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BY 4.0 license Open Access Published by De Gruyter June 5, 2023

Consensus document for lipid profile testing and reporting in Spanish clinical laboratories: what parameters should a basic lipid profile include?

  • Teresa Arrobas Velilla EMAIL logo , Carlos Guijarro , Raquel Campuzano Ruiz , Manuel Rodríguez Piñero , José Francisco Valderrama Marcos , Antonio Pérez Pérez , Antonio M. Botana López , Ana Morais López , José Antonio García Donaire , Juan Carlos Obaya , Luis Castilla Guerra , Vicente Pallares Carratalá , Isabel Egocheaga Cabello , Mercedes Salgueira Lazo , María Mar Castellanos Rodrigo , José María Mostaza Prieto , Juan José Gómez Doblas , Antonio Buño Soto and on behalf of the Multidisciplinary Task Force for Lipids and Vascular Risk
From the journal Advances in Laboratory Medicine / Avances en Medicina de Laboratorio
https://doi.org/10.1515/almed-2023-0047
A translation of this article can be found here: https://doi.org/10.1515/almed-2023-0010
Download article (PDF)

Abstract

Cardiovascular diseases (CVD) continue to be the main cause of death in our country. Adequate control of lipid metabolism disorders is a key challenge in cardiovascular prevention that is far from being achieved in real clinical practice. There is a great heterogeneity in the reports of lipid metabolism from Spanish clinical laboratories, which may contribute to its poor control. For this reason, a working group of the main scientific societies involved in the care of patients at vascular risk, has prepared this document with a consensus proposal on the determination of the basic lipid profile in cardiovascular prevention, recommendations for its realization and unification of criteria to incorporate the lipid control goals appropriate to the vascular risk of the patients in the laboratory reports.

Keywords: apolipoprotein B; biochemistry; cardiovascular diseases; cholesterol; consensus; lipoprotein (a)

Introduction

Cardiovascular diseases (CVDs), including coronary heart disease and cerebrovascular disease are the leading cause of mortality and disability in the world [1]. In Spain, CVDs continue to be the leading cause of death, followed by tumors and COVID-19 even during the height of the pandemic [2]. As the underlying pathological process in most CVDs, arteriosclerosis is a gradual process that occurs over decades. The main associated risk factors are widely known. Among them, dislipidaemia is a well-known risk factor which control has proven to reduce cardiovascular morbimortality [3, 4]. While there is a large therapeutic armamentarium for dyslipidaemia, the level of control over lipid abnormalities is clearly suboptimal, particularly in patients with a (very) high cardiovascular risk, in whom reducing absolute risk is crucial [5], [6], [7], [8].

An update of ESC Guidelines on Cardiovascular Disease Prevention in Clinical Practice was recently published [9]. These guidelines are supported by the major Spanish scientific societies involved in cardiovascular disease, including the CEIPV (Comité Español Interdisciplinario de Prevención Vascular) [10], [11], [12], [13].

Therapeutic targets for lipid-lowering therapies have been established and widely accepted. However, the reference values provided on laboratory biochemistry reports continue to be based on the distribution of values in the general population. Unfortunately, the “desirable” values according to the level of cardiovascular risk of the patient are all too often not provided. In spite of SEA (Spanish Society of Arteriosclerosis) and 2018 SEC (Spanish Society of Cardiology) recommendations [14, 15], lipid values largely exceeding “desirable” values in terms of cardiovascular prevention [16] are often reported as “normal”, whereas “desirable” values are reported as “abnormally low”. This information may be misleading and result in therapeutic abstention in patients with “normal” values, and dose reduction in patients with “abnormally low” values. For this reason, a working group of the main scientific societies involved in the care of patients with vascular risk have prepared this document, which includes a basic consensus proposal for the determination of the basic lipid profile in cardiovascular disease prevention, a set of recommendations for its implementation, and some standard criteria to incorporate lipid control targets adjusted to the vascular risk of the patient on laboratory reports.

Pre-analytical considerations

How, when and in which cases should lipid profile testing be ordered?

Lipid profile is necessary to assess the risk of developing a cardiovascular disease in apparently-healthy subjects and in high-risk clinical conditions, including candidates to cardiovascular surgery. Lipid profile is also required to assess the therapeutic effectiveness of and adherence to lipid-lowering treatments. It is essential in the prevention of CVDs, especially in subjects with a high cardiovascular risk or having relatives with a high cardiovascular risk. Likewise, it is part of the global assessment of other disorders causing secondary dyslipidaemias. Our Task Force deems that recent recommendations from the Spanish Society of Cardiology [9], recently translated [10], and supported by the Spanish Committee of Vascular Prevention [13], provide appropriate reference values (Table 1A and B).

Table 1A:

Lipid determination for assessing cardiovascular risk [17].

Patients not receiving with lipid-lowering drugs.

  1. Routine vascular risk assessment is recommended in patients presenting a major cardiovascular risk factor (i.e. familial history of early CVD, familial hypercholesterolemia, or factors such as tobacco use, arterial hypertension, diabetes mellitus, hyperlipemia, chronic renal disease, obesity or comorbidities that increase the risk for CVD).

  2. Consider routine or opportunistic assessment of CVR in men >40 years and women>50 years or postmenopausal women of the general population without CV risk factors.

  3. Consider follow-up assessment at 5 years (or earlier if the risk is close to therapeutic thresholds) in all subjects who have undergone screening for CVD risk during an opportunistic screening.

  4. Routine CVR assessment is not recommended in men <40 years and women <50 years without known CVR factors.
Monitoring of therapeutic efficacy and adherence to lipid lowering treatment

  1. Before lipid-lowering therapy is initiated perform 2 determinations within a 1–2 week interval, except in case of cardiovascular event and in patient with very high risk with indication for immediate treatment.

  2. Once lipid-lowering treatment has been initiated, repeat laboratory analysis.

    1. After an acute atherosclerotic vascular event, at 4–6 weeks.

    2. In patients who are stable in cardiovascular terms, at 8±4 weeks until targets are achieved.

  3. Once the patient has reached the optimal lipid target, how often should lipids be measured? On a yearly basis
Table 1B:

Lipid targets according to cardiovascular risk [9].

