Extreme hypertriglyceridemia: Genetic diversity, pancreatitis, pregnancy, and prevalence

Triglyceride (TG) concentrations >2000 mg/dL are extremely elevated and increase the risk of pancreatitis. We characterized five cases and two kindreds and ascertained prevalence in a reference laboratory population. Plasma lipids and DNA sequences of LPL, GPIHBP1, APOA5, APOC2, and LMF1 were det...

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Veröffentlicht in:Journal of clinical lipidology 2019-01, Vol.13 (1), p.89-99
Hauptverfasser: Chyzhyk, Vadzim, Kozmic, Sarah, Brown, Alan S., Hudgins, Lisa C., Starc, Thomas J., Davila, Ashley Deleigh, Blevins, Thomas C., Diffenderfer, Margaret R., He, Lihong, Geller, Andrew S., Rush, Caitlin, Hegele, Robert A., Schaefer, Ernst J.
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container_end_page 99
container_issue 1
container_start_page 89
container_title Journal of clinical lipidology
container_volume 13
creator Chyzhyk, Vadzim
Kozmic, Sarah
Brown, Alan S.
Hudgins, Lisa C.
Starc, Thomas J.
Davila, Ashley Deleigh
Blevins, Thomas C.
Diffenderfer, Margaret R.
He, Lihong
Geller, Andrew S.
Rush, Caitlin
Hegele, Robert A.
Schaefer, Ernst J.
description Triglyceride (TG) concentrations >2000 mg/dL are extremely elevated and increase the risk of pancreatitis. We characterized five cases and two kindreds and ascertained prevalence in a reference laboratory population. Plasma lipids and DNA sequences of LPL, GPIHBP1, APOA5, APOC2, and LMF1 were determined in cases and two kindreds. Hypertriglyceridemia prevalence was assessed in 440,240 subjects. Case 1 (female, age 28 years) had TG concentrations >2000 mg/dL and pancreatitis since infancy. She responded to diet and medium-chain triglycerides, but not medications. During two pregnancies, she required plasma exchange for TG control. She was a compound heterozygote for a p.G236Gfs*15 deletion and a p.G215E missense mutation at LPL, as was one sister with hypertriglyceridemia and pancreatitis during pregnancy. Her father was heterozygous for the deletion and had hypertriglyceridemia and recurrent pancreatitis. Other family members had either the missense mutation or the deletion, and had hypertriglyceridemia but no pancreatitis. In kindred 2, three preschool children had severe hypertriglyceridemia and were homozygous for a GPIHBP1 p.T108R missense mutation. Case 5 (male, age 43 years) presented with pancreatitis and TG levels >5000 mg/dL and had heterozygous GPIHBP1 p.G175R and APOC2 intron 2-4G>C mutations. On diet, fenofibrate, fish oil, and atorvastatin, his TG concentration was 2526 mg/dL, but normalized to 2000 mg/dL, and 66.7% were diabetic and had elevated insulin levels. Extreme hypertriglyceridemia is rare (0.014%); and during pregnancy, it may require plasma exchange. •Extreme hypertriglyceridemia (>2000 mg/dL) is associated with pancreatitis.•The prevalence of this condition in a reference laboratory population is 0.01%.•Pregnancy exacerbates hypertriglyceridemia and may require plasmapheresis.•Effective therapies include a low-fat diet, medium-chain triglyceride(s) oil, fibrates, and fish oil.•The underlying molecular defects should be characterized by DNA analysis.
