Lp(a) Awareness Day 2024

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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.

Conclusions

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 randox.com/lipoproteina/ or reach out to us at marketing@randox.com.

References

  1. World Health Organization. Cardiovascular Diseases. World Health Organization. Published June 11, 2021. https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)
  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:https://doi.org/10.1194/jlr.r067314
  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:https://doi.org/10.1016/j.ijcrp.2023.200173
  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:https://doi.org/10.3390/jcm12030764
  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:https://doi.org/10.1016/j.atherosclerosis.2023.01.014
  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:https://doi.org/10.3390/molecules28030969
  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:https://doi.org/10.1111/joim.12981
  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:https://doi.org/10.1093/eurheartj/ehac361
  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:https://doi.org/10.1016/j.jacc.2016.11.042
  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:https://doi.org/10.1194/jlr.r060582
  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:https://doi.org/10.1194/jlr.r051904
  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:https://doi.org/10.4045/tidsskr.21.0800
  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:https://doi.org/10.1016/j.plabm.2021.e00218

Copper Assay

Reagent | Copper

A Unique Test for the Determination of Copper

Benefits of the Randox Copper Assay

Exceptional correlation

A correlation coefficient of r=0.97 was displayed when the Randox copper assay was compared to commercially available methods.

Excellent precision

The Randox copper assay displayed a precision of <2.15% CV.

Wide measuring range

The Randox copper assay has a measuring range of 6.6 – 86µmol/l for the comfortable detection of clinically important results.

Standard supplied with the kit

The Randox copper kit includes the standard simplifying the ordering process. Calibrator is available for automated use.

Controls available

Controls available offering a complete testing package.

Applications available

Applications available detailing instrument-specific settings for the convenient use of the Randox copper assay on a variety of clinical chemistry analysers.

Ordering information

Cat NoSize
CU2340R1a 1 x 105ml
R1b 5 x 20ml
R2 1 x 30ml
EnquireKit Insert RequestMSDSBuy Online

Instrument Specific Applications (ISA’s) are available for a wide range of biochemistry analysers.  Contact us to enquire about your specific analyser.

  • PHYSIOLOGICAL SIGNIFICANCE
  • ANTIOXIDANT / PRO-OXIDANT
  • DEFICIENCY
  • TOXICITY

Copper (CU) is an essential trace mineral, naturally available in some foods and as dietary supplements. CU is a cofactor for several enzymes, known as cuproenzymes, which are involved in connective tissue synthesis, energy production, iron metabolism, neuropeptide activation and neurotransmitter synthesis. CU is also involved in brain development, immune system functioning, neurohormone homeostasis, pigmentation, regulation of gene expression, and several physiological processes, such as angiogenesis 1.

CU has been recognised as both an antioxidant and pro-oxidant. Naturally occurring within the body, free radicals interact with genetic material, damage cell walls and contribute to the development of several health problems. As an antioxidant, CU scavenges to neutralise the free radicals, aiding in the prevention of oxidative damage. Conversely, as a pro-oxidant, CU can promote free radical damage, inducing the development of health problems such as Alzheimer’s disease. Consequently, CU is vital as part of a balanced diet 2.

CU deficiency in Western countries is rare, however, altered CU metabolism may influence CU deficiency which negatively impacts the connective tissue, nervous, immune and cardiovascular systems. Such conditions that can predispose CU deficiency include: prematurity, gastric bypass, burns, over-the-counter vitamins containing zinc and iron and infants fed with unmodified cow milk 3.

Menkes disease is a rare x-linked recessive disorder of CU metabolism caused by mutations to the ATP7A gene. Menkes disease affects an estimated 1 in every 100,000 – 250,000 births and is characterised by sparse, kinky hair and failure to thrive and progressive deterioration of the nervous system. Symptoms commonly present during infancy, but, in some cases, the symptoms may present in early to middle childhood. If treatment is started early, the prognosis may improve 4.

Copper toxicity is also rare but can be caused by consuming too many dietary supplements high in copper, drinking contaminated water and from fungicides containing CU sulphates 3.

Wilson’s disease is an autosomal recessive disorder caused by mutations to the ATP7B gene, which is highly expressed in the liver, kidneys and placenta. Wilson’s disease affects approximately 1 in every 40,000 and is characterised by hepatic, neuropsychiatric and ophthalmic symptoms as a result of excess copper accumulation. Unlike most genetic diseases, early detection and implementation of a treatment plan for those with Wilson’s disease can prevent longer term morbidity due to copper induced end organ dysfunction 3.

