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Biomedical subjects

C L Perng

Publications and source records attributed to C L Perng.

At least 19 recordsLinked to original sources
PubMed2003

Endoscopic haemoclip versus heater probe thermocoagulation plus hypertonic saline-epinephrine injection for peptic ulcer bleeding.

BACKGROUND: Treating patients of bleeding peptic ulcers with heater probe thermocoagulation and haemoclip is considered to be safe and very effective. Yet, there is no report comparing the haemostatic effects of endoscopic haemoclip versus heater probe thermocoagulation plus hypertonic saline-epinephrine injection in these patients. AIM: To compare the clinical outcomes of both therapeutic modalities in patients with peptic ulcer bleeding. METHODS: A total of 93 patients with active bleeding or non-bleeding visible vessels were randomised to receive either endoscopic haemoclip (n = 46) or heater probe thermocoagulation plus hypertonic saline-epinephrine injection (n = 47). Five patients from the haemoclip group were excluded because of the inability to place the haemoclip. RESULTS: Initial haemostasis was achieved in 39 patients (95.1%) of the haemoclip group and 47 patients (100%) of the heater probe group (P > 0.1). Rebleeding occurred in four patients (10.3%) of the haemoclip group and three patients (6.4%) of the heater probe group (P > 0.1). The volume of blood transfused after entry into the study, duration of hospital stay, number of patients requiring urgent surgery and the mortality rates were not statistically different between the two groups. CONCLUSIONS: If the haemoclip can be applied properly, the clinical outcomes of the haemoclip group would be similar to those of the heater probe group in patients with peptic ulcer bleeding. However, if the bleeders are located at the difficult-to-approach sites, heater probe plus hypertonic saline injection is the first choice therapy.

Adolescent↗
PubMed2001

Reactivation of precore mutant hepatitis B virus in chemotherapy-treated patients.

BACKGROUND: A point mutation from G to A at nucleotide (nt) 1896 of the precore region of hepatitis B virus (HBV) DNA has been shown to be associated with fulminant and severe hepatitis. Further studies have suggested that this point mutation, together with additional mutations in the precore promoter, is probably linked to the reactivation of HBV in patients undergoing cytotoxic chemotherapy. Taiwan is an area with a high prevalence of HBV where hepatitis B flare-up has become a serious problem of HBV carriers who must rely on chemotherapy to treat their diseases. The purpose of this study was to examine if nt 1896 mutation was also present in Chinese patients in Taiwan who developed severe liver disease after chemotherapy. MATERIALS AND METHODS. Thirteen HBV carrier patients, including eight patients with lymphoma, two with germ cell tumors, two with breast carcinomas, and one with acute myeloid leukemia, received chemotherapy in the authors' hospital from February 1994 to May 2000. They all received steroid-containing regimens or antiemetics during chemotherapy. These patients were monitored closely for the development of severe hepatitis during or after chemotherapy. Their sera were harvested at different times for direct sequencing of the polymerase chain reaction products of the precore region of HBV DNA. RESULTS: Six of the 13 patients developed severe hepatitis with a fulminant course during or after the completion of chemotherapy. A point mutation from G to A at nt 1896 was detected in five of these six patients. Among those five patients, four had additional precore mutations. The other patient did not have the nt 1896 mutation but had mutations at nt 1835 (A to C). None of the other seven patients lacking the precore nt 1896 mutation developed severe hepatitis flare-up. One of those seven patients who developed moderate elevation of alanine aminotransferase (ALT) without hyperbilirubinemia did have precore mutations other than nt 1896. None of the other six patients had mutations over the precore region. CONCLUSIONS: Nucleotide mutation of the precore region, notably at position 1896, is associated with reactivation of HBV with a fulminant course during or after chemotherapy. The current data, together with other investigators' findings, suggest that patients who are HBV carriers with HBV envelope antigen (HBeAg) (-)/anti-HBV envelope antibody (Anti-HBe)(+) status should be assayed to determine if they carry mutant HBV before chemotherapy. Prophylactic use of lamivudine is strongly recommended for patients who carry mutant HBV at precore region, especially at nt 1896 (G to A), before and during chemotherapy.

Adult↗
PubMed2001

Detection and typing of vancomycin-resistance genes of enterococci from clinical and nosocomial surveillance specimens by multiplex PCR.

Ninety-three clinical isolates of vancomycin-resistant enterococci (VRE) collected from nine hospitals in Taiwan were examined for the presence of vanA, vanB, vanC1, or vanC2/vanC3 genes by a multiplex PCR. Forty-seven of these VRE isolates were vanA positive, 1 contained both vanC1 and vanA, 40 harboured vanB, 2 were vanC1, and 3 were identified to be vanC2/vanC3. Twenty-four vanA isolates were sensitive to teicoplanin and thus did not have a typical VanA phenotype. Five isolates with the VanC phenotype harboured vanB. None of the 40 clinically isolated vancomycin-susceptible E. faecium or E. faecalis and the vancomycin-resistant Leuconostoc and Pediococcus isolates were positive for any of the van genes. While performing nosocomial surveillance, VRE were isolated from 47 of 467 rectal swabs by culture. Compared with the conventional culture method, the sensitivity and specificity of the multiplex PCR for detecting and identifying vancomycin-resistance genes in enterococci directly from culture-positive broth were 97.9% and 100%, respectively. The results suggest that genotypic characterization of vancomycin-resistance is necessary for all clinical VRE isolates and that the multiplex PCR assay can be an alternative method for this purpose.

