1.Blood Pressure and the Risk of Death From Non-cardiovascular Diseases: A Population-based Cohort Study of Korean Adults.
Jeoungbin CHOI ; Jieun JANG ; Yoonsuk AN ; Sue K PARK
Journal of Preventive Medicine and Public Health 2018;51(6):298-309
OBJECTIVES: The objective of this study was to assess the relationship between systolic and diastolic blood pressure (SBP, DBP) and the risk of death from specific causes other than cardiovascular diseases. METHODS: We calculated the risk of specific death by SBP and DBP categories for 506 508 health examinees in 2002-2003 using hazard ratios (HRs) and 95% confidence intervals (CIs) in a Cox proportional hazards model. RESULTS: Compared to normal levels (SBP < 120 or DBP < 90 mmHg), stage I systolic and diastolic hypertension (SBP 140-159, DBP 85- 89 mmHg, respectively) were associated with an increased risk of death from diabetes mellitus, alcoholic liver disease, and renal failure (HR, 1.83; 95% CI, 1.51 to 2.22; HR, 1.24; 95% CI, 1.06 to 1.46; HR, 2.30; 95% CI, 1.64 to 3.21; HR, 1.67; 95% CI, 1.27 to 2.20; HR, 1.99; 95% CI, 1.41 to 2.81; HR, 1.31; 95% CI, 0.99 to 1.73, respectively), but a decreased risk of death from intestinal pneumonia (HR, 0.64; 95% CI, 0.42 to 0.98; HR, 0.59; 95% CI, 0.39 to 0.91). Only stage II systolic hypertension (SBP ≥160 mmHg) was associated with an increased risk of death from pneumonia, liver cirrhosis, and intestinal ischemia (HR, 1.54; 95% CI, 1.19 to 1.98; HR, 1.46; 95% CI, 1.00 to 2.15; HR, 3.77; 95% CI, 1.24 to 11.40, respectively), and stage I and II diastolic hypertension (SBP 140-159 and ≥160 mmHg) were associated with an increased risk of death from intestinal ischemia (HR, 3.07; 95% CI, 1.27 to 7.38; HR, 4.39; 95% CI, 1.62 to 11.88, respectively). CONCLUSIONS: An increase in blood pressure levels may alter the risk of death from certain causes other than cardiovascular diseases, a well-known outcome of hypertension, although the mechanism of these associations is not well documented.
Adult*
;
Blood Pressure*
;
Cardiovascular Diseases
;
Cohort Studies*
;
Diabetes Mellitus
;
Humans
;
Hypertension
;
Ischemia
;
Liver Cirrhosis
;
Liver Diseases, Alcoholic
;
Pneumonia
;
Proportional Hazards Models
;
Renal Insufficiency
2.Estimated Prevalence of Adolescents with Nonalcoholic Fatty Liver Disease in Korea.
Yunkoo KANG ; Sowon PARK ; Seung KIM ; Hong KOH
Journal of Korean Medical Science 2018;33(14):e109-
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) has become prevalent worldwide in the last decade. However, the recent prevalence of NAFLD in adolescents has not yet been investigated in Korea. METHODS: Data were obtained from 1,416 participants aged 10–18 years from the Korea National Health and Nutrition Examination Survey conducted in 2010 and 2015. Systolic blood pressure (SBP), diastolic blood pressure (DBP), height, weight, waist circumference (WC), body mass index (BMI), fasting glucose, total cholesterol, high-density lipoprotein (HDL), aspartate aminotransferase (AST), alanine aminotransferase (ALT) level, waist-to-height ratio (WHtR), and pediatric NAFLD fibrosis index (PNFI) were analyzed. RESULTS: SBP, weight, WC, BMI, WHtR, and total cholesterol level were significantly higher in 2015 than in 2010. Prevalence of NAFLD (BMI ≥ 85th percentile plus ALT > 30 U/L for boys and ALT > 19 U/L for girls) were 4.7% in 2010 and 5.9% in 2015 (P = 0.360). Using various cutoffs for the ALT level (> 40, > 30, > 25.8 U/L for boys and >22.1 U/L for girls) NAFLD prevalence rates were 3.0%, 4.1%, and 5.5% in 2010; 2.9%, 5.0%, and 7.1% in 2015, respectively (P = 0.899, 0.469, and 0.289). Boys had a higher SBP, DBP, height, weight, WC, BMI, WHtR, fasting glucose, total cholesterol, ALT, and lower HDL level than girls. The probability of liver fibrosis using the PNFI varies between 21.3% and 24.5% among NAFLD participants (P < 0.001). CONCLUSION: The Korean society needs to quickly control the increasing prevalence of NAFLD in adolescents and reduce its complications.
