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Page 2 of 6 Zsíros et al. Vessel Plus 2019;3:6 I http://dx.doi.org/10.20517/2574-1209.2018.78

Besides, the elimination of VLDL is decreased due to the reduced activity of lipoprotein lipase in fatty
[4]
[3]
tissue . Eventually, there is a 2-4 fold increase in triglyceride level by third trimester .
Genetic abnormalities of triglyceride metabolism can provoke severe hypertriglyceridemia in pregnancy.
In familial combined hyperlipidemia and familial hypertriglyceridemia, we see an increased formation of
triglyceride-rich lipoproteins (chylomicrons and VLDLs). Ineffective lipolysis of these particles can cause
familial chylomicronemia due to the mutations in lipoprotein lipase, apolipoprotein CII or apolipoprotein
[5]
AV . In familial dysbetalipoproteinemia, apolipoprotein E2/E2 genotype reduces hepatic clearance of
[5]
chylomicron remnants . In addition, secondary factors such as poorly controlled diabetes mellitus (via
decreasing the activity of lipoprotein lipase), hypothyroidism, nephrotic syndrome and some medications
[6]
(glucocorticoids) may aggravate gestational hypertriglyceridemia .

Hypertriglyceridemia during pregnancy increases the risk of acute pancreatitis (especially if triglyceride level
is above 11.4 mmol/L), hyperviscosity syndrome and pre-eclampsia in mother, macrosomia, premature birth
[6-9]
or fetal death in fetus .

[6]
At first, treatment of the underlying disease and fat-restricted diet are recommended . During pregnancy,
lipid-lowering medications (fibrate, nicotinic acid, statin, and ezetimibe) should be stopped due to their
[10]
possible teratogenic effects . Novel lipid-lowering agents including microsomal transfer protein and
proprotein convertase subtilisin/kexin type 9 inhibitors are also contraindicated. Therefore, in the case of
non-responding severe hypertriglyceridemia plasmapheresis should be considered. This is an extracorporeal
procedure, when plasma is separated from the blood and processed to eliminate selective components
including triglyceride-rich lipoprotein particles. The treated plasma is then reinfused although, on occasion,
it is completely eliminated and replaced by an isovolumetric solution. Most of the studies use plasmapheresis
as a treatment of hypertriglyceridemia associated pancreatitis. In some cases, they perform plasmapheresis to
prevent pancreatitis. It must be noted that the timing and frequency of plasmapheresis procedures were not
uniform in these studies [11-13] . During plasmapheresis serum triglyceride level can be decreased by 66%-70% [12,13] .

CASE REPORT
A 33-year-old woman at 37 weeks of her second pregnancy was admitted to our clinic. Her gynecologist
indicated routine laboratory examinations, which remained unsuccessful because of lipemic blood sample.
Therefore, we checked her triglyceride level and found that it was significantly elevated (57.8 mmol/L). Abdominal
pain, nausea, vomiting or any other complaints were not reported. Based on physical examination, there were
no eruptive xanthomas, palmar crease xanthomas or lipaemia retinalis. Her body mass index was within the
normal range before pregnancy (53 kg), and her total body weight gain was 9 kg during pregnancy. In her
history, there was no diabetes mellitus or any other secondary causes of hypertriglyceridemia. The diagnosis
of gestational diabetes mellitus was evaluated according to the Hungarian national recommendation.
We used the modified 1999 WHO recommendation (gestational diabetes mellitus: 75 g CH oral glucose
tolerance test (OGTT) at 24-28 gestation weeks: fasting plasma glucose ≥ 6.1 mmol/L, 120 min plasma glucose ≥
[14]
7.8 mmol/L) . Based on the fasting plasma glucose (5.2 mmol/L) and the OGTT (plasma glucose: 120 min:
7.1 mmol/L) the diagnosis of gestational diabetes mellitus was excluded. In her family history, her mother
and grandmother had mixed hyperlipidemia. Her first pregnancy had terminated without any complication
however, lipid parameter measurement was not performed. Before her pregnancy, she had not taken any
lipid-lowering medications. She had not followed a fat-restricted diet during her pregnancy. Table 1 shows
the laboratory parameters before treatment. Markedly elevated triglyceride and total cholesterol levels were
detected. Apolipoprotein B100 and lipoprotein (a) levels were also above the upper border of the normal
range. Based on the result of lipid electrophoresis, a significant increase in the level of VLDL may cause
hypertriglyceridemia.