Bacterial Proteins↗
PubMed2001

High prevalence of VanB2 vancomycin-resistant Enterococcus faecium in Taiwan.

Thirty-six VanB glycopeptide-resistant Enterococcus faecium isolates were collected from patients in five different hospitals in Taiwan. The vancomycin resistance genes were amplified by the long vanB PCR, which amplifies the 6,373-bp vanB gene cluster including the vanR(B2), vanS(B2), vanY(B2), vanW(B2), vanH(B2), vanB2, and vanX(B2) genes. The deduced amino acid sequences were found to be 95 to 98% homologous to those of the vanB1 gene cluster: VanR(B1), 97%; VanS(B1), 97%; VanY(B1), 96%; VanH(B1), 95%; VanB1, 96%; and VanX(B1), 98%. Restriction enzyme analysis of the long vanB PCR products revealed that all 36 isolates had the same vanB2-specific pattern. DNA sequence analysis of the vanB2 gene, which is a D-Ala-D-Lac ligase gene, revealed that none of the 36 sequences were identical to the previously published vanB2 sequence. Thirty-one isolates had 1 nucleotide different from the published vanB2 sequence. The sequences of the other five isolates differed from the published vanB2 sequence by 2 or 3 nucleotides. Four isolates with a low or moderate resistance to vancomycin (MIC = 4 to 32 microg/ml) were found to have the same leucine-to-methionine change at amino acid position 308 of the vanB2 gene. The genomic DNAs of all 36 isolates were digested with SmaI and then typed by pulsed-field gel electrophoresis (PFGE). Eight different PFGE types (I to VIII) were observed, and type I was found to be prevalent in all hospitals examined in this study. This result suggests that intra- and interhospital dissemination of this E. faecium strain has occurred in Taiwan.

Anti-Bacterial Agents↗
PubMed2000

Use of PCR with universal primers and restriction endonuclease digestions for detection and identification of common bacterial pathogens in cerebrospinal fluid.

We have designed a universal PCR capable of amplifying a portion of the 16S rRNA gene of eubacteria, including Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus pneumoniae, Enterococcus faecium, Enterococcus faecalis, Mycobacterium tuberculosis, Legionella pneumophila, Escherichia coli, Klebsiella pneumoniae, Serratia marcescens, Enterobacter cloacae, Pseudomonas aeruginosa, Acinetobacter baumannii, Proteus mirabilis, Haemophilus influenzae, and Neisseria meningitidis. The sizes of the amplified products from various bacteria were the same (996 bp), but the restriction patterns of most PCR products generated by HaeIII digestion were different. PCR products from S. aureus and S. epidermidis could not be digested by HaeIII but yielded different patterns when they were digested with MnlI. PCR products from S. pneumoniae, E. faecium, and E. faecalis yielded the same HaeIII digestion pattern but could be differentiated by AluI digestion. PCR products from E. coli, K. pneumoniae, S. marcescens, and E. cloacae also had the same HaeIII digestion pattern but had different patterns when digested with DdeI or BstBI. This universal PCR could detect as few as 10 E. coli or 250 S. aureus organisms. Compared with culture, the sensitivity of this universal PCR for detection and identification of bacteria directly from 150 cerebrospinal fluids was 92.3%. These results suggest that this universal PCR coupled with restriction enzyme analysis can be used to detect and identify bacterial pathogens in clinical specimens.

Aged↗
PubMed2000

Characterization of the first clinical isolate of vancomycin-resistant Enterococcus faecalis, AH803, in Taiwan.

We previously isolated a vancomycin-resistant strain of Enterococcus faecalis, designated AH803, from the sputum of a patient with pneumonia and bacteremia in Taiwan. AH803 was resistant to vancomycin (minimal inhibitory concentration, MIC = 512 micrograms/mL) but susceptible to teicoplanin (MIC = 8 micrograms/mL), and harbored the vanA gene but not the vanB gene. In this study, we further characterized E. faecalis AH803 and the plasmid it was found to contain. DNA from AH803 was analyzed for the presence of vanA and vanB resistance genes by polymerase chain reaction. The vancomycin resistant phenotype was transferable from AH803 to E. faecalis JH2-2, at a frequency of 4.8 x 10(-2). AH803 was also resistant to gentamicin and chloramphenicol, and these antibiotic resistance phenotypes cotransferred with vancomycin resistance. The genes responsible for resistance to all three antibiotics were located on a 42-kb conjugative plasmid (pBL101). This plasmid had the same restriction enzyme digestion patterns as Tn1546, found in pIP816 of E. faecalis BM4147. Epidemiologic studies of glycopeptide resistance should perhaps combine phenotypic and genotypic methods, rather than using phenotypic methods alone.