  1. In cases of very high CVR, a 50 % reduction of the baseline value is recommended, along with and a target LDL chol <1.4 mmol/L (<55 mg/dL), non-HDL ch. <85 mg/dl and ApoB <65 mg/dL.

  2. In case of high CVR, a 50 % reduction of the baseline value is recommended, along with a target LDL chol <1.8 mmol/L(<70 mg/dL), non-HDL ch. <100 mg/dl and ApoB <80 mg/dL.

  3. In case of moderate CVR, a target LDL chol <2.6 mmol/L(<100 mg/dL), non-HDL ch. <131 mg/dl and ApoB <100 mg/dL is recommended.

  4. In case of low CVR, consider a target LDL <3.0 mmol/L (<116 mg/dl).

Suspect for familial hypercholesterolemia in patients who developed arteriosclerotic cardiovascular disease before 55 years (men) or 60 years of age (women); subjects with a relative who had early CVD; subjects with relatives with tendon xamtomata; patients with very elevated LDL chol. (Adults, > 5 mmol/L [190 mg/dL]; children>4 mmol/L [150 mg/dL]) and first-degree relatives with familial hypercholesterolemia.

In children, perform testing from 5 years of age or younger, upon suspicion for homozygous familial hypercholesterolemia (HFHo).

  1. CVD, cardiovascular disease; CVR, cardiovascular risk; LDL-c, cholesterol associated to low density lipoproteins; Apo B, apolipoprotein B.

Factors influencing lipid profile determination

Laboratory parameters may be influenced by multiple factors. Thus, samples should be collected when the patient is in a “stable metabolic status” [18].

Recommendation 1: Testing lipid profile is not recommended in a context of non-cardiovascular acute inflammatory process. Lipid profile should be determined within the first 24 h after an acute arteriosclerotic ischemic event.

Lifestyle and pathophysiological status of the patient:

  1. The patient should maintain regular habits in the two previous weeks prior to the blood test.

  2. The patient should not do strenuous exercise before a blood test.

  3. The patient should remain in sitting position 15 min before the blood test.

  4. Phlebotomy should be standardised: Venous blood should be drawn with the patient in sitting position (levels of Tg and LDL-c may be lower in supine position).

  5. Exclude secondary dyslipidaemias and dyslipidaemias related to drug therapy. Annex 1 [19, 20].

  6. In case of an acute inflammatory process, phlebotomy should be performed at least 2–4 weeks after the process, since the process may cause a decrease in total cholesterol, LDL cholesterol, and HDL cholesterol, and an increase in triglycerides [21–24].

  7. In case of acute coronary syndrome (or other acute ischemic atherosclerotic event), lipid profile should be obtained within the first 24 h [25–27]. If it is performed>24 h after the acute process, levels of total cholesterol and LDL-c may be reduced with respect to the values normally found in the patient, a phenomenon that should be taken into account in clinical decision-making. In patients that have never undergone a lipid profile test, Lp (a) testing is recommended. Although Lp (a) values may increase in acute processes, variation is modest [28, 29], which enables the detection of patients with significantly elevated Lp (a) in early stages.

Is it necessary that lipid profile is tested in fasting conditions?

  1. Most lipid parameters offer little variation, regardless of the patient being in fasting conditions or not [30].

  2. The main clinical guidelines do not require fasting lipid profile, at least for an initial cardiovascular risk assessment or for diagnosis of isolated hypercholesterolemia (familial hypercholesterolemia or elevated Lp(a) in the absence of elevated triglycerides). Non-fasting lipid values may better predict the risk for ASCVD, since they provide a more accurate insight into the postprandial status of the patient and the influence of residual risk [31].

  3. Triglyceride concentration is the only parameter that changes substantially after food intake [31]. Given that the Friedewald’s formula is significantly inaccurate in patients with Tg>150 mg/dL, it is recommended that LDL-c is calculated using Martin/Hopkins formula [32] (Annex. Supplementary Material table 3) or that non-HDL cholesterol is calculated instead in these patients.

  4. Fasting is recommended if Tg≥4.5 mmol/L (≥398 mg/dL) prior to the initiation of a drug therapy that can cause severe hypertriglyceridaemia (i.e. isotretinoin) and in genetically predisposed subjects with a history of hypertriglyceridemic pancreatitis. Fasting is also advised when the laboratory request includes additional laboratory tests that require that samples are collected in fasting conditions, or when morning samples are required (i.e. fasting glucose or parameters affected by circadian rhythm).

  5. Fasting and non-fasting lipid profile should be considered as complementary rather than as mutually exclusive.

  6. Cholesterol and triglycerides are generally tested using enzymatic methods, with determinations having a variability <10 % (Annex Supplementary Material Table 2) [33]. However, within-subject variability and variability resulting from sample collection conditions (≈20% for triglycerides and ≈10% for HDL cholesterol and LDL cholesterol), make it necessary that lipid profile testing is repeated in primary prevention patients without a clear indication for immediate initiation of a lipid-lowering therapy [33].

Recommendation 2: Fasting is not required for lipid profile evaluation as an initial cardiovascular risk assessment. If levels of triglycerides exceed Tg≥4.5 mmol/L (≥398 mg/dL), a second determination is recommended in fasting conditions for confirmation of results.

Analytical considerations

Should the analytical method be reported?

Lipid profile determination should always be performed using the same methods, and a change in the testing method should always be reported. It is necessary that physicians are aware of the laboratory method used in lipid profile testing, since interferences or misinterpretations may occur.

Recommendation 3: Reporting the laboratory technique or a change of units is essential for a correct interpretation of laboratory results.

Methods for the determination of LDL cholesterol

The method of reference for testing LDL-c involves separating lipoproteins by density-gradient ultracentrifugation, a time-consuming method that is only available in specialized laboratories. For this reason, LDL-c is often estimated by measuring total cholesterol and triglycerides (using enzymatic methods), and by direct HDL cholesterol determination. Friedewald’s is the most frequently used formula [34].

Friedewald’s formula for the estimation of LDL-c (in mg/dL)

LDL cholesterol=Total cholesterol – HDL cholesterol – triglycerides/ 5

Friedewald formula assumes the absence of chylomicrons and a specific of cholesterol/Tg ratio in VLDL-c(1/5 in mg/dL; 1/2.2 in mmol/L). In VLDL, the Tg/ cholesterol ratio progressively increases as hypertriglyceridaemia exacerbates; therefore, in patients with hypertriglyceridaemia, the formula overestimates VLDL-c and thus underestimates LDL cholesterol. The formula has an acceptable accuracy when Tg concentration is <200 mg/dL and it should not be used if Tg>400 mg/dL (Recommendation 4).

