Acusera 24Ā·7 and Data Innovations – Automated QC Data Upload
Acusera 24Ā·7 and Data Innovations – Automated QC Data Upload
Automated QC Data Upload to Acusera 24·7
Now Available via Instrument Manager™ from Data Innovations
Randox Laboratories in conjunction with Data Innovations are pleased to announce the launch of a new driver that enables seamless, automated QC data upload via API from any instrument connected to Instrument Manager (IM) directly into Acusera 24.7. This new feature eliminates the need for manual data entry, reduces transcription errors and improves laboratory efficiency.
What you need to know
Uni-Directional License – Anyone wishing to avail of automated QC data upload to Acusera 24.7 will need a uni-directional license for Instrument Manager. A new license can be requested directly from a Data Innovations representative, or an existing license previously used for an analyser may be re-purposed.
Driver Download – Once a license has been secured, you will be required to download the Acusera 24.7 Driver from the MY DI Community website – https://datainnovations.my.site.com/s/drivers. To locate the driver simply select Randox from the Manufacturer drop down menu and then select Acusera 24.7 from the list of available drivers.
Configuration – Once the driver has been downloaded, you will receive help files that document the process to be followed. The same steps are to be followed as with connecting any instrument or analyser to Instrument Manager.
Once the driver has been successfully set up, Instrument Manager will automatically send QC data to Acusera 24.7, removing the need for manual data entry.
Key Considerations
- You must have have an Acusera 24.7 license and configured your Acusera 24.7 account before connecting to Instrument manager.
This new capability allows laboratories to optimise workflows, reduce errors, and streamline QC data management.
About Data Innovations
Data Innovations is a global software company that is passionate about excellence in patient care. Through innovative solutions and world-class service, they enable enterprise management of hospitals and independent laboratories. Founded in 1989 with headquarters in Vermont, Data Innovations serves more than 6,000 hospitals and laboratories in 80+ countries.
What is Instrument Manager?
Laboratory Information Management Systems (LIMS) by Data Innovations LLC
Instrument Manager™ (IM) is a truly vendor-neutral middleware platform that allows for the connection of any clinical lab instrument to any Lab Information System (LIS), with a library of over 1,000 instrument drivers. IM offers a suite of lab enablement solutions spanning productivity, quality, analytics, performance and reliability.
Labs using IM auto verification with time-saving workflows are able to achieve quicker turnaround times and increased productivity. IM quality assurance programs ensure that all connected instruments deliver the most accurate possible test results.
Candida auris: An Urgent Fungal Threat
An Urgent Fungal Threat: Tackling Candida auris in Healthcare Environments
Candida auris (C. auris), is an emerging fungal threat that has garnered global attention due to its multidrug-resistant nature and ability to cause severe, life-threatening infections. First identified in 2009, C. auris has quickly spread worldwide, particularly in healthcare settings, posing a significant challenge to both clinicians and public health professionals.
Understanding Candida auris
Candida auris is a yeast-like fungus that can lead to severe infections, especially in patients with compromised immune systems or underlying health conditions. It is frequently found in healthcare environments such as hospitals and long-term care facilities. The most concerning aspect of C. auris is its ability to persist on surfaces, increasing the risk of outbreaks in these environments. Once introduced into a healthcare setting, it can rapidly spread from one patient to another, making infection control a significant challenge.
In Illinois alone, 921 C. auris cases were confirmed between 2016 and 2022 (1). Additionally, in 2022, 2377 cases of C. auris were reported to the CDC (2), further highlighting the increase in cases each year. In Europe, survey responses were received from all 30 invited EU/EEA countries. From 2013 to 2021, a total of 1,812 Candida auris cases were reported by 15 of these countries. The number of cases nearly doubled from 335 in 2020 to 655 in 2021, indicating a significant increase compared to previous years (3).
C. auris primarily causes bloodstream infections, but it can also infect wounds, the respiratory tract, and the ear. Patients in critical care, especially those using invasive medical devices such as ventilators, catheters, or feeding tubes, are particularly susceptible. In fact, data indicates that more than one in three people with an invasive C. auris infection affecting the blood, heart, or brain, do not survive (1).
The Growing Threat of Multidrug Resistance
One of the major concerns surrounding C. auris is its resistance to multiple classes of antifungal medications, which are typically used to treat Candida infections. This multidrug resistance often leads to treatment failure and poor outcomes in affected patients. In addition to its drug resistance, Candida auris is often misidentified as other Candida species using standard laboratory methods, further delaying appropriate treatment.
The Importance of Rapid and Accurate Detection
Given the risks posed by Candida auris, rapid detection is crucial for preventing the spread of this dangerous fungus. Early identification allows healthcare professionals to implement strict infection control measures such as isolating patients, cleaning and disinfecting affected areas, and preventing further transmission within healthcare facilities. However, traditional detection methods may be slow and prone to misidentification, making timely response difficult.
Enter Vivalytic
The early identification and containment of Candida auris are essential to prevent large-scale outbreaks. This is especially important in healthcare environments where patients may be vulnerable. The Vivalytic’s rapid detection of C. auris colonisation and infection allows for earlier implementation of infection control measures. This reduces the burden on public health systems and helps save lives.
At Randox Laboratories, the focus is on advancing the detection of infectious diseases like Candida auris. The Vivalytic, developed with Bosch, offers a reliable and accurate testing solution. This supports healthcare providers in protecting patients and controlling the spread of the fungus. Real-time PCR technology is used by the Vivalytic Candida auris test to detect DNA from swabs. These swabs may be taken from the axilla, groin, nasal, or rectal regions.
Key Benefits of Vivalytic Testing for Candida auris:
- Quick Results: The Vivalytic provides results in under 1 hour, enabling healthcare providers to make swift, informed decisions about patient care and infection control. This quick turnaround is essential for both treating the patient and containing the spread of Candida auris within a healthcare facility.
