Just as hyperbetalipoproteinemia is the most common kind of familiar hyperlipoproteinemia, hyperprebetalipoproteinemia or increased very low density lipoprotein (VLDL) and its associated hypertriglyceridemia is an abnormality frequently found in association with several metabolic and nutritional disorders. This VLDL abnormality is demonstrable in high percentage of insulin dependent diabetic children before they receive treatment. It is also observed in many older, overweight, insulin resistant diabetic, with poor control of diabetes. An elevation of VLDL was also observed after ethanol intake. A mild to moderate degree of VLDL elevation is the most frequently observed from of clinical hyperlipidemia. Many investigators reported that hyperprebetalipoproteinemia (hypertriglyceridemia) is associated with an increasing incidence of coronary artery disease. As opposed to hyperbetalipoproteinemia, hyperprebetalipoproteinemia is prone to influence on the development of atherosclerosis in the middle and older aged persons which indicates the importance of triglyceride determination in these aged groups. There has been relatively rare study reported on the triglyceride metabolism in patients with congestive heart failure, essential hypertension and liver disease in Korea. This study was designed to determine serum triglyceride, free fatty acid and glycerol in the disease mentioned in Busan University Hospital between jan. 1975 and December 1976 and analized the change of lipid profile in each different condition. The results were as follows; 1. The mean of serum FFA, triglyceride and glycerol in the 37 normal were as follows 502.32+/-146.54microEq/L, 111.84+/-40.53mg% and 432.00+/-212.13microM/ml. 2. 23 patients with congestive heart failure showed a significant reduction in serum triglycerides (91.96+/-27.80mg%) and a significant increase in serum free fatty acid (576.77+/-129.67microEqL) and glycerol (432.50+/-212.13microM/ml). 3. In 15 patients with essential hypertension a significant elevation of serum triglycerides (149.38+/-42.28mg%) was noted. 4. In 13 patients with liver cirrhosis, a reduction in serum triglycerides (80.50+/-34.27mg%) was noted.
Atherosclerosis ; Busan ; Child ; Coronary Artery Disease ; Estrogens, Conjugated (USP)* ; Ethanol ; Glycerol* ; Heart Failure* ; Humans ; Hyperlipidemias ; Hyperlipoproteinemia Type II ; Hyperlipoproteinemia Type IV ; Hyperlipoproteinemias ; Hypertension* ; Hypertriglyceridemia ; Incidence ; Insulin ; Korea ; Lipoproteins ; Liver Cirrhosis* ; Liver Diseases ; Liver* ; Metabolism ; Nutrition Disorders ; Overweight ; Research Personnel ; Triglycerides*

Familial combined hyperlipidemia, otherwise known as type IIb hyperlipoproteinemia or multiple lipoprotein-type hyperlipidemia is an inherited disorder of high serum cholesterol or high blood triglycerides. This disease is genetic and inherited, although the specific defective genes have not been identified. The person's cholesterol or triglyceride become elevated during the teenage years and continue to be high throughout life. The types of elevated lipoproteins may vary between affected family members. Its clinical manifestations include lipid disposition on the skin or tendons called "xanthomas" as well as on the arteries. People with this condition have an increased risk of cardiovascular disease so that it is essential to recognize early this type of disorder. We report a case of a 37 year-old male who presented with a bilateral yellowish to reddish nodules on the elbows, knees, ankles, malleoili, ventral aspect of both hands, fingers, feet and toes, metacarpophalangeal & proximal interphalangeal joints, back and buttocks of six years duration with an elevated levels.

Human ; Male ; Adult ; Ankle ; Arteries ; Buttocks ; Cardiovascular Diseases ; Cholesterol ; Hypercholesterolemia ; Hyperlipidemia, Familial Combined ; Hyperlipoproteinemias ; Lipoproteins ; Tendons ; Toes ; Triglycerides ; Xanthomatosis