The Martin-Hopkins formula replaces number 5 in the Friedewald’s formula (c-VLDL= Tg/5) with divisors that vary according to the levels of Tg and non-HDL cholesterol of the patient (Annex. Supplementary Material Table) [32]. The Martin-Hopkins formula is more accurate than Friedewald’s when Tg>150 mg/dL, LDL-c <100 mg/dL, and especially when <70 mg/dL.

The Sampson formula is more complex and provides similar results to those of Martin-Hopkins for patients with Tg<400 mg/dL. As a result, the former is less frequently used. In patients with Tg>400 mg/dL, the use of formulas for the estimation of LDL-c is not recommended, due to their poor reliability.

Ultracentrifugation, the classical reference method for LDL-c determination, is labour intensive and is only used in very specialized laboratories. There is a direct, accurate, and widely-available measurement method. The use of this marker is recommended if Tg>400 mg/ dL or LDL<70 mg/dL, when LDL-c determination methods are more inaccurate [32].

When a direct method cannot be used to determine LDL cholesterol, the use of non-HDL cholesterol as a marker of “atherogenic” cholesterol is recommended [35]. Determination of apolipoprotein B can also be used (Apo B). Non-HDL cholesterol does not require Tg determination nor is it influenced by fasting. Moreover, it strongly correlates with levels of Apo B.

Recommendation 4: The Friedewald formula is accurate in most patients with LDL-c > 100 mg/dL and Tg<150 mg/dL. The modified Martin-Hopkins formula is superior for the estimation of LDL cholesterol, especially in patients with low LDL-c concentrations<70 mg/dL, Tg concentrations 150–400 mg/dL, and in non-fasting conditions. Direct LDL-c assays should be used to determine LDL-c if Tg≥400 mg/dL.

In patients with significantly elevated Lp(a) concentrations, LDL-c estimation should be corrected using the following formula:

L D L − c   c o r r e c t e d   f o r   L p ( a )   ( m g / d L ) = L D L − c   ( m g / d L ) − [ L p   ( a )   ( m g / d L ) × 0.30 ]

L D L − c   c o r r e c t e d   f o r   L p ( a )   ( n m o l / L ) = L D L − c   ( n m o l / L ) − [ L p   ( a )   ( m g / d L ) × 0.0078 ]

Potential Lp(a) elevation should be especially considered in Subsaharian patients, patients with the nephrotic syndrome, on peritoneal dyalisis, or with a poor decrease of LDL-c after having received a lipid-lowering therapy.

Post-analytical considerations

Markers of “normality” and alerts

The clinical laboratory plays a crucial role in the assessment of cardiovascular risk in patients with dyslipidaemia. It is essential that specific reference values are established for the pediatric population.

Desirable values should be provided in terms of cardiovascular risk and prevention on lipid profile reports [14], [15], [16]. Table 2 shows the desirable values for the main lipid parameters established for adults by the European Society of Cardiology, Arteriosclerosis and the Spanish Society of Laboratory Medicine (2019) [17, 33, 36].

Table 2:

Desirable lipid values in adults, according to the European Societies of Arteriosclerosis and Laboratory Medicine [17, 33, 36].

Parameter Desirable value in adults
Serum total cholesterol <200 mg/dL (5.17 mmol/L)
HDL cholesterol >50 mg/dL women (>1.29 mmol/L)
>40 mg/dL men (1.03 mmol/L)
LDL cholesterol Recommended values based on CVR

  1. Secondary prevention and very-high CVR<55 mg/dL (<1.4 mmol/L)

  2. High CVR<70 mg/dL (<1.8 mmol/L)

  3. Moderate CVR<100 mg/dL (<2.6 mmol/L)

  4. Low CVR<116 mg/dL (<3 mmol/L)
Non-HDL cholesterol Recommended values based on cardiovascular risk

  1. Secondary prevention and very-high CVR<85 mg/dL (<2.2 mmol/L)

  2. High CVR<100 mg/dL; (<2.6 mmol/L)

  3. Moderate CVR<131 mg/dL (<3.4 mmol/L)

  4. Secondary prevention and very-high CVR<85 mg/dL (<2.2 mmol/L)
Triglycerides Fasting TG <150 mg/dL (<1.69 mmol/L)
(Non-fasting TG <175 mg/dL) (<1.97 mmol/L)
Apolipoprotein B Recommended values based on CVR

  1. Secondary prevention and very-high CVR <65 mg/dL

  2. High CVR <80 mg/dL

  3. Moderate CVR <100 mg/dL (<3.4 mmol/L)
Lipoprotein (a) <50 mg/dL (<105 nmol/L)
<30 mg/dL in fasting conditions
<35 mg/dL in non-fasting conditions

  1. CVR, cardiovascular risk.

Critical values should be flagged and reported as such to the requesting physician, as shown in Table 3 .

Table 3:

Recommended alerts of the information system/laboratory report.

Parameter Critical value
Serum total cholesterol 310 mg/dL Patient with high cardiovascular risk
Triglycerides >880 mg/dL Severe hypertriglyceridaemia with risk of acute pancreatitis
Adult LDL cholesterol >190 mg/dL Consider heterozygous familial hypercholesterolemia
Adult LDL cholesterol >500 mg/dL Consider homozygous familial hypercholesterolemia
Atherogenic lipid triad If: Tg>150 mg/dL and HDL<30 mg/dL, LDL/Apo B<1.3 or Tg/HDL>2 Lipid triad suggestive of atherogenic dyslipidemia with a very high vascular risk
Lipoprotein (a) >120 mg/dL (260 nmol/L)a Very high CV risk of atherosclerotic cardiovascular disease and aortic valve stenosis
Apolipoprotein A 1 <10 mg/dL Consider hypoalphalipoproteinemia
Apolipoprotein B <10 mg/dL Consider hypo betalipoproteinemia

  1. LDL, low density lipoproten; Apo, apolipoprotein; Tg, triglycerides; CV, cardiovascular. aEstimation based on EAS/EFLM consesus document.