- Simple, 4-Step Process: The test uses a convenient 4-step process, from scanning the sample to receiving the results, making it easy to use in both laboratory and non-laboratory settings. The system’s fully automated, cartridge-based platform minimises the risk of contamination and simplifies workflow.
- Accurate Detection: The real-time PCR method used by Vivalytic ensures precise detection of Candida auris, even in cases where traditional methods might misidentify the fungus. This accuracy is vital in initiating appropriate antifungal treatment and curbing the infection.
- Convenient for Various Settings: The Vivalytic platform is designed to be used in a wide range of settings, from large laboratories to point-of-care environments, making it versatile and adaptable to the needs of different healthcare providers.
| Detectable Pathogens |
|---|
| Candida auris |
References
- dph.illinois.gov. (n.d.). Candida auris (C. auris). [online] Available at: https://dph.illinois.gov/topics-services/diseases-and-conditions/infectious-diseases/candida-auris.html.
- CDC (2024). Tracking C. auris. [online] Candida auris (C. auris). Available at: https://www.cdc.gov/candida-auris/tracking-c-auris/index.html.
- Kohlenberg, A., Monnet, D.L. and Plachouras, D. (2022). Increasing number of cases and outbreaks caused by Candida auris in the EU/EEA, 2020 to 2021. Eurosurveillance, 27(46). doi:https://doi.org/10.2807/1560-7917.es.2022.27.46.2200846.
Randox Attend 2024 Grand National Winning Yard
Randox Laboratories Visits W.P. Mullins’ Yard – Celebrating Success at the 2024 Grand National
Randox Laboratories were thrilled to attend the prestigious 2024 Grand National Winners Yard at W.P. Mullins’ state-of-the-art stables in County Carlow. As the proud sponsors of the Grand National, we had the opportunity to witness first-hand the dedication, precision, and care that go into training champions.
W.P. Mullins, continues to set the standard with his exceptional achievements, including the 2024 winner of the world’s greatest steeplechase I am Maximus.
Randox are grateful to have the opportunity to celebrate the hard work and passion that define winners like W.P. Mullins and his team.
Thank you to everyone at the yard for a warm welcome and an exciting experience!
Check out some of the highlights of our trip below!
Randox Testing Services – Drug and Alcohol Testing
At Randox Testing Services, we provide reliable and cost-effective drug and alcohol testing solutions for a wide range of industries. Sectors we work with include aviation, maritime, manufacturing, and more. Additionally, our Collection Officer Network operates 24 hours a day, 365 days of the year with a target call-out time of 2 hours. With over 40 years of experience in the diagnostics industry, our services not only ensure safety but also compliance in workplaces across the UK and Ireland.
We understand that every industry has unique needs, which is why we craft customised testing packages to meet specific workplace requirements. Whether it’s random testing to deter substance abuse or post-incident testing following an accident, we offer flexible solutions that cater to your business’s safety priorities. Furthermore, our expertise is trusted by industries ranging from safety-critical sectors to the medico-legal field such as family law, ensuring that our clients receive accurate, reliable, and legally defensible results.
- Pre-Employment Testing: Essential for ensuring candidate suitability and maintaining a safe environment for your current workforce.
- Random Testing: A highly effective deterrent for substance abuse, as employees are aware they could be tested at any time, ensuring integrity across all levels of the organisation.
- With-Cause Testing: Conducted when there is suspicion or allegations of drug or alcohol abuse in the workplace, or when drugs and alcohol have been found.
- Post-Incident Testing: Occurs after an accident or incident to determine if drugs or alcohol played a role.
- Abstinence Testing: Used to monitor employees who previously tested positive to ensure they remain abstinent from substance misuse.
We utilise discreet and non-invasive methods for sample collection, offering options such as urine, hair, oral fluid, breath or a combination of these. This enables both short-term and long-term drug profiling. Moreover, our testing methods are designed to suit your organisation’s needs and ensure accuracy and reliability in detecting drug and alcohol use. Each sample is handled following strict chain of custody procedures to guarantee sample integrity from collection to reporting.
We follow a thorough and professional process to deliver tailored drug and alcohol testing solutions:
-
- Consultation: We start with a free consultation to discuss your requirements and create a customised testing package.
- Policy Creation: We help develop a clear and concise workplace drug and alcohol policy that outlines employer rights while protecting employees.
- Policy Implementation: Our training and educational services help you effectively communicate the policy to your team.
- Sample Collection: Our trained officers collect samples at a time and location that suits you, maintaining sample integrity throughout the process.
- Sample Analysis: Using our advanced Biochip Array Technology, we screen samples for a wide range of substances, ensuring reliable and accurate results.
- Results Reporting: Results are delivered confidentially via our secure web portal, with options for alternative methods if preferred.
We test for a wide range of drugs across different panels using both instant testing kits and lab-based confirmatory analysis. This flexibility allows us to meet the diverse needs of our clients, ensuring all substances of concern are covered. Substances include:
| Substances Tested | |||
|---|---|---|---|
| Amphetamine | Phencyclidine | Alcohol | LSD |
| Buprenorphine | Cannabinoids | Barbiturates | Opioids |
| Benzodiazepine | Oxycodone | Benzodiazepine 1 | Mephedrone |
| Cocaine Metabolite | Tramadol | Benzodiazepine 2 | Pregabalin |
| Methadone | EDDP | Methaqualone | Gabapentin |
| Methamphetamine | Ketamine | Fentanyl | Zolpidem |
| Opiates | MDMA/Ecstasy | Propoxyphene | Zopiclone |
- Expertise across various industries, including workplace and medico-legal
- Accurate and reliable testing methods
- Global network of trained sample collection officers
- Customised training and education seminars
- Free policy review and consultation
Randox Testing Services is committed to helping businesses enhance workplace safety, reduce absenteeism, and ensure compliance with drug and alcohol regulations. Contact us today at testingservices@randox.com or call +44 (0) 28 9445 1011 to speak with one of our experts.