It is well recognized that there is an association between hyperlipidemia and pancreatitis. However, it is not so easy to define clearly whether lipid abnormalities are the cause or the result of pancreatitis. Generally, a serum level of more than 1,000 mg/dL of triglyceride is an identifiable risk factor of hyperlipidemic pancreatitis in patients with type I, IV, or V hyperlipidemia classified by Fredrick's criteria. The clinical course as well as the management of hyperlipidemic pancreatitis is not different from that of pancreatitis of other causes. A thorough family history of lipid abnormalities should be obtained and an attempt to identify secondary causes should be made. The mainstay of treatment includes dietary restriction of fat and lipid-lowering medications. In Korea, there have been reported several cases of hyperlipidemic pancreatitis but familial history of hyperlipidemia has never been identified. We experienced a case of acute type IV hyperlipidemic pancreatitis in a patient suspected of familial combined hyperlipidemia. So, we report this case with the review of related literature.
Humans ; Hyperlipidemia, Familial Combined* ; Hyperlipidemias ; Korea ; Pancreatitis* ; Risk Factors ; Triglycerides

Study on 210 patients including 120 atheromatous patients, 90 non-atheromatous patients at Transfusion Blood Center in HCMC. Research results showed that: the lipid-lipoprotein disorders had colleration to atheromatous. It was statistical. Hypercholesterolemia 62.6%, hypertriglycerid 51.6%, hypo HDL-C 48.3%, hyper LDL-C 45.8%. The lipid-lipoprotein disorders and atheroscelrosis on the over forty year old patients were higher than the young patients but there was no difference between male and female
Dyslipidemias ; Hyperlipidemia, Familial Combined ; Disease

Familial combined hyperlipidemia is one af the manogenic disorders frequently found in humans and is seen in 0.5~2% of the general populatian, accounting for at least 10% of persons with pemature atlmmcletusis. The distinguishing feature of familial combined hyperlipidemia, in camparison with other single-gene abnarmalities of lipoprotein metabolism, is that not all affected members have the same plasma lipid phenotype; some individuals have an elevation of cholesterol concentration alane(type IIa lipoprotein pattern), while some athers have an elevation of triglyceride concentration alone(type IV pattem), and still others have elevations of both values(type IIb pattem). In any one persan, the lipid phenotype can change as a result of dietary or drug treatment. Familial combined hyperlipidemia should be suspected in those subjects with moderate hypertriglyceridemia and/or moderate hypercholestaolemia (lipoprotein types IIa, Ilb, IV), especially when premature coronary heart disease is evident in the family histary. Low plasma HDL-cholesterol, obesity, insulin resistance and hyperuricemia are often . Family members affected by familial combined hyperlipidemia should be identified and be treated, since tbe condition is associated with premature caronary heart diasease. We have found one family of familial combined hyperlipidemia with one member(case 1) associated with insulin resistance, hyperuricemia and gout, and another member(case 2) associated with diabetes mellitus and infertiTity.
Cholesterol ; Coronary Disease ; Diabetes Mellitus ; Gout ; Heart ; Humans ; Hyperlipidemia, Familial Combined* ; Hypertriglyceridemia ; Hyperuricemia ; Insulin Resistance ; Lipoproteins ; Metabolism ; Obesity ; Phenotype ; Plasma ; Triglycerides

A 61-year-old female patient presented with the type III hyperlipoproteinemia (HLP) in association with generalized eruptive and tuberous xanthomas. She had hypercholesterolemia and hypertriglyceridemia, and extensive coronary atherosclerosis. Further studies revealed a positive standing plasma test, abnormal beta-very low density lipoprotein (VLDL) on lipoprotein electrophoresis, markedly elevated very low density lipoprotein-cholesterol (VLDL-C) to plasma triglycerides (TG) ratio (0.86) and homozygosity for apolipoprotein E2. After about one year of therapy with lipid-lowering agents and diet restriction, a significant reduction of serum cholesterol and TG was observed and the yellowish orange discolorations of palmar creases disappeared from her palms.
Apolipoprotein E2 ; Cholesterol ; Citrus sinensis ; Coronary Artery Disease ; Diet ; Electrophoresis ; Female ; Humans ; Hypercholesterolemia ; Hyperlipoproteinemia Type III* ; Hypertriglyceridemia ; Lipoproteins ; Middle Aged ; Plasma ; Triglycerides ; Xanthomatosis*

