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Kwan Soo Byun

Publications and source records attributed to Kwan Soo Byun.

9 recordsLinked to original sources
PubMed2003

Complete genome sequence and phylogenetic analysis of hepatitis B virus (HBV) isolates from patients with chronic HBV infection in Korea.

Although there is a report of high rate of hepatitis B virus (HBV) infection in South Korea, only a few entire genome sequences of HBV isolates from Korea have been reported. To obtain the complete nucleotide sequence of the Korean HBV, viral DNA was extracted from sera of Korean patients with chronic HBV infection who have not been exposed to any antiviral treatment. Complete genomic sequences were determined on three Korean HBV isolates. The entire genomic length of Korean HBV isolates, designated as KUHB84, KUHB81, and KUHB95, was 3,215 base pairs. No deletions and insertions were observed. Core promoter mutations (T1762/A1764) were detected in two isolates, KUHB84 and KUHB95. Phylogenetic analysis based on the entire genomic sequences showed that the Korean HBV isolates were genotype C and related closely to the Japanese HBV.

Amino Acid Substitution↗
PubMed2003

[Clinical usefulness of plasma activities of gelatinase (matrix metalloproteinase-2 and 9) in chronic liver disease].

BACKGROUND/AIMS: Gelatinase (matrix metalloproteinase (MMP) -2 and 9) has an important role in the pathogenesis of liver cirrhosis (LC) and hepatocellular carcinoma (HCC). In this study, we evaluated the relationship of gelatinase to chronic liver disease. METHODS: Four groups of subjects were examined; healthy control (10 cases), chronic hepatitis (18 cases), LC (15 cases), and HCC (28 cases). The plasma of each subject was obtained, and the equal quantification of plasma protein was done. The plasma activities of MMP-2 and 9 were measured by zymography. RESULTS: The activities of plasma MMP-2 in patients with LC were significantly higher than those in controls (p=0.009) and in patients with chronic hepatitis (p=0.011), but not different from those in patients with HCC. The activities of plasma MMP-9 in patients with LC were significantly higher than those in controls, but not different from those in patients with chronic hepatitis or HCC. In patients with LC (regardless of having HCC), the activities of MMP-2 correlated with total bilirubin (r=0.323, p=0.048) and Child-Pugh score (r=0.414, p=0.012). The activities of MMP-2 and 9 were higher in patients with LC (regardless of having HCC) caused by alcohol than caused by HBV (p=0.009 and 0.002 for each one). CONCLUSIONS: The plasma activity of MMP-2 may be a useful marker for the diagnosis and determination of the severity of LC. The plasma activity of MMP-9 was not useful for HCC, but may be a marker for alcoholic LC. Further study is needed to determine why the plasma activity of gelatinase was higher in patients with LC caused by alcohol than by HBV.

Adult↗
PubMed2003

[Polymorphism in codons 10 and 25 of the transforming growth factor-beta1 gene in Korean population and in patients with liver cirrhosis and hepatocellular carcinoma].

BACKGROUND/AIMS: The genetic polymorphism of transforming growth factor-beta1 (TGF-beta1) at codons 10 and 25 which influences the production of TGF-beta1 is related to fibrogenesis in the lung and liver. We evaluated the genetic polymorphism at codons 10 and 25 in controls and in patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC). METHODS: Blood samples were collected from controls (n=35), patients with LC (n=64), and HCC (n=49). Genomic DNA was isolated and polymerase chain reaction (PCR) was done for a segment including codons 10 and 25. The results of direct sequencing for PCR products were compared between the controls and the patients. RESULTS: There was no genetic polymorphism at codon 25 and three types of genetic polymorphism at codon 10. The leucine homozygous genotype (CTG/CTG) at codon 10 was more common in patients with LC than the controls (p=0.01) and especially in patients with LC caused by HBV (p=0.004). The polymorphism at codons 10 in patients with HCC was similar to the controls. However, leucine homozygous genotype was more common in patients with HCC of uninodular morphology than those of massive morphology (p=0.007). CONCLUSIONS: The genetic polymorphism of TGF-beta1 at codon 10 might be associated with LC and morphology of HCC. The potential usefulness of TGF-beta1 genotyping needs further studies in large scale.

