scholarly journals Increased risk of acute arterial events in young patients and severely active IBD: a nationwide French cohort study

Gut ◽  
2017 ◽  
Vol 67 (7) ◽  
pp. 1261-1268 ◽  
Author(s):  
Julien Kirchgesner ◽  
Laurent Beaugerie ◽  
Fabrice Carrat ◽  
Nynne Nyboe Andersen ◽  
Tine Jess ◽  
...  

ObjectiveMagnitude and independent drivers of the risk of acute arterial events in IBD are still unclear. We addressed this question in patients with IBD compared with the general population at a nationwide level.DesignUsing the French National Hospital Discharge Database from 2008 to 2013, all patients aged 15 years or older and diagnosed with IBD were identified and followed up until 31 December 2013. The rates of incident acute arterial events were calculated and the impact of time with active disease (period around hospitalisation for IBD flare or IBD-related surgery) on the risk was assessed by Cox regression adjusted for traditional cardiovascular risk factors.ResultsAmong 210 162 individuals with IBD (Crohn’s disease (CD), n=97 708; UC, n=112 454), 5554 incident acute arterial events were identified. Both patients with CD and UC had a statistically significant overall increased risk of acute arterial events (standardised incidence ratio (SIR) 1.35; 95% CI 1.30 to 1.41 and SIR 1.10; 95 CI 1.06 to 1.13, respectively). The highest risk was observed in patients under the age of 55 years, both in CD and UC. The 3-month periods before and after IBD-related hospitalisation were associated with an increased risk of acute arterial events in both CD and UC (HR 1.74; 95 CI 1.44 to 2.09 and 1.87; 95% CI 1.58 to 2.22, respectively).ConclusionPatients with IBD are at increased risk of acute arterial events, with the highest risk in young patients. Disease activity may also have an independent impact on the risk.

2018 ◽  
Vol 52 (1) ◽  
pp. 1702070 ◽  
Author(s):  
Keely Loewen ◽  
Barret Monchka ◽  
Salaheddin M. Mahmud ◽  
Geert 't Jong ◽  
Meghan B. Azad

Antibiotic use during infancy alters gut microbiota and immune development and is associated with an increased risk of childhood asthma. The impact of prenatal antibiotic exposure is unclear. We sought to characterise the association between prenatal antibiotic exposure and childhood asthma.We performed a population-based cohort study using prescription records, hospitalisation records and physician billing claims from 213 661 mother–child dyads born in Manitoba, Canada between 1996 and 2012. Associations were determined using Cox regression, adjusting for maternal asthma, postnatal antibiotics and other potential confounders. Sensitivity analyses evaluated maternal antibiotic use before and after pregnancy.36.8% of children were exposed prenatally to antibiotics and 10.1% developed asthma. Prenatal antibiotic exposure was associated with an increased risk of asthma (adjusted hazard ratio (aHR) 1.23, 95% CI 1.20–1.27). There was an apparent dose response (aHR 1.15, 95% CI 1.11–1.18 for one course; aHR 1.26, 95% CI 1.21–1.32 for two courses; and aHR 1.51, 95% CI 1.44–1.59 for three or more courses). Maternal antibiotic use during 9 months before pregnancy (aHR 1.27, 95% CI 1.24–1.31) and 9 months postpartum (aHR 1.32, 95% CI 1.28–1.36) were similarly associated with asthma.Prenatal antibiotic exposure was associated with a dose-dependent increase in asthma risk. However, similar associations were observed for maternal antibiotic use before and after pregnancy, suggesting the association is either not directly causal, or not specific to pregnancy.


Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Takaya Kitano ◽  
Tsutomu Sasaki ◽  
Yasufumi Gon ◽  
Kenichi Todo ◽  
Shuhei Okazaki ◽  
...  

