**4. Causes of dyslipidaemia**

Dyslipidaemias in children and adolescents can be inherited and/or acquired. Acquired causes of dyslipidaemia can be nutritional or secondary to other diseases. Excessive dietary intake of saturated and trans fats can be a major cause of dyslipidaemia. Hereditary types are referred to as primary dyslipidaemias which includes monogenetic and polygenic defects.

In the clinical setting, a primary metabolic disorder indicates that there is a deficiency in the lipid metabolism, and this is designated familial hypercholesterolemia (FH). The FH follows an autosomal dominant pattern of inheritance and is characterised by an increase of high TC and LDL-C since birth. Earlier onset of atherosclerotic cardiovascular disease (ASCVD) is also seen [20, 21]. Studies show that FH arises from genetic mutations in the LDL receptor (LDLR) and from the action of proprotein convertase known as proprotein convertase 9 (PCSK9) when it mutates [22, 23]. Also, FH has been associated with mutations in the apolipoprotein B gene which impedes the binding of LDL particles to the LDL receptor gene [22, 23].


**113**

**Table 3.**

*Dyslipidaemia in African Children and Adolescents DOI: http://dx.doi.org/10.5772/intechopen.96804*

**5. Screening for dyslipidaemia in children**

over several years with modifications [29].

1. Hypertension requiring drug therapy (i.e., BP ≥99th percentile +5 mmHg)

2. Current cigarette smoker 3. BMI ≥97th percentile

4. Presence of high-risk conditions 5. Family history of premature CVD

2. BMI ≥95th percentile, but <97th

4. Presence of moderate-risk conditions

*Risk factors and conditions for dyslipidaemia screening.*

*adolescents. J Clin Endocrinol Metab, 93(11), 4200–4209 [28].*

1. Hypertension not requiring

*High-level risk factors*

*Moderate-level risk factors*

drug therapy

percentile 3. HDL-C < 40 mg/dl

**Risk factors Risk conditions**

**Table 2** [24].

To date, reports of FH cases in Africa have been rare. There may be several explanations for this. Perhaps, the gene implicated in the aetiology of FH is rare in African population. Even though cardiovascular diseases affect many Africans, it is still important for more studies to be performed on genetic factors that can cause dyslipi-

Secondary causes of dyslipidaemia are due to "non-lipid" underlying conditions rather than an inborn lipid metabolism disorder, some of which are shown in

Usually, screening tests are performed on people who do not show any symptoms of disease to detect health problems or illnesses. The key goal of screening is early detection, to reduce the risk of illness, or to identify it early enough to treat it more effectively. Childhood lipid disorder screening is focused on the rationale for reducing the risk and severity of cardiovascular disease (CVD) in adulthood by early detection and management of paediatric dyslipidaemia. Universal screening for dyslipidaemia became the recommended practice in 2011 [25]. Currently, in most parts of Africa, screening for hyperlipidemia in children and adolescents is not routinely performed in clinical settings. However, it is appropriate to become aware of the latest guidelines for the diagnosis and treatment of dyslipidaemia by child health practitioners. The National Cholesterol Education Program Expert Panel on Blood Cholesterol in Children and Adolescents issued the first guidelines for paediatric lipid screening in 1992 [26]. By 2011, when the American Heart Association [27] and the American Academy of Paediatrics included parameters to identify high and moderate risk individuals as seen in **Table 3**, thereafter, the guideline developed

The findings of National Heart Lung and Blood Institute (NHLBI) panel which performed a systematic review and grading of evidence related to the screening and treatment of CVD risk factors, including dyslipidaemia, were released in 2011 in a combined effort to improve the assessment and management of cardiovascular disease risk factors [30, 31]. The universal screening for lipid disorders as recommended in the guidelines means that all children between the ages of 9–11 should

*High-risk conditions*

postrenal transplant 3.Post-orthotopic heart transplant 4.Kawasaki disease with current aneurysms

*Moderate-risk conditions*

4.Nephrotic syndrome

3.HIV

*Adapted from Kwiterovich, P. O., Jr. (2008). Recognition and management of dyslipidaemia in children and* 

1.Type 1 and 2 diabetes mellitus

2.Chronic kidney disease/end-stage renal disease/

1.Kawasaki disease with regressed coronary aneurysms

2.Chronic inflammatory diseases, such as: • Systemic lupus erythematosus • Juvenile rheumatoid arthritis

daemia. This would reduce the burden of cardiovascular disease in Africa.

