In the study, HPV-positive women with CINtec PLUS Cytology negative triage test results showed a very low cumulative 1-year risk for disease, which was significantly lower than the risks associated with a negative Pap cytology triage test result in HPV-positive women. Recommended clinical guidelines have also been evolving in favor of HPV tests for primary screening, supported by an interest to improve outcomes and the availability of technologies to help laboratories achieve the efficiency and scale they need to meet the demands of high-volume cervical screening programs.
This abnormality is associated with HPV infections that are transforming and can, if left untreated, progress to pre-cancer or cancer. A positive result of these two biomarkers in a single cell signals that a woman is more significantly at risk for disease. The ability of CINtec PLUS Cytology to distinguish those women who are at a higher risk for cervical disease, in conjunction with the clinician's assessment of patient screening history and other risk factors, provides labs, physicians and women with the information needed to guide patient management.
Women with negative dual-stain results are at significantly lower risk for cervical disease and their bodies can be given more time to clear the HPV infection on their own. This could reduce the number and frequency of follow-up visits, saving some patients worry and time.
This eliminates the need for additional or repeat sample collection or time spent waiting to find out if an infection is clearing. The combined strengths of pharmaceuticals and diagnostics, as well as growing capabilities in the area of data-driven medical insights help Roche deliver truly personalised healthcare. Roche is working with partners across the healthcare sector to provide the best care for each person.
Roche is also the world leader in in vitro diagnostics and tissue-based cancer diagnostics, and a frontrunner in diabetes management. In recent years, Roche has invested in genomic profiling and real-world data partnerships and has become an industry-leading partner for medical insights.
Founded in , Roche continues to search for better ways to prevent, diagnose and treat diseases and make a sustainable contribution to society. The company also aims to improve patient access to medical innovations by working with all relevant stakeholders. More than thirty medicines developed by Roche are included in the World Health Organization Model Lists of Essential Medicines, among them life-saving antibiotics, antimalarials and cancer medicines. The Roche Group, headquartered in Basel, Switzerland, is active in over countries and in employed more than , people worldwide.
In , Roche invested CHF Genentech, in the United States, is a wholly owned member of the Roche Group. Roche is the majority shareholder in Chugai Pharmaceutical, Japan. For more information, please visit www. All trademarks used or mentioned in this release are protected by law. CI confidence interval. Rate ratio for on-treatment exacerbations by quartile.
Rate of on-treatment exacerbations by 3. Rate of on-treatment exacerbations from Week 16 by Week 16 fibrinogen 3. Rate ratio for on-treatment exacerbations by 3. Time-to-first on-treatment exacerbation by quartile. Time-to-first on-treatment exacerbation from Week 16 by Week 16 fibrinogen quartile.
Interaction of treatment with fibrinogen quartile p-values for a — c are 0. Analysis of time-to-first exacerbations using the 3. Similarly, analysis of ACM using the fibrinogen 3. All-cause mortality on and off-treatment by a fibrinogen quartile; b fibrinogen 3. In this current analysis, incidence of AESIs were similar across all fibrinogen quartiles.
For CV events, the overall incidence was similar in each quartile, but Quartile 4 had a slightly higher event rate This post hoc analysis of the IMPACT trial was undertaken to investigate whether plasma fibrinogen could be used to stratify a high-risk COPD population and identify those most likely to have future events.
Our findings indicate an increased rate and risk of exacerbation in patients with higher fibrinogen levels, which is seen regardless of whether fibrinogen is analyzed by quartiles or by a 3. The results from this study support the rationale for using fibrinogen levels as a predictive biomarker for clinical trial recruitment as it provides an indicator of patients at an increased risk of COPD exacerbations [ 11 ].
This could be beneficial as an enrichment strategy in clinical trials looking at exacerbation outcomes, as more exacerbation outputs could be gained from fewer patients, and fewer patients would be required to demonstrate treatment effects.
Importantly, findings from this study support the utility of fibrinogen as a predictive marker for exacerbations in clinical practice; aiding the identification of a subgroup of patients with COPD that are at a higher risk of experiencing exacerbations and would benefit from appropriate treatment to reduce future risk [ 4 ].
These results are in agreement with the studies by Mannino et al. The analysis of exacerbations by continuous fibrinogen levels provides further support for increased exacerbation rates in patients with higher fibrinogen levels.