Most cases of hypertriglyceridemia (HTG)-induced gestational pancreatitis occur when a person with hyperlipidemia is overweight due to pregnancy or has secondary triggers associated with triglycerides (TGs). In Korea, 6 cases of HTG-induced gestational pancreatitis have been reported, but none of the affected patients had TG levels below 1,000 mg/dL. A 36-year-old female at 30 weeks of gestation was admitted due to pain in her upper abdomen. Initial biochemical analysis revealed a TG level of 260 mg/dL, an amylase level of 2,951 U/L and a lipase level of 3,500 U/L. Abdominal ultrasonography showed pancreatic swelling with a hypoechogenic rim. After several days, the patient was discharged and had a normal delivery at 38 weeks of gestation. This case report is the first to describe acute pancreatitis occurring in the presence of type IV hyperlipoproteinemia even though the TG level was less than 500 mg/dL, contrary to findings in previously reported cases.
Abdomen ; Adult ; Amylases ; Female ; Humans ; Hyperlipidemias ; Hyperlipoproteinemia Type IV ; Hypertriglyceridemia ; Korea ; Lipase ; Overweight ; Pancreatitis ; Pregnancy ; Triglycerides ; Ultrasonography

No abstract available.
Hyperlipoproteinemia Type IV* ; Hyperlipoproteinemias ; Xanthomatosis*

Glucose and lipid metabolism are linked to each other in many ways. The most important clinical manifestation of this interaction is diabetic dyslipidemia, characterized by elevated triglycerides, low high density lipoprotein cholesterol (HDL-C), and predominance of small-dense LDL particles. However, in the last decade we have learned that the interaction is much more complex. Hypertriglyceridemia and low HDL-C cannot only be the consequence but also the cause of a disturbed glucose metabolism. Furthermore, it is now well established that statins are associated with a small but significant increase in the risk for new onset diabetes. The underlying mechanisms are not completely understood but modulation of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA)-reductase may play a central role as genetic data indicate that mutations resulting in lower HMG CoA-reductase activity are also associated with obesity, higher glucose concentrations and diabetes. Very interestingly, this statin induced increased risk for new onset type 2 diabetes is not detectable in subjects with familial hypercholesterolemia. Furthermore, patients with familial hypercholesterolemia seem to have a lower risk for type 2 diabetes, a phenomenon which seems to be dose-dependent (the higher the low density lipoprotein cholesterol, the lower the risk). Whether there is also an interaction between lipoprotein(a) and diabetes is still a matter of debate.
Cholesterol, HDL ; Cholesterol, LDL ; Diabetes Mellitus ; Dyslipidemias* ; Glucose* ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Hyperlipoproteinemia Type II ; Hyperlipoproteinemias ; Hypertriglyceridemia ; Lipid Metabolism* ; Lipoprotein(a) ; Metabolism ; Obesity ; Triglycerides

Statins have been shown to be very effective and safe in numerous randomized clinical trials, and became the implacable first-line treatment against atherogenic dyslipidemia. However, even with optimal statin treatment, 60% to 80% of residual cardiovascular risk still exists. The patients with familial hypercholesterolemia which results in extremely high level of low density lipoprotein cholesterol (LDL-C) level and the patients who are intolerant or unresponsive to statins are the other hurdles of statin treatment. Recently, new classes of lipid-lowering drugs have been developed and some of them are available for the clinical practice. The pro-protein convertase subtilisin/kexintype 9 (PCSK9) inhibitor increases the expression of low density lipoprotein (LDL) receptor in hepatocytes by enhancing LDL receptor recycling. The microsomal triglyceride transport protein (MTP) inhibitor and antisense oligonucleotide against apolipoprotein B (ApoB) reduce the ApoB containing lipoprotein by blocking the hepatic very low density lipoprotein synthesis pathway. The apolipoprotein A1 (ApoA1) mimetics pursuing the beneficial effect of high density lipoprotein cholesterol and can reverse the course of atherosclerosis. ApoA1 mimetics had many controversial clinical data and need more validation in humans. The PCSK9 inhibitor recently showed promising results of significant LDL-C lowering in familial hypercholesterolemia (FH) patients from the long-term phase III trials. The MTP inhibitor and antisesnse oligonucleotide against ApoB were approved for the treatment of homozygous FH but still needs more consolidated evidences about hepatic safety such as hepatosteatosis. We would discuss the benefits and concerns of these new lipid-lowering drugs anticipating additional benefits beyond statin treatment.
Apolipoprotein A-I ; Apolipoproteins ; Apolipoproteins B ; Atherosclerosis ; Cholesterol, HDL ; Cholesterol, LDL ; Dyslipidemias* ; Hepatocytes ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors* ; Hyperlipoproteinemia Type II ; Lipoproteins ; Receptors, LDL ; Recycling ; Triglycerides