The effect of the diagnosis and treatment of lower urinary tract symptoms (LUTS) on the diagnosis of prostate cancer in a population cohort with 20-year follow-up.

2012 ◽  
Vol 30 (5_suppl) ◽  
pp. 137-137
Author(s):  
Christopher J. Weight ◽  
Simon P. Kim ◽  
Stephen A. Boorjian ◽  
R. Jeffrey Karnes ◽  
Debra Jacobson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Older Men ◽  
Population Based ◽  
Self Report ◽  
Diagnosis And Treatment ◽  
Symptom Index ◽  
Increased Risk ◽  
Younger Men ◽  
History Of ◽  
American Urological Association

137 Background: LUTS are one of the most common reasons patients visit urologists. These symptoms have not been typically associated with the development of prostate cancer (CaP). However, we hypothesized that visiting a physician for LUTS may modify the diagnostic intensity for CaP compared to population controls. Methods: We examined data from a longitudinal, population-based cohort of 2,447 men between 40 and 79 years old who were followed prospectively from 1990 to 2010. Participants completed the American Urological Association Symptom Index (AUASI) every two years. Self-reported moderate/severe LUTS were defined as an AUASI score >7 (n=1627). Data including the treatment for LUTS (n=874), prostate biopsy (PBx), family history of CaP and diagnosis of CaP were obtained through self-report and review of medical records. Associations between self-reported LUTS, treatment for LUTS, and risk of PBx or CaP were estimated using multivariate Cox proportional hazard models. Results: An interaction was noted between age and LUTS and PBx and CaP diagnosis. In younger men, the diagnosis and treatment of LUTS was associated with increased risk of PBx (HR 2.39: 95% CI 1.83, 3.13) and CaP (HR 3.47: 95% CI 2.38, 5.07). Conversely in older men, treatment for LUTS was associated with a decreased risk of PBx and CaP (Table). Self reported LUTS was not significantly associated with CaP diagnosis in younger men and was protective in older men (Table). Conclusions: There is a differential effect of LUTS on prostate cancer testing and diagnosis when stratified by age. The reason for this difference is unclear, but appears to be due largely to diagnostic intensity rather than a true biologic association between LUTS and CaP. [Table: see text]

Increased risk of prostate cancer following sexually transmitted infection in an Asian population

2013 ◽  
Vol 141 (12) ◽  
pp. 2663-2670 ◽  
Author(s):  
S. D. CHUNG ◽  
Y. K. LIN ◽  
C. C. HUANG ◽  
H. C. LIN
Keyword(s):  
Prostate Cancer ◽  
Proportional Hazards ◽  
Asian Population ◽  
Population Based ◽  
Cox Proportional Hazards ◽  
Study Cohort ◽  
Transmitted Infection ◽  
Sexually Transmitted ◽  
Increased Risk ◽  
History Of

SUMMARYThe relationship between sexually transmitted infections (STIs) and prostate cancer (PC) remains inconclusive. Moreover, all such studies to date have been conducted in Western populations. This study aimed to investigate the risk of PC following STI using a population-based matched-cohort design in Taiwan. The study cohort comprised 1055 patients with STIs, and 10 550 randomly selected subjects were used as a comparison cohort. Cox proportional hazards regression analysis revealed that the hazard ratio for PC during the 5-year follow-up period for patients with a STI was 1·95 (95% confidence interval 1·18–3·23), that of comparison subjects after adjusting for urbanization level, geographical region, monthly income, hypertension, diabetes, hyperlipidaemia, obesity, chronic prostatitis, history of vasectomy, tobacco use disorder, and alcohol abuse. We concluded that the risk of PC was higher for men who were diagnosed with a STI in an Asian population.