Randox Health features in Sunday Times article
One writerās first health MoT showed her cholesterol in the red. It forced a dramatic lifestyle rejig, but the hard part was making the changes stick
In February my colleague Matt Rudd sent a pleading email: āHelp! I need volunteers for a blood health panel screening. Hooked on the fact that a million people in the UK have undiagnosed T2 diabetes.ā
My Italian grandmother had diabetes. I had never had a proper health check in my life. It probably wasnāt a bad idea to have an MoT.
By my reckoning, I was in reasonable nick for a 37-year-old mother of a two and a five-year-old: I cooked from scratch, didnāt eat red meat and cycled (occasionally and slowly) to work. I banked on getting the health equivalent of a B+.
But I very much did not get a B+. The results from my Ā£65 āvitalā Randox Health check were graded byĀ a traffic light system. Ten per cent of me was, firmly, in the alarming red zone and 13 per cent was amber. The (main) issue was not pre-diabetes, butĀ high cholesterol. My total was 6.22 mmol (millimoles per litre) when it should have been less than 5.
āIām really freaking out,ā I messaged my partner, Tom. āIām going to get heart disease. Or have a stroke.ā
Closer inspection showed that my LDL, which Google informed me was the bad kind of cholesterol, the kind that clogs up the arteries and kills you, was 3.56. It should have been below 3. My iron levels were also low, again throwing up more red. And I wasnāt fit. My body mass index was in the green but I had the metabolic age of a 40-year-old. āThis is really sub-optimal,ā I added to Tom.
But it was the high cholesterol, which is usually without symptoms, that bothered me. Nearly 50 per cent of the population is estimated to have high cholesterol and it often runs in families, explains Julie Ward, a cardiac nurse at the British Health Foundation. āItās really prevalent in society, but often people, especially younger people, have no idea at all until they get checked. The key is to talk to your relatives, to your parents. Ask them if thereās a family history.ā
I peppered my trim mum with anxious messages. Why didnāt I know about this? āI told you that I had high cholesterol,ā she replied. When? āYou were 14.ā Somewhere between the Smirnoff Ice and Marlboro Lights, that particular health concern apparently hadnāt lodged in my mind.
I told my twin brother about our genetic predisposition, which he seemed relaxed about. I was anything but relaxed. I think it was the recognition that I could no longer āwing itā that struck me. Call it my coming of age. And my worries spiralled from there: I wanted to be around and healthy for my children as they grew up. Which meant that as Sir Keir Starmer said about the NHS, I had two options: reform or die.
The question was: what to do about it? Changing habits, some of which developed in childhood, is extremely challenging. I took a hard-nosed look at my lifestyle. Exercise didnāt really feature, other than the 25-minute cycle to the office and a bit of tennis. None of which, Tom pointed out, made me break into a sweat.
I ate lots of vegetables, fish and pulses, but I also ate cheese straws, crisps and pasta. At restaurants, I was all about fried and/or beige: croquetas, any kind of tempura, burrata, tuna tostadas. The bread basket. Nor did I ever contemplate the long rigmarole of putting our kids to bed without eating a hefty wedge of toasted sourdough, butter and mature cheddar.
So what could I do? The answers were predictable: exercise, cut out saturated fats (found in cakes, biscuits, pastries, processed food), eat more pulses and vegetables, and eat plenty more seeds, nuts, oily fish and avocado, all sources of good cholesterol, the kind that takes the bad away from the arteries.
Letās retest in six months, suggested Matt Rudd. Here was a competition, something I could get on board with.
āIām making radical changes,ā I told Tom as I filled our online Sainsburyās cart with butter beans, chickpeas and beetroot (none of which I much liked). āNo more bread, white pasta, potatoes, white rice. No cheese, no deep-fried food. No moreTonyās Chocolonely. And Iām going to work out two mornings a week.ā
The first major test came two days later when we went on a rare childfree trip to Venice, home of cichetti and Aperol Spritz. At 6pm, drinking white wine beside the lagoon, I was presented with a (free) plate of tiny smoked salmon white bread sandwiches and bruschette piled with salted cod.Oh tentazione!
But I had decided to go cold turkey. Any other approach and I knew my willpower would evaporate before Tom could say āstrokeā. Dinner was torture: obviously I wanted the spaghetti alle vongole but instead I made myself order cuttlefish stew (no carbs!).
Back in London, I carried on. Toast with butter and marmite was replaced with chia and flaxseed-heavy oat bircher. My mid-afternoon snack of pop chips became walnuts and almonds. A salad for the old me was 60 per cent crouton.
Dinner became something like veggie chilli, no rice, or spicy butter beans with spinach and tofu. Biscuits, cakes and puddings were taken off my menu. As was my after-supper chocolate.
Classpass, a monthly subscription that gets you access to various gym classes, also worked for me. Mainly because its policy is to fine you for missing a class. Brutal but effective.
It takes 60 days to form a habit, Tom kept telling me when I wavered: donāt give up. A dogma confirmed by Jenna Hope, a nutritionist who advises her clients on how to break and reform habits. āItās hard, but there are tricks,ā she says. One is to focus on what is making you sit down on the sofa with a tub of ice cream after work. āIf that is what you do for relaxation, you need to replace the ice cream with something else, something healthy. Donāt just say, āIām not having ice cream any moreā, thatās much harder.ā
Each person is different, she says, some need to make changes slowly. Others, like me, need to go nuclear. Either way, the key is consistency.
Competitiveness also drove me. I wanted to beat Matt Rudd. Though when he opened his desk drawer to reveal a supermarket-sized stack of Jammy Dodgers, Mini Cheddars and Haribo, I realised heād given up.
By two months in, I was feeling a hell of a lot of better. I no longer had stomach aches and I was fitter and had lost weight. Iād also developed a taste for crouton-free salad.
