Mortality among patients with idiopathic intracranial hypertension enrolled in the IH Registry

Neurology ◽  
2020 ◽  
Vol 95 (7) ◽  
pp. e921-e929 ◽  
Author(s):  
Sam M. Hermes ◽  
Nick R. Miller ◽  
Carin S. Waslo ◽  
Susan C. Benes ◽  
Emanuel Tanne

ObjectiveTo determine (1) if mortality among patients with idiopathic intracranial hypertension (IIH) enrolled in the Intracranial Hypertension Registry (IHR) is different from that of the general population of the United States and (2) what the leading underlying causes of death are among this cohort.MethodsMortality and underlying causes of death were ascertained from the National Death Index. Indirect standardization using age- and sex-specific nationwide all-cause and cause-specific mortality data extracted from the Centers for Disease Control and Prevention Wonder Online Database allowed for calculation of standardized mortality ratios (SMR).ResultsThere were 47 deaths (96% female) among 1437 IHR participants that met inclusion criteria. The average age at death was 46 years (range, 20–95 years). Participants of the IHR experienced higher all-cause mortality than the general population (SMR, 1.5; 95% confidence interval [CI], 1.2–2.1). Suicide, accidents, and deaths from medical/surgical complications were the most common underlying causes, accounting for 43% of all deaths. When compared to the general population, the risk of suicide was over 6 times greater (SMR, 6.1; 95% CI, 2.9–12.7) and the risk of death from accidental overdose was over 3 times greater (SMR, 3.5; 95% CI, 1.6–7.7). The risk of suicide by overdose was over 15 times greater among the IHR cohort than in the general population (SMR, 15.3; 95% CI, 6.4–36.7).ConclusionsPatients with IIH in the IHR possess significantly increased risks of death from suicide and accidental overdose compared to the general population. Complications of medical/surgical treatments were also major contributors to mortality. Depression and disability were common among decedents. These findings should be interpreted with caution as the IHR database is likely subject to selection bias.

2020 ◽  
Vol 32 (1) ◽  
pp. 154-160
Author(s):  
Deepak Gupta ◽  
Sarwan Kumar ◽  
Shushovan Chakrabortty

While SEARCHING OUR-OWN HEALTH AFTER MEDICINE (SOHAM), we as aging physicians have to first explore and expose our mortality with underlying uniqueness of causes for physician mortality. Herein, publicly available data at Centers for Disease Control and Prevention from National Occupational Mortality Surveillance program of the National Institute for Occupational Safety and Health comes in handy. As compared to all occupational workers in the United States, intentional self-harm, Parkinson’s disease, Alzheimer’s and other degenerative disease were more likely causes of death while chronic obstructive pulmonary disease, diseases of the respiratory system, ischemic heart disease and diseases of the heart were less likely causes of death among physicians in the United States. Summarily, we as physicians may have somewhat overcome sufferings of our lungs and hearts but surrendered to sufferings of our brains and minds and therefore must envisage devising physical, psychological, socioeconomic and spiritual interventions for constantly bettering our living.


2019 ◽  
Vol 135 (1) ◽  
pp. 150-160
Author(s):  
Wanda K. Jones ◽  
Robert A. Hahn ◽  
R. Gibson Parrish ◽  
Steven M. Teutsch ◽  
Man-Huei Chang

Objectives: Male mortality fell substantially during the past century, and major causes of death changed. Building on our recent analysis of female mortality trends in the United States, we examined all-cause and cause-specific mortality trends at each decade from 1900 to 2010 among US males. Methods: We conducted a descriptive study of age-adjusted death rates (AADRs) for 11 categories of disease and injury stratified by race (white, nonwhite, and, when available, black), the excess of male mortality over female mortality ([male AADR − female AADR]/female AADR), and potential causes of persistent excess of male mortality. We used national mortality data for each decade. Results: From 1900 to 2010, the all-cause AADR declined 66.4% among white males and 74.5% among nonwhite males. Five major causes of death in 1900 were pneumonia and influenza, heart disease, stroke, tuberculosis, and unintentional nonmotor vehicle injuries; in 2010, infectious conditions were replaced by cancers and chronic lower respiratory diseases. The all-cause excess of male mortality rose from 9.1% in 1900 to 65.5% in 1980 among white males and a peak of 63.7% in 1990 among nonwhite males, subsequently falling among all groups. Conclusion: During the last century, AADRs among males declined more slowly than among females. Although the gap diminished in recent decades, exploration of social and behavioral factors may inform interventions that could further reduce death rates among males.


