Moderate alcohol consumption has been suggested to protect against venous thromboembolism (VTE). However, it is not known how alcohol abuse and its associated somatic complications affect the risk of VTE. The present study determined the risk of pulmonary embolism (PE) and deep vein thrombosis (DVT) of the lower extremities in patients with alcohol use disorders (AUDs) in Sweden. All inpatients with AUDs in 2002-2010 without a previous VTE event (72,024 patients) were matched to five controls without AUD and followed until the end of follow-up (December 31, 2010), death, emigration or a VTE event. Cox regression was used to determine adjusted hazard ratios (HRs) for VTE. AUD patients were further divided into those without alcohol-related somatic complications (AUD-) and those with alcohol-related somatic complications (AUD+, i.e., encephalopathy, epilepsy, polyneuropathy, myopathy, cardiomyopathy, gastritis, liver disease, acute pancreatitis, and chronic pancreatitis). The adjusted HR for VTE was significantly increased for both AUD- (HR 1.70, 95 % CI 1.55-1.87) and AUD+ (HR 1.73, 95 % CI 1.37-2.19) patients. The risk of DVT was increased in both AUD+ and AUD- patients (HR 1.62, 95 % CI 1.45-1.83 and HR 1.99, 95 % CI 1.53-2.59, respectively). However, the risk of PE was only significantly increased in AUD- patients (HR 1.87, 95 % 1.59-1.20) and not in AUD+ patients (HR 1.16, 95 % 0.70-1.91). In conclusion, the present study shows that AUD increases the risk of VTE, even in the absence of alcohol-related somatic complications. Our findings suggest that severe alcohol abuse increases the risk of VTE.
Studies on short-term prognosis of venous thromboembolism (VTE) that take family history of VTE and Charlson Comorbidity Index (CCI) into account are sparse. The aim was to investigate the importance of family history of VTE and CCI for short-term mortality after a first episode of VTE. Using Swedish medical databases, we conducted a 90-day nationwide cohort study of 41,700 Swedish born patients with a first-time VTE (July 2005-August 2012). Patients diagnosed with VTE and prescribed anticoagulant treatment were included. Mortality hazard ratios (HRs) with 95% confidence intervals (CIs) were determined with Cox regression. Patients with first-degree (sibling/parent) family history of VTE (n?=?11,405, 27.4%) had significantly lower CCI than those without family history. Independent risk factors for 90-day mortality in the adjusted model were: female sex (HR?=?1.19, 95% CI: 1.09-1.29), increasing age (HR?=?1.02, 95% CI: 1.01-1.02 per year), pulmonary embolism (HR?=?1.21, 95% CI: 1.11-1.32) or combined pulmonary embolism and deep venous thrombosis (HR?=?1.60, 95% CI: 1.27-2.01) compared with deep venous thrombosis, CCI?=?1 (HR?=?2.93, 95% CI: 2.32-3.72), CCI?=?2 (HR?=?8.65, 95% CI: 7.16-10.46) or CCI?=?3 (HR?=?22.25, 95% CI: 18.73-26.44) compared with CCI?=?0. Having one or two or more affected first-degree relatives with VTE was associated with lower mortality, HR?=?0.83 (95% CI: 0.74-0.92) and HR?=?0.65 (95% CI: 0.51-0.85), respectively. The mortality rate was 0.70% in patients with a CCI of zero. In receiver operating characteristic (ROC) analysis, the area under the ROC curve for CCI was 0.84 (0.83-0.95). Family history of VTE is associated with lower mortality while CCI is a strong predictor for short-term mortality in VTE. Co-morbidities are important for risk assessment of VTE.
Recent studies suggest de novo mutations may involve the pathogenesis of autism and attention-deficit/hyperactivity disorder (ADHD). Based on the evidence that excessive alcohol consumption may be associated with an increased rate of de novo mutations in germ cells (sperms or eggs), we examine here whether the risks of autism and ADHD are increased among individuals with a family history of alcohol use disorders (AUDs). The standardized incidence ratios (SIRs) of autism and ADHD among individuals with a biological parental history of AUDs were 1.39 (95% CI 1.34-1.44) and 2.19 (95% CI 2.15-2.23), respectively, compared to individuals without an affected parent. Among offspring whose parents were diagnosed with AUDs before their birth, the corresponding risks were 1.46 (95% CI 1.36-1.58) and 2.70 (95% CI 2.59-2.81), respectively. Our study calls for extra surveillance for children with a family history of AUDs, and further studies examining the underlying mechanisms are needed.