Recommendation 5: On laboratory reports, the reference values for lipid parameters should always be referred to the cardiovascular risk of the patient, rather than to normal reference values for the general population. The use of asterisks marking values outside the population normality range is discouraged. The use of flagging systems is recommended for extreme lipid concentrations suggestive of severe dyslipidaemias. Specific values should be established for the pediatric population.

What parameters should a basic lipid profile include?

The basic lipid profile should include the determination of total cholesterol, HDL cholesterol, triglycerides, non-HDL cholesterol and LDL-c [9, 17, 37–39] (Figure 1).

Figure 1: Basic recommendations for lipid profile reporting in Spanish clinical laboratories.
Figure 1:

Basic recommendations for lipid profile reporting in Spanish clinical laboratories.

The Consensus Statements of the European Society of Arteriosclerosis and the European Society of Laboratory Medicine also recommend the estimation of remnant particles [9–16, 36]. Elevated lipoprotein (a) confers an increased vascular risk. Therefore, it is recommended that it is measured at least once in life, since levels are substantially determined by genetic factors [9–16, 36].

In patients with Tg>400 mg/dL, direct determination of LCL cholesterol is recommended in order to obtain more reliable values [40]. If available, Apo B is a marker of special interest, since it is the best marker of the number of atherogenic lipoproteins [41]. When direct determination of LDL-c or Apo B is not available, non-HDL cholesterol can be used as an approximation.

Recommendation 6: The basic lipid profile should include the determination of total cholesterol, HDL cholesterol, triglycerides, non-HDL cholesterol and LDL-c estimation. In patients with mild/moderate hypertriglyceridaemia, testing non-HDL cholesterol and Apo B is recommended for assessing residual cardiovascular risk.

What is non-HDL cholesterol tested for?

The estimation of non-HDL cholesterol involves a simple calculation (total cholesterol – HDL cholesterol) that reflects the cholesterol of atherogenic lipoproteins. Non-HDL cholesterol strongly correlates with Apo B concentrations. Also, it is the parameter of reference in the vascular risk assessment formulas SCORE2 (Systematic Coronary Risk Evaluation) and SCOREOP (Systematic Coronary Risk Evaluation old people) [9, 42, 43]. An additional advantage of this parameter is that it is not influenced by fasting. Moreover, it can be determined in patients with Tg>400 mg/dL or be useful as a guideline in laboratories where direct LDL or Apo B determination is not available [44].

When should apolipoprotein B used?

Apo B is an excellent predictor of cardiovascular events, since this apoprotein is found in the main atherogenic lipoproteins, namely: LDL, lipoprotein (a), VLDL-cand IDL [41], [42], [43], [44], [45]. Testing Apo B is equivalent to measuring the amount of atherogenic lipoproteins, since each one contains a single molecule of Apo B. Apo B values are not affected by fasting. The amount of lipoparticles can also be measured by MRI (magnetic resonance imaging). However, this technique is not available in routine clinical practice [46].

Apo B is especially relevant in patients with elevated triglycerides, diabetes mellitus, obesity, metabolic syndrome, or very low LDL cholesterol. In these cases, measurement or estimation of LDL-c may be inaccurate and not consider the atherogenic component of other lipoproteins.

Apo B test is rarely included in standard lipid profiles or ASCVD risk assessment tests. Monogenic disorders such as familial hypercholesterolemia (FH) can be easily recognized using a standard panel of lipids. In these cases, measuring Apo B is not necessary (Annex. Supplementary Material, Table 4) [47]. On another note, Apo B concentration helps classify severe dyslipidaemias, such as combined familial hyperlipidaemia and familial dysbetalipoproteinemia [48] (Annex. Supplementary Material. Figure).

Recommendation 7: Testing Apo B is recommended for assessing vascular risk; classify dyslipidaemias and characterize particle size. It is also preferable to non-HDL cholesterol testing in patients with mild-to-moderate hypertriglyceridaemia (175–880 mg/dL), diabetes, obesity, metabolic syndrome, or very low LDL-c (<70 mg/dL).

When should lipoprotein (a) be determined?

Testing Lp (a) is recommended at least once in life to estimate vascular risk [9, 49], [50], [51], [52]. This determination is especially relevant in patients with early-onset cardiovascular disease, familial hypercholesterolemia, poor response to statin therapy, aortic stenosis or recurrent ischemic events, and in relatives to patients with elevated Lp (a). The cardiovascular risk of patients with very elevated Lp (a) (>180 mg/dL/ >430 nmol/L) is similar to that of patients with heterozygous familial hypercholesterolemia [53, 54]. One of the challenges of Lp(a) determination is the variability of results across the different detection techniques. Another disadvantage is the unavailability of a direct equivalence between values reported in mg/dL and in nmol/L, according to the different apoprotein (a) isoforms.

Lp (a) should only be measured once in life, given that it is substantially determined by genetics and there are no specific drug therapies available as yet. Exceptions to this rule include transition to menopause, pregnancy, use of oral contraceptives, chronic kidney disease/ nephrotic syndrome, or when a specific treatment is used to reduce Lp (a) or modulate the recommended therapeutic options, such as PCSK9 inhibitors [55].

Recommendation 8: Lp (a) should be determined only once in life, except when its levels may be affected by significant changes, as the development of nephrotic syndrome or the use of a therapy to reduce Lp (a). The most appropriate units of measurement are nmol/L (Annex. Supplementary Material. Comment).

Should inflammation be assessed in patients with arteriosclerosis?

Chronic inflammatory processes are associated with an increased cardiovascular risk, regardless of the risk attributable to conventional risk factors [56]. High-sensitivity C-reactive protein is the analytical parameter most frequently used as a maker of low-intensity inflammation. It has a high variability, and there is no defined consensus on the values that should be considered ‘elevated’ for the estimation of vascular risk assessment [17].

Innovations in the diagnosis of dyslipidaemias: parameters for an e-consultation

For an e-consultation to be rapid and effective, the basic parameters to be included for the diagnosis of dyslipidaemias are shown in Table 4.

Table 4:

Reference data required for assessing cardiovascular risks in an e-consultation.