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D-3-Hydroxybutyrate & Diabetic Ketoacidosis

Diabetic Ketoacidosis is characterised by an accumulation of ketone bodies in response to insulin deficiency, most commonly occurring in T1DM patients, but is becoming increasingly prevalent among sufferers of T2DM.

Diabetic ketoacidosis is associated with symptoms such as polyuria, polydipsia, fever, vomiting, abdominal pain and fatigue with the most severe cases resulting in disastrous consequences such as cerebral oedema and death.

D-3-Hydroxybutyrate is considered to be the predominant ketone bodies associated with diabetic ketoacidosis and novel methods of detection utilise this biomarker to provide robust and accurate quantification of ketone bodies and aid in confident diagnosis of diabetic ketoacidosis.

This guide discusses the physiological and pathological processes associated with diabetic ketoacidosis and the relevant biomarkers, the complications associated with this condition and classic and novel detection methods.

To download this guide, simply click the image at the top of this post!
For more information on this assay visit https://www.randox.com/d-3-hydroxybutyrate-ranbut/
To read about some of our other superior performance reagents visit https://www.randox.com/superior-performance-and-unique-
Or, to view our wide range of diagnostic solutions visit https://www.randox.com/

 

Randox Reagents H-FABP & AKI

Determining bilirubin concentration in paediatric facilities – Vanadate Oxidation Method

The quantification of bilirubin has a wide range of diagnostic utility. In paediatric settings, bilirubin concentrations are commonly used to identify cases of bilirubin encephalopathy or kernicterus.

Historically, bilirubin quantification has been achieved through various techniques derived from the diazo method, first described by Van der Bergh and Muller in 1918. New technologies and novel methods, like the Vanadate Oxidation method, have emerged and have been shown to display superior diagnostic power, driven by its lower sensitivity to interference caused by haemolysis and lipemia when compared with other methods.

This week, we present our educational guide, ‘Determining bilirubin concentrations in paediatric facilities’ which details the key points relating to bilirubin quantification, along with descriptions and comparisons of the methods mentioned above.

To download this guide, simply click the image at the top of this post!
For more information on our Vanadate Oxidation Bilirubin assay visit: www.randox.com/bilirubin
To view our wide range of diagnostic solutions visit: www.randox.com/
Or, if you’d like to discuss this assay, or any of our other products, please contact us at: marketing@randox.com
Randox Reagents H-FABP & AKI

Randox Health partners with REVIV

Randox Health have entered into an exciting new partnership with REVIV

Randox Health Clinics are pioneering preventative health care, bringing the world’s most advanced and personalized health programs directly to the public – with the goal of harnessing the power of testing and data to shift healthcare away from sickness management and towards a more proactive approach.

This partnership with REVIV, who championed commercialised IV therapy, will allow people to see real-time results from taking steps to protect their health and to experience the future of wellness.

The IVD drip therapies include:

  • The Megaboost, that was designed with wellness in mind this infusion is packed with B vitamins, Vitamin C, Antioxidants and minerals to accomplish restoration of the body’s essential nutrients in one drip.
  • The Miniboost, similar to its larger counterpart, the Megaboost, this Miniboost is not to be underestimated! Containing B Vitamins, Vitamin C and antioxidants, it can support energy levels and the immune system whilst aiding protection against cell-damaging free radicals.
  • The Royal Flush which supercharges recovery and nutritional balance by providing the ingredients you need directly into your bloodstream. This all-in-one infusion has been directly designed to rehydrate, decreame inflammation and aid detoxification.
  • The Hydromax IV which aims to replenish your body’s salts and water.
  • The Vitaglow can support detoxification of free radicals that accumulate in the body from exposure to pollutants, daily stresses and chemicals including pesticides.
  • The Ultraviv and The Ultraviv pro, both recovery infusions. The Ultraviv can be used to aid recovery against the common cold, sore throats and even the after effects of alcohol. The Ultraviv pro combines a number of prescribed medications with essential vitamins and nutrients delivered alongside the maximum of hydration.

A full list of all REVIV drip therapies and IM booster shots will be available in the Randox Health clinics.

On REVIV partnering with Randox, David Ferguson, Chief Operating Officer, said: “Over the past few years, we’ve seen a dramatic change in people’s behaviours as they seek to understand their health and wellbeing better. At Randox Health, we provide a range of specialised health packages that enable you to take control of your health.

