Medical Laboratory Professionals Week 2024

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Medical Laboratory Professionals Week 2024

Med Lab Professional Week 2024 - blog header

Medical Laboratory Professionals Week (MLPW) is recognised every year in the last full week of April. It’s an opportunity to increase the public understanding of, and appreciation for, the hard work of clinical laboratory staff around the world. It’s also an opportunity to inject a little fun into the laboratory. So, this year, we’ve created a Lab Professionals QC Bingo card. Have a go and see how many your laboratory can get!

How many boxes does your lab tick?

Medical Lab Professionals QC Bingo

If you’re calling Bingo! you must be an Acusera 24.7 customer. If not, keep reading to find out how you can make daily life in your laboratory more straightforward.

What are Medical Laboratory Professionals?

Medicine wouldn’t be where it is today without the work of these laboratory professionals. They’re on the frontline. Around 70% of medical decisions are based on results provided by medical laboratory staff. That’s a lot of pressure on the labs to make sure their results are accurate. Clinical laboratory staff not only perform the tests used to guide diagnosis and disease prevention, but they also check all the tests they use through rigorous quality control (QC) procedures.

This involves testing samples of known values to prove that the test system and its components perform as they should and provide accurate results. To do this, laboratories require QC material. It’s important that what’s in a QC is as similar to what you’d find in a patient sample as possible. This is known as commutability. Good commutability helps limit cross-reactivity in the test and inaccurate results.

It’s also important to make sure the QC material has concentrations of analytes at similar values to those used to make diagnostic decisions. If you wanted to validate the length of the ruler on your desk, it wouldn’t be helpful to set it down on a 100m running track. Similarly, when laboratory professionals want to ensure a test is producing accurate results, they want to test the system at the critical values used to make medical decisions so that they can be confident the results at these values are accurate.

Once lab staff have confirmed the accuracy of their tests, they can begin testing patient samples. For most people, what happens to a sample after it’s taken is a bit of a mystery. MLPW is the perfect opportunity to unravel this a little:

After your sample is collected, it gets sent over to the lab. Even just moving it there needs careful handling to make sure it’s still good for testing when it arrives. Once it’s in the lab, the team checks the equipment to make sure it’s working right and giving accurate results. The QC procedure varies depending on what they’re testing for, but they always make sure their tests are legitimate. Once they’ve checked everything and carried out the tests, a pathologist looks at the results to figure out what’s going on. They use this information to help decide on the best treatment plan for you.

Even this watered-down explanation makes it sound like a lot of work, right? At Randox, we recognise the vital role and dedicated efforts of medical laboratory professionals, and the invaluable contributions they make to society, and we hope that now, you do too.

Acusera 24.7

Bingo! That’s exactly how our customers feel when they realise how much time Acusera 24.7 can save them. Our innovative and intuitive QC data software is cloud-based, allowing you to log in from anywhere in the world to review your QC data.

Along with a wide range of interactive charts, including Levey-Jennings charts, Acusera 24.7 determines measurement uncertainty and sigma metrics for you, saving you the time and stress of manually calculating these tricky statistical analyses. And that’s just the beginning. Acusera 24.7 can link to LIMS for  automated data entry, meaning lab staff don’t have to manual type long datasets, unless they want to of course; we also provide both semi-automated data upload and manual data entry options.

Access to a range of reports has never been easier. Acusera 24.7 is particularly useful when gaining or renewing your accreditation, and live peer group QC data, to give additional confidence in the accuracy of your results.

But this article is supposed to be about laboratory professionals, so we won’t bang on about it anymore. We just want everyone to know about Acusera 24.7 so they can get that daily bingo! feeling for themselves. If you want to learn more about our reports, charts, advanced statistical analysis, Acusera 24.7 more generally, or how Acusera 24.7 can help you achieve your accreditation, you can follow the links to the relevant blog post.

Last year, we interviewed two of our laboratory staff, Dean and Meadhbh, to find out what a normal day looked like for them. To find out what a day in the life of a laboratory professional is like, take a look at the interviews here

If you’d like to get in touch with us to discuss the advantages of Acusera 24.7, or you’ve made up your mind and want to get in on the action, reach out to us at We’re always happy to brag about how great Acusera 24.7 is, and how we make life simpler for more and more laboratories every day.

Lp(a) Awareness Day 2024

Lp(a) Awareness Day

Novel and classical insights into Lp(a) concentration and the effects on various cardiovascular conditions.

Despite advances in understanding and technology, cardiovascular diseases (CVDs) remain a major source of mortality across the world. The World Health Organisation (WHO) estimate that 17.9 million people died due to CVDs in 2019, accounting for around 32% of deaths that year1. First described in 1963, Lipoprotein(a) (Lp(a)) is a macromolecular lipoprotein complex2 which is thought to display proatherogenic, proinflammatory3 and prothrombotic4 potential and is considered an independent causal risk factor for various types of CVD5. 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.

Lp(a) concentrations in plasma are principally regulated by variation in LPA gene and levels remain relatively stable throughout one’s lifetime with lifestyle factors having little effect on their concentration6. Due to the highly heritable nature of Lp(a) concentration, those with a family history of Familial Hypercholesterolaemia (FH), elevated LDL-C levels, or Atherosclerotic cardiovascular disease (ASCVD) should be screened, their plasma Lp(a) concentration determined, and their risk of CVD established.

In the last 10 years, there have been many advances in the understanding of this ambiguous lipoprotein which support the causal association with CVD, clarify the established evidence and introduce novel mechanisms of action in relation to Lp(a), shedding light on its obscure pathophysiology. However, there are still diagnostic complications associated with Lp(a) measurement as there is little standardisation in methods of determination5.

Physiology and Genetics

Synthesised mainly in the liver, Lp(a), like LDL, 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 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 enzyme2. Like plasminogen, apo(a) contains unique domains named kringles5. While plasminogen contains 5 different kringle structures (KI to KV), apo(a) has lost KI to 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 and are expressed codominantly2. 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 isoforms8 due to the increased rate at which the smaller molecules can be synthesised5. 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)5. 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 translation5,8.

Lp(a) vs LDL-C

Lp(a) Pathophysiology

Lp(a) is thought to contribute to the risk of CVD through multiple mechanisms. Firstly, Lp(a) molecules display all the same atherosclerotic risk as LDL-C molecules due to their similar fundamental composition, for example, their propensity for oxidisation upon entering the vessel wall, and promotion of atherosclerosis through inflammatory and immunogenic mechanisms 9. However, Lp(a) displays more proatherogenic potential due to the presence of the apo(a) molecule. The structure of apo(a) results in decreased fibrinolysis. Due to its structural similarities, apo(a) competes with plasminogen for binding sites, competitively inhibiting plasminogen, ultimately resulting in reduced fibrinolysis9.

Lp(a) is thought to be a preferential carrier of oxidised phospholipids2 (OxPLs) which covalently bind to apo(a), increase expression of inflammatory proteins, and stimulate the secretion of IL-8 and monocyte chemoattractant protein-1, enhancing its ability to cross the vessel wall9. Some claims require further investigation, however, studies have been carried out which show inhibition of plasminogen activation in the presence of Lp(a)10. It is this indirect mechanism that Lp(a) is thought to conduct its prothrombotic activity8,9.

Clinical Evidence

Many studies have been carried out to determine the association of Lp(a) concentration and CVD risk. Studies such as the Copenhagen General Population Study, the Copenhagen City Heart Study, Dallas Heart Study, and Ischemic Heart Disease Studies provide strong evidence for Lp(a) as a causal risk factor for CVD. Data analysis of the Copenhagen General Population Study reveal that 20% of subjects displayed Lp(a) concentrations of more than 42mg/dl, or around 105nmol/L11, which is considered to result in increased risk of atherosclerotic disease5. It is important to note, there is no accepted conversion factor for converting Lp(a) concentration from mg/dl to nmol/L due to the variability of apo(a) kringles. The unitage will depend on the assay method used5. Another study in a healthcare organisation in Israel showed that Myocardial Infarction (MI) and Coronary Artery Disease was 2.5 times more common in those with high levels of Lp(a) than in the age and sex matched control group3. This study3, along with others5,6,12 describes a linear relationship between Lp(a) concentration and CVD risk, showing at least a 3-fold increase in ASCVD and MI events in adults with Lp(a) concentrations in the top 1% when compared with those in the with concentrations in the bottom 20%3.

The major variation in Lp(a) concentration seen throughout the population, is further evident between ethnicities and sexes. On average, Caucasian subjects display the lowest Lp(a) concentrations, with Black subjects displaying the highest concentrations5. However, the large number of functional variants are consistent across ethnicities suggesting that it is the KIV2 repeats and SNPs that are the major factors contributing to Lp(a) concentration regardless of ethnicity. Lp(a) concentrations are higher in women than men8 with levels increasing post-menopause thought to be caused by a decrease in oestrogen3.

Lp(a) Testing and Screening

The European Atherosclerosis Society (EAS) recommend that all adults are tested at least once in their lifetime to identify individuals who have high levels of Lp(a) and therefore high CVD risk. Screening is also recommended in children who have a family history of Ischaemic stroke, premature ASCVD or high Lp(a) levels in the absence of other identifiable risk factors8. Testing has been associated with reduced mortality rates. This is thought to be because of increased and intensified therapy for those who are identified as high risk due to high plasma Lp(a) concentration6.

