500-fold higher than that in individuals with Swedish parents. Even the early onset of these conditions identified them as familial autoinflammatory diseases. Conclusions: FAP cases were highly concentrated in the two northernmost provinces. Non-neuropathic familial autoinflammatory diseases were of early-onset and immigrant origin most likely related to periodic fever syndromes. Paradoxically, FAP has remained endemic, in spite of population movements within the country, while familial autoinflammatory diseases, with an incidence exceeding that of FAP, were brought into the country as a result of immigration mainly from the Eastern Mediterranean area.
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15.
  • Hemminki, Kari, et al. (author)
  • Obesity and familial obesity and risk of cancer.
  • 2011
  • In: European Journal of Cancer Prevention. - 1473-5709. ; 20, s. 438-443
  • Journal article (peer-reviewed)abstract
    • Obesity is associated with a risk of at least 20 different cancers. We aimed at defining cancer risks in prospectively recruited patients with a novel subgroup, those with a family history of obesity. We defined a cohort of 30 020 patients who had been hospitalized since 1964. Cancer risks in these patients were followed through 2006. Standardized incidence ratios were calculated for cancer using those not hospitalized for obesity as a reference population. We could also identify persons who had been hospitalized for type 2 diabetes. A total of 1721 patients were diagnosed with cancer after hospitalization for obesity, showing an increased risk for 12 cancers and a decrease for breast cancer. The largest increases were found for nervous system hemangioma (13.64, 95% confidence interval 2.57-40.37) and other male genital (3.94, 1.24-9.26), bone (3.41, 1.23-7.47), small intestinal (2.93, 1.60-4.93), kidney (2.46, 1.97-3.02), and endometrial (2.32, 2.01-2.66) cancers. Among endocrine cancers, adrenal tumors showed the highest risk, of 3.74 (1.86-6.72). The overall risk was 1.19 (1.13-1.25). Family history of obesity was associated with formerly unrecognized increased risks of gallbladder and colon cancers and ocular melanoma. Cancer risks in this relatively young obese population differed quantitatively from those found after type 2 diabetes. The novel findings included rare and relatively benign tumors, probably found in endocrinological and other medical examinations for obesity and related conditions. Similarly, male genital cancer may be related to sexual behavior, and bone cancers, found in old individuals, could be related to propensity for fractures.
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16.
  • Hemminki, Kari, et al. (author)
  • Risk of asthma and autoimmune diseases and related conditions in patients hospitalized for obesity
  • 2012
  • In: Annals of Medicine. - : Informa UK Limited. - 1365-2060 .- 0785-3890. ; 44:3, s. 289-295
  • Journal article (peer-reviewed)abstract
    • Background. Although there are putative mechanistic links between obesity and autoimmune diseases, obesity is not considered a risk factor for most autoimmune diseases. Methods. Using the nation-wide Hospital Discharge Register we defined a cohort of 29,665 patients hospitalized for obesity since year 1964. The patients were followed for hospitalization for any of 34 autoimmune or related conditions through year 2007. Standardized incidence ratios (SIRs) were calculated for autoimmune diseases in obese individuals compared to those who had not been hospitalized for obesity. Results. Among 22 immune diseases diagnosed after hospitalization for obesity and in at least 5 patients, the overall SIR was 2.05. Of the individual diseases studied, the risk of 16 was significantly increased; none displayed a decreased risk. Psoriasis (4.54) and Behcet's disease (4.49) exhibited the highest risks, followed by Hashimoto's disease/hypothyroidism (4.12) and asthma (3.39). Small but significant increases in SIRs were also noted for the common autoimmune diseases Graves' sdisease/hyperthyroidism (1.28) and rheumatoid arthritis (1.37). Conclusions. The present population of obese individuals, subsequently diagnosed with a number of autoimmune diseases and related conditions, was hospitalized at a relatively young age. Further studies are needed to describe the morbidity in the obese population at large.
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17.
  • Hemminki, Kari, et al. (author)
  • Risk of Cancer Following Hospitalization for Type 2 Diabetes
  • 2010
  • In: The Oncologist. - : Oxford University Press (OUP). - 1083-7159 .- 1549-490X. ; 15:6, s. 548-555
  • Journal article (peer-reviewed)abstract
    • Objectives. Cancer and type 2 diabetes (T2D) are two common diseases that may share risk factors. We aimed at determining subsequent cancer risks in patients hospitalized for T2D in Sweden. Methods. T2D patients were obtained from the nationwide Hospital Discharge Register; cancers were recorded from the Swedish Cancer Registry. Standardized incidence ratios (SIRs) were calculated for cancer following last hospitalization for T2D. The comparison group was the general Swedish population. Results. The number of hospitalized T2D patients from 1964 to 2007 was 125,126, of whom 26,641 had an affected family member. Altogether 24 cancers showed an elevated risk when follow-up was started after the last hospitalization. The highest SIRs were for pancreatic (6.08) and liver (4.25) cancers. The incidences of these cancers were even elevated when follow-up was started 5 years after the last hospitalization for T2D, with primary liver cancer showing the highest SIR of 4.66. Also increased were the incidences of upper aerodigestive tract, esophageal, colon, rectal, pancreatic, lung, cervical, endometrial, ovarian, and kidney cancers. Prostate cancer showed a lower risk. Familial T2D patients showed no exceptional elevated cancer risks but their prostate cancer and melanoma risks were lower. Conclusions. This study, covering approximately one half of Swedish T2D patients, showed an elevated risk for several cancers after hospitalization for T2D, probably indicating the profound metabolic disturbances of the underlying disease. The highest risks were found for liver and pancreatic cancers. No excess cancer risks were observed in familial diabetics. The lower risk for prostate cancer remains intriguing. The Oncologist 2010;15:548-555
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18.