Male Osteoporosis

2013 ◽  
Vol 22 (04) ◽  
pp. 260-266 ◽  
Author(s):  
S. P. Tuck ◽  
R. M. Francis ◽  
B. C. Hanusch
Keyword(s):  
Prostate Cancer ◽  
Older Men ◽  
Good Evidence ◽  
Male Osteoporosis ◽  
Fracture Rate ◽  
Common Cause ◽  
Increased Risk ◽  
Osteoporosis In Men ◽  
Considerable Morbidity ◽  
Secondary Causes

SummaryMale osteoporosis is common and results in considerable morbidity and mortality. There are distinct differences in the normal aging of bone between the genders, which result in a lower fracture rate in men. Men who suffer from osteoporosis are much more likely than women to have secondary causes. The identification and treatment of these secondary causes, wherever possible, will result in substantial improvements in BMD. There is now evidence for use of many of the existing agents to treat osteoporosis in men. In younger hypogonadal men testosterone replacement is worth considering, but in older men especially the over sixties this is less effective and there is an increased risk of adverse cardiovascular and prostatic outcomes. Prostate cancer is an increasingly common cause, which is partially the result of the success of ADT. There is now good evidence for the use of bisphosphonates and denosumab in this group of patients. HIV, whilst not being specific to men, is an increasingly recognised cause of male osteoporosis. The reasons for this are multifactorial and some may well be attributable to the anti-retroviral therapy itself. There is emerging evidence of an increased fracture risk in HIV infected individuals. The bone loss can be prevented by the use of bisphosphonates.

Prostate Carcinogenesis: Insights in relation to Epigenetics and Inflammation.

2020 ◽  
Vol 20 ◽  
Author(s):  
Mirazkar D. Pandareesh ◽  
Vivek Hamse Kameshwar ◽  
Kullaiah K. Byrappa
Keyword(s):  
Prostate Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Human Cancer ◽  
Control Cell ◽  
Diagnosis And Treatment ◽  
Epigenetic Changes ◽  
Mesenchymal Transition ◽  
Prostate Carcinogenesis ◽  
History Of ◽  
Clinical Potential

: Prostate cancer is a multifactorial disease that mainly occurs due to the accumulation of somatic, genetic and epigenetic changes, resulting in the inactivation of tumor-suppressor genes and activation of oncogenes. Mutations in genes, specifically those that control cell growth and division or the repair of damaged DNA, make the cells grow and divide uncontrollably to form a tumor. The risk of developing prostate cancer depends upon the gene that has undergone the mutation. Identifying such genetic risk factors for prostate cancer pose a challenge for the researchers. Besides genetic mutations, many epigenetic alterations including DNA methylation, histone modifications (methylation, acetylation, ubiquitylation, sumoylation, and phosphorylation) nucleosomal remodelling, and chromosomal looping, have been significantly contributed to the onset of prostate cancer as well as the prognosis, diagnosis, and treatment of prostate cancer. Chronic inflammation also plays a major role in the onset and progression of human cancer, via. modifications in the tumor microenvironment by initiating epithelial-mesenchymal transition and remodelling the extracellular matrix. In this article, the authors present a brief history of the mechanisms and potential links between the genetic aberrations, epigenetic changes, inflammation and inflammasomes that are known to contribute to the prognosis of prostate cancer. Furthermore, the authors examine and discuss clinical potential of prostate carcinogenesis in relation to epigenetics and inflammation for its diagnosis and treatment.

Elevation of pulse pressure in middle age is associated with the risk of dementia: data from a population-based cohort

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
D Kim ◽  
H Jung ◽  
P.S Yang ◽  
H.T Yu ◽  
T.H Kim ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pulse Pressure ◽  
Middle Age ◽  
Population Based ◽  
Entire Cohort ◽  
Incident Dementia ◽  
Increased Risk ◽  
Diagnosis Of Dementia ◽  
History Of ◽  
The Mean