2019 ◽  
Vol 35 (5) ◽  
Author(s):  
Ana Luiza Bierrenbach ◽  
Gizelton Pereira Alencar ◽  
Cátia Martinez ◽  
Maria de Fátima Marinho de Souza ◽  
Gabriela Moreira Policena ◽  
...  

Heart failure is considered a garbage code when assigned as the underlying cause of death. Reassigning garbage codes to plausible causes reduces bias and increases comparability of mortality data. Two redistribution methods were applied to Brazilian data, from 2008 to 2012, for decedents aged 55 years and older. In the multiple causes of death method, heart failure deaths were redistributed based on the proportion of underlying causes found in matched deaths that had heart failure listed as an intermediate cause. In the hospitalization data method, heart failure deaths were redistributed based on data from the decedents’ corresponding hospitalization record. There were 123,269 (3.7%) heart failure deaths. The method with multiple causes of death redistributed 25.3% to hypertensive heart and kidney diseases, 22.6% to coronary heart diseases and 9.6% to diabetes. The total of 41,324 heart failure deaths were linked to hospitalization records. Heart failure was listed as the principal diagnosis in 45.8% of the corresponding hospitalization records. For those, no redistribution occurred. For the remaining ones, the hospitalization data method redistributed 21.2% to a group with other (non-cardiac) diseases, 6.5% to lower respiratory infections and 9.3% to other garbage codes. Heart failure is a frequently used garbage code in Brazil. We used two redistribution methods, which were straightforwardly applied but led to different results. These methods need to be validated, which can be done in the wake of a recent national study that will investigate a big sample of hospital deaths with garbage codes listed as underlying causes.


2020 ◽  
Author(s):  
Nam Pho ◽  
Arjun K Manrai ◽  
John T Leppert ◽  
Glenn M Chertow ◽  
John P A Ioannidis ◽  
...  

Abstract Background Physicians sometimes consider whether or not to perform diagnostic testing in healthy people, but it is unknown whether nonextreme values of diagnostic tests typically encountered in such populations have any predictive ability, in particular for risk of death. The goal of this study was to quantify the associations among population reference intervals of 152 common biomarkers with all-cause mortality in a representative, nondiseased sample of adults in the United States. Methods The study used an observational cohort derived from the National Health and Nutrition Examination Survey (NHANES), a representative sample of the United States population consisting of 6 survey waves from 1999 to 2010 with linked mortality data (unweighted N = 30 651) and a median followup of 6.1 years. We deployed an X-wide association study (XWAS) approach to systematically perform association testing of 152 diagnostic tests with all-cause mortality. Results After controlling for multiple hypotheses, we found that the values within reference intervals (10–90th percentiles) of 20 common biomarkers used as diagnostic tests or clinical measures were associated with all-cause mortality, including serum albumin, red cell distribution width, serum alkaline phosphatase, and others after adjusting for age (linear and quadratic terms), sex, race, income, chronic illness, and prior-year healthcare utilization. All biomarkers combined, however, explained only an additional 0.8% of the variance of mortality risk. We found modest year-to-year changes, or changes in association from survey wave to survey wave from 1999 to 2010 in the association sizes of biomarkers. Conclusions Reference and nonoutlying variation in common biomarkers are consistently associated with mortality risk in the US population, but their additive contribution in explaining mortality risk is minor.


2020 ◽  
Author(s):  
Xin Hu ◽  
Yong Lin ◽  
Lanjing Zhang

AbstractOverall mortality among U.S. adults was stable in the past years, while racial disparity was found in 10 leading causes of death or age-specific mortality in U.S. Blacks or African Americans. However, the trends in sex- and race-adjusted age-standardized cause-specific mortality are poorly understood. This study was aimed at identifying the UCD with sex- and race-adjusted, age-standardized mortality that was changing in recent years. We extracted the data of underlying causes of death (UCD) from the Multiple Cause of Death database of the Centers for Disease Control and Prevention (CDC). Multivariable log-linear regression models were used to estimate trends in sex- and race-adjusted, age-standardized mortality during 2013-2017. A total of 31,029,133 deaths were identified. Among the list of 113 UCD compiled by the CDC, there were 29 UCD with upward trend, 33 UCD with downward trend and 56 UCD with no significant trend. The 2 UCD with largest annual percent change were both nutrition related (annual percent change= 17.73, 95% CI [15.13-20.33] for malnutrition and annual percent change= 17.49, 95% CI [14.94-20.04] for Nutritional deficiencies), followed by Accidental poisoning and exposure to noxious substances. This study thus reported the UCD with changing mortality in recent years, which was sex- and race-adjusted and age-standardized. More efforts and resources should be focused on understanding, prevention and control of the mortality linked to these UCD. Continuous monitoring of mortality trends is recommended.