Adolescent*
;
Alanine Transaminase
;
Aspartate Aminotransferases
;
Blood Pressure
;
Body Mass Index
;
Cholesterol
;
Fasting
;
Female
;
Fibrosis
;
Glucose
;
Humans
;
Korea
;
Lipoproteins
;
Liver Cirrhosis
;
Non-alcoholic Fatty Liver Disease*
;
Nutrition Surveys
;
Prevalence*
;
Waist Circumference
3.Alcohol Intake and Risk of Ischemic and Haemorrhagic Stroke: Results from a Mendelian Randomisation Study.
Anne I CHRISTENSEN ; Børge G NORDESTGAARD ; Janne S TOLSTRUP
Journal of Stroke 2018;20(2):218-227
BACKGROUND AND PURPOSE: To test whether alcohol intake, both observational and estimated by genetic instruments, is associated with risk of ischemic and haemorrhagic stroke. METHODS: We used data from the Copenhagen City Heart Study 1991 to 1994 and 2001 to 2003, and the Copenhagen General Population Study 2003 to 2012 (n=78,546). As measure of alcohol exposure, self-reported consumption and genetic variation in alcohol metabolizing genes (alcohol dehydrogenase ADH1B and ADH1C) as instrumental variables were used. Stroke diagnoses were obtained from a validated hospital register. RESULTS: During follow-up 2,535 cases of ischemic and haemorrhagic stroke occurred. Low and moderate alcohol intake (1 to 20 drinks/week) was associated with reduced risk of stroke. The hazard ratios associated with drinking 1 to 6, 7 to 13, and 14 to 20 drinks/week were 0.84 (95% confidence interval [CI], 0.76 to 0.92), 0.83 (95% CI, 0.73 to 0.94), and 0.84 (95% CI, 0.73 to 0.97), respectively, compared with drinking < 1 drink/day. ADH1B and ADH1C genotypes were not associated with risk of stroke. Further analysis to test the included measures revealed that increasing alcohol intake (per 1 drink/day) was positively associated with risk of alcoholic liver cirrhosis, but not associated with risk of stroke, and that increasing blood pressure (per systolic 10 mm Hg) was not associated with risk of alcoholic liver cirrhosis, but positively associated with risk of stroke. CONCLUSIONS: Low and moderate self-reported alcohol intake was associated with reduced risk of stroke. The result was not supported by the result from the causal genetic analysis.
Alcohol Drinking
;
Blood Pressure
;
Diagnosis
;
Drinking
;
Follow-Up Studies
;
Genetic Variation
;
Genotype
;
Heart
;
Incidence
;
Liver Cirrhosis, Alcoholic
;
Oxidoreductases
;
Prospective Studies
;
Stroke*
4.A practical clinical approach to liver fibrosis.
Rahul KUMAR ; Eng Kiong TEO ; Choon How HOW ; Teck Yee WONG ; Tiing Leong ANG
Singapore medical journal 2018;59(12):628-633
Liver fibrosis is a slow, insidious process involving accumulation of extracellular matrix protein in the liver. The stage of liver fibrosis in chronic liver disease (CLD) determines overall morbidity and mortality; the higher the stage, the worse the prognosis. Noninvasive composite scores can be used to determine whether patients with CLD have significant or advanced fibrosis. Patients with low composite scores can be safely followed up in primary care with periodic reassessment. Those with higher scores should be referred to a specialist. As the epidemic of diabetes mellitus, obesity and non-alcoholic fatty liver diseases is rising, CLD is becoming more prevalent. Easy-to-use fibrosis assessment composite scores can identify patients with minimal or advanced fibrosis, and should be an integral part of decision-making. Patients with cirrhosis, high composite scores, chronic hepatitis B with elevated alanine aminotransferase and aspartate aminotransferase, or deranged liver panel of uncertain aetiology should be referred to a specialist.