Abstract Aims Pulse pressure (PP) is a well-known risk factor for cardiovascular disease. However, the association between the PP and dementia is not well identified. This study aimed to determine the effect of PP on the risk of dementia development in different age subgroups using a longitudinal, population-based, and stroke-free cohort from the general population. Methods The association of PP with the development of incident dementia was assessed from January 1, 2005, to December 31, 2013, in 433,154 participants without a history of dementia or stroke from the Korea National Health Insurance Service-Health Screening cohort. The diagnosis of dementia was defined using the 10th revision of the International Classification of Disease codes. Results The mean age of the cohort was 55.7±9.2 years, 45.7% were women. Hypertension was 23.6%. The mean systolic and diastolic blood pressure of the entire cohort were 125.9±16.6 and 78.4±10.7 mmHg, respectively. Mean PP was 47.5±10.9 mmHg. In the middle-age group (40 to 50 year-old), increasing of 10 mmHg of PP was associated with incident dementia after adjusting mean blood pressure and clinical variables with a hazard ratio (HR) of 1.21 (95% confidence interval [CI]: 1.19–1.23, p<0.001). The association was still significant even after censoring for stroke (HR: 1.16, 95% CI: 1.08–1.22, p<0.001). In the older population, elevation of PP was not associated with dementia development (HR: 0.98, 95% CI: 0.95–1.01, p=0.247) Conclusion PP was associated with increased risk of dementia only in middle-aged population beyond that of mean arterial pressure. Funding Acknowledgement Type of funding source: None

scholarly journals Melanoma is associated with an increased risk of bullous pemphigoid: a large population-based longitudinal study

2021 ◽  
Author(s):  
Khalaf Kridin ◽  
Jennifer E. Hundt ◽  
Ralf J. Ludwig ◽  
Kyle T. Amber ◽  
Dana Tzur Bitan ◽  
...  
Keyword(s):  
Bullous Pemphigoid ◽  
Statistical Significance ◽  
Large Population ◽  
Underlying Mechanism ◽  
Population Based ◽  
Control Subjects ◽  
Increased Risk ◽  
Bidirectional Association ◽  
History Of ◽  
Incident Cases

AbstractThe association between bullous pemphigoid (BP) and melanoma is yet to be investigated. We aimed to assess assess the bidirectional association between BP and melanoma and to delineate the epidemiological features of patients with both diagnoses. A population-based cohort study was performed comparing BP patients (n = 3924) with age-, sex- and ethnicity-matched control subjects (n = 19,280) with regard to incident cases of melanoma. A case–control design was additionally adopted to estimate the risk of BP in individuals with a preexisting diagnosis of melanoma. The prevalence of preexisting melanoma was higher in patients with BP than in control subjects (1.5% vs. 1.0%, respectively; P = 0.004). A history of melanoma confers a 50% increase in the risk of subsequent BP (OR 1.53; 95% CI 1.14–2.06). This risk was higher among males (OR 1.66; 95% CI 1.09–2.54) and individuals older than 80 years (OR 1.63; 95% CI 1.11–2.38), and persisted after adjustment for multiple putative confounders including PD-1/PDL-1 antagonists (adjusted OR 1.53; 95% CI 1.14–2.06). Conversely, the risk of melanoma among patients with BP was slightly elevated, but did not reach the level of statistical significance (adjusted HR 1.13; 95% CI 0.73–1.74). Patients with a dual diagnosis of BP and melanoma were older at the onset of BP and had lower body mass index. A history of melanoma is associated with a 50% increase in the incidence of subsequent BP. Physicians managing patients with both conditions should be aware of this association. Further research is warranted to reveal the underlying mechanism of these findings.

scholarly journals SAT0589 RISK FOR PSYCHIATRIC HOSPITALIZATION FOLLOWING A RHEUMA-RELATED HOSPITALIZATION: RESULTS FROM A CZECH NATIONWIDE, COHORT STUDY

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1253.2-1254
Author(s):  
T. Formánek ◽  
K. Mladá ◽  
M. Husakova
Keyword(s):  
Rheumatoid Arthritis ◽  
Cohort Study ◽  
Ankylosing Spondylitis ◽  
Rheumatic Disease ◽  
Rheumatic Diseases ◽  
Psychiatric Hospitalization ◽  
Population Based ◽  
Index Hospitalization ◽  
Increased Risk ◽  
History Of