Take the Randox test, my editor kept asking me. But I was worried: what if, after all this effort and self-denial, my cholesterol hadnāt changed? Can you even do anything about it when it runs in your family?
Last week, I caved andtook the test. The great news was that I had reduced my metabolic age from 40 to 23. And my cholesterol? Still red but definitely leaning more pink: from a total of 6.22 it had dropped to 5.6. And the bad kind was now at the healthy level, below 3, at 2.79 mmol.
āThatās a really good level,ā said Joanna Lilburn, a scientific consultant at Randox. āAnd I wouldnāt worry about the total level because a lot of that is good cholesterol.ā
Which is what I wanted to hear. Lifestyle changes were working. Albeit slowly. What I didnāt want to hear is that cholesterol levels increase as you age. Which means that now, warned Lilburn, comes the hard part. āItās about keeping it going.ā
Read full article here: I had high cholesterol at 37. The cure was tougher than I imagined (thetimes.com)
Understanding Xanthochromia
Understanding Xanthochromia
When faced with a potential subarachnoid haemorrhage (SAH), the tools we use to diagnose can quite literally be life-saving. Cerebrospinal fluid (CSF) analysis plays a pivotal role, especially when common diagnostic tools like Computed Tomography (CT) scans might not catch early signs.
Traditionally, xanthochromia detection relied on visual assessment – a method that suffers from inconsistency due to subjective interpretation and lacks uniformity across the industry. Today, spectrophotometry has emerged as the preferred method for its precision and reliability in detecting xanthochromia. To ensure the highest accuracy, this technique requires stringent quality control measures. Here, we discuss xanthochromia and SAH, before introducing our dedicated Xanthochromia true third-party control.
What is Xanthochromia?
Xanthochromia, derived from the Greek word, ‘xanthos,’ meaning yellow, refers to the yellow, or sometimes pink, discolouration of CSF, primarily due to bilirubin, a by-product of haemoglobin breakdown. Why does this matter? Because it’s a tell-tale sign of bleeding within the brain, often indicating SAH when CT scans don’t. Understanding this can help us catch and treat critical conditions before they worsen. Xanthochromia may also be an indicator of intracerebral haemorrhage, brain tumours, infection, or severe systemic jaundice1.
Subarachnoid Haemorrhage
SAH is a spontaneous intracranial bleed characterised by significant mortality and morbidity rates. Approximately 12% of patients die before receiving medical attention, 33% within 48 hours, and 50% within 30 days of an SAH. Among the survivors, half suffer from permanent disabilities, with an estimated lifetime cost more than double that of an ischemic stroke2. Patients which have displayed symptoms often complain of severe headache, nausea, vomiting, photophobia and/or phonophobia3.
CT scans, particularly non-contrasted CTs of the brain or CT angiograms (CTAs), are often the first line of diagnostic tools for suspected SAH. However, up to 5% of SAH cases may not show any signs of haemorrhage on these scans within the first 24 hours, with this figure rising to 50% by the end of the first week and remaining around 30% by the second week4.
In contrast, xanthochromia in the CSF can be detected as early as two hours after a bleed and is observed in over 90% of patients within 12 hours of an SAH event. This detection can persist for up to three to four weeks, offering a critical diagnostic window that imaging alone might miss. The conversion from haem to bilirubin in CSF takes roughly 6 to 12 hours, suggesting that xanthochromia is most reliably identified between 6- and 12-hours post-bleed. More than 75% of patients may still present with xanthochromia at 21 days following an SAH1.
Pathophysiology explained
A ruptured cerebral aneurysm will begin to leak blood into the CSF. This blood is gradually degraded by macrophages to yield various by-products including oxyhaemoglobin, which is subsequently converted to bilirubin in a process lasting between 6 and 12 hours1. Crucially, this conversion to bilirubin can only occur in vivo, providing a unique marker for diagnosing subarachnoid haemorrhage when observed in the CSF1.
The Importance of Accurate Detection
In many parts of the world, including the US, visual detection remains a common initial test for xanthochromia in CSF.
- Procedure: Spinning a CSF sample in a centrifuge and comparing the supernatant against a vial of water, held against a white backdrop to detect a yellow or pink tint.
- Indication: A change in colour indicates that blood has been present in the spinal fluid for at least two hours, with all patients showing signs by 12 hours post-bleed1.
However, this method is prone to false positives due to:
- Dietary influences: High intake of carotenoids (like carrots and spinach).
- Medication: Use of Rifampin.
- Medical conditions: Clinical jaundice or high protein levels in CSF, which can be seen in conditions like carcinomatosis and meningitis1.
Spectrophotometry
Spectrophotometry offers a more precise alternative by measuring light absorption in materials at specific wavelengths:
- It can detect the presence of bilirubin, which absorbs light at 440 to 460 nm, a definitive indicator of xanthochromia.
- Advantages over visual detection: This method eliminates the interference from other pigments or proteins and can distinguish bilirubin from oxyhaemoglobin, crucial for accurate diagnosis.
Quality control is crucial in spectrophotometry to ensure the accuracy and reliability of xanthochromia tests:
- Regular Maintenance: Routine checks and maintenance of the spectrophotometer are fundamental to its operation. This helps in maintaining the instrument’s precision in measuring light absorption at specific wavelengths crucial for detecting bilirubin in CSF.
- Calibration: Calibrating the spectrophotometer with known standards is essential. This process adjusts the instrument to measure the absorption accurately, particularly vital given bilirubin’s narrow detection window between 440 and 460 nm.
Implementing these stringent QC measures enhances the diagnostic precision of spectrophotometry, boosting confidence in the results. Such practices ensure that patients are diagnosed accurately and receive timely, appropriate treatment, solidifying the value of advanced diagnostic techniques in medical settings.