Alanine Transaminase
;
blood
;
Aspartate Aminotransferases
;
blood
;
Decision Making
;
End Stage Liver Disease
;
complications
;
diagnosis
;
therapy
;
Hepatitis B
;
complications
;
Humans
;
Liver
;
pathology
;
Liver Cirrhosis
;
complications
;
diagnosis
;
therapy
;
Non-alcoholic Fatty Liver Disease
;
complications
;
diagnosis
;
therapy
;
Prognosis
;
Referral and Consultation
;
Treatment Outcome
5.Hemorheological Alteration in Patients Clinically Diagnosed with Chronic Liver Diseases.
Bohyun JANG ; Ji Won HAN ; Pil Soo SUNG ; Jeong Won JANG ; Si Hyun BAE ; Jong Young CHOI ; Young I CHO ; Seung Kew YOON
Journal of Korean Medical Science 2016;31(12):1943-1948
Since liver function is changed by chronic liver diseases, chronic liver disease can lead to different hemorheological alterations during the course of the progression. This study aims to compare alterations in whole blood viscosity in patients with chronic liver disease, focusing on the gender effect. Chronic liver diseases were classified into three categories by patient’s history, serologic markers, and radiologic findings: nonalcoholic fatty liver disease (NAFLD) (n = 63), chronic viral hepatitis B and C (n = 50), and liver cirrhosis (LC) (n = 35). Whole blood viscosity was measured by automated scanning capillary tube viscometer, while liver stiffness was measured by transient elastography using FibroScan®. Both systolic and diastolic whole blood viscosities were significantly lower in patients with LC than NAFLD and chronic viral hepatitis (P < 0.001) in male patients, but not in female patients. In correlation analysis, there were inverse relationships between both systolic and diastolic whole blood viscosity and liver stiffness (systolic: r = −0.25, diastolic: r = −0.22). Whole blood viscosity was significantly lower in male patients with LC than NAFLD or chronic viral hepatitis. Our data suggest that whole blood viscosity test can become a useful tool for classifying chronic liver disease and determining the prognosis for different types of chronic liver diseases.
Blood Viscosity
;
Capillaries
;
Elasticity Imaging Techniques
;
Female
;
Hemorheology
;
Hepatitis
;
Hepatitis B
;
Humans
;
Liver Cirrhosis
;
Liver Diseases*
;
Liver*
;
Male
;
Non-alcoholic Fatty Liver Disease
;
Prognosis
6.Flavobacterium ceti From Blood Samples of a Korean Patient With Alcoholic Liver Cirrhosis.
Ji Yeon SUNG ; Taek Soo KIM ; Sue SHIN ; Eun Youn ROH ; Jong Hyun YOON ; Eui Chong KIM
Annals of Laboratory Medicine 2015;35(3):384-386
No abstract available.
Asian Continental Ancestry Group
;
Flavobacteriaceae Infections
;
Flavobacterium/*genetics/isolation & purification
;
Humans
;
Liver Cirrhosis, Alcoholic/blood/*diagnosis/microbiology
;
Male
;
Middle Aged
;
RNA, Ribosomal, 16S/chemistry/genetics/metabolism
;
Republic of Korea
;
Sequence Analysis, DNA
7.Living-donor Sequential ABO-incompatible Kidney Transplantation after Liver Transplantation in a Patient with Alcoholic Liver Cirrhosis and End-stage Renal Disease.
Jin Ho KWAK ; Hyuk Jai JANG ; Gun Moo CHOI ; Chun Soo PARK ; Dae Woon EOM ; Seong Su KIM ; Duck Jong HAN ; In Koo KIM
The Journal of the Korean Society for Transplantation 2015;29(1):28-32
A 47-year-old man developed chronic alcoholic liver cirrhosis and end-stage renal disease. He underwent blood-type-compatible liver transplantation with a graft from his daughter. After 8 months, sequential ABO-incompatible (ABOi) kidney transplantation was performed, with his brother as the donor (A to O). The patient had anti-A antibody titers (1:256). We performed pretransplant desensitization, including administration of rituximab, mycophenolate mofetil, tacrolimus, and prednisolone 2 weeks before the scheduled transplantation, and plasmaphresis (PP) and administered an intravenous immunoglobulin injection. The patient underwent PP before kidney transplantation until the anti-A antibody titer was <1:8. The patient achieved normal renal function within 4 posttransplantation days. Postoperative bleeding (diffuse hemorrhage) requiring additional blood transfusions and radiological intervention (drainage procedure) occurred 9 days after transplantation. The patient was discharged on day 20 of hospitalization. Nine months after the kidney transplantation, the recipient's and donor's liver and kidney functions were normal. ABOi renal transplantation after liver transplantation can be successfully performed in patients with high baseline anti-ABO antibody titers after preconditioning with rituximab and PP, and quadruple immunosuppressive therapy. However, caution is required regarding an increased risk of bleeding complications.
