Severe Hypertriglyceridemia Secondary to Antiretroviral Drugs in an Adolescent with Hereditary...
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Transcript of Severe Hypertriglyceridemia Secondary to Antiretroviral Drugs in an Adolescent with Hereditary...
262 Journal of Clinical Lipidology, Vol 7, No 3, June 2013
abnormal lipid levels 61% counseled for lifestyle changesconsisting mainly of reduced cholesterol diet (37%).
Conclusions: The results of this survey (largest to date)on approaches to lipid screening and treatment in childrenshow: 1) insufficient awareness and implementation ofpublished pediatric lipid guidelines among PPP, and 2)despite recognizing that treatment of lipid disorders inchildhood may reduce future CV risk, only 2/3 of PPPperform lipid screening, and a small minority recommenddrug therapy. These findings emphasize the need tofurther educate PPP and provide easily accessible infor-mation on the screening and treatment of lipid disordersin children.
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Analysis of Generic Simvastatin and Atorvastatin VersusBranded Rosuvastatin in Hyperlipidemic Patients: ABudget Impact Model from a U.S.-Managed CareOrganization Perspective
Calypso Montouchet, Lewis Ruff, MSc,Sanjeev Balu, PhD, MBA, (Wilmington, Delaware)
Lead Author’s Disclosures: NoneStudy Funding: This study was supported by AstraZe-neca Pharmaceuticals.
Synopsis: Managed healthcare (MHC) decision-makersmay utilize a step-edit approach for the initiation of lipid-lowering therapy, placing all new hyperlipidemic patientson a generic statin regardless of their cardiovascular (CV)risk. Patients who do not reach their National CholesterolEducation Program (NCEP) Adult Treatment Panel III low-density lipoprotein cholesterol (LDL-C) goal subsequentlyreceive an increased dose of their initial statin, or switch toother alternatives.
Purpose: A deterministic model was developed to esti-mate the budget impact and cost effectiveness over 3 yearsof initiating high-risk patients in a hypothetical managedhealth care (MHC) plan on rosuvastatin rather thansimvastatin or atorvastatin.
Methods: Among 1,000,000 health plan members aged$18 years, 1,000 patients (0.1%) were assumed to initiatetreatment with statins. The average baseline LDL-C levelwas 189 mg/dL. Two scenarios were modeled: in scenario1, all patients were initiated on simvastatin or atorvastatinand titrated to a higher dose, or switched to atorvastatin (ifinitiated on simvastatin) or rosuvastatin; in scenario 2,100% of the 520 high-risk patients—based on NCEPguidelines—were initiated on rosuvastatin. Productlabeling, clinical trial results, national prescription claimsdata, and published literature was used to populate themodel. Drug acquisition, administration, and event costswere considered. Per member per month (PMPM) total(medication plus event costs) cost (budget impact) and theincremental total cost per additional patient reachingLDL-C goal were evaluated.
Results: Over 3 years, 149 additional patients reachedtheir LDL-C goal in scenario 2, compared with scenario1 (709 versus 558, respectively), at an increased total costof $467,689 ($1,951,404 versus $1,483,715, respectively).The additional PMPM cost of scenario 2 to the MHC planwas $0.013. Incremental total cost per additional patientreaching LDL-C goal was $3,097 over 3 years.
Conclusions: Although the model has some limitations,it highlights the value of appropriate prescribing of statins,especially to a high-risk patient population. Initiating high-risk hyperlipidemic patients on rosuvastatin maypotentially increase the number of patients reaching LDL-C goals (defined in NCEP guidelines) at a relatively modestincrease in PMPM cost to an MHC plan, despite the lowercost of generic statins. Further studies on appropriate statintreatment strategies among hyperlipidemic patients onvarying CV risk are warranted.
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Severe Hypertriglyceridemia Secondary to AntiretroviralDrugs in an Adolescent with Hereditary Pancreatitis*
Albert Chan, MD, Marielisa Rincon, MD,Mihail Marius Subtirelu, MD, (Chattanooga, Tennessee)
Lead Author’s Disclosures: NoneStudy Funding: NoneSynopsis: Hypertriglyceridemia and lipodystrophy areknown associations to the use of highly active antiretroviraltherapy (HAART) for HIV treatment. Additionally hyper-triglycredidemia is a well known cause of pancreatitis. Herewe present an adolescent with recurrent pancreatitis ini-tially believed to be due to HAART.
Purpose: To demonstrate an alternative and rarecause of pancreatitis in an adolescent with knownhypertriglyceridemia.
Methods: Case report.
Results: Clinical Case: A 16 year old female known to beHIV positive since 5 months of age was admitted to theinpatient ward after the development of acute pancreatitis.The patient had been on HAART since her diagnosis until11 years of age. At that time, she had a first episode ofacute pancreatitis, initially thought to be secondary tohypertriglyceridemia and lipodystrophy due to HAART.She had a low HIV viral load and, therefore, the therapywas discontinued. She was started on Niaspan and Gemfi-brozil. Despite of subsequently maintaining triglycerides at,500 mg/dL and being off HAART, she had 14 episodes ofacute on chronic pancreatitis over the years. She developedpancreatic insufficiency and insulin dependent diabetesmellitus secondary to the recurrent pancreatitis. Becauseof her unusual course, genetic testing for recurrent pancre-atitis was pursued demonstrating a PRSS1 gene mutation, aknown cause of chronic pancreatitis.