There are various assays available for the determination of Lp(a) concentration which vary in accuracy and precision. Many of these assays utilise polyclonal antibodies which recognise different antigenic determinants8. Due to the variability in apo(a) structure and KIV repeats, these assays often overestimate the concentration of large isoforms and underestimate concentration of small isoforms when determining the true Lp(a) levels9. This variation can be partially nullified by using a calibrator series and by selecting a method which is traceable to WHO/IFCC reference material. This allows laboratories to confidently identify individuals considered high risk but may still prove problematic when patients’ results report closer to the assay thresholds.

One study13 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) testing13.

Current and Emerging Therapies

Statins are one of the most potent treatments for the primary prevention of ASCVD through the reduction of LDL-C concentration. However, recent studies reveal that statins have no effect on Lp(a) concentration3 and others suggest that statin administration can increase Lp(a) concentration by up to 11%5,9. Nonetheless, EAS do not recommend statin therapy be halted as their strong ameliorative effects on CVD risk are well established and surmount the risk related to increased Lp(a) concentration8.

Niacin (Nicotinic acid) is another established treatment for the reduction of CVD events and act by increasing HDL levels. Niacin can reduce Lp(a) concentration though the reduction of gene expression in a dose-dependent manner5. However, Niacin therapy has not been proven to have beneficial effects on CVD risk8.

A recent metanalysis showed a 26% reduction in serum Lp(a) concentration through treatment with PCSK9 inhibitors. This is thought to be due to a shortage of apoB-100 molecules either because of reduced synthesis or competitive binding with other LDL receptors, resulting in reduced Lp(a) concentration5. Several studies show the efficacy of PCSK9 inhibitors in reducing CVD risk, but this is not yet an approved therapy5,8.

New therapeutic strategies aim to target hepatocytes, the site of apo(a) synthesis, to reduce Lp(a) concentration. Antisense Oligonucleotides (ASOs) inhibit apo(a) mRNA in the nucleus and cytoplasm, ultimately inhibiting Lp(a) secretion5 through the cleavage of the sense strand by ribonuclease H19. While still in clinical trials, ASO therapies show promise in the battle to reduce CVD risk with some studies displaying an overall reduction in Lp(a) concentration of more than 80%9.


There have been major advances in the understanding of Lp(a) pathophysiology in the last 10 years establishing this macromolecular complex as an independent causal risk factor for various forms of CVD, however, more investigation is required to fully understand the mechanisms responsible for this association. With many national healthcare organisations and the EAS recommending universal testing for Lp(a) in adults, more emphasis should be placed on raising awareness of the importance of Lp(a) screening. Finally, more research is needed into therapies which succeed at lowering Lp(a) concentration. While some therapies are in clinical trials, there are currently no approved therapies that achieve this goal.

The Randox Lp(a) assay is calibrated in nmol/L, traceable to the WHO/IFCC reference material, and displays an excellent correlation coefficient of r=0.995 with when compared with other commercially available methods. To accompany this liquid ready-to-use reagent we also offer a dedicated 5 point calibrator with accuracy-based assigned target values (in nmol/l) is available, accurately reflecting the heterogeneity of the apo(a) isoforms.

For more information on this revolutionary assay, visit or reach out to us at


  1. World Health Organization. Cardiovascular Diseases. World Health Organization. Published June 11, 2021.
  2. Schmidt K, Noureen A, Kronenberg F, Utermann G. Structure, function, and genetics of lipoprotein (a). Journal of Lipid Research. 2016;57(8):1339-1359. doi:
  3. 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:
  4. Pino BD, Gorini F, Gaggini M, Landi P, Pingitore A, Vassalle C. Lipoprotein(a), Cardiovascular Events and Sex Differences: A Single Cardiological Unit Experience. Journal of Clinical Medicine. 2023;12(3):764. doi:
  5. 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:
  6. Lampsas S, Xenou M, Oikonomou E, et al. Lipoprotein(a) in Atherosclerotic Diseases: From Pathophysiology to Diagnosis and Treatment. Molecules. 2023;28(3):969. doi:
  7. Vuorio A, Watts GF, Schneider WJ, Tsimikas S, Kovanen PT. Familial hypercholesterolemia and elevated lipoprotein(a): double heritable risk and new therapeutic opportunities. Journal of Internal Medicine. 2019;287(1):2-18. doi:
  8. Kronenberg F, Mora S, Stroes ESG, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. European Heart Journal. 2022;43(39):3925-3946. doi:
  9. Tsimikas S. A Test in Context: Lipoprotein(a): Diagnosis, Prognosis, Controversies, and Emerging Therapies. Journal of the American College of Cardiology. 2017;69(6):692-711. doi:
  10. Boffa MB, Koschinsky ML. Lipoprotein (a): truly a direct prothrombotic factor in cardiovascular disease? Journal of Lipid Research. 2016;57(5):745-757. doi:
  11. Enkhmaa B, Anuurad E, Berglund L. Lipoprotein (a): impact by ethnicity and environmental and medical conditions. Journal of Lipid Research. 2016;57(7):1111-1125. doi:
  12. Svilaas T, Klemsdal TO, Bogsrud MP, et al. High levels of lipoprotein(a) – assessment and treatment. Tidsskrift for Den norske legeforening. Published online January 12, 2023. doi:
  13. Wyness SP, Genzen JR. Performance evaluation of five lipoprotein(a) immunoassays on the Roche cobas c501 chemistry analyzer. Practical Laboratory Medicine. 2021;25:e00218. doi:

World Tuberculosis Day 2024

World Tuberculosis Day

Tuberculosis in Brief

When we think of Tuberculosis (TB) we tend to think of an old-timey disease. Doc Holliday, the famous gunslinger, died of consumption, the old-world name for TB. As did Fantine from Victor Hugo’s “Les Misérables” and Nicole Kidman’s, Santine, in the 2001 movie, Moulin Rouge! For the videogame fans out there, you might be familiar with Arthur Morgan from Red Dead Redemption 2 who, depending on how you played the game, may have suffered a similar fate. However, this disease is still prevalent around the world today. TB is a bacterial infection caused by Mycobacterium tuberculosis estimated to infect around 10 million people and is responsible for up to 1.5 million deaths each year1.

Originally discovered in 1882, M. tuberculosis is an airborne pathogen which primarily affects the lungs but can also affect other parts of the body2. TB infection exists in 3 states: latent, subclinical, and active. A latent TB infection is asymptomatic and non-transmissible. Subclinical infections are also asymptomatic but transmissible and will produce a positive culture. Finally, active disease is a transmissible state associated with the symptoms of TB2. The World Health Organization (WHO) estimates that around ¼ of the world population is infected with M. tuberculosis3. Up to 15% of those infected with TB will progress to active disease, while those who do not are at a heightened risk of infection throughout the rest of their lives4. Compared with some other bacterial diseases, TB is not particularly infectious. An infected individual is estimated to infect between 3-10 people per year2. However, subclinical TB infections present a challenge in reducing transmission because asymptomatic individuals may unknowingly spread the disease – over 1/3 of TB infections are never formally diagnosed5.

The symptoms of an active TB infection include fever, fatigue, lack of appetite, weight loss, and where the infection effects the lungs, a persistent cough and haemoptysis (coughing up blood). HIV-infection is a major risk factor for TB infection and mortality. Up to 12% of all new cases and 25% of TB deaths occur in HIV-positive persons2. Other risk factors for the development of TB are, malnutrition, poor indoor air quality, Type 2 diabetes, excessive alcohol consumption and smoking1.

TB is present around the world. However, as you might expect from the risk factors, low-to-middle income and developing countries account for a disproportionate number of cases. According to WHO, half of all TB infections are found in 8 countries: Bangladesh, China, India, Indonesia, Nigeria, Pakistan, Philippines, and South Africa.

Without effective treatment, TB will kill and estimated 50% of those infected2. Treatment for TB typically involves first-line antibiotics such as isoniazid, rifampicin, pyrazinamide, and ethambutol, with second-line drugs including fluoroquinolones and injectable aminoglycosides6. Nonetheless, drug-resistant TB accounts for an inordinately large amount of the global AMR burden which can arise from both transmitted and acquired resistance. Resistant M. tuberculosis strains are classified as monoresistant – those resistant to 1 drug; multi-drug resistant (MDR) – those resistant to 2 or more first line treatments, commonly isoniazid and rifampicin; and extensively drug resistant (XDR) – MDR strains which are also resistant to second line therapies like fluoroquinolones and aminoglycosides6.

Global rates of TB have been declining. An estimated 75 million lives have been saved since 20001. Furthermore, between 2015 and 2020, TB incidence fell by 13.5%7. However, the progress made over the last decade has been compromised by the COVID-19 pandemic, illustrated by a, 18% drop in diagnosis between 2019 and 20207. Explanations for this decline include delayed treatment because of lack of access to public transport and healthcare facilities, disruption of laboratory services, a personal desire to avoid the stigma of disease and misdiagnosis due to the similarities in symptoms between TB and COVID-19.

The theme for World Tuberculosis Day 2024 is “Yes, we can end TB!” The WHO have set targets of an 80% decline in new cases and a 90% drop in TB-related deaths by 2030. Screening and preventative treatments are crucial to achieving these goals. Therefore, novel methods of detection which are quick, inexpensive and include drug resistance identification are needed.

Mycobacterium Tuberculosis EQA

It is important for those carrying out TB testing to ensure their instruments and methods are accurate and effective. External Quality Assessment (EQA) programmes are an essential part of this process. QCMD is an independent international EQA organisation primarily focused on molecular infectious diseases to over 2000 participants in over 100 countries.

QCMD offers 2 programmes for those testing for TB through molecular methods: Mycobacterium tuberculosis DNA and Mycobacterium Tuberculosis Drug Resistance.