Osteoporosis is common in the elderly, and it is associated with lifetime exposure to endogenous hormones and vitamin D intake, both of which are associated with cancer development. The association of osteoporosis with subsequent cancer has not been established, and hence we examined here the overall and site-specific cancer risks among Swedish individuals after hospitalization for osteoporosis. Patients with osteoporosis were identified from the Swedish Hospital Discharge Register and then linked to the Cancer Registry. Follow-up of patients was carried out from the date of first hospitalization, that is in or after 1969 to 2008. Standardized incidence ratios (SIRs) were calculated for cancers in these patients and these ratios were compared with those for individuals without osteoporosis. A total of 26 833 patients were hospitalized for osteoporosis during 1969-2008 and 3941 of them developed subsequent cancer, giving an overall SIR of 1.25; for cancer diagnosed after 1 year of follow-up the SIR was 1.06. A significant increase in risk was noted for cancers of the upper aerodigestive tract, skin (squamous cell carcinoma), and lung, and additionally for myeloma. The risk was decreased for breast, endometrial, and ovarian cancers among female patients. Patients with multiple hospitalizations showed higher risks for myeloma and skin cancer and lower risk for breast and endometrial cancers. In total, a 25% increase in cancer risk was noted among osteoporosis patients, but the increase was confined mainly to the first year after hospitalization. However, the increased risk of certain types of cancers calls for clinical attention.
Patients with autoimmune diseases are at an increased risk of cancer due to underlying dysregulation of the immune system or treatment. Data on cancer incidence, mortality and survival after autoimmune diseases would provide further information on the clinical implications. We systematically analysed data on lung cancer in patients diagnosed with 33 different autoimmune diseases. Standardised incidence ratios (SIRs), standardised mortality ratios (SMRs) and hazard ratios (HRs) were calculated for subsequent incident lung cancers or lung cancer deaths up to 2008 in patients hospitalised for autoimmune disease after 1964. Increased risks of lung cancer were recorded for SIRs after 12 autoimmune diseases, SMRs after 11 autoimmune diseases and HRs after two autoimmune diseases. The highest SIRs and SMRs, respectively, were seen after discoid lupus erythematosus (4.71 and 4.80), polymyosistis/dermatomyositis (4.20 and 4.17), systemic lupus erythematosus (2.47 and 2.69), rheumatic fever (2.07 and 2.07) and systemic sclerosis (2.19 and 1.98). Autoimmune disease did not influence survival overall but some autoimmune diseases appeared to impair survival in small cell carcinoma. All autoimmune diseases that had an SIR >2.0 are known to present with lung manifestations, suggesting that the autoimmune process contributes to lung cancer susceptibility. The data on survival are reassuring that autoimmune diseases do not influence prognosis in lung cancer.
Studies on whether family history (FH) of venous thromboembolism (VTE) affects long-term mortality after VTE are missing. The aim of this study was to determine whether FH of VTE affects long-term mortality after a first episode of VTE. Using Swedish medical databases, we conducted a 30-year nationwide cohort study of 49,159 adult Swedish born patients included in the multi-generation register (born 1932 or later) with a first-time VTE (1981-2010). Using Cox regression, we assessed mortality Hazard ratios (HRs) with 95% confidence intervals (CIs). Totally 10,093 (20.5%) patients with VTE had a first-degree FH of VTE (parent/sibling). Patients without FH of VTE had significantly more VTE provoking risk factors and comorbidities than those with FH. The mortality HR the first 10-years after first time VTE was decreased for those with FH of VTE compared to for those without FH: crude HR 0.807, 95% CI 0.771-0.845 and adjusted HR 0.864, 95% CI 0.826-0.905. After 10-years of follow-up there was no significant effect of FH of VTE on mortality: crude HR?=?1.018, 95% CI 0.905-1.145 and adjusted HR?=?0.995, 95% CI 0.884-1.119. Cancer-associated mortality was more common in those without FH the first 10 years (56.9 vs. 53.4%, p?=?0.002). After 10 years there were no difference in cancer-associated mortality (4.9 vs. 5.6%, p?=?0.604). The results suggest that patients with FH of VTE have lower thrombotic threshold and need less provoking factors and comorbidities. They have also slightly lower total and cancer mortality the first 10 years after VTE.
Some autoimmune diseases are associated with increased risk of liver cancer. However, there has been no comprehensive evaluation of autoimmune diseases among patients who develop different subtypes of hepatobiliary cancer. We examined the association between autoimmune diseases and cancers of the liver and biliary tract in the Swedish population.
We analyzed data from national datasets at the Center for Primary Health Care Research (Lund University, Sweden). Data on patients with autoimmune disorders were retrieved from the Swedish Hospital Discharge Register, from 1964 through 2008; 33 diseases were evaluated. Hepatobiliary cancer cases were retrieved from the Swedish Cancer Registry. We calculated standardized incidence ratios (SIRs) and hazard ratios for incident cancers and deaths from hepatobiliary cancers.
Among 402,462 patients with autoimmune disorders, 582 were diagnosed with primary liver cancer, 330 with gallbladder cancer, 115 with extrahepatic bile duct cancer, and 43 with ampulla of Vater cancers. We identified 14 autoimmune conditions that were significantly associated with increased risk of primary liver cancer (overall SIR [any autoimmune disease], 2.1; 95% confidence interval [CI], 2.0-2.3), 5 conditions associated with gallbladder cancer (overall SIR, 1.3; 95% CI, 1.1-1.4), and 3 associated with extrahepatic bile duct cancer (overall SIR, 1.6; 95% CI, 1.3-1.9). The autoimmune disorders with the strongest association with primary liver cancer were primary biliary cirrhosis (SIR, 39.5; 95% CI, 28.2-53.8) and autoimmune hepatitis (SIR, 29.0; 95% CI, 9.1-68.2); ulcerative colitis was strongly associated with extrahepatic bile duct cancer (SIR, 5.6; 95% CI, 3.6-8.4). Celiac disease, Crohn's disease, systemic sclerosis, and ulcerative colitis were associated with at least 2 types of cancer. Increased hazard ratios were observed only for patients with biliary tract cancer who had been hospitalized for autoimmune conditions.
