ArticleJournal of clinical lipidology
Recognition and management of persistent chylomicronemia: A Joint Expert Clinical Consensus by the National Lipid Association and the American Society for Preventive Cardiology.
Article in Journal of clinical lipidology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Dietary Interventions for Hypertriglyceridemia.Current atherosclerosis reports · 2026Review
- Heterozygosity for pathogenic variants in familial chylomicronemia syndrome genes: from carrier state to complex trait.Current opinion in lipidology · 2026Review
- Hypertriglyceridaemia-Associated Acute Pancreatitis: Risk Stratification, Drivers, and Prevention of Recurrence.Diseases (Basel, Switzerland) · 2026Review
- Course of Pregnancies and Occurrence of Acute Pancreatitis in Women With Chylomicronemia.The Journal of clinical endocrinology and metabolism · 2026Article
- Course of Pregnancy in a Woman With Familial Chylomicronemia Syndrome Treated With Plozasiran, a Small Interfering RNA Against ApoC3.JIMD reports · 2026Article
- Clinical considerations for the treatment of patients with familial chylomicronemia syndrome using a hepatic-targetedAmerican journal of preventive cardiology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Extreme hypertriglyceridemia, defined as triglyceride (TG) levels ≥1000 mg/dL, is almost always indicative of chylomicronemia. The current diagnostic approach categorizes individuals with chylomicronemia into familial chylomicronemia syndrome (FCS; prevalence 1-10 per million), caused by the biallelic combination of pathogenic variants that impair the lipolytic action of lipoprotein lipase (LPL), or multifactorial chylomicronemia syndrome (MCS, 1 in 500). A pragmatic framework should emphasize the severity of the phenotype and the risk of complications. Therefore, we endorse the term "persistent chylomicronemia (PC)" defined as TG ≥1000 mg/dL in more than half of the measurements to encompass patients with the highest risk for pancreatitis, regardless of their genetic predisposition. We suggest classification of PC into 4 subtypes: (1) genetic FCS, (2) clinical FCS, (3) PC with "alarm" features, and (4) PC without alarm features. Although patients with FCS most likely have PC, the vast majority with PC do not have genetic FCS. Proposed alarm features are: (a) history of recurrent TG-induced acute pancreatitis, (b) recurrent hospitalizations for severe abdominal pain without another identified cause, (c) childhood pancreatitis, (d) family history of TG-induced pancreatitis, and/or (e) postheparin LPL activity <20% of normal value. Alarm features constitute the strongest risk factors for future acute pancreatitis risk. Patients with PC and alarm features have very high risk of pancreatitis, comparable to that in patients with FCS. Effective, innovative treatments for PC, like apolipoprotein C-III inhibitors, have been developed. Combined with lifestyle modifications, these agents markedly lower TG levels and risk of pancreatitis in the very-high-risk groups, irrespective of the monogenic etiology. Pragmatic definitions, education, and focus on patients with PC, specifically those with alarm features, could help mitigate the risk of acute pancreatitis and other complications.
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