Blood Transfusion
;
Hemorrhage
;
Hospitalization
;
Humans
;
Immunoglobulins
;
Kidney
;
Kidney Failure, Chronic*
;
Kidney Transplantation*
;
Liver
;
Liver Cirrhosis, Alcoholic*
;
Liver Transplantation*
;
Middle Aged
;
Nuclear Family
;
Prednisolone
;
Rituximab
;
Siblings
;
Tacrolimus
;
Tissue Donors
;
Transplants
8.The Influence of Alcoholic Liver Disease on Serum PIVKA-II Levels in Patients without Hepatocellular Carcinoma.
Keunhee KANG ; Ji Hoon KIM ; Seong Hee KANG ; Beom Jae LEE ; Yeon Seok SEO ; Hyung Joon YIM ; Jong Eun YEON ; Jong Jae PARK ; Jae Seon KIM ; Young Tae BAK ; Kwan Soo BYUN
Gut and Liver 2015;9(2):224-230
BACKGROUND/AIMS: Prothrombin induced by vitamin K deficiency or antagonist II (PIVKA-II) is a widely used diagnostic marker for hepatocellular carcinoma (HCC). We evaluated the correlation between alcoholic liver disease (ALD) and serum PIVKA-II levels in chronic liver disease (CLD) patients. METHODS: We retrospectively reviewed the medical records of 2,528 CLD patients without HCC. Among these patients, 76 exhibited serum high PIVKA-II levels of >125 mAU/mL (group 1). We categorized 76 control patients matched by age, sex, and the presence of liver cirrhosis from the remaining patients who were negative for serum PIVKA-II (group 2). RESULTS: Group 1 revealed increased antibiotic usage (23.7% vs 2.6%, p<0.001) and incidence of ALD (60.5% vs 14.5%, p<0.001) as well as elevated aspartate aminotransferase (52.5 IU/L vs 30.5 IU/L, p=0.025) and gamma glutamyl transpeptidase (67.5 IU/L vs 36.5 IU/L, p=0.005) levels compared with group 2. Further, group 1 was significantly associated with a worse Child-Pugh class than group 2. In the multivariate analysis, ALD (odds ratio [OR], 7.151; p<0.001) and antibiotic usage (OR, 5.846; p<0.001) were significantly associated with positive PIVKA-II levels. CONCLUSIONS: Our study suggests that ALD and antibiotics usage may be confounding factors when interpreting high serum PIVKA-II levels in patients without HCC. Therefore, serum PIVKA-II levels in patients with ALD or in patients administered antibiotics should be interpreted with caution.
Adult
;
Age Distribution
;
Aged
;
Anti-Bacterial Agents/therapeutic use
;
Aspartate Aminotransferases/blood
;
Biomarkers/*blood
;
Carcinoma, Hepatocellular/blood
;
Diagnosis, Differential
;
Female
;
Humans
;
Liver Cirrhosis/blood
;
Liver Diseases, Alcoholic/*blood
;
Liver Neoplasms/blood
;
Male
;
Matched-Pair Analysis
;
Middle Aged
;
Multivariate Analysis
;
Protein Precursors/*blood
;
Prothrombin/analysis
;
Retrospective Studies
;
Sex Distribution
;
gamma-Glutamyltransferase/blood
9.The Influence of Alcoholic Liver Disease on Serum PIVKA-II Levels in Patients without Hepatocellular Carcinoma.