In a study of the Swedish population, we identified an increased risk of hepatobiliary cancers among individuals diagnosed with autoimmune disease. Associations among different cancer types indicate that shared immunomodulatory mechanisms determine susceptibility to hepatobiliary cancer.
Few large-scale studies have examined the prevalence of irritable bowel syndrome (IBS) and the number of visits among IBS patients in a primary health care setting. The aim of this study was to assess the prevalence of IBS in primary health care in four Swedish counties. Another aim was to study the number of visits among the IBS patients.
A register-based study. Setting. A primary health care database with information on patients from 71 primary health care centres in the Swedish counties of Stockholm, Uppsala, Värmland, and Gotland.
The primary health care database contains individual-level data for 919,954 patients for the period 2001-2007. Main outcome measures. Prevalence of IBS diagnosis.
10,987 patients had a diagnosis of IBS, which corresponds to a prevalence of 1.2%. IBS was most common in the 25-44 years age group (37% of IBS patients); 71% of IBS patients were female, and 81% of IBS patients visited their GP six or more times, compared with 46% of non-IBS patients. However, 95% of the IBS patients visited their GP three times or fewer for IBS.
The prevalence of IBS was low among Swedish primary health care patients. This might suggest that IBS patients are insufficiently diagnosed in Swedish primary health care.
Cites: Aliment Pharmacol Ther. 2005 Jun 1;21(11):1365-7515932367
Cites: Aust N Z J Psychiatry. 2005 Sep;39(9):772-8116168035
Cites: Aliment Pharmacol Ther. 2005 Nov 15;22(10):935-4216268967
To investigate the risk of small for gestational age (SGA) births in relation to maternal history of cardiovascular disease (CVD) across two generations and additionally to analyse maternal CVD risk based on number of SGA offspring.
We used register data from 1.4 million women and 2.7 million offspring. The outcome measures were risk of being SGA in relation to maternal total CVD (n = 10 436) across two generations, as well as risk of CVD in mothers in relation to the number of their SGA offspring, stratified by educational level.
Compared to no family history of CVD (reference) the hazard ratio (HR) for being SGA in female offspring was 1.11 (95% confidence interval (CI) 1.09-1.13) for a positive maternal history of CVD. The highest risk was shown in daughters when both the mother and the grandmother had a history of CVD (HR 1.32, 95% CI 1.24-1.39). There was a stepwise increased risk of CVD events in mothers in relation to the number of their SGA offspring (HR 1.41-1.86) when 'no SGA offspring' was used as reference. The risk of CVD in relation to SGA status was increased in the least educated group (HR 2.7-5.0) compared to the group with the highest level of education with no SGA offspring.
The risk of SGA offspring and the risk of maternal CVD are mutually interdependent and both conditions increased in women with a low level of education.
Cancer patients diagnosed with type 2 diabetes mellitus (T2DM) are at an increased risk of death due to cancer. However, whether T2DM comorbidity increases other causes of death in cancer patients is the novel theme of this study. Patients with T2DM were identified from the nationwide Swedish Hospital Discharge Register and linked with patients with cancer recorded from the Swedish Cancer Registry. Hazard ratios (HRs) were calculated for death due to all causes among cancer patients with and without T2DM; both underlying and multiple causes of death were examined using the Cox regression model. A total of 13 325 cancer patients were identified with comorbidity of T2DM. The total number of deaths of cancer patients was 276 021. Of these, 5900 occurred after T2DM diagnosis. For underlying causes of death, except for T2DM, the highest cause-specific HRs were found for complications of bacterial disease (HR, 3.93; 95% CI, 3.04-5.09), urinary system disease (HR, 3.39; 95% CI, 2.78-4.12), and myocardial infarction (HR, 2.93; 95% CI, 2.75-3.12). When risk of death was examined for both underlying and multiple causes of death, the highest HRs were found for hypertensive disease (HR, 3.42; 95% CI, 3.15-3.72), urinary system disease (HR, 3.39; 95% CI, 3.17-3.63), and arterial disease (HR, 3.26; 95% CI, 3.08-3.46). The diagnosis of T2DM in cancer patients is associated with an increased risk of death due to various causes, including myocardial infarction, other bacterial disease, urinary system disease, hypertensive disease, arterial disease, and so on, which may be related to both cancer and treatment. Clinicians that treat cancer patients with T2DM should pay more attention to comorbidities.
Comment In: Eur J Cancer Prev. 2012 May;21(3):30722082833