Published in PLOS One on 2026-08-26, this study is presented as an attributed evidence briefing. The excerpts below are the original researchers’ words, reproduced under their Creative Commons Attribution licence. Health Signal has selected the abstract and, where needed, opening background paragraphs; the complete methods, results, limitations and references remain in the linked paper.
Original authors: Lambert Tetteh Appiah, Florence Koryo Akumiah, Jacob Solomon Idan, Gordon Manu Amponsah, Solomon Gyabaah, Birgit Agyeiwaah Baah, Frederick Kwarteng Owusu, Benedict Kusi Ampofo, Robert Winfred Eshun, Oladotun Victor Olalusi, Bert-Jan van den Born, Charles Agyemang, Emmanuel Ofori
Source: PLOS One • DOI 10.1371/journal.pone.0356490
Read the complete primary study ↗ · Creative Commons Attribution licence
From the researchers
Abstract
Lipoprotein(a) [Lp(a)] is a low-density lipoprotein-like particle covalently bound to apolipoprotein(a) and encoded by the LPA gene. Elevated plasma levels of Lp(a) are a well-established, independent, and causal risk factor for cardiovascular disease. While the epidemiology of Lp(a) has been extensively mapped in non- African populations, the burden and distribution of Lp(a) in African populations remain under-characterized despite its unique genetic, phenotypic, ethnolinguistic and ancestral diversity. The primary objective was to synthesize existing literature to determine the prevalence and distribution of elevated Lp(a) levels in apparently healthy African individuals residing on the African continent.
This systematic review included observational studies (cross-sectional, cohort, and case-control) involving apparently healthy adults (≥18 years) in Africa. The review systematically searched PubMed/MEDLINE, Embase, Scopus, African Journals Online, and Google Scholar without language or date restrictions to capture the full breadth of historical and contemporary data. Data were extracted using a standardized form capturing study characteristics, population demographics, assay methods and quantitative outcomes. Methodological quality was assessed using the Newcastle-Ottawa Scale.
A total of 17 studies met the inclusion criteria, representing populations from West Africa (Nigeria, Ghana) Central Africa (Cameroon), Southern Africa (South Africa, Zimbabwe), and North Africa (Morocco, Tunisia). Studies in Ghana reported prevalence rates of elevated Lp(a) (>30 mg/dL) between 30–61%. Lp(a) mean levels ranged from 12.7 mg/dL to 54.5 mg/dL depending on the cohort and assay used. Females exhibited higher Lp(a) levels than males across most African cohorts. Clinically, elevated Lp(a) was associated with hypertension, type 2 diabetes mellitus, ischemic stroke, myocardial infarction and anti-retroviral drug use.
Elevated Lp(a) is a common, genetically determined trait in Africa rather than a rare dyslipidemia. Far from being a benign variant, it acts as a significant amplifier of cardiovascular risk, particularly in the presence of rising incident rates of hypertension and diabetes. Addressing this burden requires the adoption of standardized, isoform-independent assays and the development of population-specific risk thresholds to guide targeted preventive cardiovascular care.
Introduction
Cardiovascular diseases (CVD) remain the preeminent cause of morbidity and mortality worldwide [1]. The burden is disproportionately borne by low- and middle-income countries (LMICs) [2,3] which is attributable to population expansion and a myriad (or complex interplay) of genetic, environmental and lifestyle factors [4]. Lipoprotein(a) [Lp(a)] has emerged over the last decade as a genetically determined and one of the prevalent risk factors of CVD [1,5]. Structurally, Lp(a) is a unique lipoprotein subclass that resembles a low-density lipoprotein (LDL) particle in its lipid composition and the presence of apolipoprotein B-100 (apoB-100) [1]. However, it is distinguished by the presence of a second apolipoprotein(a) [apo(a)], which is covalently linked to the apoB-100 moiety via a single disulfide bond [5]. It shares a high degree of structural homology with plasminogen [1]. This unique assembly confers upon Lp(a) a pro-atherogenic properties of LDL due to its cholesterol content whiles the apo(a) moiety adds distinct pro-thrombotic and pro-inflammatory predilection [1].
Reading this evidence
Use the full paper to check the study design, participant selection, comparator and outcome definitions before drawing a practical conclusion. An association does not by itself show cause and effect. A reported performance measure needs its denominator and uncertainty. A finding from a particular facility, sample or time period should retain that scope when it is discussed elsewhere.
This briefing makes the source accessible within the wider research & evidence desk. It does not assess an individual patient or certify a product. When considering relevance to another health system, examine the original authors’ account of context and limitations, then seek local implementation evidence. The related reporting below provides other studies to read alongside this one; it is a topic connection, rather than a claim that their results are directly comparable.
© 2026 Lambert Tetteh Appiah, Florence Koryo Akumiah, Jacob Solomon Idan, Gordon Manu Amponsah, Solomon Gyabaah, Birgit Agyeiwaah Baah, Frederick Kwarteng Owusu, Benedict Kusi Ampofo, Robert Winfred Eshun, Oladotun Victor Olalusi, Bert-Jan van den Born, Charles Agyemang, Emmanuel Ofori. Excerpts reproduced under CC BY. Selection, formatting and contextual notes by Health Signal. The researchers are the authors of the source study, not members of Health Signal’s staff.
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- Evidence brief: Prevalence, treatment rates and control of dyslipidemia among diabetes patients in northern Nigeria: A cross-sectional, multicenter study