Introduction: Chemotherapy may be a cause of cancer-associated stroke, but whether it increases stroke risk remains uncertain. We aimed to clarify the impact of chemotherapy on stroke risk in cancer patients. Methods: We investigated 27,932 patients enrolled in a hospital-based cancer registry at Osaka University Hospital between 2007 and 2015. The registry collects clinical data, including cancer status (site and stage), on all patients treated for cancer. Of them, 19,006 patients with complete data were included. A validated algorithm was used to identify stroke events within 2 years of cancer diagnosis. Patients were divided based on whether their initial treatment plan included chemotherapy. The association between chemotherapy and stroke was analyzed using the Kaplan-Meier method and stratified Cox regression. Results: Of the 19,006 patients, 5,887 (31%) patients were in the chemotherapy group. Non-targeted chemotherapy was used in 5,371 patients. Stroke occurred in 44 patients (0.75%) in the chemotherapy group and 51 patients (0.39%) in the no-chemotherapy group. Kaplan-Meier curve analysis showed that patients in the chemotherapy group had a higher stroke risk than patients in the no-chemotherapy group (HR 1.84; 95% CI 1.23-2.75; Figure [A]). However, this difference was insignificant after adjustment for cancer status using inverse probability of treatment weighting with propensity scores (HR 1.20; 95% CI 0.76-1.91; Figure [B]). Similarly, in the stratified Cox regression model, chemotherapy was not associated with stroke after adjustment for cancer status (HR 1.26; 95% CI 0.78-2.03). These findings were consistent with analysis wherein the effect of chemotherapy was treated as a time-dependent covariate (HR 1.02; 95% CI 0.55-1.88). Conclusions: In this population, the elevated stroke risk in cancer patients who received chemotherapy was presumably due to advanced cancer stage; chemotherapy was not associated with the increased risk of stroke.


2019 ◽  
Vol 41 (2) ◽  
pp. 209-217 ◽  
Author(s):  
David Fitchett ◽  
Silvio E Inzucchi ◽  
Christoph Wanner ◽  
Michaela Mattheus ◽  
Jyothis T George ◽  
...  

Abstract Aims Hypoglycaemia, in patients with Type 2 diabetes (T2D) is associated with an increased risk for cardiovascular (CV) events. In EMPA-REG OUTCOME, the sodium-glucose co-transporter-2 inhibitor empagliflozin reduced the risk of CV death by 38% and heart failure hospitalization (HHF) by 35%, while decreasing glycated haemoglobin (HbA1c) without increasing hypoglycaemia. We investigated CV outcomes in patients with hypoglycaemia during the trial and the impact of hypoglycaemia on the treatment effect of empagliflozin. Methods and results About 7020 patients with T2D (HbA1c 7–10%) were treated with empagliflozin 10 or 25 mg, or placebo and followed for median 3.1 years. The relationship between on-trial hypoglycaemia and CV outcomes, and effects of empagliflozin on outcomes by incident hypoglycaemia [HYPO-broad: symptomatic hypoglycaemia with plasma glucose (PG) ≤70 mg/dL, any hypoglycaemia with PG <54 mg/dL, or severe hypoglycaemia, and HYPO-strict: hypoglycaemia with PG <54 mg/dL, or severe hypoglycaemia] was investigated using adjusted Cox regression models with time-varying covariates for hypoglycaemia and interaction with treatment. HYPO-broad occurred in 28% in each group and HYPO-strict in 19%. In the placebo group, hypoglycaemia was associated with an increased risk of HHF for both HYPO-broad [hazard ratio (HR, 95% confidence interval, CI) 1.91 (1.25–2.93)] and HYPO-strict [1.72 (1.06–2.78)]. HYPO-broad (but not HYPO-strict) was associated with an increased risk of myocardial infarction (MI) [HR 1.56 (1.06–2.29)]. Empagliflozin improved CV outcomes, regardless of occurrence of hypoglycaemia (P-for interactions >0.05). Conclusion In this post hoc exploratory analysis, hypoglycaemia was associated with an increased risk of HHF and MI. Hypoglycaemia risk was not increased with empagliflozin and incident hypoglycaemia did not attenuate its cardio-protective effects.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Esther Wong ◽  
Dorothea Nitsch