doi_str_mv 10.1016/j.jacl.2018.09.007
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We characterized five cases and two kindreds and ascertained prevalence in a reference laboratory population. Plasma lipids and DNA sequences of LPL, GPIHBP1, APOA5, APOC2, and LMF1 were determined in cases and two kindreds. Hypertriglyceridemia prevalence was assessed in 440,240 subjects. Case 1 (female, age 28 years) had TG concentrations &gt;2000 mg/dL and pancreatitis since infancy. She responded to diet and medium-chain triglycerides, but not medications. During two pregnancies, she required plasma exchange for TG control. She was a compound heterozygote for a p.G236Gfs*15 deletion and a p.G215E missense mutation at LPL, as was one sister with hypertriglyceridemia and pancreatitis during pregnancy. Her father was heterozygous for the deletion and had hypertriglyceridemia and recurrent pancreatitis. Other family members had either the missense mutation or the deletion, and had hypertriglyceridemia but no pancreatitis. In kindred 2, three preschool children had severe hypertriglyceridemia and were homozygous for a GPIHBP1 p.T108R missense mutation. Case 5 (male, age 43 years) presented with pancreatitis and TG levels &gt;5000 mg/dL and had heterozygous GPIHBP1 p.G175R and APOC2 intron 2-4G&gt;C mutations. On diet, fenofibrate, fish oil, and atorvastatin, his TG concentration was 2526 mg/dL, but normalized to &lt;100 mg/dL with added pioglitazone. In our population study, 60 subjects (0.014%) of 440,240 had TG concentrations &gt;2000 mg/dL, and 66.7% were diabetic and had elevated insulin levels. Extreme hypertriglyceridemia is rare (0.014%); and during pregnancy, it may require plasma exchange. •Extreme hypertriglyceridemia (&gt;2000 mg/dL) is associated with pancreatitis.•The prevalence of this condition in a reference laboratory population is 0.01%.•Pregnancy exacerbates hypertriglyceridemia and may require plasmapheresis.•Effective therapies include a low-fat diet, medium-chain triglyceride(s) oil, fibrates, and fish oil.•The underlying molecular defects should be characterized by DNA analysis.</description><identifier>ISSN: 1933-2874</identifier><identifier>EISSN: 1876-4789</identifier><identifier>DOI: 10.1016/j.jacl.2018.09.007</identifier><identifier>PMID: 30352774</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Apolipoprotein A-V - blood ; Apolipoprotein A-V - genetics ; Apolipoprotein C-II - blood ; Apolipoprotein C-II - genetics ; Chylomicronemia ; Disease Progression ; Female ; Genetics ; Humans ; Hypertriglyceridemia - epidemiology ; Hypertriglyceridemia - genetics ; Hypertriglyceridemia - immunology ; Lipoprotein Lipase - blood ; Lipoprotein Lipase - genetics ; Male ; Membrane Proteins - blood ; Membrane Proteins - genetics ; Mutation, Missense - genetics ; Pancreatitis ; Pedigree ; Plasma Exchange ; Plasmapheresis ; Polymorphism, Genetic ; Population prevalence ; Pregnancy ; Pregnancy Complications ; Prevalence ; Receptors, Lipoprotein - blood ; Receptors, Lipoprotein - genetics ; Triglycerides ; Triglycerides - blood</subject><ispartof>Journal of clinical lipidology, 2019-01, Vol.13 (1), p.89-99</ispartof><rights>2018 National Lipid Association</rights><rights>Copyright © 2018 National Lipid Association. 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We characterized five cases and two kindreds and ascertained prevalence in a reference laboratory population. Plasma lipids and DNA sequences of LPL, GPIHBP1, APOA5, APOC2, and LMF1 were determined in cases and two kindreds. Hypertriglyceridemia prevalence was assessed in 440,240 subjects. Case 1 (female, age 28 years) had TG concentrations &gt;2000 mg/dL and pancreatitis since infancy. She responded to diet and medium-chain triglycerides, but not medications. During two pregnancies, she required plasma exchange for TG control. She was a compound heterozygote for a p.G236Gfs*15 deletion and a p.G215E missense mutation at LPL, as was one sister with