Introducing Randox Xanthochromia Controls
Diagnosing SAH swiftly and precisely is critical due to its significant immediate and long-term impacts. To aid precise detection, our Liquid Frozen Xanthochromia Positive & Negative Controls are essential tools for laboratories conducting CSF analysis. Here’s what makes them stand out:
- Dedicated Xanthochromia true third-party control with only 2 analytes for limited cross-reactivity – Bilirubin & Oxyhaemoglobin
- 2-day open vial stability at 2° to 8°C and a 11-week shelf life from date of manufacture when stored at -18ºC to -24ºC.
- Liquid frozen control provides suitable matrix in an easy-to-use format.
- Consistent, clinically significant values.
- Suitable for use with UV spectrophotometers, these controls help monitor bilirubin and oxyhaemoglobin levels effectively.
The Randox Xanthochromia Controls are ideally suited for laboratories, both public and private, as well as researchers who perform CSF analysis. Their use is crucial in ensuring the precision of SAH testing, which contributes to more accurate diagnostics and ultimately leads to better patient outcomes.
Considering the crucial role of accurate xanthochromia detection in diagnosing SAH, isn’t it time to review your lab’s capabilities? Explore how Randox Xanthochromia Controls can enhance your diagnostic processes. For more details on how to get these tools in your lab, contact us at marketing@randox.com.
In the fight against conditions like SAH, every second and every test counts. Equip your lab with Randox Xanthochromia Controls to ensure that your diagnostics are as precise and reliable as possible, helping save lives and improve healthcare outcomes.
References
-
- Dugas C, Jamal Z, Bollu PC. Xanthochromia. StatPearls Publishing; 2024. Accessed August 5, 2024. https://www.ncbi.nlm.nih.gov/books/NBK526048/
- Sehba FA, Hou J, Pluta RM, Zhang JH. The importance of early brain injury after subarachnoid hemorrhage. Prog Neurobiol. 2012;97(1):14-37. doi:10.1016/j.pneurobio.2012.02.003
- NHS. Subarachnoid haemorrhage. https://www.nhs.uk/conditions/subarachnoid-haemorrhage/.
- Chakraborty T, Daneshmand A, Lanzino G, Hocker S. CT-Negative Subarachnoid Hemorrhage in the First Six Hours. Journal of Stroke and Cerebrovascular Diseases. 2020;29(12):105300. doi:10.1016/j.jstrokecerebrovasdis.2020.105300
Routine healthcare could save billions and boost survival rates for cancer and serious diseases.
Reports show that “improvement in life expectancy have ground to a halt” and more than one in five deaths are considered “avoidable”. It warns that since the 1960 the UK has “declined from being ranked first for life expectancy among G7 countries to being ranked second last”.Ā
Dr. FitzGerald said: “This is a shameful drop of quality care, and it should be a national disgrace that our healthcare provider has failed us so badly.”
Pushing for the UK to follow the example of Japan, where the average person can expect to live more than 84 years, he said: “Japan is leading the way in healthcare testing. It has the highest life expectancy of all G7 nations, and it routinely tests for far more than we do in the UK.
“Major benefits for them have included a massive 25 per cent fall in diabetes rates among those at risk of developing the disease.”
The Office for National Statistics sounded the alarm bell about declining life expectancy in the UK earlier this year. Life expectancy at birth for men in the 2020-22 period fell by 38 weeks to 78.6 compared with 2017-2019;Ā for women, it went down by 23 weeks to 82.6 years.
There is strong concern that in Britain people are much more likely to enjoy long lives if they are better off. In 2021, there was alarm when it was reported that a man living in Kensington and Chelsea, one of the country’s richest areas, could be expected to live 27 years longer than a counterpart in Blackpool.
Dr. FitzGerald is pushing for a far more ambitious programme of testing than the health MOTs offered to people aged 40-plus on the NHS.
Claiming that the “NHS is creaking at the seams”, he said: “By investing in preventative measures, the NHS will be far more effective and therefore far better value for money for the taxpayer.”
The biochemist, who in 1982 founded his company in a converted chicken house in Crumlin in Northern Ireland, argues Britain “must do better”. He said, “Improving the health and prosperity of the nation is an important goal – and this initiative can more than pay for itself. More importantly, it will be greater than a simple money saving exercise.
It can and will save lives. It is time for government to step up and deliver for the British people. A Department for Health and Social Care spokeswoman said: “We will transform the NHS from a late diagnosis, late treatment health service, to one that catches illness earlier and prevents it in the first place. We will start by doubling the number of diagnostic scanners to help speed up diagnosis and treatment.”
Dr. FitzGerald is pushing for a far more ambitious programme of testing than the health MOTs offered to people aged 40–plus on the NHS. Claiming that the ‘NHS’ is creaking at the seems, he said: “By investing in preventative measures, the NHS will be far more effective and therefore far better value for money for the taxpayer.
“More importantly, it will be greater than simple money saving exercise.Ā It can and will save lives. It is time for the government to step up and deliver for the British people. A Department for Health and Social Care spokeswoman said: “We will transform the NHS from a late diagnosis, late treatment health service, to one that catches illness earlier and prevents it in the first place. We will start by doubling the number of diagnostic scanners to help speed up diagnosis and treatment.”
Health Secretary Wes Streeting has ordered a ‘full and independent investigation into the state of the NHS to uncover the biggest challenges facing the health service.
Words by David Williamson, The Sunday Express
Randox Health ā Optimising Performance as Official Diagnostic Health partner of Team GB for Paris 2024
Randox Healthās unique diagnostic technologies have been supporting Team GB throughout their journey to the Paris 2024 Olympic Games ā from preparation to their hard-earned success of over 40 Olympic medals and will continue to help optimise the teamās performance during the remainder of the competition.Ā
Randoxās Vivalytic diagnostics machine has been in action during Paris 2024. These fully automated, all-in-one molecular diagnostic machines are powered by Randoxās unique Biochip Technology and are capable of checking for a wide range of respiratory infections, enabling multiple test results from just one sample.