(1) Age, sex, BMI and waist circumference of the patient
(2) Short summary of familial and personal medical history
(3) Risk factors: Tobacco use, alcohol use (quantified),
(4) Short summary of the lipid history and previous lipid-lowering treatments
(5) Full outline of patient treatment
(6) Possible side effects of lipid-lowering therapy.
(7) Current basic lipid profile) Total cholesterol, LDL cholesterol, HDL cholesterol, Non-HDL cholesterol and triglycerides
(8) Active problem
(9) Availability of personal or familial genetic studies.
(10) In case familial hypercholesterolemia is suspected, Dutch lipid clinic network score (DLCN)/WHO (47)
(11) On case of suspicion of hypertriglyceridemia: Moulin score for the diagnosis of familial quilomicronemia (57).

  1. BMI, body mass index; LDL, low density lipoprotein; HDL, high density lipoprotein; WHO, World Health Organization.

Corresponding author: Teresa Arrobas Velilla, Spanish Society of Laboratory Medicine (SEQCML), Laboratory of Clinical Biochemistry, Virgen Macarena University Hospital, Seville, Spain, E-mail:
Teresa Arrobas Velilla, Carlos Guijarro and Raquel Campuzano Ruiz contributed equally to this work. This article is co-published, within the framework of the corresponding publication and copyright agreement, in the following journals: Clinica e Investigación en Arteriosclerosis, Advances in Laboratory Medicine, REC: CardioClinics, Angiology, Cardiovascular Surgery, Endocrinology, Diabetes and Nutrition, Hypertension and Vascular Risk, Revista Clínica de Medicina de Familia, Revista Clínica Española, Medicina General y de Familia, Nefrología, Medicina General y de Familia, Nefrología, Revista Clínica Española, Medicina General y de Familia, Nefrología y Neurología Perspectivas. The members of the Multidisciplinary Working Group on Lipids and Vascular Risk are presented in the Contributors Section. https://doi.org/10.1016/j.arteri.2022.10.002, 0214–9168/© 2023. Published by Elsevier España, S.L.U. on behalf of the Spanish Society of Arteriosclerosis and Arteriovascular Arteriosclerosis.

Acknowledgments

To all the scientific societies involved in the preparation of the documents and presidents of their respective societies for their support in the preparation of the document.

Committee of Lipids and Vascular Diseases of the Spanish Society of Laboratory Medicine and Task Force for Cardiac Rehabilitation of the Spanish Society of Cardiology:

Nuria Amigó Grau, Biosfer Teslab, IISPV, CIBERDEM, Universidad Rovira i Virgili, Tarragona, Spain. Pilar Calmarza Calmarza, Departamento de Bioquímica.Hospital Universitario Miguel Servet, Zaragoza, Spain. Silvia Camòs Anguila, Servicio de Bioquímica Clínica, Hospital Hospital Universitari de Girona Josep Trueta, Beatriz Candás Estebanez, Laboratorio Clínico, Hospital de Barcelona, María José Castro Castro, Laboratorio Clínico Hospital Universitario de Bellvitge, Barcelona, Spain. Carla Fernández Prendes, Laboratorio de Bioquímica Hospital Universitario Germans Trias i Pujol, Barcelona, Spain. Irene González Martínez, Servicio de análisis clínicos, Hospital 12 de Octubre, Spain. María Martín Palencia, Hospital Universitario de Burgos, Spain. Carlos Romero Román, Laboratory of Clinical Biochemistry, Hospital de Albacete, Spain. José Puzo Foncillas, Laboratorio Hospital General San Jorge, Huesca, Spain. Almudena Castro Conde, Unidad de Rehabilitación Cardiaca, Servicio de Cardiología, Hospital Universitario La Paz, Madrid, Spain. Rosa Fernández Olmo, Servicio Cardiología Hospital Universitario de Jaén, Spain.

  1. Article Note: The original article can be found here: https://doi.org/10.1515/almed-2023-0010.

  2. Research funding: None declared.

  3. Author contributions: All authors have accepted responsibility for the entire content of this manuscript and approved its submission.

  4. Competing interests: Authors state no conflict of interest.

  5. Informed consent: Informed consent was obtained from all individuals included in this study.

  6. Ethical approval: The local Institutional Review Board deemed the study exempt from review.

References

1. Roth, GA, Abate, D, Abate, KH, Abay, SM, Abbafati, C, Abbasi, N, et al.. GBD 2017 Causes of Death Collaborators Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Lond Engl 2018;392:1736–88. https://doi.org/10.1016/S0140-6736(18)32203-7.Search in Google Scholar PubMed PubMed Central

2. INE Defunciones por causas (lista reducida) por sexo y grupos de edad(7947). INE Available from: https://www.ine.es/jaxiT3/Datos.htm?t=7947#!tabs-tabla [accedido 16 febrero 2022].Search in Google Scholar

3. Borén, J, Chapman, MJ, Krauss, RM, Packard, CJ, Bentzon, JF, Binder, CJ, et al.. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J 2020;41:2313–30. https://doi.org/10.1093/eurheartj/ehz962.Search in Google Scholar PubMed PubMed Central

4. Royo Bordonada, MÁ, Lobos Bejarano, JM, Millán Núñez-Cortés, J, Villar Álvarez, F, Brotons Cuixart, C, Camafort Babkowski, M, et al.. Dislipidemias: un reto pendiente en prevención cardiovascular. Documento de consenso CEIPC/SEA. Med Clínica 2011;137:30.e1–13, https://doi.org/10.1016/j.medcli.2011.02.008.Search in Google Scholar PubMed

5. De Backer, G, Jankowski, P, Kotseva, K, Mirrakhimov, E, Reiner, Ž, Rydén, L, et al.. Management of dyslipidaemia in patients with coronary heart disease: results from the ESC-EORP EUROASPIRE V survey in 27 countries. Atherosclerosis 2019;285:135–46. https://doi.org/10.1016/j.atherosclerosis.2019.03.014.Search in Google Scholar PubMed

6. Ray, KK, Molemans, B, Schoonen, WM, Giovas, P, Bray, S, Kiru, G, et al.. EU-wide cross- sectional observational study of lipid-modifying therapy use in secondary and primary care: the DA VINCI study. Eur J Prev Cardiol 2021;28:1279–89. https://doi.org/10.1093/eurjpc/zwaa047.Search in Google Scholar PubMed