Mycobacterium tuberculosis DNA EQA Programme

Mycobacterium tuberculosis DNA EQA Programme

Mycobacterium Tuberculosis Drug Resistance EQA Programme

Mycobacterium Tuberculosis Drug Resistance EQA Programme

Mycobacterium Tuberculosis Quality Controls

Those conducting research into TB infections and new methods of detection, screening and drug resistance profiling need to be confident that the equipment they are using is up to the task. Qnostics is a leading provider of Quality Control solutions for molecular infectious disease testing. Our range comprises hundreds of characterised viral, bacterial, and fungal targets covering a wide range of diseases.

Q Controls

Our range of positive run, whole pathogen, third party controls are designed to monitor assay performance on a routine basis. As true third-party controls, assay drift is detected, monitored, and managed, helping to ensure accurate and reliable results. The use of third-party controls will also help to support ISO 15189:2012 regulatory requirements.

Mycobacterium tuberculosis (MTB) Q Control 01

Target Pathogen – Mycobacterium tuberculosis (MTB)

Matrix – Synthetic Sputum

Stability – Single use control designed to be used immediately minimising the risk of contamination

Shelf Life – Up to 2 years from date of manufacture

Regulatory Status – Research Use Only

Mycobacterium tuberculosis (MTB) Q Control 01

Mycobacterium tuberculosis (MTB) Rifampicin Resistant Q Control

Compatible for use with Cepheid analysers, this whole pathogen positive control is designed to monitor the performance of molecular assays used in the detection of Rifampicin resistant Mycobacterium tuberculosis.

Target Pathogen – Mycobacterium tuberculosis (MTB)

Target Genotype – Rifampicin Resistance

Matrix – Synthetic Sputum

Stability – Single use control designed to be used immediately minimising the risk of contamination

Shelf Life – Up to 2 years from date of manufacture

Regulatory Status – Research Use Only

Mycobacterium tuberculosis (MTB) Rifampicin Resistant Q Control

Mycobacterium tuberculosis (MTB) Evaluation Panel Control

QNOSTICS Evaluation Panels cover a range of genotypes and/or levels, and may be used to evaluate assay characteristics, confirm performance claims, and ultimately ensure the assay is fit for purpose. Evaluation Panels may also be used in the validation of clinical assays and the development of new diagnostic tests.

This dedicated MTB Evaluation Panel comprises 3 targets relating to Mycobacterium tuberculosis for validating a new assay or instrument to ensure that everything is working as expected. High and medium concentrations are provided alongside a negative sample.

Target Pathogens – MTB, M. bovis, Rifampicin (Rif) resistant MTB, Isoniazid (INH) resistant MTB, Negative

Matrix – Synthetic Sputum

Panel Members – 8 (Including a negative)

Stability – Single use. Once thawed, use immediately

Shelf Life – up to 2 years from date of manufacture

Regulatory Status – Research Use Only

Mycobacterium tuberculosis (MTB) Evaluation Panel Control

If you are interested in any of the TB quality control products shown above, or any other products from our wide catalogue of molecular controls and EQA programmes, get in touch with us today at To learn more, see the links below which will take you to the relevant sites and brochures.

QNOSTICS Brochure Download


QCMD Brochure Download


  1. World Health Organisation. Tuberculosis. Fact Sheets. Published November 7, 2023. Accessed March 21, 2024.
  2. Pai M, Behr MA, Dowdy D, et al. Tuberculosis. Nat Rev Dis Primers. 2016;2(1):16076. doi:10.1038/nrdp.2016.76
  3. World Health Organisation. Tuberculosis.
  4. Andrews JR, Noubary F, Walensky RP, Cerda R, Losina E, Horsburgh CR. Risk of Progression to Active Tuberculosis Following Reinfection With Mycobacterium tuberculosis. Clinical Infectious Diseases. 2012;54(6):784-791. doi:10.1093/cid/cir951
  5. Adigun R, Singh R. Tuberculosis. StatPearls Publishing; 2024.
  6. Liebenberg D, Gordhan BG, Kana BD. Drug resistant tuberculosis: Implications for transmission, diagnosis, and disease management. Front Cell Infect Microbiol. 2022;12. doi:10.3389/fcimb.2022.943545
  7. World Health Organisation. Global Tuberculosis Report 2022.; 2022. Accessed March 21, 2024.


A Peculiar Problem in Pregnancy and the Placenta

Complications and Diagnosis of Pre-eclampsia

When we consider our most important organ its intuitive to choose the heart, the lungs or even the kidneys. However, there’s another without which none of us would be here to have the discussion. This ephemeral organ provides us with the nutrients necessary for development, removes malevolent agents, provides our initial immunity and much more, before being cast off as we enter the world. We are, of course, talking about the placenta. Indeed, all our organs work together to support life and it’s arbitrary to imbue one with more importance than the others. Nevertheless, as our first organ, the significance of the placenta is irrefutable.

Placental dysfunction, along with several other factors, is known to contribute to the development of pre-eclampsia – a complex, multisystem hypertensive disorder of pregnancy. While the aetiology of pre-eclampsia remains largely unknown, the grave complications associated with it have driven development of novel methods for predicting its onset.

Pre-eclampsia and Epidemiology

Pre-eclampsia is traditionally defined as new onset hypertension and proteinuria in pregnancy1, however, the International Federation of Gynaecology and Obstetrics’ (FIGO) clinical definition describes it as sudden onset hypertension (>20 weeks of gestation) and at least one of the following: proteinuria, maternal organ dysfunction or uteroplacental dysfunction2. It is responsible for an estimated 70’000 maternal deaths, and 500’000 foetal deaths globally3. Pre-eclampsia affects around 4% of pregnancies in the US and is more common in low-to-middle income countries (LMICs), displaying an overall pooled incidence of 13% in a cohort from sub-Saharan Africa4. The risk factors for pre-eclampsia are shown in the graphic below.

Pre-eclampsia is associated with increased morbidity and mortality worldwide. In the US, pre-eclampsia is the foremost cause of maternal death, severe maternal morbidity, maternal intensive care admissions and prematurity5.

Classical classification of pre-eclampsia included early-onset (<34 weeks gestation) and late-onset (>34 weeks gestation). However, this classification lacks clinical utility as it does not accurately illustrate maternal or foetal prognosis. Therefore, the International Society for the study of Hypertension in Pregnancy (ISSHP) and contemporary studies prefer to classify pre-eclampsia as preterm (delivery <37 weeks of gestation), term (delivery ≥37 weeks of gestation) and postpartum pre-eclampsia (after delivery).


Pre-eclampsia has been associated with acute and chronic complications for both mother and child. Worldwide risk of maternal and foetal morbidity displays adjusted odds ratios of 3.73 and 3.12, respectively (pre-eclampsia vs non pre-eclampsia)6.

Acute Maternal Complications

A range of neurological complications are associated with pre-eclampsia. The most obvious is eclampsia, defined as seizures in pregnant women commonly from 20 weeks of gestation or after birth7. Eclampsia has two proposed mechanisms: abnormal placentation reduces blood supply and causes oxidative stress, leading to endothelial damage; and elevated blood pressure in pre-eclampsia disrupts cerebral vasculature, causing hypoperfusion and damage8. In high-income countries (HICs), most women make a full recovery, however, more severe cases of eclampsia can result in permanent disability or brain damage7.

Stroke is a significant complication of pre-eclampsia, constituting 36% of strokes related to pregnancy9. The hypertension characteristic of pre-eclampsia can weaken the walls of blood vessels causing subarachnoid or intracerebral haemorrhage resulting in haemorrhagic stroke. Ischaemic stroke is also of concern due to blood clotting complications which will be discussed later.

Additonal neurological complications include visual scotoma, cortical blindness, cerebral venous sinus thrombosis, cerebral vasoconstriction syndrome and posterior reversible encephalopathic syndrome (PRES). Notably, the last three in this list frequently manifest postpartum without warning6.

HELLP (Haemolysis, Elevated Liver enzymes and Low Platelets) syndrome is a liver and blood clotting disorder and life-threatening complication of pre-eclampsia. HELLP syndrome most commonly presents immediately postpartum but can manifest any time after 20 weeks of gestation7. Microangiopathy, or small blood vessel disorder, leads to ischaemia and a subsequent increase in oxidative stress and inflammation, causing an increase in liver enzymes and participates in the initiation of HELLP. Thrombocytopenia, or platelet deficiency, is considered a product of platelet depletion resulting from heightened platelet activation triggered by widespread endothelial damage6.

Another blood clotting condition associated with pre-eclampsia is Disseminated intravascular coagulation (DIC)7, described as the dysfunction of the maternal blood clotting system resulting in multiple organ dysfunction syndrome10. DIC can cause excessive bleeding due to lack of clotting proteins, or the formation of clots due to overactive clotting proteins, ultimately causing organ damage10.

As described earlier, proteinuria is included in the diagnostic criteria for pre-eclampsia, suggesting involvement of the kidneys. This is caused by high concentrations of soluble FMS like Tyrosine kinase 1 (sFLT-1), a placental angiogenic factor, which inhibits proteins of the podocyte slit diaphragm6; the machinery involved in preventing the leakage of proteins into the urine11. Reduced levels of Vascular Endothelial Growth Factor (VEGF) and Placental Growth Factor (PlGF) stimulates Endothelin 1 expression6, known to promote podocyte detachment, further contributing to proteinuria12.

Finally, Pulmonary oedema, excessive fluid accumulation in the lungs, is an acute and life-threatening complication associated with pre-eclampsia, the likelihood of which is increased via administration of antihypertensive medications6.