“Our innovative diagnostic technologies can deliver hundreds of results to give you a comprehensive overview of your health and help detect the earliest signs of illness. Collaborating with REVIV is a natural next step, combining our world-class diagnostic services with REVIV signature IV therapies to help our customers protect their current and future health.”

For more information please contact us at: marketing@randox.com


The Importance of Maintaining Regular Dietary Patterns to reduce CVD risk

Cardiovascular disease (CVD) is the leading cause of mortality worldwide. An estimated 17.9 million people died from some form of CVD in 2019, accounting for 32% of all-cause mortality that year1. Associations between diet and risk of cardiovascular complications have long been established, largely relating to alterations in lipid profiles.

For as long as anyone can remember, breakfast has been considered the most important meal of the day. Previous studies2 have shown an association between skipping breakfast and increased CVD risk prompting recommendations that up to 30% of one’s daily energy intake should be consumed during the first meal of the day. It has been reported that over 25% of adults skip breakfast. These individuals are often socioeconomically disadvantaged, shift workers, individuals who work particularly long hours, those who suffer from depression or those with poor health literacy2. Another study3 showed that skipping breakfast, when compared with consuming a high-energy breakfast, was associated with a 1.6x and 2.6x higher probability of non-coronary and general atherosclerosis respectively, when all other CVD risk factor had been controlled. This suggests a close relationship between eating breakfast and reducing CVD risk, however, the mechanisms and magnitude of this relationship are poorly understood.

Small, dense low-density lipoprotein cholesterol (sdLDL-C) is a smaller form of LDL-C which boasts greater propensity for uptake by arterial tissue, increased proteoglycan binding, and increased susceptibility for oxidation4. sdLDL-C concentration is strongly associated with CVD risk, yet once again, the mechanisms of this association remain enigmatic. It is thought that all of the metabolic changes associated with alterations in sdLDL-C concentration collectively contribute to the increased risk of CVD, with the main drivers being its propensity for uptake by arterial tissues and its long circulatory stability4

Skipping breakfast and sdLDL-C

A recent study investigated the relationship between skipping breakfast and the effects on lipid parameters5. In a cohort of around 28’000 people from the Japanese population, this study looked at the several markers, including sdLDL-C, to develop an understanding of the importance of regular dietary patterns for reducing the risk of CVD.

The study participants were divided into two main categories: breakfast eaters and breakfast skippers. These categories were further subdivided to differentiate men and women, over and under 55 years old, and those who eat staple products (rice, pasta, bread, etc.) and those who did not. The participants contributed blood samples which were tested for several cardiovascular biomarkers: Creatinine, Liver ALT, Total Cholesterol, Triglycerides, direct LDL-C, HDL-C and sdLDL-C.

They found that around 26% of men and 16.9% of women skipped breakfast regularly. Of these, most were considered young and had significant increases in concentration of triglycerides, LDL-C and sdLDL-C compared with those who ate breakfast almost every day.

Table 1. Median concentration of triglycerides, LDL-C, and sdLDL-C for breakfast skippers and eaters5

Analyte Breakfast Skippers (mg/dL) Breakfast Eaters (mg/dL)
Triglycerides 103 93
LDL-C 124 122
sdLDL-C 34.7 32

This investigation also revealed that in this cohort, 20% of men and 27.3% of women did not regularly consume staple foods as part of their diet and had higher median sdLDL-C concentration.

Table 2. Median concentration of sdLDL-C in men and women who eat or skip staple food products in their diet5

Gender Staple Skippers (mg/dL) Staple Eaters (mg/dL)
Men 34.1 31.6
Women 25.8 24.7

The data from this study supports the finding that individuals who skipped breakfast had higher sdLDL-C concentrations than those who ate breakfast consistently. Skipping breakfast can therefore be associated with troublesome lipid parameters in both genders and all age groups in the Japanese population. This study suggests that eating breakfast every day is crucial to maintain beneficial lipid parameters and reduce the risk of developing CVD.

The data also show that individuals who skipped staple foods in their meals presented with higher concentrations of sdLDL-C and a higher sdLDL-C/LDL-C ratio, in men and postmenopausal women, when compared with those who included staple foods in their meals. It is becoming increasingly common to remove staple foods from one’s diet due to their high carbohydrate content and the prevalence of low-carbohydrate diets. This data exhibits the importance of maintaining a nutritionally balanced diet to help reduce the risk of developing CVD.