Abstract Background and Aims Incidence of Acute Kidney Injury (AKI) is known to be seasonal, peaking in winter months among hospitalised patients. Previous studies have suggested that the seasonality of AKI is likely to be influenced by the seasonality of the underlying acute illnesses that are associated with AKI. Mortality of patients with AKI has also been reported as being higher in winter, reflecting well-described excess winter mortality associations. Here we describe the seasonal variations of AKI alerts in England and the associated mortality rate using linked national databases. Method Serum creatinine changes compatible with KDIGO AKI stage 1, 2 and 3 are sent by laboratories in England as AKI alerts to the treating clinicians and the UK Renal Registry (UKRR). We linked the electronic AKI alerts to the Hospital Episode Statistics (HES) data, to identify patients who were hospitalised. We carried out descriptive statistics, and investigate the seasonal effect to the 30-day patient mortality from date of getting AKI alert, using multivariable Cox regression and sequentially adjusting for age, sex, Index of multiple deprivation (IMD) and peak AKI stage Results Winter has the highest number of AKI episodes (N=81,276), which is 6% higher than that in summer (N=76,329) (Table 1). For patients who had an AKI episode and admitted to hospitals, the crude 30-day mortality is higher in the winter season when compared to the summer [HR 1.28 (1.25-1.31), p<0.01] (Figure 1). After adjusting season by age, peak AKI stage, IMD and sex, winter season still has significantly higher 30-day mortality than summer [HR 1.24 (1.21-1.27), p<0.01]. Winter mortality peak is confounded by age and AKI severity, which explained the drop of hazard ratio at winter peaks; whereas season is not confounded by deprivation and sex. The pattern of seasonality varies with age, in age group 18-39, there were 26.1% of AKI episodes in summer and 23.3% in winter, whereas in age group >75, there were 23.7% in summer and 27.1% in winter. Conclusion Analysis of England data confirms seasonal peak in AKI during winter months. Additionally it shows increased risk of mortality for patients with AKI in winter months. Future work will investigate the impact of comorbidities and case-mix on outcomes. By understanding the seasonal variation of AKI, we can potentially plan preventive care and improve clinical practice.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yaerim Kim ◽  
Jeongsoo Yoon ◽  
Jin Hyuk Paek ◽  
Woo Yeong Park ◽  
Kyubok Jin ◽  
...  

Abstract Background and Aims Glomerular hyperfiltration is associated with all-cause mortality. Herein, we evaluated the association between glomerular hyperfiltration and the development of malignant disease, the most common cause of death, in an Asian population. Method We retrospectively reviewed the National Health Insurance Service database of Korea for people who received national health screenings from 2012 to 2013. Glomerular hyperfiltration was defined as the 95th percentile and greater after adjusting for age and sex. We performed a multivariate Cox regression analysis using glomerular hyperfiltration at the first health screening as the exposure variable and cancer development as the outcome variable to evaluate the impact of glomerular hyperfiltration on the development of malignant disease. Results A total of 1,953,123 examinations who followed-up for 4.9 years were included in this study. Among the 8 different site-specific malignant disease categories, digestive organs and female genital organs showed a significant associations between glomerular hyperfiltration and malignancy. The population with glomerular hyperfiltration showed an increased risk for stomach cancer (adjusted hazard ratio [aHR], 1.27), colorectal cancer (aHR, 1.23), and liver or intrahepatic malignancy (aHR, 1.40). In addition, the risk for uterine and ovarian cancer was significantly increased in the population with glomerular hyperfiltration (aHR, 1.36). Conclusion Glomerular hyperfiltration was associated with an increased risk for the development of malignant diseases in specific organs, such as the stomach, colorectum, uterus, and ovary. Glomerular hyperfiltration needs to be considered a significant sign of the need to evaluate the possibility of hidden adverse health conditions, including malignancies.