Acute Neonatal Complications

There are several documented complications affecting the baby of a pre-eclamptic mother. Firstly, Intrauterine growth restriction (IUGR) can result in underdevelopment of the foetus because of deficient transfer of oxygen and other nutrients from mother to child13. This can result in low birth weight, particularly when pre-eclampsia occurs prior to 37 weeks of gestation7. In pre-eclampsia with severe symptoms, delivery frequently occurs prematurely, either spontaneously or through induction. Preterm delivery can result in complications such as neonatal respiratory distress syndrome and neonates often require ICU admission7. Additionally, there is increased risk of stillbirth in pre-eclamptic pregnancies with relative risk shown to be 1.45 (95% Cl 1.20-1.76)14. Other complications documented in neonates born through pre-eclamptic pregnancies include neonatal thrombocytopenia, bronchopulmonary dysplasia, and a range of neurodevelopment outcomes15.

Long-term Complications

The only known cure for pre-eclampsia is delivery. However, the complications for both mother and child can last long after even an uncomplicated delivery. After a pre-eclamptic pregnancy, women are increased risk of end stage renal disease (4.7-fold), stroke (4-fold) and vascular dementia (3-fold) later in life5. Women are also at increased risk of other cardiovascular disease (CVD) including chronic hypertension, coronary artery disease, congestive heart failure5, and ischaemic heart disease13. In offspring, IUGR increases the risk of development of hypertension and other CVD13. Finally, offspring have been shown to be at higher risk of increased body mass index, changes in neuroanatomy, reductions in cognitive function, and hormonal abnormalities13.

sFLT-1/PlGF ratio

The pathophysiology of pre-eclampsia is complex and enigmatic. However, placental dysfunction is known to be a factor in pre-eclampsia development. The placental-related angiogenic factors, sFLT-1 (anti-angiogenic) and PlGF (pro-angiogenic), have been implicated in this development. This ratio provides a useful measure of placental dysfunction as a sharp increase in sFLT-1 and decrease in PlGF has been shown approximately 5 weeks before onset of pre-eclampsia16.

Until recently, diagnosis of pre-eclampsia was one of clinical manifestation. However, studies such as PROGNOSIS17 and PROGNOSIS Asia18, along with others19,20, have shown strong utility of this ratio. The PROGNOSIS study showed that a ratio cutoff of ≥38 was useful for ruling out pre-eclampsia within 1 week with a negative predictive value (NPV) of 99.3% or 4 weeks with a positive predictive value (PPV) of 36.7%17. The definitions of pre-eclampsia used by ICCHP and American College of Obstetricians and Gynaecologists (ACOG) have a PPV of around 20%, but when used in combination with the sFLT-1/PlGF ratio, the PPV is enhanced to 65.5% for ruling in pre-eclampsia within 4 weeks.21.

Similar results have been shown in an Asian cohort in the PROGNOSIS Asia Study. Using the same cutoff value, this study reported an NPV of 98.9%18. Furthermore, in a sub analysis of this cohort that looked at Japanese participants, a cutoff of ≥38 displayed an NPV of 100% for ruling out pre-eclampsia within 1 week and a PPV of 32.4% for ruling in within 4 weeks22.

Accurate Identification is Essential

Like all clinical assays, those used to determine the sFLT-1/PlGF ratio are subject to rigorous quality control, essential to ensure accurate results and diagnosis. The complications of pre-eclampsia are severe and often life-threating for both mother and child. Early and accurate identification is imperative for optimal monitoring, management, and timely interventions to reduce the risk of the grave consequences associated with pre-eclampsia.

The utility of the sFLT-1/PlGF ratio has been shown over various large cohorts and provides improved identification when used in combination with established clinical definitions. While the enigma of pre-eclampsia persists, the dedication of the scientific community to unravel its complexities ensures a future where expectant mothers may benefit from more effective and tailored strategies to mitigate the risks associated with this puzzling condition. Continued research endeavours will undoubtedly shape the landscape of maternal-foetal medicine, fostering advancements that hold the promise of improved outcomes for both mothers and their unborn children.

At Randox Quality Control,  we’ve introduced our Pre-eclampsia Control to the Acusera IQC range for use with in vitro diagnostic assays for the quantitative determination of PlGF and sFlt-1 in human serum and plasma.

Our true third-party Pre-eclampsia control comes with clinically relevant, assayed target values, is liquid-frozen for user convenience, utilises a human-based, commutable matrix, and has a 30-day open vial stability.

For more information on this, or any of our other controls, browse our brochure, or reach out to us today at for more information.


  1. American College of Obstetricians and Gynecologists; Task Force on Hypertension in Pregnancy. Hypertension in Pregnancy. Obstetrics & Gynecology. 2013;122(5):1122-1131. doi:10.1097/01.AOG.0000437382.03963.88
  2. Poon LC, Shennan A, Hyett JA, et al. The International Federation of Gynecology and Obstetrics (FIGO) initiative on pre‐eclampsia: A pragmatic guide for first‐trimester screening and prevention. International Journal of Gynecology & Obstetrics. 2019;145(S1):1-33. doi:10.1002/ijgo.12802
  3. Karrar SA, Hong PL. Preeclampsia. StatPearls Publishing; 2023.
  4. Jikamo B, Adefris M, Azale T, Alemu K. Incidence, trends and risk factors of preeclampsia in sub-Saharan Africa: a systematic review and meta-analysis. PAMJ – One Health. 2023;11. doi:10.11604/pamj-oh.2023.11.1.39297
  5. Rana S, Lemoine E, Granger JP, Karumanchi SA. Preeclampsia. Circ Res. 2019;124(7):1094-1112. doi:10.1161/CIRCRESAHA.118.313276
  6. Dimitriadis E, Rolnik DL, Zhou W, et al. Pre-eclampsia. Nat Rev Dis Primers. 2023;9(1):8. doi:10.1038/s41572-023-00417-6
  7. NHS. Pre-eclampsia. Health A to Z. Published September 28, 2021. Accessed January 3, 2024.
  8. Magley M, Hinson MR. Eclampsia. StatPearls Publishing; 2023.
  9. Crovetto F, Somigliana E, Peguero A, Figueras F. Stroke during pregnancy and pre-eclampsia. Curr Opin Obstet Gynecol. 2013;25(6):425-432. doi:10.1097/GCO.0000000000000024
  10. Costello RA, Nehring SM. Disseminated Intravascular Coagulation. StatPearls Publishing; 2023.
  11. Kawachi H, Fukusumi Y. New insight into podocyte slit diaphragm, a therapeutic target of proteinuria. Clin Exp Nephrol. 2020;24(3):193-204. doi:10.1007/s10157-020-01854-3
  12. Trimarchi H. Mechanisms of Podocyte Detachment, Podocyturia, and Risk of Progression of Glomerulopathies. Kidney Dis (Basel). 2020;6(5):324-329. doi:10.1159/000507997
  13. Turbeville HR, Sasser JM. Preeclampsia beyond pregnancy: long-term consequences for mother and child. American Journal of Physiology-Renal Physiology. 2020;318(6):F1315-F1326. doi:10.1152/ajprenal.00071.2020
  14. Harmon QE, Huang L, Umbach DM, et al. Risk of Fetal Death With Preeclampsia. Obstetrics & Gynecology. 2015;125(3):628-635. doi:10.1097/AOG.0000000000000696
  15. Backes CH, Markham K, Moorehead P, Cordero L, Nankervis CA, Giannone PJ. Maternal Preeclampsia and Neonatal Outcomes. J Pregnancy. 2011;2011:1-7. doi:10.1155/2011/214365
  16. Verlohren S, Galindo A, Schlembach D, et al. An automated method for the determination of the sFlt-1/PIGF ratio in the assessment of preeclampsia. Am J Obstet Gynecol. 2010;202(2):161.e1-161.e11. doi:10.1016/j.ajog.2009.09.016
  17. Zeisler H, Llurba E, Chantraine F, et al. Predictive Value of the sFlt-1:PlGF Ratio in Women with Suspected Preeclampsia. New England Journal of Medicine. 2016;374(1):13-22. doi:10.1056/NEJMoa1414838
  18. Bian X, Biswas A, Huang X, et al. Short-Term Prediction of Adverse Outcomes Using the sFlt-1 (Soluble fms-Like Tyrosine Kinase 1)/PlGF (Placental Growth Factor) Ratio in Asian Women With Suspected Preeclampsia. Hypertension. 2019;74(1):164-172. doi:10.1161/HYPERTENSIONAHA.119.12760
  19. Hughes RCE, Phillips I, Florkowski CM, Gullam J. The predictive value of the sFlt‐1/PlGF ratio in suspected preeclampsia in a New Zealand population: A prospective cohort study. Australian and New Zealand Journal of Obstetrics and Gynaecology. 2023;63(1):34-41. doi:10.1111/ajo.13549
  20. Nikuei P, Rajaei M, Roozbeh N, et al. Diagnostic accuracy of sFlt1/PlGF ratio as a marker for preeclampsia. BMC Pregnancy Childbirth. 2020;20(1):80. doi:10.1186/s12884-020-2744-2
  21. Verlohren S, Brennecke SP, Galindo A, et al. Clinical interpretation and implementation of the sFlt-1/PlGF ratio in the prediction, diagnosis and management of preeclampsia. Pregnancy Hypertens. 2022;27:42-50. doi:10.1016/j.preghy.2021.12.003
  22. Ohkuchi A, Saito S, Yamamoto T, et al. Short-term prediction of preeclampsia using the sFlt-1/PlGF ratio: a subanalysis of pregnant Japanese women from the PROGNOSIS Asia study. Hypertension Research. 2021;44(7):813-821. doi:10.1038/s41440-021-00629-x



International Day of Women and Girls in Science 2024

For the 9th consecutive year, the field of science has taken this day to celebrate women in the STEM industries and their achievements. The representation of women in STEM is climbing, however it remains low, with estimates claiming women make up only around 26% of the workforce. By celebrating the accomplishments of women in these fields, we hope to encourage more girls to enter the world of science and engineering and challenge the adversity women in STEM all too often face.