Background:Cohort studies using nationwide health registers have shown an increased risk for affective and anxiety disorders in people with ankylosing spondylitis (AS) and rheumatoid arthritis (RA) (1-3). Moreover, a nationwide cohort study demonstrated an increased risk for mental disorders in people with rheumatic diseases (4).Objectives:We aimed to investigate the risk for psychiatric hospitalization following a hospitalization for rheumatic disease.Methods:Using data from the Czech nationwide register of all-cause hospitalizations, we obtained 4 971 individuals hospitalized (index hospitalization) between 2004 and 2012 for rheumatic diseases - RA, spondyloarthritis (including AS, psoriatic arthritis and undifferentiated spondyloarthritis), systemic lupus erythematosus and systemic sclerodermia, with no history of psychiatric and rheuma-related hospitalization in the previous 10 years from the index hospitalization. On these individuals, we randomly matched (on age, gender and year of index hospitalization) controls that were hospitalized in the same time period for a non-rheumatic disease and have no history of psychiatric and rheumatic hospitalization in the last 10 years from their index hospitalization, in the ratio of 1:5. We employed conditional logistic regression for assessing the risk for psychiatric hospitalization in the subsequent 3 years from the index hospitalization. To strengthen our results, we repeated the matching step 100 times and run the analysis on each resulting dataset separately, and pooled the results. The findings are expressed as odds ratios (OR) with 95% confidence intervals (95% CI).Results:We identified an elevated risk for psychiatric (OR = 1.34, 95% CI = 1; 1.78) and for affective disorders (OR = 2.19, 95% CI = 1.17; 4.1) in people hospitalized for rheumatic diseases. We did not find a statistically significant association with organic, psychotic and anxiety disorders.Conclusion:There is an increased risk for experiencing a psychiatric disorder in the period of 3 years after a rheuma-related hospitalization.References:[1]Shen C-C, Hu L-Y, Yang AC, Kuo BI-T, Chiang Y-Y, Tsai S-J. Risk of Psychiatric Disorders following Ankylosing Spondylitis: A Nationwide Population-based Retrospective Cohort Study. The Journal of Rheumatology. 2016;43(3).[2]Park J-S, Jang H-D, Hong J-Y, Park Y-S, Han K, Suh S-W, et al. Impact of ankylosing spondylitis on depression: a nationwide cohort study. Scientific Reports. 2019;9(1):6736.[3]Hsu C-C, Chen S-C, Liu C-J, Lu T, Shen C-C, Hu Y-W, et al. Rheumatoid Arthritis and the Risk of Bipolar Disorder: A Nationwide Population-Based Study. PLOS ONE. 2014;9(9).[4]Sundquist K, Li X, Hemminki K, Sundquist J. Subsequent Risk of Hospitalization for Neuropsychiatric Disorders in Patients With Rheumatic Diseases: A Nationwide Study From Sweden. Archives of General Psychiatry. 2008;65(5):501-7.Acknowledgments:Supported by the project (Ministry of Health Czech Republic) for conceptual development of research organization 00023728 (Institute of Rheumatology).Disclosure of Interests:Tomáš Formánek: None declared, Karolina Mladá: None declared, Marketa Husakova Speakers bureau: Novartis

scholarly journals CHEK2∗1100delC Mutation and Risk of Prostate Cancer

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Victoria Hale ◽  
Maren Weischer ◽  
Jong Y. Park
Keyword(s):  
Prostate Cancer ◽  
Current Knowledge ◽  
Prostate Cancer Screening ◽  
Critical Role ◽  
Prostate Cancer Risk ◽  
Conclusive Evidence ◽  
Increased Risk ◽  
History Of ◽  
Cancer Studies

Although the causes of prostate cancer are largely unknown, previous studies support the role of genetic factors in the development of prostate cancer.CHEK2plays a critical role in DNA replication by responding to double-stranded breaks. In this review, we provide an overview of the current knowledge of the role of a genetic variant, 1100delC, ofCHEK2on prostate cancer risk and discuss the implication for potential translation of this knowledge into clinical practice. Currently, twelve articles that discussedCHEK2∗1100delC and its association with prostate cancer were identified. Of the twelve prostate cancer studies, five studies had independent data to draw conclusive evidence from. The pooled results of OR and 95% CI were 1.98 (1.23–3.18) for unselected cases and 3.39 (1.78–6.47) for familial cases, indicating thatCHEK2∗1100delC mutation is associated with increased risk of prostate cancer. Screening for CHEK2∗1100delC should be considered in men with a familial history of prostate cancer.