As the first large scale study of its kind, this analysis provides clear insight into the increased risk of CVD associated with not only skipping breakfast, but failing to maintain a nutritionally balanced diet. The major limitation of this analysis is that it only includes individuals from the Japanese population and the same affects may not be seen in populations from other ethnicities. Therefore, further in-depth analysis is required to confirm these findings in other ethnicities

 

Randox sdLDL-C Assay

The Randox sdLDL-C assay employs the clearance method which displays good correlation with the gold standard in sdLDL-C quantification, giving laboratories increased confidence in their results first time, every time. Supplied as liquid ready-to-use reagents, this this test can be applied to a wide range of clinical chemistry analysers, producing results in as little as 10 minutes. Relevant controls and calibrators are also available from Randox as part of the Acusera range.

Randox sdLDL-C Assay Key Features

  • Direct, automated test for convenience and efficiency.
  • Rapid analysis results can be produced in as little as ten minutes, facilitating faster patient diagnosis and treatment plan implementation.
  • Liquid ready-to-use reagents for convenience and ease of use.
  • Applications available detailing instrument specific settings for a wide range of clinical chemistry analysers.
  • sdLDL-C controls and calibrator available.

References

  1. World Health Organization. Cardiovascular Diseases. World Health Organization. Published June 11, 2021. https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)
  2. Ofori-Asenso R, Owen AJ, Liew D. Skipping Breakfast and the Risk of Cardiovascular Disease and Death: A Systematic Review of Prospective Cohort Studies in Primary Prevention Settings. Journal of Cardiovascular Development and Disease. 2019;6(3):30. doi:https://doi.org/10.3390/jcdd6030030
  3. Uzhova I, Fuster V, Fernández-Ortiz A, et al. The Importance of Breakfast in Atherosclerosis Disease. Journal of the American College of Cardiology. 2017;70(15):1833-1842. doi:https://doi.org/10.1016/j.jacc.2017.08.027
  4. Rizvi AA, Stoian AP, Janez A, Rizzo M. Lipoproteins and cardiovascular disease: An update on the clinical significance of atherogenic small, dense LDL and new therapeutical options. Biomedicines. 2021;9:1579. doi:https://doi.org/10.3390/biomedicines9111579
  5. Arimoto M, Yamamoto Y, Imaoka W, et al. Small dense low-density lipoprotein cholesterol levels in breakfast skippers and staple food skippers. Journal of Atherosclerosis and Thrombosis. 2023;30. doi:https://doi.org/10.5551/jat.64024

For more information on our sdLDL-C assay or any of our other products, please contact us at: marketing@randox.com

 

 

 

Randox Reagents H-FABP & AKI

Foal IGG

 

 

 

VeraSTAT-V | Foal IgG test 

Foal’s Future, In Stable Hands

 

 

Benefits of the VeraSTAT-V Foal IgG test

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    Measure the failure of passive transfer (FTP) of antibodies which occurs in 10 to 20% of new-born foals in 6 minutes
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    Lightweight, portable and convenient POC device delivering results when and where they are required

     

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    Delays in sending samples for lab testing are eliminated, providing immediate on-site Foal IgG testing to assess FTP
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    Test results are exported via Bluetooth connectivity so that results can be saved and tracked overtime
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    Tests are effective with 10 μl of blood sample to ensure foals receive sufficient transfer
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    Intuitive interface provides guidance though the entire testing process, enabling ease of use an interpretation of results

An Introduction to the NEW Foal IgG test

The latest edition to the VeraSTAT-V testing menu is the foal IgG test. Essential IgG antibodies are not transferred maternally to a foal within the womb, meaning the foal is born with no immune system to defend itself from potential bacterial infections outside the womb. Low IgG levels can lead to further complications such as pneumonia and arthritis.

The new born foal only has 24-48 hours in which its intestinal mucosa remains permeable enough to absorb the antibodies, it is therefore crucial to measure whether a foal has received enough IgGs during this timeframe to protect its immune system until it is old enough to produce its own.

Why this test is essential 

The VeraSTAT-V device measures quantitative levels of IgG in blood to determine whether a sufficient transfer of antibodies have been achieved. Ideally the IgG levels should exceed 800mg/dL2. Levels below 400 mg/dL indicate inadequate passive transfer and the need for IgG supplementation.

Foals with low IgG levels are usually unable to fight infection and are therefore more likely require veterinary intervention. In this case immunoglobins should be tested regularly to ensure that enough antibodies have been received before the foal can be discharged.

