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Articles by Daniel Gaudet
Total Records ( 3 ) for Daniel Gaudet
  Karine Tremblay , Julie Methot , Diane Brisson and Daniel Gaudet
 

Background

Plasma lactescence is a clinical sign of severe hypertriglyceridemia (hyperTG; TG >10 mmol/L), which is likely to be observed more frequently in the next decades because of the growing prevalence of obesity and diabetes worldwide.

Objective

The objective of this study was to describe the clinical expression of plasma lactescence.

Methods

A total of 354 subjects with lactescent plasma hyperTG (mean TG ± SD: 17.1 ± 1.8 mmol/L) were classified according to blood appearance, etiology, and biochemical characteristics. The resulting phenotypes were compared with those of 364 normolipidemic controls (TG ≤2 mmol/L) and 487 clear plasma hyperTG subjects (5 < TG ≤9 mmol/L). The association of lactescent plasma with clinical covariates (obesity, coronary artery disease, peripheral artery disease, hypertension, diabetes, glucose intolerance, pancreatitis, and response to TG-lowering drugs) was performed by the use of multiple regression models.

Results

The risk of pancreatitis increased as a function of the plasma creamy white collar and was the greatest among nonobese individuals with early-onset lactescence not responding to current TG-lowering drugs (familial hyperchylomicronemia). Patients with lactescent plasma and yellowish palmar xanthomas (dysbetalipoproteinemia) responded significantly better to fibrates than the other severe hyperTG phenotypes but were at greater risk of peripheral atherosclerosis. Overweight and obese patients with a creamy supernatant and a cloudy, cream of tomato, infranatant caused by hyper apolipoprotein B showed the most deleterious cardiometabolic risk profile, followed by the severe hyperTG-normal apolipoprotein B phenotype, the most frequent cause of lactescent plasma.

Conclusion

Lactescent plasma hyperTG represents a clinically heterogeneous group of high-risk patients.

  Charles Meyers , Daniel Gaudet , Karine Tremblay , Ahmed Amer , Jin Chen and Feng Aimin
  Familial chylomicronemia syndrome (FCS, type I hyperlipoproteinemia) is a rare autosomal-recessive lipoprotein lipase (LPL) deficiency resulting in chylomicron accumulation, extreme triglyceride (TG) elevation, and greatly increased risk of life-threatening pancreatitis. No currently available TG-lowering drug is effective in the treatment of FCS, and the standard of care, the consumption of a very low-fat diet, is difficult to maintain over a lifetime. Because diacylglycerol-acyltransferase (DGAT) 1 plays a key role in the synthesis and secretion of chylomicron TG, inhibition of DGAT1 is an attractive option for the treatment of FCS.
  D. Meeike Kusters , Barbarba A. Hutten , Brian W. McCrindle , David Cassiman , Gordon A. Francis , Claude Gagne , Daniel Gaudet , Katherine M. Morrison , Gisle Langslet , John J. Kastelein and Albert Wiegman
 

Background

Statin therapy is recommended for children with familial hypercholesterolemia (FH), but most children do not reach treatment targets.

Objective

Here we present the design and results at baseline of the ongoing CHARON study, to evaluate the safety and efficacy of rosuvastatin.

Methods

This study comprises an international 2-year open label, titration-to-goal study in 198 children with heterozygous FH aged 6 to 18 years, with rosuvastatin in a maximum dose of 10 mg (<10 years of age) or 20 mg (older children). In addition, 64 unaffected siblings were enrolled as controls. The primary efficacy outcome is the change from baseline in low-density lipoprotein cholesterol, and the secondary outcome is the change in carotid intima-media thickness (c-IMT) in patients with FH compared with their siblings. The primary safety outcomes are growth and sexual maturation; secondary outcomes are the change in other lipoprotein levels and the incidence of adverse events, discontinuation rates, and abnormal laboratory values.

Results

At baseline, mean age of patients with FH was 12.1 ± 3.3 years, 44% were boys, and mean low-density lipoprotein cholesterol levels were 6.1 ± 1.3 mmol/L (235.9 ± 48.7 mg/dL). Mean c-IMT was 0.399 mm (95% CI, 0.392-0.406 mm) in children with FH versus 0.377 (95% CI, 0.366-0.388 mm) in unaffected siblings (P = .001).

Conclusions

At baseline, as expected according to on previous observations, children with FH proved to have a greater c-IMT than their healthy siblings. These differences had already occurred at a very young age, which emphasizes the importance of considering early statin initiation in this high-risk population.

 
 
 
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