Abstracts 263
This patients will have a total pancreatectomy this year tostop episodes of recurrent pancreatitis, as she is alreadyreceiving fully pancreatic function replacement.
Conclusions: This case illustrates the need to consideralternative causes of recurrent pancreatitis in hypertrigly-ceridemic patients. If triglyceride levels are not criticallyhigh to predict pancreatitis, the judicious clinicianshould include other considerations in the differentialdiagnosis.
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Oral Contraceptives: A Cause of Elevated LDL-ParticleNumber in Two Young Dyslipidemic Women*
Kathleen M. Chiu, FNP, Thomas Dayspring, MD,James Underberg, MD, (New York, New York)
Lead Author’s Disclosures: NoneStudy Funding: NoneSynopsis: The link between postmenopausal hormonetherapy and increased risk for cardiovascular events has beenreported in the Women’s Health Initiative. Increased cardi-ovascular risk in women taking oral contraceptives (OC’s)has been described, decreasing with the discontinuation ofOC’s. OC’s may raise TG’s, and this may lead to increasedlevels of ApoB containing lipoprotein particles. Twowomenof child bearing age taking oral contraceptives (OC’s) withno other cardiovascular risk factors and no family history ofhypercholesterolemia presented to our clinic with markedlyincreased LDL-Particle (LDL-P) concentrations withoutchanges in LDL size. Discontinuation of OC use in bothpatients was associated with significant reductions in LDL-Pconcentration.
Purpose: We report two cases of likely contraceptiveinduced hyperbetalipoproteinemia in otherwise premeno-pausal healthy women with hypercholesterolemia withprudent lifestyle and no significant family history ofcardiovascular disease.
Methods: Advanced lipoprotein testing utilizing NuclearMagnetic Resonance (NMR) Spectroscopy (LipoScience,Raleigh, NC) was performed on two premenopausalwomen with hyperlipidemia referred to the lipid clinic.
Results: Patients 1 and 2 presented on OC therapy (1-20mg-mcg norethindrone acetetate-ethinyl estradiol and 0.25-
Chart 1 Baseline Characteristics and Off-OCP Lipids & Lipoproteins
Patient Designation Total Cholesterol
Patient 11-20 mg-mcg norethindroneacetetate-ethinyl estradiol
On OCP 228Off OCP 214% Change -6%
Patient 20.25-35 mg-mcgnorgestimate-ethinyl estradiol
On OCP 223Off OCP 181% Change -18%
LDL-C, Low Density Lipoprotein Cholesterol; HDL-C, High Density Lipoprotei
35 mg-mcg norgestimate-ethinyl estradiol) with increasedLDL cholesterol (LDL-C). The remainder of the lipidpanels were otherwise unremarkable (Chart 1). Bothpatients had significantly elevated LDL-P concentrations.One month after discontinuation of OC therapy bothpatients had significant reductions in LDL-P and LDL-C.The change in LDL-P was significantly greater than thechange in LDL-C (44% and 48% decrease in LDL-P,respectively compared to changes in LDL-C).
Conclusions: OC’s should be considered as a potentialcause of dyslipidemia with possible discordance betweenLDL-P and LDL-C. A repeat lipid panel after discontinuingOC’s should be obtained to determine cause and effect. OC’sare known to reduce LDL-C, increase high densitylipoprotein-cholesterol (HDL-C) and raise triglycerides. TheWHI sub-study on lipoproteins showed discordance betweenLDL-C and LDL-Particle concentration in patients treatedwith menopausal hormone therapy. Data suggests that LDL-Pconcentration may be a useful predictor of cardiovascular riskin patients when such discordance exists. We postulate that inPatient 2 the OC-induced hypertriglyceridemia induced TG-rich, cholesterol-depleted LDLs leading to high LDL-P.Etiology of Patient 1’s changes is speculative. This is apotential cardiovascular risk factor that patients and providersshould be aware of. A prospective proof of concept studywould further clarify this relationship.
145
Management of Aminotransferase Elevations Observedin a Phase 3 Study of Patients with Homozygous FamilialHypercholesterolemia Treated with Lomitapide
Marina Cuchel, MD, PhD, Emma A. Meagher, MD,Prediman Krishan Shah, MD, LeAnne T. Bloedon, MS, RD,Daniel J. Rader, MD, for the Phase 3 HoFH LomitapideStudy Investigators, (Philadelphia, Pennsylvania)
Lead Author’s Disclosures: Dr. Cuchel receivedresearch grant, speaker honoraria, and travel support forattending scientific meetings from Aegerion Pharmaceuti-cals. Dr. Rader is an inventor on a patent related tolomitapide and serves as the chair of the scientific advisoryboard for Aegerion Pharmaceuticals.
LDL-C HDL-C TGs LDL-P HDL-P LDL Size
159 58 56 2498 39.0 21.4140 58 78 1387 38.2 21.4-11% 0% 140% -44% -2% 0%100 63 298 2499 34.5 21.1116 54 54 1288 31.8 21.0116% -14% -81% -48% -7% -0.4%
n Cholesterol; TGs, Triglycerides; LDL-P, Low Density Lipoprotein Particle.