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PubMed1978

Inheritance of apolipoprotein C-II deficiency with hypertriglyceridemia and pancreatitis.

A study of the relatives of a patient with apolipoprotein C-II deficiency showed that the defect is inherited as an autosomal recessive trait. The kindred studied originated from an isolated population in which considerable inbreeding has occurred for 140 years. Seven homozygotes had marked fasting chylomicronemia and triglyceridemia, and lacked detectable apolipoprotein C-II by several assay methods. Five homozygotes had experienced one to many attacks of pancreatitis from as early as six years of age. Obligate heterozygotes had apolipoprotein C-II concentrations about 30 to 50 per cent of normal values and had normal plasma triglyceride concentrations. This metabolic defect should be considered in patients with markedly elevated plasma triglycerides who have apparent lipoprotein lipase deficiency, and usually also have pancreatitis.

Adolescent↗
PubMed1975

Hypertriglyceridemia in patients with chronic renal insufficiency.

The development of hypertiglyceridemia was studied in 38 patients who were at different deteriorative stages of chronic renal insufficiency, as measured by corrected creatinine clearance. Patients in the mild stages of chronic renal insufficiency showed a 53% decrease in postheparin lipolytic activity, and no change in plasma triglyceride levels. In the moderate and severe stages, plasmia triglycerides were significantly elevated but there was no further decrease in PHLA. Those patients undergoing chronic hemodialysis showed a further increase in plasma triglycerides and postheparin lipolytic activity decreased to near zero. Serum electrophoretic studies indicated that in the moderate and severe stages of chronic renal insufficiency, prior to initiating hemodialysis, the chylomicron and very low density lipoprotein fraction were elevated. In those patients receiving chronic hemodialysis hyperchylomicronemia was the predominant finding.

Cholesterol↗
PubMed1995

Primary chylomicronemia in patients with severe familial hypertriglyceridemia responds to long-term treatment with (n-3) fatty acids.

Because it disturbs microcirculation, chylomicronemia can cause severe clinical complications such as acute pancreatitis. Dietary measures are very important in the prevention and treatment of this condition. Dietary supplementation with (n-3) fatty acids has been shown to be of benefit in short-term treatment of chylomicronemia. To evaluate the long-term efficacy of (n-3) fatty acids we added 2.16 or 4.32 g/d (for 3 mo) and 3.24 g/d (for a further 8 mo after 1 mo of no treatment) (n-3) fatty acids to the diet of eight patients with primary chylomicronemia. Serum triglycerides decreased significantly from 15.0 +/- 2.5 to 9.9 +/- 2.8 mmol/L (P < 0.01) after 11 mo of treatment, and VLDL triglycerides decreased from 12.3 +/- 2.8 to 9.0 +/- 2.4 mmol/L (P < 0.01), resulting in a significant decrease of plasma viscosity from 1.56 +/- 0.17 mPa-s to 1.47 +/- 0.12 mPa.s (P < 0.01). Total cholesterol, HDL and LDL cholesterol as well as lipoprotein (a) and fibrinogen concentrations were not affected by fish oil treatment. The presence of chylomicrons and chylomicron remnants (apolipoprotein B 48 concentration in the lipoprotein fraction with a density lower than 1.006 kg/L) was significantly reduced from 4.82 +/- 1.08 to 1.06 +/- 0.38 mg/L (P < 0.01). Body weight increased significantly from 71.0 +/- 4.6 kg to 75.2 +/- 5.3 kg after 11 mo of treatment with (n-3) fatty acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