Click here to download Windows App:

  1. Download VeraSTAT-V Analyzer windows application to your computer.
  2. Extract the zipped file and double click VeraSTAT-V setup
  3. Follow the application install instruction to install the application on device
Download

Interpretation of Results

Ordering Information

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VeraSTAT-Sports Performance

Best in the Field

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    Eliminate delays in sending samples to labs and receive rapid results for rapid recovery in 6 minutes.

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    Requires just a few drops of whole blood or serum, ideal for use at the point of care.

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    Lightweight, portable and convenient, the Randox VeraSTAT delivers diagnostic results where and when they are required.

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    The Randox VeraSTAT allows for results to be exported via bluetooth connectivity.

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    Intuitive user interface guides the operator through the entire testing process.

VeraSTAT-Improve your performance

As the best it’s field, the Randox VeraSTAT device allows athletes to overcome the limitations of other generation tests, providing accurate, cost effective and reliable results that will help users receive the care necessary to get them back on their feet and back to their best.

Monitoring response to exercise is vitally important to an athlete and trainer. While a heavy training schedule can lead to chronic immunosuppression in athletes, it is essential that they receive the appropriate care in the case of a dip in health state. Eliminating the risk of inflammation and infection is essential to preventing disruptions to practice and performance.

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VeraSTAT Test Menu

The VeraSTAT testing menu is designed to monitor an athletes immune response to exercise. C-Reactive Protein (CRP) levels are used to guide the treatment of bacterial infections or inflammation associated with tissue injury and other inflammatory disorders. On the other hand, Mxyovirus Resistance Protein 1 (MxA) is used as a key indicator of viral infections. These tests used in combination, can allow healthcare clinicians to determine the best course of treatment and get the athlete back to full health

C-Reactive Protein (CRP)

CRP is a Key indicator of inflammation and stress, often resulting from the breakdown in tissues. Overtraining can lead to elevated levels of CRP in the body.

 

Myxovirus Resistance Protein I (MxA)

MxA is a key indicator of a viral infection which may impact physical performance and activity levels. Unexplained failures are often attributed to recent or current infections.

Glycated Hemoglobin (HbA1c)

*In Development

For the quantitative determination of Hemoglobin A1c in whole blood samples

COMING SOON

Creatine Kinase MB (CKMB)

* In Development

For the quantitative measurement of CK-MB in whole blood samples to assist diagnosis of an acute myocardial infarction

COMING SOON

World Heart Day 2022

World Heart Day 2022

World Heart Day – Raising awareness of Cardiovascular Diseases

On 29th September, World Heart Day is an opportunity for everyone to stop and consider how best to use heart for humanity, for nature, and for yourself. Beating cardiovascular disease is something that matters to every beating heart.

In May 2012, world leaders committed to reducing global mortality from non-communicable diseases (NCDs) by 25% by 2025. Cardiovascular disease (CVD) is accountable for nearly half of all NCD deaths making it the world’s number one killer. World Heart Day is, therefore, the perfect platform for the CVD community to unite in the fight against CVD and reduce the global disease burden.

World Heart Day is a global campaign created by the World Heart Federation in which it informs people around the globe that CVD, including heart disease and stroke, is the world’s leading cause of death claiming 18.6 million lives each year. It aims to highlight the actions that individuals can take to prevent and control CVD as well as to drive action to educate people by controlling risk factors such as tobacco use, unhealthy diet, and physical inactivity.

What are cardiovascular diseases?

Cardiovascular diseases (CVDs) are a group of disorders relating to the heart and blood vessels and they include:

  • coronary heart disease – disease of the blood vessels supplying the heart muscle
  • cerebrovascular disease – disease of the blood vessels supplying the brain
  • peripheral arterial disease – disease of blood vessels supplying the arms and legs
  • rheumatic heart disease – damage to the heart muscle and heart valves from rheumatic fever, caused by streptococcal bacteria
  • congenital heart disease – malformations of heart structure existing at birth
  • deep vein thrombosis and pulmonary embolism – blood clots in the leg veins, which can dislodge and move to the heart and lungs

How can Randox help with these current global challenges

Cardiovascular disease, including heart disease, is easier to treat when detected early. Here at Randox, we utilise innovative diagnostic tests for early risk assessment capable of diagnosing disease at the earliest possible stages, because we understand that “prevention is better than cure”.

