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Polypharmacy is becoming a global health problem. The aims of this study were to evaluate the temporal trends in the prevalence of polypharmacy in Sweden and to explore polypharmacy disparities by age, gender, education, and immigration status. Polypharmacy and excessive polypharmacy were evaluated using data extracted from the Swedish Prescribed Drug Register between 2006 and 2014. Polypharmacy was defined as being exposed to five or more drugs and excessive polypharmacy was defined as being exposed to 10 or more drugs during 1 month respectively. Average annual percent change (AAPC) was calculated using Joinpoint Statistical Software. The prevalence of polypharmacy increased from 16.9% in 2006 to 19.0% in 2014 with an AAPC of 1.3; the prevalence of excess polypharmacy increased from 3.8% in 2006 to 5.1% in 2014 with an AAPC of 3.4. The prevalence of polypharmacy and excessive polypharmacy increased dramatically with age and peaked up to 79.6% and 36.4% in individuals aged 90 and above respectively. Females and individuals with lower education level were associated with a higher rate of polypharmacy and excessive polypharmacy. Immigrants from Middle-Eastern countries had the highest rate of polypharmacy and excessive polypharmacy, whereas individuals from Western Europe countries had the lowest rate. The prevalence of polypharmacy has increased gradually in Sweden during the past decade. Individuals with older age, female sex, or lower education have a higher rate of polypharmacy and excessive polypharmacy. Immigrants from Middle-Eastern countries showed a higher rate of polypharmacy.

Preterm birth has previously been linked with cardiovascular disease (CVD) in adulthood. However, associations with lipid disorders (e.g., high cholesterol or triglycerides), which are major risk factors for CVD, have seldom been examined and are conflicting. Clinicians will increasingly encounter adult survivors of preterm birth and will need to understand the long-term health sequelae. We conducted the first large population-based study to determine whether preterm birth is associated with an increased risk of lipid disorders. A retrospective national cohort study was conducted of all 2,235,012 persons born as singletons in Sweden during 1973 to 1995 (48.6% women), who were followed up for lipid disorders identified from nationwide inpatient, outpatient, and pharmacy data through 2016 (maximum age 44 years). Cox regression was used to adjust for other perinatal and maternal factors, and co-sibling analyses assessed the potential influence of unmeasured shared familial (genetic and/or environmental) factors. A total of 25,050 (1.1%) persons were identified with lipid disorders in 30.3 million person-years of follow-up. Each additional 5 weeks of gestation were associated with a 14% reduction in risk of lipid disorders (adjusted hazard ratio [HR], 0.86; 95% CI, 0.83-0.89; P < 0.001). Relative to full-term birth (gestational age 39-41 weeks), the adjusted HR associated with preterm birth (<37 weeks) was 1.23 (95% CI, 1.16-1.29; P < 0.001), and further stratified was 2.00 (1.41-2.85; P < 0.001) for extremely preterm (22-27 weeks), 1.33 (1.19-1.49; P < 0.001) for very preterm (28-33 weeks), and 1.19 (1.12-1.26; P < 0.001) for late preterm (34-36 weeks). These findings were similar in men and women (e.g., preterm versus full-term, men: HR, 1.22; 95% CI, 1.14-1.31; P < 0.001; women: HR, 1.23; 1.12-1.32; P < 0.001). Co-sibling analyses suggested that they were substantially though not completely explained by shared genetic or environmental factors in families. The main study limitation was the unavailability of laboratory data to assess specific types or severity of lipid disorders. In this large national cohort, preterm birth was associated with an increased risk of lipid disorders in early- to midadulthood. Persons born prematurely may need early preventive evaluation and long-term monitoring for lipid disorders to reduce their future cardiovascular risks.

