Topical Area: Medical Nutrition/Case Study Vignettes
(P16-025-20) An Algorithmic Approach for Lipid Metabolism and Management of Patients with Xanthelasma Palpebrarum (XP)
Objectives: XP (flat, yellowish plaques around the eyes) is difficult to treat and often recurs. We describe an algorithmic approach to explore the lipid metabolism and management of XP.
Methods: A 64 yo female with hypothyroidism, obesity, and metabolic syndrome was successful with weight loss and glycemia but noted recurrence of XP after a surgical excision. Her lipid profile (on rosuvastatin) revealed: total cholesterol 150 mg/dL, LDL 54 mg/dL, triglycerides 74 mg/dL, HDL 81 mg/dL. Apolipoprotein (Apo) A1 was 213 mg/dL (nl female >140). Apo B100 was 63 mg/dL (nl < 130). Lp(a) was 29 mg/dL (nl < 30). LDL particles were 958 nmol/L (nl < 1000). LDL particle size was 20.9 nm (nl >20.5). Small dense LDL particles were 598 nmol/L (nl < 528). There was presence of serum campesterol (3.7 mg/L; nl 0-7.0) and sitosterol (2.1 mg/L; nl 0-5.0), but not desmosterol or lathosterol. Oral ezetimibe (EZ), 10 mg/day was administered. After 8 months of therapy, campesterol and sitosterol dropped significantly (campesterol: 2.1, - 44%; sitosterol: 1.3, - 39%). XP lesions resolved completely .
Results: We developed an algorithmic approach to XP management. The sequence is as follows: 1) examine standard lipid levels, 2) examine levels of pro-atherogenic particles, 3) explore net cholesterol tissue transport, 4) confirm hepatic cholesterol synthesis suppression, 5) examine plant sterols, 6) treat the abnormalities detected.
In this example case phytosterols were responsible for XP recurrence. Sitosterol and campesterol should be minimally absorbed by the gut through the Nieman Pick C1 Like 1 (NPC1L1)sterol influx transporter and eliminated by the sterol efflux transporters, adenosine triphosphate-binding cassette (ABC) ABCG5/ABCG8. If phytosterols are retained in the body, they may predispose to resistant XP.
An algorithmic approach to XP suggested that hyper-absorption of plant sterols by the NPC1L1 transporter was present. This was clinically confirmed because inhibition of NPC1L1 transport (by EZ) significantly reduced plant sterol levels. Plant sterols were also clinically confirmed as the cause of her XP, since their reduction and led to XP resolution.
Conclusions: We present an algorithmic approach to help detail the metabolic etiology of XP and direct its management. The example case demonstrates its value to reduce XP recurrence and resolve XP in selected cases.
Funding Sources: None
Michael M. Rothkopf
Director, Metabolic Medicine Consultants Newark Beth Israel Medical Center North Caldwell, New Jersey