**Table 2.**

*Causes of secondary dyslipidaemia in children and adolescents.*

*adolescents, national heart, lung, and blood institute [3].*

*Management of Dyslipidemia*

**4. Causes of dyslipidaemia**

monogenetic and polygenic defects.

• Alcohol

antiretroviral agents

hyperlipidemia was 12.1% for TC, 4.5% for TG, 28.4% for HDL-C and 9.2% for LDL-C [17]. Another study conducted among adolescent school children in the Eti-Osa Local Government Area of Lagos State, Nigeria, recorded that only 3.6 per cent of participants had TC greater than 200 mg/dL [18]. The highest prevalence of high TC among Angolan pre-pubertal adolescents, 7 to 11 years of age, was estimated to be 69.2% [19].

Dyslipidaemias in children and adolescents can be inherited and/or acquired. Acquired causes of dyslipidaemia can be nutritional or secondary to other diseases. Excessive dietary intake of saturated and trans fats can be a major cause of dyslipidaemia. Hereditary types are referred to as primary dyslipidaemias which includes

In the clinical setting, a primary metabolic disorder indicates that there is a deficiency in the lipid metabolism, and this is designated familial hypercholesterolemia (FH). The FH follows an autosomal dominant pattern of inheritance and is characterised by an increase of high TC and LDL-C since birth. Earlier onset of atherosclerotic cardiovascular disease (ASCVD) is also seen [20, 21]. Studies show that FH arises from genetic mutations in the LDL receptor (LDLR) and from the action of proprotein convertase known as proprotein convertase 9 (PCSK9) when it mutates [22, 23]. Also, FH has been associated with mutations in the apolipoprotein B gene which impedes the binding of LDL particles to the LDL receptor gene [22, 23].

**Exogenous causes Hepatic causes**

**Endocrine/Metabolic causes Inflammatory disease** • Hypothyroidism/hypopituitarism • Systemic lupus erythematosus • Diabetes mellitus types 1 and 2 • Juvenile rheumatoid arthritis

• Polycystic ovary syndrome Glycogen storage disease • Lipodystrophy • Gaucher disease • Acute intermittent porphyria • Cystine storage disease **Renal causes** • Juvenile Tay-Sachs disease • Chronic renal disease • Niemann-Pick disease

• Acute viral/bacterial infection • Childhood cancer survivor • HIV infection • Idiopathic hypercalcemia • Hepatitis • Klinefelter syndrome *Adapted from expert panel on integrated guidelines for cardiovascular health and risk reduction in children and* 

• Pregnancy **Storage disease**

• Haemolytic uremic syndrome **Other causes** • Nephrotic syndrome • Kawasaki disease **Infectious causes** • Anorexia nervosa

• Obstructive liver disease/cholestatic

conditions • Biliary cirrhosis • Alagille syndrome

• Drug therapy including corticosteroids, isotretinoin, some oral contraceptives, select chemotherapeutic agents, and select

*adolescents, national heart, lung, and blood institute [3].*

*Causes of secondary dyslipidaemia in children and adolescents.*

**112**

**Table 2.**

To date, reports of FH cases in Africa have been rare. There may be several explanations for this. Perhaps, the gene implicated in the aetiology of FH is rare in African population. Even though cardiovascular diseases affect many Africans, it is still important for more studies to be performed on genetic factors that can cause dyslipidaemia. This would reduce the burden of cardiovascular disease in Africa.

Secondary causes of dyslipidaemia are due to "non-lipid" underlying conditions rather than an inborn lipid metabolism disorder, some of which are shown in **Table 2** [24].
