• Journal of the Korean Society of Radiology
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• v.13 no.5
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• pp.729-737
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• 2019

Fatty pancreas is an abnormal process of lipid deposition in cells, resulting in increased fat tissue and obesity. The result is a risk factor for cardiovascular and metabolic diseases. The aim of this study was to evaluate the usefulness of pancreatic fat as a predictor of cardiovascular disease and metabolic syndrome in pancreatic ultrasonography. In 407 patients who underwent a comprehensive screening at the W Health Care Center in Busan from September 2. 2018 to December 31, 2018, the degree of fat deposition in the pancreas was evaluated as the degree of mild, moderate. Data on non-obstructive atherosclerosis, BMI, hyperlipidemia, hypertension, and diabetes were collected to assess the association of pancreatic fat deposition with cardiovascular disease and metabolic syndrome. In addition, we tried to analyze the correlation between liver dysfunction and thyroid dysfunction as the degree of fat pancreas increased. We examined the relationship between six parameters including atherosclerosis, BMI, hyperlipidemia, hypertension, diabetes, liver dysfunction, and thyroid dysfunction among patients with fatty pancreas. We concluded that the carotid intima-media thickness of atherosclerosis, which is a risk factor of cardiovascular disease, is most closely related to fatty pancreas.

• YAKHAK HOEJI
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• v.54 no.4
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• pp.270-281
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• 2010

Total parenteral nutrition (TPN) is necessary to neonates in neonatal intensive care unit (NICU) for survival and growth because of impossible of enteral feeding. Long-term TPN can be associated with a broad spectrum of hepatobiliary disorder, ranging from mild hepatic dysfunction to severe end-stage liver disease. Cholestasis developed most commonly in neonate, ursodeoxycholic acid (UDCA) is widely used in adult with cholestatic and non-cholestatic liver diseases but there have been limited data on the effects in neonate with PNAC. This study was performed retrospectively to review all medical histories of the total 30 neonates with was administrated UDCA for treatment to parenteral nutrition associated cholestasis (PNAC) at Chungbuk National University Hospital NICU from April 2002 to December 2008. UDCA was administrated at bilirubin is over 2 mg/dl. The criterias for drug evaluation were included hepatic biochemical marker such as direct bilirubin, total bilirubin, AST, ALT, ALP and GGT, TPN therapy period, cholestasis development period, UDCA treatment period, UDCA dosage and adverse effect. In the results, Post-UDCA treatment significant was decreased direct bilirubin, total bilirubin, AST and ALP (p<0.05), and was decreased GGT (p>0.05) and slightly was increased ALT (p>0.05). Reffective timect biDCA was appear at mean $10.5{\pm}1.3$ days, iDCA administration period was mean $64.4{\pm}5.9$ days, cholestasis period was mean $71.9{\pm}6.4$ days and UDCA dosage was mean $22.9{\pm}0.9$ mg/kg/day. Common adverse effects is diarrhea, 5 patients arised mild diarrhea but it possible also related with increased enteral feeding. In conclusion, iDCA can decrease direct bilirubin that major parameter t bcholestasis and oher hepatic biochemical makers. UDCA is effective on PNAC without any serious side effect and cost-effective. Although no greatly shortening cholestasis period, but can protect to develop into severe liver disease and other complication or death. Based on these result, UDCA is recommended for treatment of cholestasis at direct bilirubin is over 2 mg/dl.

• Journal of Korean Public Health Nursing
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• v.16 no.2
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• pp.436-444
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• 2002