āAs a Sport and Exercise Medicine Consultant working with elite athletes, itās important we know the pathogen driving the disease process to be able to target management appropriately. With Randox supplying this useful technology in our performance environments, we can optimally manage both the athletes and wider team safely and efficiently.ā
āOur aim, along with the teams of experts assisting our athletes is simple ā to ensure that Team GB is in peak physical and mental condition as they get to the starting line.ā Dr. Lisa Hyland, who is working as a Team GB HQ Doctor
Find out how Randox Technologies help Team GB reach Olympic success with our Vivalytic Point of Care testing
Team GBās Chief Medical Officer, Niall Elliott, said that Randox was helping in three critical areas of health testing for athletes ā iron metabolism, vitamin D levels ā critical to the immune system and muscle power ā and glucose or energy levels. āIt is a fascinating journey, the testing we can do.ā
Over the last year, Randox have been working closely with Team GB brand ambassadors, to ensure they are perfectly placed to perform their utmost at the Olympic Games. Each of them have undertaken a Randox Health Everyman and Everywoman diagnostic health test package at one of the Randox Health clinics, to measure their conditions as they get to that starting line in Paris.
As one star, Duncan Scott, Team GBās most decorated Olympic swimmer, put it: āIf it makes one per cent difference itās 100% worth it.ā
āEverything you do as a swimmer is being channelled through the window of your technique but thereās external factors such as nutrition, recovery, sleep that contribute those one percents towards how youāre going to be inside the pool when it matters the most. With that in mind, I think the Randox Health Everyman check was spot on and Iām glad that Iāve done it.ā
Team GB sprinter and double Olympic medallist Daryll Neita the Everywoman test, calling it, āthe most in-depth testing Iāve ever had.ā
āItās amazing that the Everywoman test discovers things that could help my performance whether itās how I recover to deficiencies but also our sport is about marginal gains, centimetres, millimetres, the finest of margins and through tests like this, it lets you stay on-top of your health helping you achieve optimal performance or even a mental boost that youāre healthy.ā
Adds Dr. Peter FitzGerald, Founder and Managing Director of Randox Health, āAnd these technologies are not just for athletes ā our diagnostic packages and analysers are designed to make a difference to everyoneās life ā to help us make the most of all the opportunities life has to offer.ā
Lipoprotein (a): Molar or Mass?
Lipoprotein (a): Molar or Mass?
Lipoprotein (a) was first identified in 1963. However, it’s been in the last decade we’ve seen significant advances in our understanding of this ambiguous molecule and its relationship with cardiovascular disease (CVD) risk.
Lp(a) is a macromolecular lipoprotein complex1 which is thought to display proatherogenic, proinflammatory2 and prothrombotic3 potential and is considered an independent causal risk factor for various types of CVD4. These properties provide several mechanisms in which elevated Lp(a) levels may contribute to CVD however the true nature of Lp(a)’s relationship to CVD remains largely enigmatic.
Although some of the first studies failed to find a causal relationship, advances in quantification methods soon led to data which showed this relationship did in fact exist. It has been shown that those with the highest levels of Lp(a) are at a 1.5x increased risk of cardiovascular-related death, 1.6x risk of stroke, and up to 4x risk of heart attack when compared with those with the lowest levels5.
Accurate measurement of Lp(a) is crucial in determining CVD risk. Quantification methods which account for the size-related variability of Lp(a) molecules are known to produce less bias when compared with those which do not. The Randox Lp(a) reagent is based on the Denka Seiken method which has been shown to produce minimal size-related bias. This assay has FDA 510(K) clearance, illustrating its reliability and safety. Furthermore, the Randox Lp(a) assay is reported in nmol/L, is traceable to the WHO/IFCC reference material, and provides acceptable bias compared with the Northwest Lipid Metabolism Diabetes Research Laboratory (NLMDRKL) gold standard method.
Physiology and Genetics
Synthesised mainly in the liver, Lp(a), like Low-density lipoprotein (LDL) cholesterol, is composed of a lipid centre made of cholesteryl esters and triacylglycerols, surrounded by a shell of phospholipids, free cholesterol, and an apoB-100 molecule. The major difference between other LDL cholesterol molecules and Lp(a) is the presence of a polymorphic glycoprotein, apo(a), bound to apoB-100 by a single disulphide bond5. It is this apo(a) molecule which contributes to Lp(a)’s pathophysiology.
Apo(a) is thought to have evolved from the plasminogen gene (PLG) around 40 million years ago and shares 78-100% sequence homology within the untranslated and coding regions of the fibrinolytic enzyme1. Like plasminogen, apo(a) contains unique domains named kringles4. While plasminogen contains 5 different kringle structures (KI to KV), apo(a) has lost KI through KIII and instead contains several forms of KIV, namely, 1 copy of KIV1 and KIV3-10, 1-40 copies of KIV2, 1 copy of KV and an inactive protein domain at the carboxyl terminus of the molecule7. These hydrophilic subunits are highly polymorphic due to the variation in KIV2 repeats.
Individuals may possess two different isoforms of apo(a), one of which will have been passed down from each parent, that are expressed codominantly1. These isoforms are dependent on the number of KIV2 repeats they contain2. Isoforms with less KIV2 repeats produce smaller apo(a) isoforms which are found at a higher concentration compared with larger isoforms6 due to the increased rate at which the smaller molecules can be synthesised4. The polymorphisms in KIV2 repeats account for up to 70% of the variation seen in concentration between individuals, with the remainder being attributed to differences in protein folding, transport, and single nucleotide polymorphisms (SNPs)4. SNPs are central in the heterogeneity of apo(a), effecting RNA splicing, nonsense mutations and 5’ untranslated region of the LPA gene resulting in shorter gene translation4,6.
Mass versus Molar?
The quantification of Lp(a) levels is essential in evaluating CVD risk, yet the units of measurement—mass (mg/dL) versus molar (nmol/L) – play a critical role in the accuracy and reliability of these assessments. Historically, Lp(a) levels have been expressed in mass units (mg/dL), but recent advances advocate for the use of molar units (nmol/L) due to their ability to account for molecular variability7.