7. González-Juanatey, JR, Millán, J, Alegría, E, Guijarro, C, Lozano, JV, Vitale, GC. Prevalence and characteristics of lipid abnormalities in patients treated with statins in primary and secondary prevention in Spain. DYSIS-Spain study. Rev Esp Cardiol Engl Ed 2011;64:286–94. https://doi.org/10.1016/j.rec.2010.10.030.Search in Google Scholar

8. Robinson, JG, Huijgen, R, Ray, K, Persons, J, Kastelein, JJP, Pencina, MJ. Determining when to add nonstatin therapy: a quantitative approach. J Am Coll Cardiol 2016;68:2412–21. https://doi.org/10.1016/j.jacc.2016.09.928.Search in Google Scholar PubMed

9. Visseren, FLJ, Mach, F, Smulders, YM, Carballo, D, Koskinas, KC, Bäck, M, et al.. ESC Guidelines on cardiovascular disease prevention in clinical practice: developed by the Task Force for cardiovascular disease prevention in clinical practice with representatives of the European Society of Cardiology and 12 medical societies with the special contribution of the European Association of Preventive Cardiology (EAPC). Eur Heart J 2021;42:3227–337. https://doi.org/10.1093/eurheartj/ehab484.Search in Google Scholar PubMed

10. Visseren, LJF, Mach, F, Smulders, MY, Carballo, D, Koskinas, CK, Bäck, M, et al.. Guía ESC 2021 sobre la prevención de la enfermedad cardiovascular en la práctica clínica: con la contribución especial de la European Association of Preventive Cardiology (EAPC). Rev Esp Cardiol 2022;75:429.e1–104. https://doi.org/10.1016/j.recesp.2021.10.016.Search in Google Scholar

11. Palacio-Portilla, EJ, Roquer, J, Amaro, S, Arenillas, JF, Ayo-Martín, O, Castellanos, M, et al.. Dislipidemias y prevención del ictus: recomendaciones del Grupo de Estudio de Enfermedades Cerebrovasculares de la Sociedad Española de Neurología. Neurología. 2022;37:61–72. https://doi.org/10.1016/j.nrl.2020.07.027.Search in Google Scholar PubMed

12. Mostaza, JM, Pintó, X, Armario, P, Masana, L, Real, JT, Valdivielso, P, et al.. Estándares SEA 2022 para el control global del riesgo cardiovascular. Clínica E Investig En Arterioscler 2022;34:130–79. https://doi.org/10.1016/j.arteri.2021.11.003.Search in Google Scholar PubMed

13. Armario, P, Brotons, C, Elosua, R, Alonso de Leciñana, M, Castro, A, Clarà, A, et al.. Statement of the Spanish interdisciplinary vascular prevention committee on the updated European cardiovascular prevention guidelines. Clin E Investig En Arterioscler Publicacion Soc Espanola Arterioscler 2021;33:85–107. https://doi.org/10.1016/j.arteri.2020.11.004.Search in Google Scholar PubMed

14. Pedro-Botet, J, Rodríguez-Padial, L, Brotons, C, Esteban-Salán, M, García-Lerín, A, Pintó, X, et al.. Homogeneización de los valores del perfil lipídico. Clínica E Investig En Arterioscler 2018;30:36–48. https://doi.org/10.1016/j.arteri.2017.12.001.Search in Google Scholar PubMed

15. Pedro-Botet, J, Rodríguez-Padial, L, Brotons, C, Esteban-Salán, M, García-Lerín, A, Pintó, X, et al.. El informe analítico ideal del perfil lipídico. Necesidad de un consenso. Rev Esp Cardiol 2018;71:512–4. https://doi.org/10.1016/j.recesp.2018.01.004.Search in Google Scholar

16. Wright, IS. Correct levels of serum cholesterol: average vs. normal vs. optimal. J Am Med Assoc 1976;236:261–2. https://doi.org/10.1001/jama.1976.03270030015018.Search in Google Scholar

17. Mach, F, Baigent, C, Catapano, AL, Koskinas, KC, Casula, M, Badimon, L, et al.. ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J 2020;41:111–88. https://doi.org/10.1093/eurheartj/ehz455.Search in Google Scholar PubMed

18. Cooper, GR, Myers, GL, Smith, SJ, Schlant, RC. Blood lipid measurements: variations and practical utility. J Am Med Assoc 1992;267:1652–60. https://doi.org/10.1001/jama.1992.03480120090039.Search in Google Scholar

19. Bays, HE, Jones, PH, Orringer, CE, Brown, WV, Jacobson, TA. National lipid association annual summary of clinical lipidology 2016. J Clin Lipidol. 2016;10:S1-43, https://doi.org/10.1016/j.jacl.2015.08.002.Search in Google Scholar PubMed

20. Herink, M, Ito, MK. Medication induced changes in lipid and lipoproteins. In: Feingold, KR, Anawalt, B, Boyce, A, Chrousos, G, de, Herder WW, Dhatariya, K, et al.. editors. Endotext. South Dartmouth (MA): MDText.com, Inc.; 2000.Search in Google Scholar

21. Khovidhunkit, W, Kim, M-S, Memon, RA, Shigenaga, JK, Moser, AH, Feingold, KR, et al.. Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. J Lipid Res 2004;45:1169–96. https://doi.org/10.1194/jlr.R300019-JLR200.Search in Google Scholar PubMed

22. Feingold, KR, Grunfeld, C. The effect of inflammation and infection on lipids and lipoproteins. In: Feingold, KR, Anawalt, B, Boyce, Ade, Herder WW Dhatariya, K, et al.. editors. Endotext. South Dartmouth (MA): MDText.com, Inc.; 2000.Search in Google Scholar

23. van Leeuwen, HJ, Heezius, ECJM, Dallinga, GM, van Strijp, JAG, Verhoef, J, van Kessel, KPM. Lipoprotein metabolism in patients with severe sepsis. Crit Care Med 2003;31:1359–66. https://doi.org/10.1097/01.CCM.0000059724.08290.51.Search in Google Scholar PubMed

