Hyperlipidemia status

A 10-year-old child had status epilepticus controlled with a combination of valproate, oxcarbazepine, and 48 hours of propofol infusion in a dose of 5.5 mg/kg/ hour. After weaning from propofol, a classic ketogenic diet was instituted in an attempt to provide long-term control of the seizures. A day later status epilepticus recurred and propofol was restarted at a rate of 6-9 mg/ kg/hour to suppress seizure activity (the diet, valproate, and oxcarbazepine were also continued). Shortly thereafter, he developed the classical constellation of malignant ventricular arrhythmias, hyperlipidemia, rhabdomyolysis, lactic acidosis, and biventricular cardiac failure. He did not survive. 

Adipocytes have vitamin D receptors, and there is evidence that vitamin D may act as a suppressor of adipocyte development (Kawada et al., 1996). It has been suggested that vitamin D inadequacy may be a factor in the development of the metabolic syndrome ( syndrome X, the combination of insulin resistance, hyperlipidemia, and atherosclerosis associated with abdominal obesity). Sunlight exposure, and hence vitamin D status, may be a factor in the difference in incidence of atherosclerosis and myocardial infarction between northern and southern European countries in addition to effects on adipocyte development, calcitriol also enhances insulin secretion through induction of calbindin-D (Section 3.3.7.1), and there is some evidence vitamin D supplements can improve glucose tolerance (Boucher, 1998). 

Vitamins Bg, B12 and folate have specific and vital functions in the metabolism a deficiency (or excess) causes specific diseases such as hyperlipidemia, hypertension, obesity or cardiovascular diseases, which are related to a modern lifestyle and common in industrialized countries. As observed in several studies, cobalamin (B12) deficiency in most cases coincides with an insufficient folate status (Ball 2006 Howard et al. 1998 Morris et al. 2007). 

A negative correlation between deficient biotin status and blood lipid concentrations was found in rats (Marshall et al. 1976) as well as in humans (Marshall et al. 1980). A decrease in plasma lipids was observed in human healthy volunteers within 30 min of absorption of 100 mg of biotin infusion. It was shown that oral biotin supplementation affected plasma lipid concentrations. The administration of 5 mg/day of biotin decreased hypercholesterolemia in atherosclerosis and hyperlipidemia patients (Dukusova and Krivoruchenko 1972). A 15 mg/day treatment by biotin for 28 days decreased hypertriglyceridemia of subjects whose triacylglycerol concentrations were more than 25% above the normal of 1.8mmol/L (Baez-Saldana 2004). 

Diet-Related Risk Factors for Human Atherosclerosis Hyperlipidemia, Hypertension, Hyperglycemia — Current Status. ... 

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