Mass measurement of Lp(a) quantifies the total mass of Lp(a) particles in a given volume of blood, expressed in milligrams per decilitre (mg/dL). This method has been widely used and aligns with other lipid measurements such as cholesterol and triglycerides8. However, it does not account for the significant variability in the size and composition of Lp(a) particles. This can result in an overestimation of Lp(a) concentration in those with large apo(a) isoforms, and conversely underestimation of concentrations in patients with small apo(a) isoforms9. Consequently, two individuals with the same mass concentration of Lp(a) may have vastly different particle numbers and sizes, leading to potential discrepancies in risk assessment10.
In contrast, molar measurement expresses the concentration of Lp(a) particles in terms of their molar quantity, measured in nanomoles per litre (nmol/L). This approach provides a more accurate reflection of the number of Lp(a) particles present, irrespective of their size11. By focusing on particle count rather than mass, molar measurement offers a standardised and minimally biased method that better accounts for the heterogeneity of Lp(a) particles12.
The conversion between mass and molar units is not straightforward due to the variability in the molecular weight of Lp(a) particles. A commonly used conversion factor is approximately 2.5, meaning 1 mg/dL of Lp(a) is roughly equivalent to 2.5 nmol/L13. However, this factor can vary depending on the specific characteristics of the Lp(a) particles in a given sample. For this reason, converting between units is discouraged by various relevant organisations including the European Atherosclerosis (EAS)6.
Clinical guidelines and risk assessments have traditionally been based on mass concentrations, but the shift towards molar units is gaining traction. The Randox Lp(a) assay, which reports in nmol/L and is traceable to the WHO/IFCC reference material, exemplifies this trend. This assay not only provides a more accurate measurement but also aligns with the NLMDRKL gold standard method, ensuring minimal size-related bias14.
The choice between mass and molar measurements has significant clinical implications. Accurate assessment of Lp(a) levels is crucial for identifying individuals at risk of CVD and implementing appropriate interventions. As the understanding of Lp(a) continues to evolve, the adoption of molar measurement is expected to enhance the precision and reliability of Lp(a) testing, ultimately improving patient outcomes.
Randox Lp(a) Reagent
For the reasons above, the European Atherosclerosis Society (EAS) recommends that Lp(a) measurement is of the particles (molar) rather than the total mass, to provide a result with minimal size-related bias.
The Randox Lp(a) assay has FDA 510(K) clearance and is one of the only methodologies on the market that detects the non-variable part of the Lp(a) molecule and therefore suffers minimal size related bias providing more accurate and consistent results. The Randox Lp(a) kit is standardised to the WHO/IFCC reference material, SRM 2B, and is the closest in terms of agreement to the ELISA reference method. We also provide a five-point calibrator with accuracy-based assigned target values which accurately reflects the heterogeneity of isoforms present in the general population. Applications are available for a wide range of biochemistry analysers which details instrument-specific settings for the convenient use of the Randox Lp(a) assay on a variety of systems. Measuring units in nmol/L are available upon request.
Features
- Excellent Correlation and Precision: The Randox Lp(a) assay demonstrates excellent performance, evidenced by a correlation coefficient of r=0.995 when compared with other commercially available methods and a within-run precision of less than 2.54%.
- 510(K) Cleared: Randox’s Lp(a) assay has received FDA 510(k) clearance, signifying its safety and effectiveness and ensuring healthcare professionals can trust its accurate and reliable cardiovascular risk assessments.
- Dedicated Five-Point Calibrator Available: Five-point calibrator with accuracy-based assigned target values (in nmol/l) is available, accurately reflecting the heterogeneity of the apo(a) isoforms. Dedicated Lp(a) control is available offering a complete testing package.
- WHO/IFCC Reference Material: The Randox Lp(a) assay is reported in nmol/l and traceable to the WHO/IFCC reference material (IFCC SRM 2B) and provides an acceptable bias compared with the Northwest Lipid Metabolism Diabetes Research Laboratory (NLMDRKL) gold standard method.
- Applications Available: Applications are available detailing instrument-specific settings for the convenient use of the Randox Lp(a) assay on a wide range of clinical chemistry analysers.
- Liquid Ready-To-Use: The Randox Lp(a) assay is available in a liquid ready-to-use format for convenience and ease-of-use.
One study15 compared 5 commercially available Lp(a) assays on an automated clinical chemistry analyser. The assays tested were manufactured by Diazyme, Kamiya, MedTest, Roche, and Randox. The authors show that all the assays tested met the manufacturers claims for sensitivity, linearity, and precision. However, significant bias was observed in 4 out of 5 assays. The only assay which did not display significant bias was the Randox Lp(a) Assay which is traceable to WHO/IFCC reference material. This report highlights the importance of measuring and reporting Lp(a) in molar concentration rather than in mass units to facilitate standardisation and harmonisation in Lp(a) testing15.
Conclusions
In conclusion, understanding and accurately measuring Lp(a) is crucial for assessing CVD risk. Despite its enigmatic nature, recent advancements have clarified Lp(a)’s role as a significant independent risk factor for CVD. The shift from mass to molar measurement units is enhancing the precision and reliability of Lp(a) assessments, with the Randox Lp(a) assay leading the way in providing minimal size-related bias and accurate results.
To ensure the most accurate and reliable assessment of your patients’ cardiovascular risk, consider integrating the Randox Lp(a) assay into your diagnostic toolkit. With its FDA 510(k) clearance, traceability to WHO/IFCC reference material, and high precision, the Randox Lp(a) assay is an essential component for any modern clinical laboratory.
Integrate the Randox Lp(a) assay into your practice today to enhance the precision of your cardiovascular risk evaluations.