24. Páez-Guillán, E-M, Campos-Franco, J, Alende, R, Garitaonaindía, Y, González-Quintela, A. Transient hypertriglyceridemia: a common finding during Epstein-Barr virus-induced infectious mononucleosis. Lipids Health Dis 2021;20:177. https://doi.org/10.1186/s12944-021-01603-9.Search in Google Scholar PubMed PubMed Central

25. Shrivastava, AK, Singh, HV, Raizada, A, Singh, SK. Serial measurement of lipid profile and inflammatory markers in patients with acute myocardial infarction. EXCLI J 2015;14:517–26. https://doi.org/10.17179/excli2014-671.Search in Google Scholar PubMed PubMed Central

26. Wattanasuwan, N, Khan, IA, Gowda, RM, Vasavada, BC, Sacchi, TJ. Effect of acute myocardial infarction on cholesterol ratios. Chest 2001;120:1196–9. https://doi.org/10.1378/chest.120.4.1196.Search in Google Scholar PubMed

27. Rosenson, RS. Myocardial injury: the acute phase response and lipoprotein metabolism. J Am Coll Cardiol 1993;22:933–40. https://doi.org/10.1016/0735-1097(93)90213-k.Search in Google Scholar PubMed

28. Enkhmaa, B, Anuurad, E, Berglund, L. Lipoprotein (a): impact by thnicity and environmental and medical conditions. J Lipid Res 2016;57:1111–25. https://doi.org/10.1194/jlr.R051904.Search in Google Scholar PubMed PubMed Central

29. Langsted, A, Kamstrup, PR, Nordestgaard, BG. Lipoprotein(a): fasting and nonfasting levels, inflammation, and cardiovascular risk. Atherosclerosis 2014;234:95–101. https://doi.org/10.1016/j.atherosclerosis.2014.01.049.Search in Google Scholar PubMed

30. Nordestgaard, BG, Langsted, A, Mora, S, Kolovou, G, Baum, H, Bruckert, E, et al.. Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points—a joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. Eur Heart J 2016;37:1944–58. https://doi.org/10.1093/eurheartj/ehw152.Search in Google Scholar PubMed PubMed Central

31. Mora, S, Rifai, N, Buring, JE, Ridker, PM. Fasting compared with nonfasting lipids and apolipoproteins for predicting incident cardiovascular events. Circulation 2008;118:993–1001. https://doi.org/10.1161/CIRCULATIONAHA.108.777334.Search in Google Scholar PubMed PubMed Central

32. Martin, SS, Blaha, MJ, Elshazly, MB, Toth, PP, Kwiterovich, PO, Blumenthal, RS, et al.. Comparison of a novel method vs the Friedewald equation for estimating low-density lipoprotein cholesterol levels from the standard lipid profile. J Am Med Assoc 2013;310:2061–8. https://doi.org/10.1001/jama.2013.280532.Search in Google Scholar PubMed PubMed Central

33. Wilson, PWF, Jacobson, TA, Martin, SS, Jackson, EJ, Le, N-A, Davidson, MH, et al.. Lipid measurements in the management of cardiovascular diseases: practical recommendations a scientific statement from the national lipid association writing group. J Clin Lipidol 2021;15:629–48. https://doi.org/10.1016/j.jacl.2021.09.046.Search in Google Scholar PubMed

34. Martin, SS, Blaha, MJ, Elshazly, MB, Brinton, EA, Toth, PP, McEvoy, JW, et al.. Friedewald- estimated versus directly measured low-density lipoprotein cholesterol and treatment implications. J Am Coll Cardiol 2013;62:732–9. https://doi.org/10.1016/j.jacc.2013.01.079.Search in Google Scholar PubMed

35. Sniderman, AD, Williams, K, Contois, JH, Monroe, HM, McQueen, MJ, De Graaf, J, et al.. A meta-analysis of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein b as markers of cardiovascular risk. Circ Cardiovasc Qual OuTgomes 2011;4:337–45. https://doi.org/10.1161/CIRCOUTgOMES.110.959247.Search in Google Scholar

36. Nordestgaard, BG, Langlois, MR, Langsted, A, Chapman, MJ, Aakre, KM, Baum, H, et al.. Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM. Atherosclerosis 2020;294:46–61. https://doi.org/10.1016/j.atherosclerosis.2019.12.005.Search in Google Scholar PubMed

37. Arnett, DK, Blumenthal, RS, Albert, MA, Buroker, AB, Goldberger, ZD, Hahn, EJ, et al.. ACC/AHA guideline on the primary prevention of cardiovascular disease. Circulation 2019;140:e596-600.10.1161/CIR.0000000000000678Search in Google Scholar PubMed PubMed Central

38. Grundy, SM, Stone, NJ, Bailey, AL, Beam, C, BirTgher, KK, Blumenthal, RS, et al.. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol: a report of the American college of Cardiology/American heart association Task Force on clinical practice guidelines. Circulation 2019;139:e1082–143. https://doi.org/10.1161/CIR.0000000000000625.Search in Google Scholar PubMed PubMed Central

39. Pearson, GJ, Thanassoulis, G, Anderson, TJ, Barry, AR, Couture, P, Dayan, N, et al.. Canadian cardiovascular society guidelines for the management of dyslipidemia for the prevention of cardiovascular disease in adults. Can J Cardiol 2021;S0828–282X:00165–3. https://doi.org/10.1016/j.cjca.2021.03.016.Search in Google Scholar PubMed

40. Langlois, MR, Nordestgaard, BG, Langsted, A, Chapman, MJ, Aakre, KM, Baum, H, et al.. Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM. Clin Chem Lab Med 2020;58:496–517. https://doi.org/10.1515/cclm-2019-1253.Search in Google Scholar PubMed

41. Marston, NA, Giugliano, RP, Melloni, GEM, Park, J-G, Morrill, V, Blazing, MA, et al.. Association of apolipoprotein B–containing lipoproteins and risk of myocardial infarction in individuals with and without atherosclerosis: distinguishing between particle concentration, type, and content. JAMA Cardiol 2022;7:250–6. https://doi.org/10.1001/jamacardio.2021.5083.Search in Google Scholar PubMed PubMed Central

42. SCORE2 working group and ESC Cardiovascular risk collaboration SCORE2 risk prediction algorithms: new models to estimate 10-year risk of cardiovascular disease in Europe. Eur Heart J 2021;42:2439–54, https://doi.org/10.1093/eurheartj/ehab309.Search in Google Scholar PubMed PubMed Central