This differs from results shown in other studies that found that higher levels of plasma fibrinogen were associated with an increased risk of death [ 11 , 17 ]. These differences could potentially be due to the fact that the Week 16 fibrinogen population may not represent all patients; furthermore, patients who died prior to Week 16, and therefore did not have fibrinogen data available, were not included in this analysis.
Finally, it should be noted that this analysis considers a short duration of follow-up from Week 16 to Week 52 , and that there were few events, which may have limited power. The analysis of exacerbation rates by treatment and fibrinogen threshold of 3.
The explanation for this is unclear. Due to the lack of data before Week 16, these results should be interpreted with caution as this limits inferences that may be made around treatment effect; there was a lower rate of treatment discontinuation in patients treated with triple versus dual therapy [ 3 ], possibly confounding any potential treatment effects.
Finally, patients with higher fibrinogen levels had more exacerbations, and it is possible to speculate that these could be biologically different events that did not respond as well to ICS. Fibrinogen is a known risk factor in CV disease, and fibrinogen levels have been shown to be higher in patients with CV disease than those without [ 18 ].
In our analyses, the highest fibrinogen quartile had similar incidence of CV events compared with the other quartiles, with only a small increase in annual event rate 0. Only SAEs and deaths were independently adjudicated in the IMPACT trial; therefore, the lack of an observable increase in AESIs with increasing levels of fibrinogen in our analysis could potentially be due to AEs being misclassified by the clinician as respiratory in nature when in fact they were CV events because of overlapping clinical symptoms between the diseases [ 19 , 20 ].
Systemic inflammation has been associated with CV disease, cancer, and metabolic syndrome as well as COPD [ 9 , 21 — 23 ]. The relationship between reduced fibrinogen and protection from exacerbations [ 9 , 11 , 24 ], suggests that there might be a low-grade inflammatory condition in the lung or extrapulmonary that predisposes patients to exacerbations. However, the absence of an effect of treatment on fibrinogen levels suggests that the site of this ongoing inflammatory response may not reside in the lung.
It should be noted that patients with COPD may also suffer from comorbid diseases that could drive an increase in fibrinogen levels, such as cardiac failure or diabetes; therefore, higher fibrinogen levels may also be an indicator of a comorbidity [ 4 ].
The sample size for the IMPACT trial was large allowing for these subgroup analyses; however, there are limitations that should be considered when interpreting these data. Fibrinogen data were only collected at Week However, it is worth noting that the exacerbation incidence within the first 16 weeks was higher in patients who withdrew from the study compared with those who remained in the study.
Furthermore, patients did not have fibrinogen data; had data been available for these patients, a different result may have been observed. Additionally, survival bias may mean that patients included in this analysis are not representative of a general patient population with COPD. Furthermore, overall data from the IMPACT trial indicates there was a clear separation between treatment arms for both moderate or severe exacerbations and mortality by Week 16, with ACM significantly lower for FF-containing therapies, which could have influenced the results [ 3 ].
There appeared to be no association between fibrinogen levels and risk of death, although the lack of data prior to Week 16 and the relatively small number of deaths overall limit interpretation on risk of death, in addition to the assessment of any potential treatment effects.
The incidence of AESIs was similar between fibrinogen levels, with pneumonia and CV events slightly more common at the highest fibrinogen quartile. Overall, our findings confirm the utility of fibrinogen as a predictive biomarker of exacerbation risk but not for risk of mortality. Editorial support in the form of preparation of the first draft based on input from all authors, and collation and incorporation of author feedback to develop subsequent drafts, was provided by Eloise Morecroft and Chrystelle Rasamison, of Fishawack Indicia Ltd, UK, part of Fishawack Health, and was funded by GSK.
The authors meet criteria for authorship as recommended by the International Committee of Medical Journal Editors. All authors had full access to the data in this study and take complete responsibility for the integrity of the data and accuracy of the data analysis. All authors contributed to data analysis and interpretation. GC, and MD also contributed to the acquisition of data.
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Study Description. Drug Information available for: Empagliflozin. FDA Resources. Arms and Interventions. Outcome Measures. Low risk patients were discharged if troponin test results were below the 99th percentile of a normal reference population, with a letter to their general practitioner stating that further objective testing was not indicated.
