Cardiovascular disease (CVD) is the most common cause of death worldwide, and dyslipidemia is a major risk factor. Atherosclerosis can begin in childhood and continue into adulthood, thereby contributing to CVD development. Obesity is the most common cause of dyslipidemia, and the prevalence of childhood obesity and dyslipidemia is increasing worldwide, making it a public health concern. As clinical evidence has accumulated, guidelines for dyslipidemia in children have been continuously revised since 1992. The limitations of screening tests for individuals with a family history of dyslipidemia emphasize the necessity of universal screening, and non-HDL cholesterol assessment is recommended as a screening test for dyslipidemia in children. The guidelines for dyslipidemia in Korean children and adolescents published in 2017 recommend that non-HDL cholesterol screening tests be performed in non-fasting conditions at 9–11 years and 17–21 years of age. The main purpose of this article is to describe the history and rationale of lipid screening recommendations in children and adolescents and to review the currently recommended screening methods and treatments for dyslipidemia. (Ewha Med J 2022;45(3):e4)
: This study aimed to characteristic the systolic blood pressure (SBP), diastolic pressure, pulse pressure, glucose, creatine, and lipid profile. This study also aimed to investigate the prevalence of hypertension and the relationship between hypertension and the lipid profile in Uzbekistan.
The subjects consisted of 58 Uzbekistan subjects recruited from Ewha Medical Care patients. Blood samples were collected from the patients for the lipid profile and random glucose and creatinine levels. Paired t tests were used for the group means and a chi-square or Fisher’s exact test for categorical variables. A multiple logistic regression analysis was performed.
Among the 58 patients constituting the baseline population, hypertension developed in 42 patients. Among them, the triglyceride (TG) level was significantly higher in the hypertension group than normal group (173.19 vs. 127.06 mg/dL, P=0.014). The SBP had a positive correlation with the TG (r=0.979, P<0.01) and creatinine (r=0.002, P<0.05) levels and also, the pulse pressure had a positive correlation with the cholesterol level (r=0.539, P<0.05). A multivariate analysis (adjusted for age and sex) indicated that there was a positive correlation between the SBP and TG level (r=0.941, P<0.05).
There was a positive correlation between the SBP and TG level in the Uzbekistan population according to this study.
Hyperlipidemia can be a cause of acute pancreatitis. For example, dyslipidemia classified Fredrickson/WHO classification type I, V can induce acute pancreatitis spontaneously. Secondary hyperlipidemia (DM, alcohol, estrogen, etc.) also can induce acute pancreatitis. High serum amylase level and triglyceride level are hall markers of diagnosis. But lactescent serum interferes with accurate laboratory analysis of amylase. Serum amylase was normal or low in 50% of cases. Clinical course and treatment are similar with other causes of acute pancreatitis. Lipoprotein electrophoresis helps classify dyslipidemia by Fredrickson/WHO classification. In some cases, to prevent hyperlipidemic pancreatitis, serum triglyceride should be lower than 500 mg/dl. We report two cases of acute pancreatitis caused by dyslipidemia.