References
- Schmidt K, Noureen A, Kronenberg F, Utermann G. Structure, function, and genetics of lipoprotein (a). J Lipid Res. 2016;57(8):1339-1359. doi:10.1194/jlr.R067314
- Zafrir B, Aker A, Saliba W. Extreme lipoprotein(a) in clinical practice: A cross sectional study. International Journal of Cardiology Cardiovascular Risk and Prevention. 2023;16:200173. doi:10.1016/j.ijcrp.2023.200173
- Dal Pino B, Gorini F, Gaggini M, Landi P, Pingitore A, Vassalle C. Lipoprotein(a), Cardiovascular Events and Sex Differences: A Single Cardiological Unit Experience. J Clin Med. 2023;12(3):764. doi:10.3390/jcm12030764
- Stürzebecher PE, Schorr JJ, Klebs SHG, Laufs U. Trends and consequences of lipoprotein(a) testing: Cross-sectional and longitudinal health insurance claims database analyses. Atherosclerosis. 2023;367:24-33. doi:10.1016/j.atherosclerosis.2023.01.014
- Scheel P, Meyer J, Blumenthal R, Martin S. Lipoprotein(a) in Clinical Practice. Latest in Cardiology. Published online July 2, 2019. Accessed March 22, 2024. https://www.acc.org/Latest-in-Cardiology/Articles/2019/07/02/08/05/Lipoproteina-in-Clinical-Practice
- Kronenberg F, Mora S, Stroes ESG, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur Heart J. 2022;43(39):3925-3946. doi:10.1093/eurheartj/ehac361
- Kronenberg F. Lipoprotein(a) measurement issues: Are we making a mountain out of a molehill? Atherosclerosis. 2022;349:123-135. doi:10.1016/j.atherosclerosis.2022.04.008
- Scharnagl H, Stojakovic T, Dieplinger B, et al. Comparison of lipoprotein (a) serum concentrations measured by six commercially available immunoassays. Atherosclerosis. 2019;289:206-213. doi:10.1016/j.atherosclerosis.2019.08.015
- Tsimikas S. A Test in Context: Lipoprotein(a). J Am Coll Cardiol. 2017;69(6):692-711. doi:10.1016/j.jacc.2016.11.042
- Kamstrup PR. Lipoprotein(a) and Cardiovascular Disease. Clin Chem. 2021;67(1):154-166. doi:10.1093/clinchem/hvaa247
- Langsted A, Kamstrup PR, Nordestgaard BG. High lipoprotein(a) and high risk of mortality. Eur Heart J. 2019;40(33):2760-2770. doi:10.1093/eurheartj/ehy902
- Afshar M, Rong J, Zhan Y, et al. Risks of Incident Cardiovascular Disease Associated With Concomitant Elevations in Lipoprotein(a) and Low‐Density Lipoprotein Cholesterol—The Framingham Heart Study. J Am Heart Assoc. 2020;9(18). doi:10.1161/JAHA.119.014711
- Zheng W, Chilazi M, Park J, et al. Assessing the Accuracy of Estimated Lipoprotein(a) Cholesterol and Lipoprotein(a)‐Free Low‐Density Lipoprotein Cholesterol. J Am Heart Assoc. 2022;11(2). doi:10.1161/JAHA.121.023136
- Madsen CM, Kamstrup PR, Langsted A, Varbo A, Nordestgaard BG. Lipoprotein(a)-Lowering by 50 mg/dL (105 nmol/L) May Be Needed to Reduce Cardiovascular Disease 20% in Secondary Prevention. Arterioscler Thromb Vasc Biol. 2020;40(1):255-266. doi:10.1161/ATVBAHA.119.312951
- Wyness SP, Genzen JR. Performance evaluation of five lipoprotein(a) immunoassays on the Roche cobas c501 chemistry analyzer. Pract Lab Med. 2021;25:e00218. doi:10.1016/j.plabm.2021.e00218
Blood test for over-40s could save the economy Ā£12bn a year if offered on NHS – OCO report
The NHS currently offers health MOTs to patients aged 40 to 75. However, the five-yearly check is normally limited to blood pressure and cholesterol, along with height, weight and waist measurements.
Diagnostic firms sell private blood tests which can check for 200 types of disease, including most common cancers.
A report by OCO Global, an independent consultancy firm, says that if the NHS provided these more comprehensive health checks, problems would be detected far earlier, ultimately saving lives and money.
The research, which has been sent to Wes Streeting, the Health Secretary says that although each check would cost around Ā£230 – a bill for the NHS of around Ā£650 million a year – they would reap major rewards.
Modelling suggests that, after 16 years, the annual boost to the economy would amount to Ā£11.7 billion – Ā£1.83 billion in treatment costs, around Ā£5.8 billion wider savings from health improvements and an indirect benefit of Ā£4 billion – based on the assumption that around half of people take up the tests.
The report was commissioned by Randox, the UK’s biggest diagnostics firm, which carried out millions of PCR tests during the Covid-19 pandemic.
It claims that the blood testās 200 data points would enable far earlier diagnosis, similar to an approach in countries such as Japan and South Korea, where the checks are mandatory and linked to health insurance.
In Japan, which has the highest life expectancy of all G7 nations, such checks have seen a 25 per cent fall in diabetes rates, among those suffering from pre-diabetes rates, among those suffering from pre-diabetes.
The report highlights the intense pressures on the NHS, with waiting list of more than seven million, and 185 million working days lost to sickness every year.
“For too long the UK has been behind the curve on health testing, with less testing carried out than any other developed country. This means that serious diseases are detected too late, with the consequence of more cost for the NHS, more suffering for the patient, and often premature death.ā David Davis, former chairman of the Commons Public Accounts Committee
āImproving the health and prosperity of the nation is a lofty goal – and the report shows this initiative can more than pay for itself.āDr Peter FitzGerald, Randoxās managing director
Words by Laura Donnelly, The Telegraph
Read full article here: https://www.telegraph.co.uk/news/2024/08/04/nhs-cancer-blood-test-save-12bn-research/