This study surveyed 146 obese elementary school children(94 male and 52 female) in Seoul, and measured height, body weight, degree of obesity, blood pressure, fasting blood sugar, serum lipid profiles and liver function. The hypertension was above 95 percentile depending on age and sex. and the hyperglycemia was defined as above 110mg/dl. The hypercholesterolemia and hypertriglyceridemia were defined as above 200mg/dl, 160mg/dl, repectively. The abnormal liver function was considered as elevated alanine aminotransferase(ALT>35IU/L)or aspartate aminotransferase(AST>35IU/L). The results were as follows: 1. The mean degree of obesity was $29.56\pm12.56\%$, and the percentage of overweight was $18.5\%$, mild obesity $41.1\%$, moderate obesity $35.6\%$, severe obesity $4.8\%$ respectively in surveyed children. 2. The systolic blood pressure was $108.34\pm13.73mmHg$, diastolic blood pressure was $67.46\pm8.27mmHg$. 3. FBS was $93.79\pm6.51mg/dl$. 4. Total cholesterol, triglyceride, ALT and AST were $183.34\pm31.38mg/dl$. $115.55\pm56.43mg/dl,\;24.08\pm18.42IU/L,\; 28.73\pm10.45IU/L,$ respectively. 5. The prevalence of complications was $47.2\%$ : hypertension$(13\%)$, hyperglycemia$(0.7\%)$, hypercholesterolemia$(23.3\%)$, hypertriglyceridemia$(17.1\%)$, and liver dysfunction$(21.9\%)$. In conclusion. childhood obesity is associated with various risk factors. Therefore, the aggressive approaches to successful prevention, early detection, and effective treatment of obesity in children are urgently required.

• Journal of Nutrition and Health
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• v.37 no.9
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• pp.786-793
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• 2004

Women with menopause or rats with ovariectomy is associated with increased body weight, body fat and insulin resistance, which are components of metabolic syndrome. Increased prevalence of metabolic syndrome after menopause might be associated with mitochondrial dysfunction, since mitochondrial oxidative and phosphorylation activity is strongly correlated with insulin sensitivity. Although estradiol replacement prevents the metabolic syndrome, harmful effect of estradiol hampers the casual usage to prevent the metabolic syndrome. It has been reported that genistein has a mild estrogenic activity, decreases fat mass in mice and has an antidiabetic role in diabetic rats. Although insulin resistance is closely related to mitochondrial functions, there has not been yet any study in regard to the effect of dietary genistein on mitochondrial function in the insulin resistant female subjects induced by ovariectomy or similar situation. The present study investigated whether the supplementation of genistein in the high fat diet affected the mitochondrial function of high fat fed ovariectomized rats. Female Sprague Dawley rats (8 weeks old) were assigned to the following groups: sham-operated+ high fat diet (S, n=6); sham-operated + high fat diet with 0.1% genistein (S + G, n=7); ovariectomized + high fat diet (OVX, n=8); ovariectomized + high fat diet with 0.1% genistein (OVX+ G, n=8). Ovariectomy significantly increased body weight compared with S group. Genistein consumption in ovariectomized (OVX + G) rats decreased body weight gain compared with OVX rats. Liver weights were increased by ovariectomy. The hepatic mitochondrial protein density expressed as mg per g liver was lower in the OVX group than in the S group. However, OVX + G group showed the increased mitochondrial protein density similar to the level of S group. When mRNA levels of genes related to mitochondria such as peroxisome proliferator-activated receptor ${\gamma}$ coactivator 1 (PGC-1) and cytochrome c oxidase subunit III (COX III) were measured, there were decreases in the mRNA levels of PGC-1 and COX III in S + G, OVX and OVX + G group. The activity of cytochrome c oxidase was not different between groups. We could observe the decrease in succinate dehydrogenase (SDH) activity per g liver in OVX rats. Genistein supplement increased SDH activity. In conclusion, genistein supplementation to the OVX rats enhanced mitochondrial function by increasing mitochondrial protein density and SDH activity. The improvement in mitochondrial function by genistein can contribute to the improvement in metabolic syndrome.