2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Alicia V. Gayle ◽  
Cosetta Minelli ◽  
Jennifer K. Quint

Abstract Background Distinguishing between mortality attributed to respiratory causes and other causes among people with asthma, COPD, and asthma-COPD overlap (ACO) is important. This study used electronic health records in England to estimate excess risk of death from respiratory-related causes after accounting for other causes of death. Methods We used linked Clinical Practice Research Datalink (CPRD) primary care and Office for National Statistics mortality data to identify adults with asthma and COPD from 2005 to 2015. Causes of death were ascertained using death certificates. Hazard ratios (HR) and excess risk of death were estimated using Fine-Gray competing risk models and adjusting for age, sex, smoking status, body mass index and socioeconomic status. Results 65,021 people with asthma and 45,649 with COPD in the CPRD dataset were frequency matched 5:1 with people without the disease on age, sex and general practice. Only 14 in 100,000 people with asthma are predicted to experience a respiratory-related death up to 10 years post-diagnosis, whereas in COPD this is 98 in 100,000. Asthma is associated with an 0.01% excess incidence of respiratory related mortality whereas COPD is associated with an 0.07% excess. Among people with asthma-COPD overlap (N = 22,145) we observed an increased risk of respiratory-related death compared to those with asthma alone (HR = 1.30; 95% CI 1.21–1.40) but not COPD alone (HR = 0.89; 95% CI 0.83–0.94). Conclusions Asthma and COPD are associated with an increased risk of respiratory-related death after accounting for other causes; however, diagnosis of COPD carries a much higher probability. ACO is associated with a lower risk compared to COPD alone but higher risk compared to asthma alone.


2020 ◽  
Vol 11 ◽  
Author(s):  
Arash Ghaffari-Rafi ◽  
Rana Mehdizadeh ◽  
Andrew Wai Kei Ko ◽  
Shadeh Ghaffari-Rafi ◽  
Jose Leon-Rojas

2018 ◽  
Vol 48 (6) ◽  
pp. 472-481 ◽  
Author(s):  
Ahmed A. Awan ◽  
Jingbo Niu ◽  
Jenny S. Pan ◽  
Kevin F. Erickson ◽  
Sreedhar Mandayam ◽  
...  

Background: Death with graft function remains an important cause of graft loss among kidney transplant recipients (KTRs). Little is known about the trend of specific causes of death in KTRs in recent years. Methods: We analyzed United States Renal Data System data (1996–2014) to determine 1- and 10-year all-cause and cause-specific mortality in adult KTRs who died with a functioning allograft. We also studied 1- and 10-year trends in the various causes of mortality. Results: Of 210,327 KTRs who received their first kidney transplant from 1996 to 2014, 3.2% died within 1 year after transplant. Cardiovascular deaths constituted the majority (24.7%), followed by infectious (15.2%) and malignant (2.9%) causes; 40.1% of deaths had no reported cause. Using 1996 as the referent year, all-cause as well as cardiovascular mortality declined, whereas mortality due to malignancy did not. For analyses of 10-year mortality, we studied 94,384 patients who received a first kidney transplant from 1996 to 2005. Of those, 22.1% died over 10 years and the causative patterns of their causes of death were similar to those associated with 1-year mortality. Conclusions: Despite the downtrend in mortality over the last 2 decades, a significant percentage of KTRs die in 10-years with a functioning graft, and cardiovascular mortality remains the leading cause of death. These data also highlight the need for diligent collection of mortality data in KTRs.