Randox Laboratories is a world leader in innovative diagnostics with 40 years’ experience and a leading provider of diagnostic reagents for the assessment of cardiovascular disease risk. Randox offer an extensive menu of cardiac biomarkers within the cardiology reagents panel including:

Risk Assessment

  • CK-MB – useful in patients with chest pain; Creatine Kinase is an enzyme produced in many different types of cells, of which high levels indicate muscle trauma or damage.
  • Myoglobin – a small protein which leaks out of muscle cells after injury, is also considered a biomarker for the detection of Myocardinal Infraction.
  • Routine lipid tests to determine the patient’s cholesterol and triglyceride levels HDL Cholesterol, LDL Cholesterol, Total Cholesterol and Triglycerides
  • Independent risk assessment tests such as sdLDL Cholesterol and Lipoprotein(a) to determine any genetic factors which may increase their risk of CVD. Please note, this is necessary even for patients who have good cholesterol levels
  • Secondary tests, such as High Sensitivity CRP, in addition to risk assessment markers and lipid evaluation – secondary tests are important in predicting future cardiac events of individuals with no previous history of CVD and those deemed healthy because of primary tests; approximately half of all heart attacks occur in patients classified as low risk. In addition, they can also be used to evaluate the risk of a recurrent cardiac event
  • Homocysteine – elevated levels of homocysteine have been linked to various disease states including CVD. Extremely high levels are found in patients with homocystinuria, of which many suffer from early arteriosclerosis.

More information

If you are a clinician or lab interested in our Cardiology & Lipids Panel, we have a wealth of resources available:

Download our Reagents Brochure 

Download our Cardiology & Lipid Testing Brochure

If you would like to get in touch with a Sales representative please email us reagents@randox.com

 

 

Cardiac QC

Acusera Cardiac Controls is designed to deliver an assayed solution for Tropinin I and NT-proBNP testing. Its intended use with Roche, Abbott and Siemens. This control is manufactured using only the highest quality material and offers a 7-day thawed stability at +2ºC to +8ºC.

Four levels are available covering the clinically relevant range, including High Sensitivity Troponin I.

Features and Benefits

  • Liquid for ease-of-use stability
  • Aqueous material
  • 4 Clinically relevant levels (including Ultra-Low)
  • Stable to expiry date at -18-24ºC storage
  • Thawed stability of 7 days at 2°C – 8°C

For more information, visit our Cardiac Quality Control website 

If you have any other queries, don’t hesitate on contacting us at qualitycontrol@randox.com

Heart Health Test

High Cholesterol is a major risk factor for heart disease and stroke therefore at Randox Health we have the Heart Health Test to keep our cholesterol at a healthy level. This is done from the convenience of your home with our home sample collection kit. Heart Health measures your total cholesterol, HDL (good) cholesterol, LDL (bad cholesterol) and triglycerides.

Why we get tested?

There is so much importance in identifying cholesterol imbalance early which allows you to make appropriate dietary and lifestyle changes which in turn reduces your risk of heart disease and stroke. It is essential to acknowledge that regardless of your age and physical health, anyone can have high cholesterol; high levels may be a result of genetics or lifestyle which can often display with no underlying symptoms. Those with a family history of heart disease, who are overweight/ obese, drink alcohol, smoke regularly, lead a sedentary lifestyle or have diabetes are at an increased risk and should get tested.

Find out more here

Want to know more about Randox?

Contact us or visit our homepage to view more.


CRP & MxA VeraSTAT

VeraSTAT | CRP & MxA 

Rapid Differentiation of Viral & Bacterial Respiratory Infections

MxA protein has the potential to greatly enhance the rapid detection of viral respiratory infections and increases significantly when there is actuate viral infection.
CRP is the dominant acute phase protein often used to guide treatment of a bacterial infection or inflammation associated with tissue injury, inflammatory disorders, and associated diseases.

Together, allow clinicians to make appropriate decision in supporting antimicrobial stewardship and guide thappropriate use of antibiotics.

MxA

VeraSTAT MxA kit is an in vitro near-patient diagnostic test for the quantitative determination of Myxovirus resistance protein A (MxA) from whole blood.  The MxA Kit is used for detection of acute respiratory tract viral infections from symptomatic patients.

CRP

VeraSTAT CRP kit is an in vitro near-patient diagnostic test for the quantitative determination of C-reactive protein (CRP) from whole blood to assess the inflammatory status of the body.

Sample Volume- 7 μL

Sample Type- Whole Blood

Measuring Time- 11 minutes

Ordering Information: VS1004

Sample Volume- 5 μL

Sample Type- Whole Blood

Measuring Time- 6 minutes 

Ordering Information: VS1003

Enquire Now

MxA Test- Training Video

CRP Test- Training Video

Useful Resources

VERASTAT-V

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VERASTAT BROCHURE


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