• Journal of Gastric Cancer
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• v.21 no.1
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• pp.74-83
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• 2021

Purpose: No consensus exists on whether to preserve or ligate an aberrant left hepatic artery (ALHA), which is the most commonly encountered hepatic arterial variation during gastric surgery. Therefore, we aimed to evaluate the clinical effects of ALHA ligation by analyzing the perioperative outcomes. Materials and Methods: We retrospectively reviewed the data of 5,310 patients who underwent subtotal/total gastrectomy for gastric cancer. Patients in whom the ALHA was ligated (n=486) were categorized into 2 groups according to peak aspartate aminotransferase (AST) or alanine aminotransferase (ALT) levels: moderate-to-severe (MS) elevation (≥5 times the upper limit of normal [ULN]; MS group, n=42) and no-to-mild (NM) elevation (<5 times the ULN; NM group, n=444). The groups were matched 1:3 using propensity score-matching analysis to minimize confounding factors that can affect the perioperative outcomes. Results: The mean operation time (P=0.646) and blood loss amount (P=0.937) were similar between the 2 groups. The length of hospital stay was longer in the MS group (13.0 vs. 7.8 days, P=0.022). No postoperative mortality occurred. The incidence of grade ≥ IIIa postoperative complications (19.0% vs. 5.1%, P=0.001), especially pulmonary complications (11.9% vs. 2.5%, P=0.003), was significantly higher in the MS group. This group also showed a higher Comprehensive Complication Index (29.0 vs. 13.9, P<0.001). Conclusions: Among patients with a ligated ALHA, those with peak AST/ALT ≥5 times the ULN showed worse perioperative outcomes in terms of hospital stay and severity of complications. More precise perioperative decision-making tools are needed to better determine whether to preserve or ligate an ALHA.

• Pediatric Infection and Vaccine
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• v.29 no.3
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• pp.155-160
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• 2022

Children and adolescents with coronavirus disease 2019 (COVID-19) generally have mild symptoms. Severe infection due to severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) involving multiorgan dysfunction is rare in this population. Herein, we present an unusual case of severe SARS-CoV-2 infection with multiorgan involvement followed by multisystem inflammatory syndrome in children (MIS-C) in a vaccinated 16-year-old boy. The patient was unconscious on initial presentation, and had severe paralytic ileus. On laboratory examination, there was severe metabolic acidosis, lymphocytopenia, thrombocytopenia, elevated inflammatory markers, elevated liver enzymes, and evidence of acute kidney injury with proteinuria and hematuria. His symptoms improved with the administration of remdesivir and dexamethasone. The patient briefly experienced MIS-C 2 weeks after the diagnosis of COVID-19, but the patient was discharged without any complications.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.9-17
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• 2015

Glycogen storage disease (GSD) type Ia is rare inborn metabolic disorder, caused by glucose-6-phosphatase deficiency. It characterized by hepatomegaly, hypoglycemia, lactic acidosis, hypertriglyceridemia, and hyperuricemia and it is usually manifested in the infantile period. In addition, it is also associated with growth failure, pubertal delay, anemia, platelet dysfunction, osteopenia, and pulmonary hypertension. Hepatocellular adenoma and renal dysfunction are frequent late complications. Delayed diagnosis and inappropriate therapy lead to many complications such as growth failure, osteoporosis, refractory gout, renal failure, hepatocellular carcinoma (HCC), and pulmonary hypertension. Here, two Korean sisters diagnosed with GSD Ia, aged 33 and 36 respectively, were described and compared to recent articles about four adults with late diagnosis of GSD Ia. One sister had typical manifestations of GSD Ia including short stature (height, 145 cm), multiple hepatic adenoma, chronic kidney disease stage IV, and severe osteoporosis, whereas the older sister had normal stature (162 cm), one tiny hepatic nodule, and normal renal function. Direct sequencing of G6PC in two sisters identified a homozygous splicing mutation, c.645G>T, which is a prevalent mutation in Korea. Interestingly, our cases and four adults from recent reports had asymptomatic mild hypoglycemia and various manifestations including renal failure, HCC, fatty liver, or uncontrolled hyperlipidemia. These adult cases represent not only heterogenous phenotype to genotype within family members with GSD Ia but also long-term complications such as gouty arthritis, renal failure, and osteoporosis in untreated adult GSD Ia patients. In addition, lactic academia and hypertriglyceridemia are good markers of GSD Ia to distinguish from metabolic disease.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.13 no.1
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• pp.51-57
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• 2010