In honour of International Day of Women and Girls in Science 2024, we’ve looked at some of the most important achievements in the life sciences. Some of the names you’ll be familiar with, others may be new. We’ll travel to Ancient Greece where we will learn about the first female science writer and surgeon, before coming back to today to recognise some of the most groundbreaking innovations in medicine. For far too long the door to a career in the life sciences has been all but closed for women, as you will discover in this article. Yet some of the discoveries and triumphs over adversity we’ll look at are arguably some of the most important achieved by humanity.


In Ancient Greece, it was believed that science was derived directly from the gods. This meant, like other divine disciplines, women were not allowed to practice medicine. However, such a technicality did not stop our first heroine of science. Before her exploits in Greece, Metrodora was likely born and educated in Egypt where men and woman were equals, unlike much of the ancient world. In fact, some believe Metrodora to be an alias of the famous Cleopatra VII, Queen of Egypt. There is some debate about when Metrodora lived; some say between 200-400 CE, others claim it was more likely to be during the 7th century CE. The name Metrodora is particularly fitting for a woman of her accolades. In Greek, metro can be translated as womb, and dora means gift.

Metrodora was the author of a textbook, making her the first female science writer, spanning 2 volumes and 108 chapters entitled On the Disease and Cures of Women, in which she describes in detail her theories and findings on the topics of female health and the reproductive system. She is thought to have devised treatments for sterility, infections of the female reproductive system, menorrhagia (heavy periods) as well as a method for determining sexual abuse in women. Not to be limited by writing and medicine, Metrodora was also a surgeon, cited as removing dead embryos to save the lives of mothers who miscarried, removing cancers of the breast and uterus and was even among the first to perform cosmetic surgery. Metrodora reconciled this with her Hippocratic duty to help women who had been abused through aesthetic facial and breast reconstruction and the restructuring of the hymen of women who had suffered this fate.

Her pioneering work, however, was quite nearly forgotten forever as she was largely overlooked by her contemporaries. But thankfully, some of her texts are preserved in the Laurentian Library in Florence. Metrodora’s commitment to medicine and female health is summed up perfectly in the opening words of her text, “some of them are intricate to treat and others are fatal, by these notes we will recognise each one”.




Elizabeth Blackwell (1821-1910)

Elizabeth Blackwell was always destined to shake the status quo. Her father, Samuel, was a Quaker and an antislavery activist. Among her siblings are Henry, an abolitionist and women’s suffrage supporter; her sister, Emily, who followed Elizabeth into medicine; and her sister-in-law, Antoinette Brown Blackwell, who was the first female minister in mainstream Protestantism.

She was inspired into a life of medicine after a close friend had confessed embarrassment of her treatment by male doctors and suggested she’d have been more comfortable if attended to by a female physician. After a series of rejections from numerous medical schools, Elizabeth was finally accepted to Geneva College, New York. However, this acceptance was intended as a practical joke. Not to be discouraged, Elizabeth proved them all wrong, graduating top of her class in 1849 and becoming the first woman to graduate medical school. Dr Blackwell then practiced in London and Paris and was one of the first advocates for the importance of hygiene in medicine, noting that male doctors frequently failed to wash their hands, which led to the spread of epidemics.

In 1851, Elizabeth made the trip back to New York where discrimination was still rife. Once again, her persistence led to the opening of the New York Infirmary for Women and Children in 1857 with Dr Emily Blackwell and Dr Marie Zakrzewska. This institution was a haven for women who needed medical treatment but were often too poor to afford it, and for female physicians struggling to get work in the field. Among her laurels, she played a role in the inception of the National Health Society, established in 1871, which aimed to spread knowledge of public health, and is considered the predecessor to the National Health Service.



Marie Curie (1867-1934)

Marie Curie is among the most famous of the women in science, so we won’t spend too much time on her life and accomplishments here. However, its impossible to have the discussion without mentioning her invaluable contribution to science. In often poor laboratory conditions with worse equipment, she, and her husband Pierre Curie, made some pivotal discoveries including the isolation of polonium and radium. Marie Curie developed techniques to separate radium from radioactive residues which allowed it to be studied extensively and eventually, its use as a therapeutic agent.

In 1903, Marie and Pierre Curie were awarded half of the Nobel Prize for Physics for their work on spontaneous radiation. Then, in 1911, Marie Curie was given a second Nobel Prize, this one for chemistry, for her work on radioactivity. In recognition of her groundbreaking work leading to novel cancer therapies, the charity Marie Curie was named in her honour, immortalising her and her contributions to the field.

Marie Curie, 1867-1934

Gerty Cori (1896-1957)

Here we find another woman whose name outshines that of her husband, Carl, with whom she collaborated for most of her scientific career. Gerty graduated from medical school in 1920, along with her husband, before they emigrated to America in 1922. Here, they initially delved into the fate of sugar within the animal body, exploring the impacts of insulin and epinephrine. They made groundbreaking discoveries, including the demonstration of glycolysis in tumours in vivo. Their research on carbohydrate metabolism evolved from whole animal studies to experiments on isolated tissues, and eventually to tissue extracts and isolated enzymes, including some in crystalline form. In a pivotal moment in 1936, they isolated glucose-1-phosphate, known as “Cori ester,” and linked its formation to the activity of phosphorylase, which plays a crucial role in the breakdown and synthesis of polysaccharides. This discovery paved the way for the enzymatic synthesis of glycogen and starch in vitro.

Their research extended into the realm of hormone action mechanisms, with several studies focusing on the pituitary gland. They observed significant changes in rats that have had their pituitary gland removed, including a marked decrease in glycogen and a drop in blood sugar levels, accompanied by an increased rate of glucose oxidation. Further investigations into the effects of hormones on hexokinase revealed that certain pituitary extracts could inhibit this enzyme both in vivo and in vitro, while insulin was found to counteract this inhibition.

Beyond their groundbreaking research, the Cori’s served as an endless source of inspiration to their peers in the vibrant hubs of biochemical research they led. Their contributions to The Journal of Biological Chemistry and numerous other scientific journals have left an indelible mark on the field, showcasing their innovative work and collaborative spirit throughout their careers.


Gertrude Belle Elion (1918-1999)

Gertrude provides us with another tale of the triumph over adversity. After graduating with a degree in biochemistry in 1937, she failed to obtain a graduate position because she was a woman. After roles in laboratories and teaching, she joined the Burroughs Wellcome Laboratories in 1944 and became the assistant to Dr George Hitchings. Over the following 40 years, the pair were successful in the development of a vast array of new drugs and treatments. Much of their success is attributed to their methods. At the time, normal practice is best described as trial and error. However, Hitchings and Elion studied and intimately understood the difference between normal and pathogenic biochemistry, allowing them to envision and create targeted treatments for, to name just a few, leukaemia, urinary-tract infection, gout, malaria and viral herpes.

Although she never achieved her doctorate, in 1967 Elion was promoted to Head of the Department of Experimental Therapy, where she remained until her retirement in 1983. But Elion didn’t let a silly old thing like retirement get in her way. She remained at the Burroughs Wellcome Laboratories as a Scientist Emeritus and Consultant, including overseeing the development of azidothymidine, the first drug used to treat AIDS. Elion also became a Research Professor of Medicine and Pharmacology at Duke University, working with medical students in the field of tumour biochemistry and pharmacology, while continuing to write and lecture. Gertrude B. Elion passed away in 1999, bringing an end to a happy and fruitful career as one of the most influential women in science.


GSK Heritage Archives
GSK Heritage Archives

Rosalind Franklin (1920-1958)

Rosalind Franklin, another well-known name and one synonymous with the discovery of the DNA double helix, was an exceptional scientist whose meticulous work in X-ray crystallography laid the groundwork for one of the 20th century’s most significant scientific discoveries. Franklin graduated from Cambridge University in 1941, where she initially delved into the study of coal, gases, and carbon compounds, significantly contributing to the understanding of the molecular structures of these materials. Her early research not only showcased her exceptional skills in physical chemistry but also set the stage for her pioneering work in biology.

In 1951, Franklin joined King’s College London, where she was tasked with improving the X-ray crystallography unit. It was here that Franklin embarked on her most famous work: the study of the structure of DNA. Using her expertise in X-ray diffraction techniques, she captured Photograph 51, a critical piece of evidence revealing the helical structure of DNA. This image was crucial in identifying the double helix structure, although her contributions were not fully acknowledged until after her death.

Franklin’s research extended beyond DNA to the study of viruses, making significant strides in understanding the polio virus and the tobacco mosaic virus. Her work in virology, much like her work on DNA, was pioneering, employing her crystallography skills to uncover the detailed structure of viral particles. This work provided valuable insights into how viruses replicate and infect cells, contributing to the broader field of virology and paving the way for future research in virus structure and function.

Despite facing considerable challenges as a woman in a predominantly male scientific community, Franklin’s contributions were profound. Her relentless pursuit of scientific truth, combined with her exceptional experimental skills, left a legacy in the fields of chemistry, virology, and genetics. Beyond her scientific achievements, Franklin is remembered as a trailblazer who paved the way for future generations of women in science, demonstrating the critical role of perseverance and dedication in the pursuit of knowledge.