Colorectal cancer (CRC) incidence is increasing among young adults below screening age, despite the effectiveness of screening in older populations. Individuals with diabetes mellitus are at increased risk of early-onset CRC. We aimed to determine how many years earlier than the general population patients with diabetes with/without family history of CRC reach the threshold risk at which CRC screening is recommended to the general population. A nationwide cohort study (follow-up:1964-2015) involving all Swedish residents born after 1931 and their parents was carried out using record linkage of Swedish Population Register, Cancer Registry, National Patient Register, and Multi-Generation Register. Of 12,614,256 individuals who were followed between 1964 and 2015 (51% men; age range at baseline 0-107 years), 162,226 developed CRC, and 559,375 developed diabetes. Age-specific 10-year cumulative risk curves were used to draw conclusions about how many years earlier patients with diabetes reach the 10-year cumulative risks of CRC in 50-year-old men and women (most common age of first screening), which were 0.44% and 0.41%, respectively. Diabetic patients attained the screening level of CRC risk earlier than the general Swedish population. Men with diabetes reached 0.44% risk at age 45 (5 years earlier than the recommended age of screening). In women with diabetes, the risk advancement was 4 years. Risk was more pronounced for those with additional family history of CRC (12-21 years earlier depending on sex and benchmark starting age of screening). The study limitations include lack of detailed information on diabetes type, lifestyle factors, and colonoscopy data. Using high-quality registers, this study is, to our knowledge, the first one that provides novel evidence-based information for risk-adapted starting ages of CRC screening for patients with diabetes, who are at higher risk of early-onset CRC than the general population.

Background The overall aim of this study is to present descriptive data regarding the treated prevalence of nine common psychiatric and substance use disorders in the first Primary Care Registry (PCR) in Sweden: Major Depression (MD), Anxiety Disorders (AD), Obsessive-Compulsive Disorder (OCD), Adjustment Disorder (AdjD), Eating Disorders (ED), Personality Disorder (PD), Attention Deficit Hyperactivity Disorder (ADHD), Alcohol Use Disorder (AUD) and Drug Abuse (DA). Method We selected 5,397,675 individuals aged ≥18. We examined patterns of comorbidity among these disorders and explored the association between diagnoses in the PCR and diagnoses obtained from Hospital and Specialist care. We explored the proportion of patients with these nine disorders that are only treated in primary health care. Results For four of our disorders, 80% or more of the cases were present only in the PCR: AdjD, DA, AD and MD. For two disorders (OCD and ED), 65–70% of cases were only found in the PCR. For three disorders (PD, AUD, and ADHD), 45–55% of the patients were only present in the PCR. Conclusion The PCR will, in the future, likely prove to be an important tool for studies in psychiatric epidemiology.

Phosphodiesterase-5 (PDE5) inhibitors are suggested to have anti-tumor effects and to inhibit surgery-induced immunosuppression. We aimed to explore whether post-diagnostic use of PDE5 inhibitors was associated with a better prognosis among male patients with colorectal cancer (CRC) and the role of open surgery in the association. Here we show that post-diagnostic use of PDE5 inhibitors is associated with a decreased risk of CRC-specific mortality (adjusted HR = 0.82, 95% CI 0.67-0.99) as well as a decreased risk of metastasis (adjusted HR = 0.85, 95% CI 0.74-0.98). Specifically, post-operative use of PDE5 inhibitors has a strong anti-cancer effect. The reduced risk of metastasis is mainly due to distant metastasis but not regional lymphatic metastasis. PDE5 inhibitors have the potential to be an adjuvant drug for patients with CRC to improve prognosis, especially those who have undergone open surgery. Phosphodiesterase-5 (PDE5) inhibitors have been suggested to have an anti-tumor effect and block surgery-induced immunosuppression. Here, the authors show that postdiagnostic use of PDE5 inhibitors is associated with a decreased risk of colorectal cancerspecific mortality as well as a decreased risk of metastasis.