Purpose: It has been reported that children with hypopituitarism have features of metabolic syndrome, including obesity, impaired glucose tolerance, and dyslipidemia. The aim of this study was to investigate the clinical features and liver histology of pediatric non-alcoholic fatty liver disease (NAFLD) associated with hypopituitarism. Methods: We reviewed the clinical data of 11 children diagnosed with NAFLD among patients with hypopituitarism. Results: The mean age at the time of diagnosis of hypopituitarism was 10.4${\pm}$3.2 years, and the mean age at the time of diagnosis of NAFLD was 13.1${\pm}$2.7 years. A craniopharyngioma was the most common cause of pituitary dysfunction. At the time of diagnosis of NAFLD, 9 patients (82%) had a body mass index greater than the 85th percentile, 5 patients (45%) had elevated fasting blood glucose levels, and 9 patients (82%) had hypertriglyceridemia. The mean height SD score was significantly lower at the time of diagnosis of NAFLD than at the time of diagnosis of hypopituitarism. Of the six patients who were biopsied, one had cirrhosis, two had non-alcoholic steatohepatitis (NASH) with bridging fibrosis, two had NASH with mild portal fibrosis, and one had simple steatosis. Conclusion: Children with hypopituitarism are at risk of short stature, obesity, dyslipidemia, and NAFLD. The early diagnosis of NAFLD is important in children with hypopituitarism because advanced fibrosis is common.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.14 no.2
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• pp.186-190
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• 2014

Citrullinemia type 2 (citrin deficiency) is an autosomal recessive inborn error metabolism, caused by the SLC25A13 gene mutation. Citrin deficiency is associated with two clinical phenotype; neonatal-onset type II citrullinemia (CTLN2), also known as neonatal intraphepatic cholestasis caused by citrin deficiency (NICCD) and adult-onset CTLN2. Clinical manifestations of NICCD include poor growth, intrahepatic cholestasis, liver dysfunction and increased plasma citrulline, methionine, threonine, arginine. The molecular diagnosis could be confirmed by SLC25A13 gene mutation analysis. A 3-month-old male infant with persistent jaundice was referred for evaluation. Newborn screening was normal at birth. Mild elevation of serum ammonia and AST/ALT were observed. Plasma amino acid analysis showed significantly elevated citrulline, methionine, threonine. DNA sequence analysis of the SLC25A13 gene revealed two compound heterozygous mutations, c.[852_855del]($p.Met285Profs^*2$) and [1180+1G>A]. We suggest that NICCD should be considered as one of the cause of in infants with cholestatic jaundice, although the newborn screening was normal.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.29-34
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• 2015

Citrullinemia type1 is an autosomal recessive disorder of the urea cycle characterized by neonatal or late onset of hyperammonemia caused by a deficiency of the enzyme argininosuccinate synthetase (ASS). An ASS1 deficiency demonstrates fatal clinical manifestations that are characterized by the neonatal metabolic coma and early death when untreated. It causes a broad spectrum of effects, ranging from a mild disorder to a severe mental retardation, epilepsy, neurologic deficits. An acute neonatal form is the most common. Infants are normal at birth followed by an acute illness characterized by vomiting, lethargy, seizures and coma. These medical problems are life-threatening in many cases. A later onset form is less frequent and may be milder than the neonatal form. This later-onset form is associated with severe headaches, visual dysfunction, motor dysfunction, and lack of energy. Citrullinemia type1 is caused by mutations in the ASS1 gene located on chromosome 9q34.1 that encodes argininosuccinate synthetase, the third enzyme of the urea cycle catalyzing the formation of argininosuccinic acid from citrulline and aspartic acid. The enzyme is distributed in tissues including liver and fibroblasts. This mutation leads to hyperammonemia, arginine deficiency and elevated citrulline level. In the urea cycle, argininosuccinate synthetase catalyses the conversion of citrulline and aspartate to argininosuccinate.. Here, we describe a female newborn patient with lethargy, rigidity and hyperammonemia who was diagnosed as citrullinemia type1 with a c.[421-2A>G], c.[1128-6_1188dup] mutation.