2020 ◽  
Vol 41 (17) ◽  
pp. 1673-1683 ◽  
Author(s):  
Michael Böhm ◽  
João Pedro Ferreira ◽  
Felix Mahfoud ◽  
Kevin Duarte ◽  
Bertram Pitt ◽  
...  

Abstract Aims The described association of low diastolic blood pressure (DBP) with increased cardiovascular outcomes could be due to reduced coronary perfusion or is simply due to reverse causation. If DBP is physiologically relevant, coronary reperfusion after myocardial infarction (MI) might influence DBP–risk association. Methods and results The relation of achieved DBP with cardiovascular death or cardiovascular hospitalization, cardiovascular death, and all-cause death was explored in 5929 patients after acute myocardial infarction (AMI) with impaired left ventricular function, signs and symptoms of heart failure, or diabetes in the EPHESUS trial according to their reperfusion status. Cox regression models were used to assess the impact of reperfusion status on the association of DBP and systolic blood pressure (SBP) with outcomes in an adjusted fashion. In patients without reperfusion, lower DBP <70 mmHg was associated with increased risk for all-cause death [adjusted hazard ratios (HRs) 1.80, 95% confidence interval (CI) 1.41–2.30; P < 0.001], cardiovascular death (HR 1.70, 95% CI 1.3–3.22; P < 0.001), cardiovascular death or cardiovascular hospitalization (HR 1.54, 95% CI 1.26–1.87; P < 0.001). In patients with reperfusion, the risk increase at low DBP was not observed. At low SBP, risk increased independently of reperfusion. A sensitivity analysis in the subgroup of patients with optimal SBP of 120–130 mmHg showed again risk reduction of reperfusion at low DBP. Adding the treatment allocation to eplerenone or placebo into the models had no effects on the results. Conclusion Patients after AMIs with a low DBP had an increased risk, which was sensitive to reperfusion therapy. Low blood pressure after MI identifies in patients with particular higher risk. These data support the hypothesis that low DBP in patients with stenotic coronary lesions is associated with risk, potentially involving coronary perfusion pressure and the recommendations provided by guidelines suggesting lower DBP boundaries for these high-risk patients.


2018 ◽  
Vol 33 (6) ◽  
pp. 385-393 ◽  
Author(s):  
Jakub Kazmierski ◽  
Chaido Messini-Zachou ◽  
Mara Gkioka ◽  
Magda Tsolaki

Cholinesterase inhibitors (ChEIs) are the mainstays of symptomatic treatment of Alzheimer’s disease (AD); however, their efficacy is limited, and their use was associated with deaths in some groups of patients. The aim of the current study was to assess the impact of the long-term use of ChEIs on mortality in patients with AD. This observational, longitudinal study included 1171 adult patients with a diagnosis of AD treated with donepezil or rivastigmine. Each patient was observed for 24 months or until death. The cognitive and functional assessments, the use of ChEIs, memantine, antipsychotics, antidepressants, and anxiolytics were recorded. The total number of deaths at the end of the observational period was 99 (8.45%). The patients who had received rivastigmine treatment were at an increased risk of death in the follow-up period. The higher risk of death in the rivastigmine group remained significant in multivariate Cox regression models.


2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Henrique Cotchi Simbo Muela ◽  
Jose Jayme Galvão De Lima ◽  
Luis Henrique W. Gowdak ◽  
Flávio J. de Paula ◽  
Luiz Aparecido Bortolotto

Background.High serum uric acid (UA) is associated with increased cardiovascular (CV) risk in the general population. The impact of UA on CV events and mortality in CKD is unclear.Objective.To assess the relationship between UA and prognosis in hemodialysis (HD) patients before and after renal transplantation (TX).Methods.1020 HD patients assessed for CV risk and followed from the time of inception until CV event, death, or TX (HD) or date of TX, CV event, death, or return to dialysis (TX).Results.821 patients remained on HD while 199 underwent TX. High UA (≥428 mmol/L) was not associated with either composite CV events or mortality in HD patients. In TX patients high UA predicted an increased risk of events (P=0.03, HR 1.6, and 95% CI 1.03–2.54) but not with death. In the Cox proportional model UA was no longer significantly associated with CV events. Instead, a reduced GFR (<50 mL/min) emerged as the independent risk factor for events (P=0.02, HR 1.79, and % CI 1.07–3.21).Conclusion.In recipients of TX an increased posttransplant UA is related to higher probability of major CV events but this association probably caused concurrent reduction in GFR.