Population‐based data on metastatic patterns are lacking because cancer registries seldom record metastases. This study uses a novel population‐based approach to identify metastases and describes metastatic pathways from 14 common primary cancers to 12 specific metastatic sites. A total of 179 581 patients with metastatic cancer were identified from the Swedish Cancer Registry and metastatic sites were identified using the Cause of Death Register and the National Patient Register. Patterns of metastatic spread were described across age and sex. In men, colorectal cancer was the main source of lung, peritoneal, and liver metastases. Lung cancer was the main origin of pleural and nervous system metastases. Prostate cancer dominated bone metastases but had minor contribution to other metastatic sites. Among women, breast cancer was the dominant origin of most metastatic sites, with the exception of peritoneum which was ruled by metastases from the ovary. As other exceptions, for nervous system metastases, lung cancer was the origin of metastases somewhat more frequently than breast cancer and for liver metastases, colorectal cancer was the main origin instead of breast cancer. The present achievement was to implement the first nationwide description of clinical landscape of cancer metastases, with an aim to serve as a reliable source for clinicians and researchers. This study uses a novel population‐based approach to identify metastases and describes metastatic pathways from 14 common primary cancers to 12 specific metastatic sites. The present achievement was to implement the first nationwide description of clinical landscape of cancer metastases, with an aim to serve as a reliable source for clinicians and researchers.

ObjectiveTransitions in the spectrum of valvular heart diseases (VHDs) in developed countries over the 20th century have been reported from clinical case series, but large, contemporary population-based studies are lacking.MethodsWe used nationwide registers to identify all patients with a first diagnosis of VHD at Swedish hospitals between 2003 and 2010. Age-stratified and sex-stratified incidence of each VHD and adjusted comorbidity profiles were assessed.ResultsIn the Swedish population (n=10 164 211), the incidence of VHD was 63.9 per 100 000 person-years, with aortic stenosis (AS; 47.2%), mitral regurgitation (MR; 24.2%) and aortic regurgitation (AR; 18.0%) contributing most of the VHD diagnoses. The majority of VHDs were diagnosed in the elderly (68.9% in subjects aged ≥65 years), but pulmonary valve disease incidence peaked in newborns. Incidences of AR, AS and MR were higher in men who were also more frequently diagnosed at an earlier age. Mitral stenosis (MS) incidence was higher in women. Rheumatic fever was rare. Half of AS cases had concomitant atherosclerotic vascular disease (48.4%), whereas concomitant heart failure and atrial fibrillation were common in mitral valve disease and tricuspid regurgitation. Other common comorbidities were thoracic aortic aneurysms in AR (10.3%), autoimmune disorders in MS (24.5%) and abdominal hernias or prolapse in MR (10.7%) and TR (10.3%).ConclusionsClinically diagnosed VHD was primarily a disease of the elderly. Rheumatic fever was rare in Sweden, but specific VHDs showed a range of different comorbidity profiles . Pronounced sex-specific patterns were observed for AR and MS, for which the mechanisms remain incompletely understood.

Some autoimmune disorders have been linked to venous thromboembolism. We examined whether there is an association between autoimmune disorders and risk of pulmonary embolism. We followed up all individuals in Sweden without previous hospital admission for venous thromboembolism and with a primary or secondary diagnosis of an autoimmune disorder between Jan 1, 1964, and Dec 31, 2008, for hospital admission for pulmonary embolism. We obtained data from the MigMed2 database, which has individual-level information about all registered residents of Sweden. The reference population was the total population of Sweden. We calculated standardised incidence ratios (SIRs) for pulmonary embolism, adjusted for individual variables, including age and sex. 535 538 individuals were admitted to hospital because of an autoimmune disorder. Overall risk of pulmonary embolism during the first year after admission for an autoimmune disorder was 6·38 (95% CI 6·19–6·57). All the 33 autoimmune disorders were associated with a significantly increased risk of pulmonary embolism during the first year after admission. However, some had a particularly high risk—eg, immune thrombocytopenic purpura (10·79, 95% CI 7·98–14·28), polyarteritis nodosa (13·26, 9·33–18·29), polymyositis or dermatomyositis (16·44, 11·57–22·69), and systemic lupus erythematosus (10·23, 8·31–12·45). Overall risk decreased over time, from 1·53 (1·48–1·57) at 1–5 years, to 1·15 (1·11–1·20) at 5–10 years, and 1·04 (1·00–1·07) at 10 years and later. The risk was increased for both sexes and all age groups. Autoimmune disorders are associated with a high risk of pulmonary embolism in the first year after hospital admission. Our findings suggest that these disorders in general should be regarded as hypercoagulable disorders. Swedish Research Council, Swedish Council for Working Life and Social Research, Swedish Research Council Formas, Region Skåne.