The Editors of Encyclopaedia Britannica. "Rosalind Franklin, British Scientist," Encyclopaedia Britannica (article created 20 Jul 1998, accessed 08 Jan 2024); :
The Editors of Encyclopaedia Britannica. "Rosalind Franklin, British Scientist," Encyclopaedia Britannica (article created 20 Jul 1998, accessed 08 Jan 2024); :

Françoise Barré-Sinoussi (1947-)

When discussing women who changed science, it’s impossible not to mention Françoise Barré-Sinoussi. She was born in Paris in 1947 and attended university there. Her passion for science saw her skip class to work at the Pasteur Institute, participating in investigations of retroviruses that caused leukaemia in mice. Although, this didn’t seem to affect her exams scores, and she received her PhD in 1974.

Françoise Barré-Sinoussi is hailed as the woman who discovered the viral cause of the AIDS epidemic. In 1982, the Pasteur Institute was approached by a virologist from a hospital in Paris, seeking help in identifying the cause of a worrying new epidemic. In a mere 2 weeks, Barré-Sinoussi, and her colleagues at the Pasteur Institute, isolated and grew a retrovirus from a biopsied lymph node of a patient at risk of AIDS. The virus, later named HIV-1, was found to be the cause of the AIDS epidemic.

Barré-Sinoussi has been contributing to virology research ever since, including areas such as the function of the host’s innate immune defences in managing HIV/AIDS, the elements contributing to the transmission of HIV from mother to child, and traits enabling a select group of HIV-positive individuals to restrain HIV replication without the need for antiretroviral medications. In 1992, Barré-Sinoussi was appointed Head of the Biology of Retrovirus Unit, renamed the Regulation of Retroviral Infections Unit in 2005.

However, Barré-Sinoussi didn’t stop at the science. She became a prominent activist for public education about AIDS prevention and helped to establish centres for diagnosing and treating AIDS around the world. In 2006, Barré-Sinoussi was elected to the International AIDS Society (IAS) Governing Council and served as president of the IAS from 2012-2016.,_2008-1.jpg,_2008-1.jpg

Jennifer Douda and Emmanuelle Charpentier

Most people have heard of CRISPR-Cas9. But many aren’t aware that we have women to thank for this scientific innovation. In 2012, Jennifer Douda (left) and Emmanuelle Charpentier (right) discovered the ingenious CRISPR-Cas9 technology – a groundbreaking tool in genetic engineering, which holds the promise of revolutionising medicine and biology. By enabling precise editing of the DNA in the cells of living organisms, CRISPR-Cas9 could lead to cures for genetic disorders, enhance crop resistance to pests and diseases, and advance our understanding of complex genetic conditions. It offers the potential to correct genetic defects, combat infectious diseases, and even manipulate traits in plants and animals, paving the way for significant advancements in therapeutic treatments, agricultural productivity, and the study of genetics. This discovery saw both women share the Nobel Prize in Chemistry in 2020.


Photograph by Christopher Michel

We’ve only looked at a subsection of science, but one where the importance of the innovations and discoveries is felt by people every day. The scientists we’ve discussed here are only a small sample of the inspirational women that have graced the STEM field. We hope that by elucidating some of their work, we can inspire more girls and women to pursue a career in STEM. Careers in this field are challenging and rewarding, perfect for those with a curious mind and those in whom discovery sparks delight.

World Hepatitis Day 2023


World Hepatitis Day, observed on July 28th, serves as a crucial reminder of the ongoing battle against hepatitis (HBV), a viral infection that affects millions of people worldwide. In 2019, it was estimated that 296 million people were living with chronic hepatitis B, resulting in over 800,000 fatalities1. In this article, we will delve into the intricate mechanisms behind hepatitis, explore the viral species responsible for its occurrence, discuss methods for diagnosis, and shed light on treatment and management strategies.

Understanding Hepatitis

Hepatitis refers to the inflammation of the liver, often caused by viral infections. Among the primary hepatitis viruses are Hepatitis A, B, C, D, and E, each with distinct modes of transmission and characteristics2.

Mechanisms of Hepatitis Infection

Hepatitis A and E: Hepatitis A and E viruses are primarily transmitted via the faecal-oral route, often through contaminated food or water. Ingestion of these viruses leads to acute infection, and while self-limiting in most cases, they can cause significant morbidity and mortality in certain populations5,6.

Hepatitis B, C, and D: Hepatitis B, C, and D viruses are predominantly spread through blood and bodily fluids. Hepatitis B can also be transmitted from mother to child during childbirth which in endemic areas, HBV infection from mother to child transmission accounted for approximately half of chronic infections. These viruses can cause chronic infections, leading to long-term liver damage, cirrhosis, and an increased risk of hepatocellular carcinoma7,8.

Diagnosis of Hepatitis

Accurate and timely diagnosis of hepatitis is crucial for appropriate management. Diagnostic methods include:

Serology: Serological tests, such as enzyme immunoassays, are employed to detect specific viral antigens or antibodies in blood samples, aiding in the identification of different hepatitis viruses and determining the stage of infection9.

Nucleic Acid Testing: Highly sensitive molecular techniques like polymerase chain reaction (PCR) enable the detection and quantification of viral genetic material, aiding in the diagnosis and monitoring of chronic hepatitis10.

Treatment and Management of Hepatitis

The management of hepatitis depends on several factors, including the virus involved, the stage of infection, the presence of co-infections, and the individual patient’s health status. Treatment strategies encompass:

Antiviral Medications: For hepatitis B and C, antiviral drugs such as interferons and direct-acting antivirals have revolutionized the treatment landscape, offering higher cure rates and improved outcomes11,12.

Supportive Care: Hepatitis patients may require supportive care to alleviate symptoms, maintain proper nutrition, and manage complications. Vaccination against hepatitis A and B is highly recommended for prevention13.

Liver Transplantation: In cases of end-stage liver disease or hepatocellular carcinoma resulting from chronic hepatitis, liver transplantation may be considered a lifesaving option14.

Randox Hepatitis Solutions


Acusera provides a range of positive and negative serology controls comprising various infectious diseases including Hepatitis. The table below details the suitable controls, and more information can be found on our website: Serology Quality Controls – Randox Laboratories


The RIQAS HIV/Hepatitis EQA programme is designed to monitor the performance of tests used to detect HIV/Hepatitis antibodies and specific antigens. All samples are conveniently supplied liquid ready-to-use and are suitable for qualitative methods of analysis.


  • Anti-HIV-1
  • Anti-HCV
  • Anti-HTLV-II
  • HBsAg
  • Anti-HIV-2
  • Anti-HBc
  • Anti-HTLV-1&2 (combined)
  • Anti-HIV-1&2 (combined)
  • Anti-HTLV-I
  • Anti-CMV
  • Anti-HAV IgM
  • Anti-HAV (Total)
  • Anti-HBc (Total)
  • Anti-HBe (Total)
  • Anti-HBs (Total)
  • P24

For more information, please visit our website at: HIV Hepatitis EQA | RIQAS (


Monitoring for the presence of Blood Borne Virus (BBV) nucleic acid is an essential parameter in guiding clinical treatment and patient outcomes. The use of appropriate quality control measures is important in ensuring the appropriate daily performance of the molecular assay used in the laboratory independent of the technology.

Qnostics’ Blood Borne Virus Molecular Controls comprises a range of pathogens which are classically detected directly from the blood including those related to hepatitis. The table below lists the Qnostics products related to hepatitis testing. For more information visit our website: Qnostics | Molecular Infectious Disease Controls – Randox Laboratories


QCMD is a world-leading External Quality Assessment (EQA) / Proficiency Testing (PT) scheme, dedicated to improving the quality of molecular diagnostic assays used in the detection of infectious diseases. With an extensive database of over 2000 participants in over 100 countries, QCMD is one of the largest providers of molecular EQA in the field of molecular diagnostics. QCMD programmes related to hepatitis testing are listed below:

  • HBV Drug resistance Typing EQA programme.
  • HCV Drug resistance Typing EQA programme.
  • Hepatitis B Virus DNA EQA Programme
  • Hepatitis B Virus Dried Blood Spot EQA Pilot Study
  • Hepatitis B virus Genotype EQA Programme
  • Hepatitis C Virus Dried Blood Spot EQA Pilot Study
  • Hepatitis C Virus RNA EQA Programme
  • Hepatitis C virus Genotype EQA Programme
  • Hepatitis D Virus EQA Programme
  • Hepatitis E virus RNA EQA Programme

For more information on any of these EQA programmes please visit: QCMD – Molecular EQA Scheme | Randox Quality Control


World Hepatitis Day serves as a reminder of the global impact of hepatitis and the urgent need to raise awareness, prevent transmission, and improve the diagnosis and management of this disease. By understanding the mechanisms, bacterial species involved, diagnostic techniques, and treatment approaches, we can work towards a future free from the burden of hepatitis. Let us unite in our efforts to combat this disease and strive for a healthier world.