  • Hemminki, Kari, et al. (author)
  • Subsequent Autoimmune or Related Disease in Asthma Patients: Clustering of Diseases or Medical Care?
  • 2010
  • In: Annals of Epidemiology. - : Elsevier BV. - 1047-2797 .- 1873-2585. ; 20, s. 217-222
  • Journal article (peer-reviewed)abstract
    • PURPOSE: Asthma includes immunological components that may share mechanisms with autoimmune diseases. We analyzed the subsequent occurrence of any of 22 autoimmune and related conditions in hospitalized asthma patients. METHODS: A nationwide study was conducted in Sweden on subsequent diseases of asthma patients on the basis of the Hospital Discharge Register. Standardized incidence ratios (SIRs) were calculated for subsequent autoimmune diseases. RESULTS: A total of 4006 patients were hospitalized for an autoimmune condition after last hospitalization for asthma. The SIRs were increased for 11 subsequent autoimmune conditions, diagnosed at least 5 years after asthma. The highest SIRs were noted for polyarteritis nodosa (4.29) and Addison disease (3.62). SIRs for these diseases and others, including the most common autoimmune disease rheumatoid arthritis, were increased even when the follow-up was started 5 years after the last asthma hospitalization. Addison disease and Crohn disease were increased in asthma patients hospitalized at various ages, whereas young asthma patients presented with celiac disease and immune thrombocytopenic purpura. CONCLUSIONS: Hospitalized asthma patients presented with a number of subsequent autoimmune and related diseases. Although we were unable to exclude the effects of environmental factors, the data suggest that shared genetic factors or gene-environment interactions may explain coexistence of some of these diseases.
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19.
  • Hemminki, Kari, et al. (author)
  • The epidemiology of Graves' disease: Evidence of a genetic and an environmental contribution.
  • 2010
  • In: Journal of Autoimmunity. - : Elsevier BV. - 0896-8411 .- 1095-9157. ; 34, s. 307-313
  • Journal article (peer-reviewed)abstract
    • Previous family and twin studies have indicated that Graves' disease has a heritable component. Family studies have also shown that some autoimmune disease cluster in families and genetic studies have been able to show shared susceptibility genes. In the present nation-wide study we describe familial risk for Graves' disease among parents and offspring, singleton siblings, twins and spouses with regard to age of onset, gender and number and type of affected family members. Additionally familial association of Graves' disease with any of 33 other autoimmune and related conditions was analyzed. The Swedish Multigeneration Register on 0-75-year-old subjects was linked to the Hospital Discharge Register from years 1987-2007. Standardized incidence ratios (SIRs) were calculated for individuals whose relatives were hospitalized for Graves' disease compared to those whose relatives were unaffected. The total number of hospitalized Graves' patients was 15,743. Offspring with an affected family member constituted 3.6% of all patients among offspring. The familial SIR was 5.04 for individuals whose sibling was affected but it increased to 310 when two or more siblings were affected; the SIR in twins was 16.45. Familial risks were higher for males than for females. The SIR was increased to 6.22 or 30.20 when parental age was limited to 50 or 20 years, respectively. Graves' disease associated with 19 other autoimmune and related conditions, including Addison's disease, type 1 diabetes mellitus, Hashimoto/hypothyroidism, pernicious anemia, polymyositis/dermatomyositis, myasthenia gravis, discoid lupus erythematosus and localized scleroderma. Remarkably, there was a high disease concordance of 2.75 between spouses. The clustering between spouses suggests environmental effects on Graves' disease which may contribute to the observed gender effects. The demonstrated high risks should be considered in clinical counseling and in prevention plans.
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20.
  • Kawakami, Naomi, et al. (author)
  • Health-promoting and health-damaging neighbourhood resources and coronary heart disease: a follow-up study of 2 165 000 people.
  • 2011
  • In: Journal of Epidemiology and Community Health. - : BMJ. - 1470-2738 .- 0143-005X. ; 65, s. 866-872
  • Journal article (peer-reviewed)abstract
    • Background It has been hypothesised that the presence of health-damaging factors and lack of health-promoting factors lie in the causal pathway between neighbourhood deprivation and coronary heart disease (CHD). This study is the first to examine the associations between individual-level CHD risk and neighbourhood availability of fast-food restaurants, bars/pubs, physical activity facilities and healthcare resources. Methods Multilevel logistic regression models were used for the follow-up of 1 065 000 men and 1 100 000 women (aged 35-80 years) between 1 December 2005 and 31 December 2007, for individual-level CHD events (both morbidity and mortality). Results The relatively weak associations between neighbourhood availability of potentially health-damaging and health-promoting goods, services and resources, and CHD incidence no longer remained significant after adjustment for neighbourhood-level deprivation and individual-level age and income. Conclusions The presence of potentially health-damaging factors and lack of potentially health-promoting factors do not seem to contribute significantly to the development of CHD. Other features of deprived neighbourhoods appear to play a greater role.
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