Background The ability of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) to decrease certain microvascular events has called for the investigation of GLP-1 RAs against diabetic retinopathy (DR), but the evidence is limited. By combining data from observational and Mendelian randomization (MR) studies, we aimed to investigate whether GLP-1 RAs decrease the risk of DR. Methods We combined data from several Swedish Registers and identified patients with incident type 2 diabetes being treated with GLP-1 RAs between 2006 and 2015, and matched them to diabetic patients who did not use GLP-1 RAs as the comparisons. The Cox proportional hazards models were applied to assess the risk of DR. We further performed the summary-data-based MR (SMR) analyses based on the Genotype-Tissue Expression databases and the Genome-Wide Association Study of DR from the FinnGen consortium. Results A total of 2390 diabetic patients were treated with GLP-1 RAs and the incidence of DR was 5.97 per 1000 person-years. Compared with diabetic patients who did not use GLP-1 RAs having an incidence of 12.85 per 1000 person-years, the adjusted hazard ratio (HR) of DR was 0.42 [95% confidence interval (CI), 0.29–0.61]. Genetically-predicted GLP1R expression (the target of GLP-1 RAs) showed an inverse association with background [odds ratio (OR)=0.83, 95% CI, 0.71–0.97] and severe nonproliferative DR (OR=0.72, 95% CI, 0.53–0.98), and a non-significant association with overall (OR=0.97, 95% CI, 0.92–1.03) and proliferative DR (OR=0.98, 95% CI, 0.91–1.05). Conclusions Both observational and mendelian randomization analyses showed a significantly lower risk of DR for patients treated with GLP-1 RAs, which calls for further studies to validate these findings.

Alcohol use disorder (AUD) is clinically heterogeneous. We examine its potential genetic heterogeneity as a function of sex, age, clinical features and mode of ascertainment. In the Swedish population born 1932-1995 ( = 5 829 952), we examined the genetic risk profiles for AUD, major depression (MD), anxiety disorders, bipolar disorder, drug use disorder (DUD), attention deficit-hyperactivity disorder (ADHD) and criminal behavior (CB) in 361 124 cases of AUD subdivided by sex, age at onset (AAO), recurrence, mode of ascertainment and medical complications. Family genetic risk scores (FGRS), calculated from 1st to 5th-degree relatives controlling of cohabitation, assesses genetic risk from phenotypes in the family, not from DNA variants. FGRS profiles differed modestly across sex with all scores higher in females. Differences were more pronounced for AAO and recurrence with the FGRS for AUD, DUD, ADHD and CB substantially higher in cases with early AAO or high recurrence rates. Genetic profiles differed considerably by mode of ascertainment, with higher FGRS for AUD and most other disorders in patients seen in hospital primary care settings. Cases of AUD with medical complications had higher FGRS for AUD. AUD cases comorbid with MD and DUD had higher FGRS risk for AUD, but this genetic may be less specific given increases in FGRS for multiple other disorders. From a genetic perspective, AUD differs substantially as a function of AAO, recurrence, mode of ascertainment and patterns of comorbidity, suggesting caution in cross-sample comparisons of AUD cohorts that differ in these features.