Research nurses collected data according to standardised reporting definitions. Blood samples were collected on presentation and at 2 hours for low and intermediate risk patients, and at 0 and 6 hours for high risk patients. All available troponin results were included in clinical decision making. ECG was performed on presentation and at 2 hours for low and intermediate risk patients, and interpreted by the treating ED clinicians. Patients with other abnormal ECG findings eg, pacing artefact, left bundle branch block detected by earlier ECG were not defined as high risk patients.
Administrative database data were assessed to determine health service use, including ED and hospital length of stay LOS. Research nurses followed up patients by telephone 30 days after presentation. All information was verified against medical record databases and cardiac investigation results. The primary outcome was an ACS within 30 days of presentation, including acute myocardial infarction AMI , cardiovascular death, unstable angina pectoris UAP , or coronary revascularisation emergency or urgent.
Type 2 AMIs, infarction secondary to an acute imbalance between oxygen supply and demand eg, ventricular arrhythmias, heart failure, coronary artery spasm , 16 were not included in the primary outcome for this study. The day outcomes were adjudicated independently according to standardised reporting definitions by local cardiologists who had access to the clinical record, ECG and troponin assay results, and all subsequent standard care investigations.
When there was disagreement between the two adjudicators, endpoints were agreed by consensus. AMI was diagnosed according to international guidelines, and was based on evidence of myocardial necrosis and ischaemia, 16 including ECG and imaging findings. Diagnosis of UAP was based on ischaemic symptoms, ECG changes, and objective investigations exercise stress testing, stress echocardiography, computed tomographic coronary angiography [CTCA], myocardial perfusion scan or angiography with normal biomarker levels.
This included patients with new symptoms or a changing symptom pattern ie, from stable to unstable angina. Patients with equivocal ECG changes but clear positive changes on exercise testing or imaging evidence of critical coronary stenosis were also classified as having UAP.
Baseline demographic data are reported for the entire cohort. Median LOS, the proportion of patients with ACS, and the proportion of patients undergoing objective testing are reported. Data were analysed in Stata 14 StataCorp. Informed consent was obtained from all participants. The mean age of the participants was Nineteen patients were incorrectly enrolled as intermediate risk patients, including five who reported syncope at presentation, nine who were in Killip class II or above, two who had elevated troponin values 0.
Objective testing of low and intermediate risk patients There were no cases of ACS in the low risk group and 14 1. ACS was identified in 13 patients in the intermediate risk group by inpatient objective testing, including eight who had an exercise stress test as their first test.
The other five patients underwent other initial testing because of physical inability one , ECG abnormalities that were not classically ischaemic one , and clinician decision three patients. One patient had discharged themselves against medical advice before objective testing, and had an outpatient exercise stress test the next day that indicated ischaemia; they were diagnosed with UAP and therefore classed as a missed case of ACS.
The combination of risk stratification, 2-hour serial troponin results, and selected early objective testing for coronary ischaemia according to the IMPACT protocol provided a safe and efficient means for assessing chest pain in the ED.
The IMPACT study is the first large trial to employ widely available diagnostic tools, to implement a strategy of no additional testing for low risk patients, and to report the outcomes.
While some of the patients stratified in the low risk group underwent objective testing, no low risk patient was subsequently diagnosed with an ACS. Clinician gestalt overall clinical judgement may allow confident discharge of about one-quarter of patients with respect to AMI 19 , but the safety of this approach has not been tested more broadly for ACS. Diagnostic strategies employing CTCA may identify low risk patients and reduce ED LOS, but it is not universally available, and is associated with increased rates of coronary angiography and revascularisation.
Our study found that expedited assessment, including inpatient objective testing, can safely identify ACS in intermediate risk patients. IMPACT enabled three-quarters of patients to be rapidly discharged from hospital without further assessment. Few studies have reported such large proportions of patients being eligible for accelerated assessment and discharge without outpatient investigation. However, IMPACT enabled the accelerated assessment of a larger group of patients by applying the approach to both low and intermediate risk patients; those in the intermediate risk group could be discharged within 8 hours without requiring outpatient testing.
If patients with UAP are not recognised and discharged early, avoidable harm of clinical and medico-legal importance may ensue. Irrespective of strategies, patients with high risk features, including elevated troponin levels, are unlikely to be discharged from the ED.
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