Adult↗
PubMed2002

Simultaneous duodenal and colon masses as late presentation of metastatic renal cell carcinoma.

We report a case of pathologically proven simultaneous duodenal and colonic metastases about four years after nephrectomy for mixed clear and granular cell type renal cell carcinoma (RCC). A 76-year-old female patient who had undergone a left radical nephrectomy 4 years previously for RCC presented with a 1-month history of dyspepsia and pain in the right upper abdomen. An abdominopelvic CT scan showed circumferential wall thickening with high enhancement at the second portion of the duodenum and additional enhancement of an irregular protruding mass into the lumen of the ascending colon. A gastroscopy showed a large and ulcerative protruding mass nearly obstructing the second portion of the duodenum. A colonoscopy revealed a polypoid, nodular and purplish mass in the ascending colon. Microscopy of the biopsy specimen showed the features identical to those of the RCC which was resected 4 years earlier in this patient. We believe this to be the first case illustrating a metastatic renal cell carcinoma as simultaneous duodenal and colon masses.

Aged↗
PubMed2002

Endoscopically observed lower esophageal capillary patterns.

BACKGROUND: It has been reported that there are four zones of distinct venous patterns around the gastroesophageal junction (GEJ); i.e. truncal, perforating, palisade (PZ) and gastric zones. Using the distal end of PZ as a marker for GEJ, this study was done to assess the length and patterns of PZ in Koreans, and to assess the prevalence of endoscopic Barrett's esophagus (E-BE) and hiatal hernia (E-HH). METHODS: 847 consecutive patients undergoing diagnostic endoscopy were included. During endoscopy, PZ, squamocolumnar junction (SCJ) and pinchcock action (PCA) were identified. Patterns were classified according to the relationships of the distal end of PZ with SCJ and PCA; A: all three at the same level, B: SCJ proximal to the other two which are at the same level, C: PCA distal to the other two which are at the same level, D: SCJ proximal to the distal end of PZ which is proximal to PCA. Cases with patterns B and D were thought to have E-BE, and those with patterns C and D to have E-HH. RESULTS: Patterns A, B, C and D were 79.2%, 12.1%, 3.8% and 4.9%, respectively. Length of PZ was 3.0 +/- 0.1 cm. E-BE and E-HH were found in 17.0% and 8.7%, respectively. Both E-BE and E-HH were more frequently found in males and in cases with reflux esophagitis. CONCLUSION: E-BE and E-HH are not so infrequent in Koreans as previously thought, if we use the distal end of PZ as an endoscopic marker of GEJ.

Barrett Esophagus↗
PubMed2002

[A study of polymorphism in UDP-glucuronosyltransferase 1 (UGT-1A1) promoter gene in Korean patients with Gilbert's syndrome].

BACKGROUND/AIMS: Hepatic glucuronidating activity, essential for efficient biliary excretion of bilirubin, is reduced to about 30 percent of normal in patients with Gilbert's syndrome. Patients with Gilbert's syndrome have an additional TA insertion in the A(TA)TAA of UDP-glucuronosyltransferase 1 (UGT-1A1) promoter gene. This results in reduced frequency and accuracy of transcription initiation and enzyme activity. The frequency and location of the mutation vary according to races. This study was done to determine the UGT-1A1 promoter gene mutation in Korean cases of Gilbert's syndrome. METHODS: Promoter regions of the gene for bilirubin UGT-1A1 in twelve patients with Gilbert's syndrome and twenty healthy subjects (controls) were sequenced. RESULTS: 1) Among twelve Gilbert's syndrome five patients were homozygous for A(TA)6/6TAA, two were homozygous for A(TA)7/7TAA, and the other five were heterozygous for A(TA)6/7TAA. The prevalence of A(TA)TAA mutation was 58.3 percent. 2) Among twenty healthy subjects seventeen were homozygous for A(TA)6/6TAA, one was homozygous for A(TA)7/7TAA, and two were heterozygous for A(TA)6/7TAA. The prevalence of A(TA)TAA mutation was 15 percent. 3) The prevalence of A(TA)TAA mutation in Gilbert's syndrome patients was significantly higher than in the controls (p=0.018). CONCLUSION: Although the prevalence of A(TA)TAA mutation in Korean patients with Gilbert's syndrome is significantly higher than in the controls, the mutations of the promoter region of UGT-1A1 gene appear not to be the main or sole cause in Gilbert's syndrome in Korea since the prevalence of A(TA)TAA mutation is not so high. Further studies to determine the relationship between other UGT-1A1 gene mutation and Gilbert's syndrome in Korea are needed.

