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Editor's Correspondence |

Concerns About Heparin Therapy for Hypertriglyceridemia

Thomas F. Whayne Jr, MD, PhD
Arch Intern Med. 2010;170(1):108-109. doi:10.1001/archinternmed.2009.461.
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Chylomicronemia is a major component of the most severe hypertriglyceridemia (HTG) and is commonly associated with diabetes mellitus (DM). In the August 10/24 issue of the Archives, Cole1 described the management approach for one such patient treated with low-level intravenous unfractionated heparin (UFH). This patient had a timely decrease in plasma triglyceride (TG) level, and UFH therapy was credited with the successful outcome. However, the patient received insulin initially. In his brief review of previous reports of heparin treatment for severe HTG, Cole1 cites 9 references, but only 2 (Loo and Tan2; Sleth et al3) did not also administer insulin. Insulin is well established as a cofactor of lipoprotein lipase (LPL) and may contribute markedly to lipolysis of chylomicrons and very low-density lipoproteins.4 Lipoprotein lipase is bound to heparan sulfate proteoglycans (very similar to heparin) on capillary walls, which is where the LPL hydrolyzes TGs in chylomicrons and very low-density lipoproteins.5 The intravenous injection of UFH produces a rapid increase in circulating LPL, then the lipolysis system appears to circulate as a heparin-apoenzyme complex followed by an exponential disappearance of LPL activity.6 The inactivation system involves the destruction of heparin by a liver heparinase and subsequent dissociation of the active complex followed by removal of the apoenzyme.6 Concerns must be raised regarding any protocol using UFH to treat severe HTG because when additional UFH is added to the assay system, human LPL released by UFH develops a marked decrease in activity.7 In his observation, Cole1 notes that longer-term heparin can decrease LPL concentration if hepatic metabolism and degradation are greater than production and release of LPL.

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January 11, 2010
Randolph P. Cole, MD
Arch Intern Med. 2010;170(1):109. doi:10.1001/archinternmed.2009.462.
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