Atherosclerosis · 2026
Statin-associated symptoms and statin intolerance in children with familial hypercholesterolemia: Insights from 15 years of clinical practice.
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van den Bosch Sibbeliene E, Kowsoleea Fianna C, Corpeleijn Willemijn E, Huisman Sophie A, Kowsoleea Astra I E, Wiegman Albert, Hutten Barbara A
Аннотация
BACKGROUND AND AIMS: To reduce the increased premature cardiovascular risk in children with heterozygous familial hypercholesterolemia (FH), statins are the first pharmacological step. This study aims to assess the incidence of statin-associated symptoms (SAS) and statin intolerance in pediatric FH patients.
METHODS: Children (<18 years) with FH who received statins in our pediatric lipid clinic at the Amsterdam UMC - location AMC between October 2009 and October 2024 were eligible. Data were retrospectively collected from electronic medical records, including medical history, statin type and dose, SAS, statin intolerance and blood samples. Data were evaluated at three time points: statin initiation (T1), following adjustment of statin dose and/or type (T2), and if changed, at the last prescribed dose (T3).
RESULTS: A total of 696 children were included (329 girls, 47.3%) with a median age (IQR) at statin initiation of 11.0 (8.3 - 14.0) years. SAS were reported in 1 in 8.5 children at T1, 1 in 8.2 children at T2, and 1 in 8.2 at T3. The majority of symptoms were transient and mild. Muscle symptoms without clinically significant creatine kinase (CK) elevation (≤3 × upper limit of normal) were most frequently reported. No cases of rhabdomyolysis or other adverse events requiring hospital admission were reported. In total, 13 children (1.9%) were statin intolerant due to persistent symptoms leading to permanent discontinuation of statin therapy.
CONCLUSIONS: This study shows that SAS were common, but generally transient and mild, whereas statin into-lerance was relatively uncommon in children with FH. Proactive management of SAS and consideration of alternative therapies are crucial to maintain adherence and reduce their increased cardiovascular risk. Future research should focus on identifying risk factors to enable personalized treatment strategies.
METHODS: Children (<18 years) with FH who received statins in our pediatric lipid clinic at the Amsterdam UMC - location AMC between October 2009 and October 2024 were eligible. Data were retrospectively collected from electronic medical records, including medical history, statin type and dose, SAS, statin intolerance and blood samples. Data were evaluated at three time points: statin initiation (T1), following adjustment of statin dose and/or type (T2), and if changed, at the last prescribed dose (T3).
RESULTS: A total of 696 children were included (329 girls, 47.3%) with a median age (IQR) at statin initiation of 11.0 (8.3 - 14.0) years. SAS were reported in 1 in 8.5 children at T1, 1 in 8.2 children at T2, and 1 in 8.2 at T3. The majority of symptoms were transient and mild. Muscle symptoms without clinically significant creatine kinase (CK) elevation (≤3 × upper limit of normal) were most frequently reported. No cases of rhabdomyolysis or other adverse events requiring hospital admission were reported. In total, 13 children (1.9%) were statin intolerant due to persistent symptoms leading to permanent discontinuation of statin therapy.
CONCLUSIONS: This study shows that SAS were common, but generally transient and mild, whereas statin into-lerance was relatively uncommon in children with FH. Proactive management of SAS and consideration of alternative therapies are crucial to maintain adherence and reduce their increased cardiovascular risk. Future research should focus on identifying risk factors to enable personalized treatment strategies.