Keunhee KANG ; Ji Hoon KIM ; Seong Hee KANG ; Beom Jae LEE ; Yeon Seok SEO ; Hyung Joon YIM ; Jong Eun YEON ; Jong Jae PARK ; Jae Seon KIM ; Young Tae BAK ; Kwan Soo BYUN
Gut and Liver 2015;9(2):224-230
BACKGROUND/AIMS: Prothrombin induced by vitamin K deficiency or antagonist II (PIVKA-II) is a widely used diagnostic marker for hepatocellular carcinoma (HCC). We evaluated the correlation between alcoholic liver disease (ALD) and serum PIVKA-II levels in chronic liver disease (CLD) patients. METHODS: We retrospectively reviewed the medical records of 2,528 CLD patients without HCC. Among these patients, 76 exhibited serum high PIVKA-II levels of >125 mAU/mL (group 1). We categorized 76 control patients matched by age, sex, and the presence of liver cirrhosis from the remaining patients who were negative for serum PIVKA-II (group 2). RESULTS: Group 1 revealed increased antibiotic usage (23.7% vs 2.6%, p<0.001) and incidence of ALD (60.5% vs 14.5%, p<0.001) as well as elevated aspartate aminotransferase (52.5 IU/L vs 30.5 IU/L, p=0.025) and gamma glutamyl transpeptidase (67.5 IU/L vs 36.5 IU/L, p=0.005) levels compared with group 2. Further, group 1 was significantly associated with a worse Child-Pugh class than group 2. In the multivariate analysis, ALD (odds ratio [OR], 7.151; p<0.001) and antibiotic usage (OR, 5.846; p<0.001) were significantly associated with positive PIVKA-II levels. CONCLUSIONS: Our study suggests that ALD and antibiotics usage may be confounding factors when interpreting high serum PIVKA-II levels in patients without HCC. Therefore, serum PIVKA-II levels in patients with ALD or in patients administered antibiotics should be interpreted with caution.
Adult
;
Age Distribution
;
Aged
;
Anti-Bacterial Agents/therapeutic use
;
Aspartate Aminotransferases/blood
;
Biomarkers/*blood
;
Carcinoma, Hepatocellular/blood
;
Diagnosis, Differential
;
Female
;
Humans
;
Liver Cirrhosis/blood
;
Liver Diseases, Alcoholic/*blood
;
Liver Neoplasms/blood
;
Male
;
Matched-Pair Analysis
;
Middle Aged
;
Multivariate Analysis
;
Protein Precursors/*blood
;
Prothrombin/analysis
;
Retrospective Studies
;
Sex Distribution
;
gamma-Glutamyltransferase/blood
10.Spontaneous Arterial Bleeding in Patients with Alcoholic Liver Cirrhosis: a Series of Three Cases.
Choon Sik SEON ; Yunju JO ; Jihyun LEE ; Young Kwan JO ; Sang Bong AHN ; Byungkwan SON ; Young Kwon CHO
Korean Journal of Medicine 2014;87(4):449-454
Spontaneous arterial bleeding has been reported rarely. In a patient consuming heavy amounts of alcohol with alcoholic liver cirrhosis, spontaneous bleeding can be evoked by thrombocytopenia, altered platelet function, and shear stress on fully dilated arteries by portal hypertension. Alcohol consumption itself can also predispose a patient to bleeding by influencing the aggregation and activation of platelets, and altering the coagulation and fibrinolysis pathway. All of these mechanisms could cause patients with alcoholic liver cirrhosis to bleed spontaneously; however, conditions inducing peripheral arterial bleeding are very rare. Here, we report three cases of spontaneous arterial bleeding in patients with liver cirrhosis consuming heavy amounts of alcohol. All of the patients bled without any physical trauma, and the involved arteries were the intercostal arteries in two cases and a gastroduodenal artery in the other case. The patients were treated by angiographic embolization. One expired due to recurrence of arterial bleeding despite repeated angiographic embolization and massive transfusion.
Alcohol Drinking
;
Arteries
;
Blood Platelets
;
Embolization, Therapeutic
;
Fibrinolysis
;
Hemorrhage*
;
Humans
;
Hypertension, Portal
;
Liver Cirrhosis
;
Liver Cirrhosis, Alcoholic*
;
Recurrence
;
Thrombocytopenia

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