Abstract 12385: Past Alcohol Consumption and Incident Atrial Fibrillation

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Shalini Dixit ◽  
Alvaro Alonso ◽  
Elsayed Z Soliman ◽  
Lin Y Chen ◽  
Gregory M Marcus
Keyword(s):  
Atrial Fibrillation ◽  
Alcohol Consumption ◽  
Alcohol Use ◽  
Population Based ◽  
Self Report ◽  
Atherosclerosis Risk In Communities ◽  
Increased Risk ◽  
Before And After ◽  
Dietary Intake Assessment ◽  
Aric Study

Introduction: Although current alcohol consumption appears to be a risk factor for incident atrial fibrillation (AF), limitations related to self-reported alcohol use and confounding in observational studies limit the certainty of conclusions regarding causality. Whether cessation of alcohol consumption can protect against incident AF remains unknown. Methods: We examined all participants in the Atherosclerosis Risk in Communities (ARIC) study, a population-based cohort of 15,792 men and women aged 45-65, without prevalent AF. Past alcohol consumption was assessed via self-report during the baseline dietary intake assessment. Cases of incident AF were ascertained via study ECGs, hospital discharge ICD-9 codes, and death certificates. Results: Among 15,262 participants with complete survey data, 2,898 (19.0%) were former drinkers. During an average follow-up of 17.4 years, there were 380 cases of incident AF in former consumers. Both before and after adjustment for potential confounders, a longer duration of alcohol abstinence was associated with a lower risk of developing AF; previously consuming alcohol for a longer duration and consuming a greater quantity of alcohol were each associated with a higher risk of developing AF (Table). Conclusions: Among former drinkers, the number of years of drinking and the amount of alcohol consumed may each confer an increased risk of AF. Given that a longer duration of abstinence was associated with a decreased risk of AF, modification of alcohol use could potentially play a role in AF prevention.

The Genes and Genetics of Malignant Melanoma

2002 ◽  
Vol 6 (3) ◽  
pp. 229-235 ◽  
Author(s):  
Peter Gibbs ◽  
Benjamin M. R. Brady ◽  
William A. Robinson
Keyword(s):  
High Risk ◽  
Sun Exposure ◽  
Population Based ◽  
Uv Exposure ◽  
Molecular Defect ◽  
Clinical Variables ◽  
Red Hair ◽  
Increased Risk ◽  
History Of ◽  
Self Examination

Background: Population-based studies have identified several clinical variables associated with an increased risk of developing cutaneous melanoma that include phenotype, amount of and response to sun exposure, and family history. However, these observations are of limited relevance to clinical practice as the risk associated with each factor is individually modest and the characteristics of these variables lack precision when applied to a particular individual. Objective: To review the literature regarding recent advances made in the understanding of the genes and genetics of clinical variables associated with an increased risk of melanoma. Conclusion: Variants of the MC1R (melanocortin-1 receptor) have been identified as major determinants of high-risk phenotypes, such as red hair and pale skin, and the ability to tan in response to UV exposure. Several studies also suggest that such variants may increase melanoma risk independent of their contribution to phenotype. A strong genetic basis for both nevus density and size has been demonstrated and the link between nevi and the development of MM has become better defined. Finally, germline defects in several genes involved in cell cycle regulation, namely, p16 and CDK4, have been demonstrated in many familial melanoma kindreds. This progress has introduced the prospect of genetic testing as a means of identifying a limited number of high-risk individuals who can be targeted with regular screening and education regarding UV exposure and skin self-examination. Ultimately, through rational genetic therapy targeted to correcting the underlying molecular defect, altering the natural history of melanoma development may be possible.

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