Adult↗
PubMed2002

[Clinical outcome in cases of viral breakthrough during lamivudine therapy in chronic hepatitis B patients].

BACKGROUND/AIMS: Long-term lamivudine therapy can induce the emergence of lamivudine resistant hepatitis B virus (HBV) mutants. Clinically emergence of the mutant is expressed by the reappearance of disappeared HBV DNA in serum. Continued lamivudine treatment has been usually recommended in cases of viral breakthrough. However, the clinical outcome in patients with viral breakthrough is not clear. The aim of this study was to investigate the clinical course of chronic hepatitis B patients after viral breakthrough during lamivudine therapy. METHODS: A total of 74 patients with chronic hepatitis B who showed viral breakthrough after at least 6 months of lamivudine treatment were included in this study. They had positive HBeAg and HBV DNA before treatment. The median follow-up duration after breakthrough was 13 months. RESULTS: After viral breakthrough, only 8 patients (11%) maintained normal ALT levels and 66 patients (89%) showed elevation of ALT. 30 patients (41%) showed acute exacerbation of hepatitis (ALT increase over five-times upper normal limit). These acute exacerbations occurred within three months after breakthrough in 19 patients (63%). In the cases of acute exacerbation, 6 patients showed decompensated progression such as elevation of serum total bilirubin. One of them died of hepatic failure. A predictive factor for acute exacerbation was not found. HBeAg seroconversion occurred in 8 patients after viral breakthrough but their clinical course was highly variable. CONCLUSIONS: Chronic hepatitis B patients who had viral breakthrough during lamivudine therapy should be followed carefully and regularly in mind of potential clinical deterioration. New strategies are needed to manage the cases of acute exacerbation after viral breakthrough.

Adult↗
PubMed2002

[Viral breakthrough in HBeAg-negative chronic hepatitis B patients receiving lamivudine therapy].

BACKGROUND/AIMS: Long-term efficacy and the rate of viral breakthrough in patients with HBeAg- negative chronic hepatitis B receiving lamivudine therapy is uncertain. This study was conducted to determine the rate of viral breakthrough according to the HBeAg status and the relation of viral breakthrough with YMDD mutants. METHODS: Two hundred and five patients with HBeAg-positive and 49 patients with HBeAg-negative chronic hepatitis B, who had received lamivudine for at least 9 months, were included. The mean durations of the lamivudine treatment were 176 months and 155 months in HBeAg-positive and negative patients, respectively. Analysis of HBV genome for YMDD mutations was performed by restriction-fragment-length polymorphism assay and direct sequencing. RESULTS: While the cumulative rates of viral breakthrough at 12th and 24th months of the lamivudine therapy were 0% and 7% in the HBeAg-negative group, they were 12% and 39% in the HBeAg-positive group. The cumulative rate of viral breakthrough in the HBeAg-negative group was significantly lower than in the HBeAg-positive group (p<0.01). In multivariate analysis, the only significant factor related to viral breakthrough was the HBeAg status (p<0.05). The YMDD mutants were detected in all patients with viral breakthrough irrespective of HBeAg status. However, in patients without viral breakthrough, the rate of YMDD mutants was significantly higher in the HBeAg-negative group than in the HBeAg-positive group (13.3% vs 5.1%; p<0.01). CONCLUSIONS: Lamivudine is expected to be more persistently effective in HBeAg-negative chronic hepatitis B because of a lower viral breakthrough rate than in HBeAg-positive chronic hepatitis B in spite of the emergence of YMDD mutants.

Adult↗