If you’d like to find out more about hepatitis or the diagnosis and testing of hepatitis, please visit our website. If you’d like more information on how Randox can improve hepatitis testing in your laboratory, please reach out to


  1.  World Health Organization. World Health Statistics 2023. World Health Organization; 2023.
  2. World Health Organization. Hepatitis. Published 2017. Accessed June 9, 2023.
  3. Wan Z, Wang X. Bacterial Hepatitis. In: Encyclopedia of Medical Microbiology. Elsevier; 2020:110-117.
  4. Russo TA, McFadden DC. Bacterial and fungal infections in patients with cirrhosis. Clin Liver Dis. 2019;14(2):71-74.
  5. World Health Organization. Hepatitis E. Published 2018. Accessed June 9, 2023.
  6. Rakesh S, Pekamwar SS. Hepatitis A. In: StatPearls [Internet]. StatPearls Publishing; 2020.
  7. World Health Organization. Hepatitis B. Published 2021. Accessed June 9, 2023.
  8. World Health Organization. Hepatitis D. Published 2021. Accessed June 9, 2023.
  9. Alfaresi MS, Elkoush AA, Khan AS. Serological diagnosis of viral hepatitis. J Clin Transl Hepatol. 2017;5(4):343-359.
  10. European Association for the Study of the Liver. EASL Recommendations on Treatment of Hepatitis C. J Hepatol. 2017;66(1):153-194.
  11. European Association for the Study of the Liver. EASL 2017 Clinical Practice Guidelines on the management of hepatitis B virus infection. J Hepatol. 2017;67(2):370-398.
  12. Vermehren J, Sarrazin C. New HCV therapies on the horizon. Clin Microbiol Infect. 2011;17(2):122-134.
  13. World Health Organization. Hepatitis A. Published 2020. Accessed June 9, 2023.
  14. Kim WR, Terrault NA. Hepatocellular carcinoma and liver transplantation. Clin Liver Dis. 2018;22(2):381-394.

Enhancing Laboratory Quality Control with Multi-Rule QC: A Comprehensive Guide


We are thrilled to announce the release of our latest educational guide, “Understanding Multi-rule QC,” which delves into the world of laboratory quality control. Designed for laboratory professionals, this comprehensive guide aims to empower you with knowledge and strategies to ensure accurate results and uphold patient safety.

Understanding the Significance of Multi-Rule QC

Laboratory quality control is paramount in maintaining the integrity of test results. The guide begins by exploring the various causes of deviations in laboratory testing processes. From instrument malfunctions to environmental factors, we shed light on potential sources of error that can impact result accuracy.

Next, we dive into the core of the guide: Multi-rule QC. This powerful framework encompasses a series of rules that serve as a robust screening tool for identifying outliers, shifts, and trends in data. Through an in-depth exploration of rules such as 1:2s, 1:3s, 2:2s, R4s, 3:1s, 4:1s, 10x, and 7T, we unveil their underlying principles and their significance in maintaining quality control within laboratory settings.

Applying the Multi-Rule QC Approach

The guide equips laboratory professionals with practical insights on applying the Multi-rule QC approach. By examining consecutive data points, analysing trends, and detecting systematic shifts, you gain the ability to proactively address issues before they compromise result accuracy. We highlight the importance of avoiding overreliance on individual rules for result rejection, emphasizing the need to consider additional factors such as clinical relevance and method performance.

Troubleshooting Out-of-Control Events

No laboratory is immune to out-of-control events. That’s why our guide goes beyond rule implementation and delves into effective troubleshooting strategies. We provide guidance on identifying root causes, implementing corrective actions, and re-establishing control in your laboratory environment. By embracing a culture of continuous improvement, you can minimize the impact of deviations and optimize laboratory performance.

Acusera 24.7 

Acusera 24.7 is a cloud-based inter-laboratory data management and peer-group reporting software designed to assist in the management of daily QC activities and aid continuous improvement in the laboratory. It includes multi-rule capabilities that can be utilized to monitor your QC data and index it as accepted, rejected, or trigger an alert, depending on the pre-defined multi-rules against which you want to check your data. These features enable the identification of nonconformities and reduce the need for laborious manual statistical analysis while enhancing the accuracy and precision of the laboratory.


In an era where accuracy and patient safety are paramount, the “Multi-rule QC” guide serves as an invaluable resource for laboratory professionals. By mastering the principles and applications of Multi-rule QC, you can enhance the quality control processes within your laboratory, mitigating risks and delivering reliable test results.

To explore the full potential of Multi-rule QC and embark on a journey of laboratory excellence, we invite you to download the guide today. Stay ahead of the curve and ensure the highest standards of quality and patient care in your laboratory!

You can download the Understanding Multi-rule QC Educational Guide below: 

If you’d like to find out more about what we can do to help your laboratory or view our range of Internal Quality Controls, don’t hesitate to contact us at or feel free to browse the range on our website


Differentiating Type 1 and Type 2 Diabetes Mellitus

An estimated 422 million people across the world are living with diabetes1. Diabetes Mellitus (DM) encompasses a collection of chronic diseases characterised by absent or ineffective insulin activity. Insulin is a hormone produced by the pancreas responsible for a host of essential physiological processes related to glucose metabolism and protein synthesis.

There are two main forms of DM, named type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) which result from different mechanisms and more importantly, require different therapeutic approaches. It is estimated that up to 40% of those diagnosed with T1DM after the age of 30 may have been misdiagnosed with T2DM2. This misdiagnosis of T1DM as T2DM will result in poor glycaemic control, frequent healthcare contact for increased treatment, inappropriate insulin regimes and risk of life-threatening ketoacidosis.

In this article, we’ll look at the similarities and differences between these two forms of DM and investigate the mechanisms by which these common diseases arise.

Insulin Pathway

The normal insulin signalling pathway, shown below, is responsible for the processing and transport of glucose in the body. Briefly, insulin binds to the insulin receptor and activates PI3K and, subsequently, serine-threonine kinase (AKT). AKT is responsible for the phosphorylation of glycogen synthase kinase 3-β (GSK-3β), inhibiting its activity and promoting the synthesis of glycogen leading to a reduction in blood glucose concentration.  Failing to inhibit GSK-3β will result in hyperglycaemia and eventually T2DM.

Type 1 Diabetes Mellitus

T1DM is most commonly diagnosed at a young age. This form of DM is the result of an autoimmune reaction to proteins produced by the pancreas which results in a lack of insulin secretion. The antibodies responsible for this autoimmunity are detailed in the table below:

A key factor in T1DM pathogenesis is changes in the T cell-mediated immunoregulation, notably in the CD4+ T cell compartment. The activation of the CD4+ T cells is responsible for inflammation of the pancreatic cells which produce insulin, known as insulitis.

Changes in the expression of IL-1 and TNFα cause structural alterations in pancreatic β-cells which result in the suppression of insulin secretion.  This insulin deficiency has subsequent effects on glucose metabolism and protein synthesis.

T1DM causes an increase in hepatic glucose levels when gluconeogenesis converts glycogen to glucose. A lack of insulin means the subsequent hepatic uptake of this glucose does not occur.

Insulin is also responsible for regulating the synthesis of many proteins. This regulation can be positive or negative but ultimately results in an increase in protein synthesis and a decrease in protein degradation. Therefore, when hypoinsulinemia occurs, decreasing insulin concentration in the blood, protein catabolism is increased leading to increased plasma amino acid concentration.

Type 2 Diabetes Mellitus

The pathogenesis of T2DM, detailed in the diagram below, is multi-factorial. It arises from a combination of genetic and environmental factors which affect insulin activity.

In T2DM, the regulatory mechanisms related to glucose metabolism fail resulting in impaired insulin activity or insulin resistance.

Mutations in genes involved in insulin production can cause the secretion of abnormal insulin molecules, known as insulinopathies. Insulinopathies are unable to effectively metabolise glucose which results in the accumulation of this sugar. Additionally, obesity is considered to be a causal factor in the development of T2DM.

Unlike those with T1DM, patients with T2DM can maintain circulating insulin levels. T2DM is characterised by glucose intolerance, impaired glucose tolerance, diabetes with minimal fasting hyperglycaemia, and DM in association with overt fasting hyperglycaemia.

Individuals with impaired glucose tolerance have hyperglycaemia despite preserving high levels of plasma insulin. These levels of insulin decline from impaired glucose tolerance to DM. It is insulin resistance is considered the primary cause of T2DM.


The misdiagnosis of these types of DM is common, due to similar symptoms. The simplest differentiating factor is when these symptoms manifest. T1DM is an autoimmune disorder and therefore, symptoms generally occur much earlier in one’s life. T2DM is typically diagnosed in later life. The common symptoms of DM are:

  • Frequent urination, particularly throughout the night.
  • Polydipsia (excessive thirst)
  • Polyphagia (excessive hunger)
  • Lethargy
  • Sudden weight loss
  • Genital itching or thrush
  • Blurred vision

The misdiagnosis of T2DM as T1DM results in unnecessary initial insulin therapy, higher drug and monitoring costs and often, an increase in the number and severity of symptoms. Conversely, the incorrect classification of T1DM as T2DM causes poor glycaemic control, frequent visits to healthcare services for treatment, inappropriate insulin regimes and risk of Diabetic Ketoacidosis.

Diabetic Ketoacidosis (DKA)

DKA is a potentially life-threatening condition caused by an accumulation of ketones in the body due to insulin deficiency, which is common in patients with T1DM, however, an increasing number of cases have been reported in patients with T2DM. Diagnosis of DKA consists of a high anion gap metabolic acidosis, ketone bodies present in serum and/or urine, and high blood glucose concentration. The symptoms of DKA include:

  • Polyuria (excessive urination) and polydipsia (thirst)
  • Weight loss
  • Fatigue
  • Dyspnoea (shortness of breath)
  • Vomiting
  • Fever
  • Abdominal pain
  • Polyphagia (excess hunger)
  • Fruity-smelling breath caused by acetone accumulation.