2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e19056-e19056
Author(s):  
Nicole H. Dalal ◽  
Graca Dores ◽  
Rochelle E. Curtis ◽  
Martha S. Linet ◽  
Lindsay M. Morton

e19056 Background: LPL and WM are rare, indolent mature B-cell lymphomas. While recent studies reveal improving survival after LPL/WM, cause-specific mortality has not been comprehensively studied. Methods: We identified 6659 adults with first primary LPL (n = 2866) or WM (n = 3793) within 17 US population-based cancer registries from 2000 to 2015. Patients were followed for vital status (mean follow-up = 5.07 years), and causes of death were determined from death certificates. Standardized mortality ratios (SMRs) estimated relative risk of death compared to the general population. We estimated cumulative mortality and absolute excess risk (AER) per 10,000 person-years. Results: We observed 2826 deaths overall, of which 43%, 13%, and 42% were due to lymphoma, cancers excluding lymphoma, and non-malignant causes, respectively. There was a 20% higher risk of death due to non-malignant causes compared to the general population (n = 1194, SMR = 1.2, 95% confidence interval [CI] = 1.1 to 1.2). The most common non-malignant causes included infectious (n = 162, SMR = 1.8, 95% CI = 1.5 to 2.1, AER = 21.0), respiratory (n = 131, SMR = 1.2, 95% CI = 1.0 to 1.5, AER = 7.4), and digestive (n = 76, SMR = 1.9, 95% CI = 1.5 to 2.4, AER = 10.7) diseases. Cause-specific mortality varied by time since and age at LPL/WM diagnosis. Risks were highest in the first year after LPL/WM for non-malignant causes (SMR = 1.4, AER = 34.3), particularly infections (SMR = 2.4, AER = 34.4) and non-neoplastic hematologic diseases (SMR = 17.3, AER = 20.7). In contrast, risk of death due to cancers excluding lymphoma increased with time since diagnosis (SMR< 1y = 1.2, SMR≥5y = 1.7; AER< 1y = 15.1, AER≥5y = 60.0). Analyses by age, focused on AERs, showed generally similar risks across age groups (cancers excluding lymphoma: AER< 65= 26, AER65-75= 28, AER≥75= 31; non-malignant causes: AER< 65= 52, AER65-75= 66, AER≥75= 23). Cumulative mortality from non-malignant causes (23.7%) exceeded that from lymphoma (22.9%) beginning 9 years after LPL/WM diagnosis. Conclusions: Using population data, we identified areas to improve survivorship care of LPL/WM patients, particularly for non-malignant causes of death.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3985-3985
Author(s):  
Ramya Varadarajan ◽  
Michael K Cummings ◽  
Andrew J Hyland ◽  
Eunice S. Wang ◽  
Meir Wetzler

Abstract Smoking is the leading preventable cause of death in the Western world. There is substantial evidence that smokers are approximately 1.5 times more likely to develop acute myeloid leukemia (AML) than non smokers. We were interested to know if there is a relationship between smoking and treatment outcome in AML. We searched the Centers for Disease Control and Prevention (CDC) and Surveillance Epidemiology and End Results (SEER) databases for data about smoking incidence and AML mortality. We collected AML mortality data for the United States (US) from SEER and state leukemia mortality data from CDC. CDC data are lumped for all types of leukemia. Since AML is the most common leukemia, and no significant improvement in AML treatment, as compared to chronic myeloid leukemia, occurred in the last two decades, we used the collective leukemia data. We compared smoking incidence and age-adjusted leukemia mortality between overall US and states with either a high (Alabama, Indiana, Ohio, Oklahoma, Kentucky) or a low (California, Connecticut, New York, Utah, Rhode Island) smoking incidence. SEER data revealed a statistically significant correlation (r=0.88) between smoking incidence and AML mortality for the different US regions (Figure 1). The correlation was significant whether we included a 10-year lag period (r= 0.75) for leukemia mortality or not. The correlation between smoking incidence and mortality rates for individual states was much more variable; data from two representative states, California (CA) with low smoking incidence (r=0.74) and Indiana (IN) with high smoking incidence (r=0.03) are shown (Figure 2). Possible causes for decreased mortality can include less pulmonary infections, less aggressive leukemia [reports of more frequent chromosomal aberrations involving chromosome 5, 7 and 8 in smokers] and better transplant outcome in non-smokers. To date, we did not find any data on association between leukemia incidence and smoking prevalence. These data suggest a possible association between smoking and leukemia mortality, and additional research is needed to determine if smoking cessation can be a tool to decrease leukemia mortality. Figure 1 Figure 1. Figure 2: Figure 2:.


Sign in / Sign up

Export Citation Format

Share Document