43. SCORE2-OP working group and ESC Cardiovascular risk collaboration SCORE2-OP risk prediction algorithms: estimating incident cardiovascular event risk in older persons in four geographical risk regions. Eur Heart J 2021;42:2455–67, https://doi.org/10.1093/eurheartj/ehab312.Search in Google Scholar PubMed PubMed Central

44. Di Angelantonio, E, Sarwar, N, Perry, P, Kaptoge, S, Ray, KK, Thompson, A, et al., Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease. J Am Med Assoc 2009;302:1993–2000. https://doi.org/10.1001/jama.2009.1619.Search in Google Scholar PubMed PubMed Central

45. Richardson, T, Sanderson, E, Palmer, TM, Ala-Korpela, M, Ference, BA, Davey Smith, G, et al.. Evaluating the relationship between circulating lipoprotein lipids and apolipoproteins with risk of coronary heart disease: a multivariable Mendelian randomisation analysis. Plos Med 2020;17. https://doi.org/10.1371/journal.pmed.1003062.Search in Google Scholar PubMed PubMed Central

46. Pintó, X, Masana, L, Civeira, F, Real, J, Ibarretxe, D, Candas, B, et al.. Consensus document of an expert group from the Spanish Society of Arteriosclerosis (SEA) on the clinical use of nuclear magnetic resonance to assess lipoprotein metabolism (Liposcale®). Clin E Investig En Arterioscler Publicacion Of Soc Espanola Arterioscler 2020;32:219–29. https://doi.org/10.1016/j.arteri.2020.04.004.Search in Google Scholar PubMed

47. WHO Human Genetics Programme Familial hypercholesterolaemia (FH) : report of a second WHO consultation, Geneva: World Health Organization; 1999.Search in Google Scholar

48. Paquette, M, Bernard, S, Blank, D, Paré, G, Baass, A. A simplified diagnosis algorithm for dysbetalipoproteinemia. J Clin Lipidol 2020;14:431–7. https://doi.org/10.1016/j.jacl.2020.06.004.Search in Google Scholar PubMed

49. Wilson, DP, Jacobson, TA, Jones, PH, Koschinsky, ML, McNeal, CJ, Nordestgaard, BG, et al.. Use of Lipoprotein(a) in clinical practice: a biomarker whose time has come. A scientific statement from the National Lipid Association. J Clin Lipidol 2019;13:374–92. https://doi.org/10.1016/j.jacl.2019.04.010.Search in Google Scholar PubMed

50. Reyes-Soffer, G, Ginsberg, HN, Berglund, L, Duell, PB, Heffron, SP, Kamstrup, PR, et al.. Lipoprotein(a): a genetically determined, causal, and prevalent risk factor for atherosclerotic cardiovascular disease: a scientific statement from the American heart association. Arterioscler Thromb Vasc Biol 2021;42:e48-60. https://doi.org/10.1161/ATV.0000000000000147.Search in Google Scholar PubMed PubMed Central

51. Cegla, J, Neely, RDG, France, M, Ferns, G, Byrne, CD, Halcox, J, et al.. HEART UK consensus statement on Lipoprotein(a): a call to action. Atherosclerosis 2019;291:62–70. https://doi.org/10.1016/j.atherosclerosis.2019.10.011.Search in Google Scholar PubMed

52. Kronenberg, F, Mora, S, Stroes, ESG, Ference, BA, Arsenault, BJ, Berglund, L, et al.. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur Heart J 2022;43:3925–46. https://doi.org/10.1093/eurheartj/ehac361.Search in Google Scholar PubMed PubMed Central

53. Burgess, S, Ference, BA, Staley, JR, Freitag, DF, Mason, AM, Nielsen, SF, et al.. Association of LPA variants with risk of coronary disease and the implications for lipoprotein(a)- lowering therapies: a mendelian randomization analysis. JAMA Cardiol 2018;3:619–27. https://doi.org/10.1001/jamacardio.2018.1470.Search in Google Scholar PubMed PubMed Central

54. Langsted, A, Kamstrup, PR, Benn, M, Tybjærg-Hansen, A, Nordestgaard, BG. High lipoprotein(a) as a possible cause of clinical familial hypercholesterolaemia: a prospective cohort study. Lancet Diabetes Endocrinol 2016;4:577–87. https://doi.org/10.1016/S2213-8587(16)30042-0.Search in Google Scholar PubMed

55. Ascaso, JF, Civeira, F, Guijarro, C, López Miranda, J, Masana, L, Mostaza, JM, et al.. Indicaciones de los inhibidores de proproteína convertasa subtilisina kexina 9 (PCSK9) en la práctica clínica. Recomendaciones de la Spanish Society of Arteriosclerosis (SEA) 2019. Clin E Investig En Arterioscler Publicacion Of Soc Espanola Arterioscler 2019;31:128–39. https://doi.org/10.1016/j.arteri.2019.04.002.Search in Google Scholar PubMed

56. Conrad, N, Verbeke, G, Molenberghs, G, Goetschalckx, L, Callender, T, Cambridge, G, et al.. Autoimmune diseases and cardiovascular risk: a population-based study on 19 autoimmune diseases and 12 cardiovascular diseases in 22 million individuals in the UK. Lancet 2022;400:733–43. https://doi.org/10.1016/S0140-6736(22)01349-6.Search in Google Scholar PubMed

57. Moulin, P, Dufour, R, Averna, M, Arca, M, Cefalù, AB, Noto, D, et al.. Identification and diagnosis of patients with familial chylomicronaemia syndrome (FCS): expert panel recommendations and proposal of an «FCS score». Atherosclerosis 2018;275:265–72. https://doi.org/10.1016/j.atherosclerosis.2018.06.814.Search in Google Scholar PubMed

Supplementary Material

This article contains supplementary material (https://doi.org/10.1515/almed-2023-0047).

Received: 2023-01-23
Accepted: 2023-03-02
Published Online: 2023-06-05

© 2023 the author(s), published by De Gruyter, Berlin/Boston

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Advances in Laboratory Medicine / Avances en Medicina de Laboratorio
Advances in Laboratory Medicine / Avances en Medicina de Laboratorio
Volume 4 Issue 2
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