hypertriglyceridemia and pancreatitis during pregnancy. Her father was heterozygous for the deletion and had hypertriglyceridemia and recurrent pancreatitis. Other family members had either the missense mutation or the deletion, and had hypertriglyceridemia but no pancreatitis. In kindred 2, three preschool children had severe hypertriglyceridemia and were homozygous for a GPIHBP1 p.T108R missense mutation. Case 5 (male, age 43 years) presented with pancreatitis and TG levels &gt;5000 mg/dL and had heterozygous GPIHBP1 p.G175R and APOC2 intron 2-4G&gt;C mutations. On diet, fenofibrate, fish oil, and atorvastatin, his TG concentration was 2526 mg/dL, but normalized to &lt;100 mg/dL with added pioglitazone. In our population study, 60 subjects (0.014%) of 440,240 had TG concentrations &gt;2000 mg/dL, and 66.7% were diabetic and had elevated insulin levels. 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We characterized five cases and two kindreds and ascertained prevalence in a reference laboratory population. Plasma lipids and DNA sequences of LPL, GPIHBP1, APOA5, APOC2, and LMF1 were determined in cases and two kindreds. Hypertriglyceridemia prevalence was assessed in 440,240 subjects. Case 1 (female, age 28 years) had TG concentrations &gt;2000 mg/dL and pancreatitis since infancy. She responded to diet and medium-chain triglycerides, but not medications. During two pregnancies, she required plasma exchange for TG control. She was a compound heterozygote for a p.G236Gfs*15 deletion and a p.G215E missense mutation at LPL, as was one sister with hypertriglyceridemia and pancreatitis during pregnancy. Her father was heterozygous for the deletion and had hypertriglyceridemia and recurrent pancreatitis. Other family members had either the missense mutation or the deletion, and had hypertriglyceridemia but no pancreatitis. In kindred 2, three preschool children had severe hypertriglyceridemia and were homozygous for a GPIHBP1 p.T108R missense mutation. Case 5 (male, age 43 years) presented with pancreatitis and TG levels &gt;5000 mg/dL and had heterozygous GPIHBP1 p.G175R and APOC2 intron 2-4G&gt;C mutations. On diet, fenofibrate, fish oil, and atorvastatin, his TG concentration was 2526 mg/dL, but normalized to &lt;100 mg/dL with added pioglitazone. In our population study, 60 subjects (0.014%) of 440,240 had TG concentrations &gt;2000 mg/dL, and 66.7% were diabetic and had elevated insulin levels. Extreme hypertriglyceridemia is rare (0.014%); and during pregnancy, it may require plasma exchange. •Extreme hypertriglyceridemia (&gt;2000 mg/dL) is associated with pancreatitis.•The prevalence of this condition in a reference laboratory population is 0.01%.•Pregnancy exacerbates hypertriglyceridemia and may require plasmapheresis.•Effective therapies include a low-fat diet, medium-chain triglyceride(s) oil, fibrates, and fish oil.•The underlying molecular defects should be characterized by DNA analysis.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>30352774</pmid><doi>10.1016/j.jacl.2018.09.007</doi><tpages>11</tpages></addata></record>
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subjects Adult
Apolipoprotein A-V - blood
Apolipoprotein A-V - genetics
Apolipoprotein C-II - blood
Apolipoprotein C-II - genetics
Chylomicronemia
Disease Progression
Female
Genetics
Humans
Hypertriglyceridemia - epidemiology
Hypertriglyceridemia - genetics
Hypertriglyceridemia - immunology
Lipoprotein Lipase - blood
Lipoprotein Lipase - genetics
Male
Membrane Proteins - blood
Membrane Proteins - genetics
Mutation, Missense - genetics
Pancreatitis
Pedigree
Plasma Exchange
Plasmapheresis
Polymorphism, Genetic
Population prevalence
Pregnancy
Pregnancy Complications
Prevalence
Receptors, Lipoprotein - blood
Receptors, Lipoprotein - genetics
Triglycerides
Triglycerides - blood
title Extreme hypertriglyceridemia: Genetic diversity, pancreatitis, pregnancy, and prevalence
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