Author(s):  
N. Stepanova ◽  
V. Novakivskyy ◽  
L. Snisar ◽  
M. Kutsenko

Abstract. We hypothesized that the use of antihypertensive medications in patients treated by hemodialysis (HD) may interfere with the activity of erythropoietin and leads to an increase in the dose of erythropoiesis stimulating agents (ESAs). The aim of our study was to analyze the impact of antihypertensive medications on the effectiveness of anemia treatment. Methods. We conducted a multicenter retrospective observational study. The archival medical data from 379 patients treated by HD or hemodiafiltration (HDF) were used. The medical records of 142 patients were excluded from the study. The study group consisted of 237 patients: 108 (45.6%) women and 129 (54.4%) men, with an average age of 54 [41-62.5] years. Results. The analysis of the mean hemoglobin (Hb) stratified by the administration of antihypertensive medications in the dynamics of dialysis treatment demonstrated a significant impact of angiotensin-converting enzyme (ACE) inhibitors (F = 3.97; p = 0.048) and amlodipine (F = 6.9; p = 0.01) on the effectiveness of anemia correction. The significant effect of amlodipine on the need to increase the dosage of iron-containing medications (OR = 3.9; 95% CI (1.27-12.06), p = 0.002; RR = 1.9 95% CI (1.27-2.9) and continuous erythropoietin receptor activator (CERA) (OR = 5.2, 95% CI (1.2-24.4), p = 0.03; RR = 1.3 95% CI (1, 08-1.6), p = 0.006) weas showed by logistic regression analysis. The increased risk of failure to achieve of the target Hb level in HD patients received amlodipine was confirmed by Cox regression model (HR = 2.7 (95% CI 1.5-4.7)). Conclusions: The results of our study demonstrated a significant increase in the frequency of appointment and amount of anti-anemia therapy in HD patients when amlodipine is co-administered. Follow-up studies to determine the effect of amlodipine mechanism for anemia will avoid unreasonable prescriptions for the treatment of НD patients. Conflict of interest statement: the authors declared no competing interests.


Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1693
Author(s):  
Daryl Ramai ◽  
Khoi P. Dang-Ho ◽  
Anjali Kewalramani ◽  
Praneeth Bandaru ◽  
Rodolfo Sacco ◽  
...  

Frailty represents a state of vulnerability to multiple internal physiologic factors, as well as external pressures, and has been associated with clinical outcomes. We aim to understand the impact of frailty on patients admitted with hepatocellular carcinoma (HCC) by using the validated Hospital Frailty Risk Score, which is implemented in several hospitals worldwide. We conducted a nation-wide retrospective cohort study to determine the effect of frailty on the risk of in-patient mortality, hepatic encephalopathy, length of stay and cost. Frailty was associated with a 4.5-fold increased risk of mortality and a 2.3-fold increased risk of hepatic encephalopathy. Adjusted Cox regression showed that frailty was correlated with increased risk of in-patient mortality (hazard ratio: 2.3, 95% CI 1.9–2.8, p < 0.001). Frail HCC patients had longer hospital stay (median 5 days) vs. non-frail HCC patients (median 3 days). Additionally, frail patients had higher total costs of hospitalization ($40,875) compared with non-frail patients ($31,667). Frailty is an independent predictor of hepatic encephalopathy and in-patient mortality. Frailty is a surrogate marker of hospital length of stay and cost.


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