Randox Type 1 Diabetes Mellitus Genetic Risk Array

T1DM is largely genetic and is associated with over 50 distinct genetic signatures, many of which are single nucleotide polymorphisms (SNPs). This is of great advantage in testing as unlike traditional biomarkers, genetic markers don’t change throughout one’s life, providing a robust method for diagnosis and risk stratification. Genetic data gathered can then be used to develop a genetic risk score, allowing an individual’s probability of developing the disease to be quantified.

Using this principle, together with our patented Biochip array technology, Randox have developed a T1DM GRS array. Using a combination of 10 SNPs from the HLA region and the non-HLA region commonly detected in T1DM patients, and a selection of other risk factors and biomarkers, this molecular array can accurately discriminate between T1DM and T2DM.


Misdiagnosis of DM can have life-threatening consequences. Both types of DM are very common and distinguishing between T1DM and T2DM is crucial.

T1DM is an autoimmune disorder with a lack of insulin secretion, while T2DM is primarily due to insulin resistance. Understanding their mechanisms is vital for accurate diagnosis and treatment. Genetic testing, like the Randox Type 1 Diabetes Mellitus Genetic Risk Array, can differentiate between T1DM and T2DM by analysing genetic markers and providing personalized treatment insights.

Accurate diabetes diagnosis is crucial for proper management, prevention of complications, and improving the lives of millions. Together, we can make a difference in the lives of those affected by diabetes!

If you’d like to learn more about the different types of DM, including the pathogenesis, pathophysiology, associated risk factors, and more, please take a look at our educational guide Diabetes Solutions.

Alternatively, feel free to reach out to our marketing team at who will be happy to help you with any queries you may have.


  1. World Health Organization. Diabetes. World Health Organisation. Published April 5, 2023. Accessed April 25, 2023.
  2. The Misdiagnosis of type 1 and type 2 diabetes in adults. The Lancet Regional Health. 2023;29:100661-100661. doi:

Sexually Transmitted Infections – Rapid Testing at the Point of Care

Urgency, Challenges and Advances in STI Testing

Sexually transmitted infections (STIs) are a major global health issue, with over 30 pathogens causing an estimated one million infections daily, a number that is rising. Surveillance programs in countries like the United States and Canada have reported an increase in STIs such as syphilis, gonorrhoea, and chlamydia. STIs can have serious consequences for sexual health, including infertility and chronic pelvic pain, particularly affecting women. The World Health Organization (WHO) has recognised the urgency of addressing this problem and has recommended measures to end the STI healthcare issue by 2030. Integrated testing, including multiplex and point-of-care testing, is considered essential. However, implementation of these recommendations at regional and national levels is lacking. Rapid point-of-care PCR tests that can detect multiple pathogens simultaneously would greatly improve STI diagnosis and containment. Currently, Randox, in collaboration with Bosch offers two STI test panels on the Vivalytic POC system: Vivalytic STI and Vivalytic MG, MH, UP/UU panels, capable of detecting multiple pathogens in a single test run, with results available within hours.

The Global Burden

  • The WHO estimates 374 million new infections of chlamydia, gonorrhoea, syphilis, and trichomoniasis annually.
  • Chlamydia is the most frequently reported STI in Europe, followed by gonorrhoea and syphilis.
  • Countries with comprehensive STI screening programs, like Denmark, have higher prevalence rates than the European average.
  • The UK has a comprehensive screening program for chlamydia targeting 15-24-year-olds, with cases accounting for 60% of total cases in the European Region.
  • The actual infection rate in countries without systematic screening is likely higher than official figures suggest.
  • Reported cases of gonorrhoea and syphilis in the European Region have increased, particularly among certain age groups and higher numbers in men than women.
Global Burden

Gaps in Current STI Testing Strategies

The European Centre for Disease Prevention (ECDC) acknowledges the growing concern of STIs in Europe and emphasises the importance of testing in their recent report. While various European countries have screening programs for chlamydia, testing options for other STI pathogens are usually limited. The lack of accessible testing, combined with the prevalence of asymptomatic infections, increases the risk of STI transmission and hampers containment efforts. Prevention campaigns and low-threshold testing opportunities are crucial to address the spread of STIs. The UK’s chlamydia screening program, implemented in 2008, demonstrated the benefits of community-based testing services and led to a significant increase in diagnosed cases, reducing the number of unreported cases.


Infections and Co-Infections

  • Co-infections, where multiple sexually transmitted pathogens are present simultaneously, are common but often go undetected due to limited testing.
  • Symptoms of co-infections can be difficult to differentiate since different pathogens can cause similar or overlapping symptoms.
  • However, most STIs, even in high-risk groups, are caused by a single sexually transmitted pathogen.
  • In cases where co-infections need to be detected, a rapid and comprehensive differential diagnosis of sexually transmitted pathogens is crucial for initiating appropriate therapy promptly.

The Importance of Rapid Results at the Point of Care

  • Rapid detection and treatment of STIs are crucial to prevent further spread.
  • Traditional STI diagnostics in specialized laboratories can result in delays of several days or up to 1-2 weeks until test results are available to the physician.
  • Delays occur due to transportation of samples, laboratory workflow, result transfer, and scheduling additional appointments.
  • The delay in treatment initiation can lead to decreased patient compliance and missed appointments.

The Vivalytic STI test provides results directly at the point of care (POC) in less than two and a half hours. It eliminates the need for sample transportation to a central laboratory. In addition, patients can receive their test results on the same day of the visit, allowing for immediate initiation of appropriate treatment.


In a Nutshell

Sexually transmitted infections (STIs) spread due to various factors. Many STIs do not show symptoms, resulting in numerous unreported and untreated cases that can have fatal consequences depending on the specific pathogen. Increasing awareness and implementing a decentralised low-threshold testing strategy can significantly reduce infections, particularly among high-risk groups. Speed and comprehensive testing of relevant pathogens are crucial for targeted therapy and containing STIs. Rapid PCR tests used at the point of care (POC) are emerging as important technologies due to their advantages. Patients receive same-day results and immediate treatment, providing clarity in just one visit. Clinicians can provide up-to-date diagnoses and treatments, even in decentralised or hospital settings, benefiting high-risk patients with limited access to healthcare.


The Bosch Vivalytic, is an advanced and automated platform for molecular diagnostics that utilises PCR to detect pathogens. It offers applications for various medical disciplines and requires only a few steps from sample collection to obtaining results. The patient sample is processed automatically within the Vivalytic analyser, and the test result is displayed on its integrated screen. The time it takes to get results depends on the specific Vivalytic application. For the STI Panel, which simultaneously detects 10 common sexually transmitted pathogens, the time to result is 2.5 hours. On the other hand, the Vivalytic MG, MH, UP/UU panel, used to detect mycoplasmas and/or ureaplasmas, provides results in approximately one hour.

By conducting fully automated analyses at the point of care, Vivalytic saves valuable time for hospitals, labs, genitourinary clinics and doctor’s offices during their routine processes.

STI PanelMG, MH, UP, UU Panel
Chlamydia trachomatisMycoplasma genitalium
Neisseria gonorrhoeaeMycoplasma hominis
Trichomonas vaginalisUreaplasma parvum/Ureaplasma
Mycoplasma genitalium
Treponema pallidum
Mycoplasma hominis
Ureaplasma urealyticum
Haemophilus ducreyi
Herpes simplex virus I
Herpes simplex virus II

At a Glance

  • The Vivalytic system allows fully automated sample analysis with minimal manual steps.
  • It eliminates the need for expensive and complex laboratory equipment.
  • Vivalytic supports both single and multiplex tests.
  • The Vivalytic does not require peripheral equipment such as a laptop, keyboard, barcode scanner, or charging station.
  • The cartridge used in the system ensures hygienic and safe operation as a closed system.
  • Cartridges can be stored and used at room temperature.
  • Vivasuite, a cloud-based solution, facilitates convenient device management.
  • The Vivalytic can be seamlessly integrated into existing IT structures using HL7, Ethernet, USB, or WLAN.
Vivalytic Reflection

For more information please contact us at:

Dementia Action Week 2023

Dementia Action Week is a national event that sees people across the UK taking action to improve the lives of people affected by dementia, as organized by the Alzheimer’s Society.

Dementia is an umbrella term for a range of progressive conditions that affect the brain.

Each type of dementia stops a person’s brain cells (neurons) working properly in specific area and affecting their ability to remember, think and speak cohesively. 

It is estimated that one in three people born this year nationwide will develop some form of Dementia at some point in their lives.


A cure for Dementia has unfortunately not yet been developed. However, in the pursuit of a cure, there is things that have the potential to vastly improve the quality of life for those living with these conditions.

Here at Randox, there is a focus on preventative healthcare. Which is why it made sense when Randox partnered with Race Against Dementia for their nominated charity of  2023.

Race Against Dementia is a global charity founded by three-times Formula 1 World Champion Sir Jackie Stewart, OBE – with the aim of funding much needed pioneering research into the prevention and cure of Dementia.


Also, in our work of towards diagnosis and treatments for those living with Dementia conditions, Randox Laboratories have launched a CE marked Alzheimer’s Disease Risk Array.

Alzheimer’s is one of the most common forms of Dementia and is an irreversible, progressive brain disorder, in which parts of the brain are damaged over time. 

Randox Laboratories’ Alzheimer’s Disease Risk Array can be used for the direct determination of ApoE4 status from plasma, eliminating the need for genetic testing, assisting in clinical research and personalized medicine strategies.

At Randox, we believe the importance of measuring ApoE4 protein expression in plasma is the way forward to screen those individuals at increased risk of Alzheimer Disease, as new beta amyloid-targeting therapies for this condition are being expected.    


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