Bacterial Proteins↗
PubMed2000

Characterization of a highly glycopeptide-resistant Enterococcus gallinarum isolate.

BACKGROUND AND PURPOSE: Adequate treatment of emergency infection involving antibiotic-resistant bacteria such as vancomycin-resistant Enterococcus requires a convergence of clinical and bacteriologic techniques. An isolate of Enterococcus gallinarum, designated as TSGH63, is known to be uncommonly vancomycin-resistant. This study investigated the genetic determinant for this unique characteristic. METHODS: After completing the conventional identification and sensitivity tests, the genomic content of E. gallinarum TSGH63 was extracted and analyzed by pulse-field electrophoresis. A set of specific primers for vanA, vanB, vanC1, and vanC2/C3 genes was then applied in a multiplex polymerase chain reaction (PCR) to differentiate its genetic content. To locate the determinant for high vancomycin resistance, the electrophoresis profile was further analyzed by Southern blot using the digoxigenin (DIG)-labeled vanA gene probe. Finally, interspecies transfer of the vancomycin-resistance determinant of E. gallinarum TSGH63 was tested by a conjugation experiment in vitro. RESULTS: A 50-kb plasmid was identified in the analysis of the genomic extract of E. gallinarum TSGH63 by pulse field electrophoresis. Using multiplex PCR, we demonstrated that E. gallinarum TSGH63 harbors a vanA gene in addition to a vanC1 gene. The DIG-labeled vanA gene-specific probe bound to the plasmid exclusively on the Southern blot. The plasmid-carried vanA gene, but not the vanC1 gene, was found to be transferable from TSGH63 to E. faecalis JH2-2 by conjugation in vitro. CONCLUSIONS: This is the first report of isolation of E. gallinarum with a high level of resistance to glycopeptides in Taiwan. The demonstrated interspecies transfer of the vancomycin-resistance gene highlights the importance of stringent control of the use of vancomycin.

Conjugation, Genetic↗
PubMed1999

Will Helicobacter pylori affect short-term rebleeding rate in peptic ulcer bleeding patients after successful endoscopic therapy?

OBJECTIVE: Helicobacter pylori (H. pylori) can augment the pH-increasing effect of omeprazole in patients with peptic ulcer. A high intragastric pH may be helpful in preventing recurrent hemorrhage by stabilizing the blood clot at the ulcer base of bleeding peptic ulcer patients. Therefore, we hypothesized that omeprazole may reduce short-term rebleeding rate in these patients with H. pylori infection after initial hemostasis had been obtained. METHODS: Between July 1996 and December 1998, 65 bleeding peptic ulcer patients (24 gastric ulcer, 41 duodenal ulcer) who had obtained initial hemostasis with endoscopic therapy were enrolled in this trial. Thirty (46.2%) of them were found to have H. pylori infection by a rapid urease test and pathological examination. For all studied patients, omeprazole was given 40 mg intravenously every 6 h for 3 days. Thereafter, omeprazole was given 20 mg per os (p.o.) once daily for 2 months. A pH meter was inserted in the fundus of each patient under fluoroscopic guidance after intravenous omeprazole had been administered. The occurrence of rebleeding episode was observed for 14 days. RESULTS: In patients with H. pylori infection, intragastric pH (median, 95% confidence interval [CI]: 6.54, 5.90-6.68) was higher than in those without H. pylori infection (6.05, 5.59-6.50, p < 0.001). However, the patients with rebleeding (2 vs 3), volume of blood transfusion (median, range: 1000 ml, 0-2250 vs 750, 0-2000), number of operations (0 vs 1), mortality caused by bleeding (0 vs 0), and hospital stay (median, range: 6 days, 3-14 vs 7, 5-16) were not statistically different from those without H. pylori infection. CONCLUSIONS: Omeprazole does increase intragastric pH in bleeding peptic ulcer patients with H. pylori infection. However, the presence of H. pylori infection does not affect the short-term rebleeding rate in these patients.

Adult↗
PubMed1999

Comparison of adrenaline injection and bipolar electrocoagulation for the arrest of peptic ulcer bleeding.

BACKGROUND: Peptic ulcers with active bleeding or a non-bleeding visible vessel require aggressive endoscopic treatment. AIMS: To determine whether endoscopic adrenaline injection alone or contact probe therapy following injection is a suitable treatment for peptic ulcer bleeding. METHODS: A total of 96 patients with active bleeding or non-bleeding visible vessels received adrenaline alone, bipolar electrocoagulation alone, or combined treatment (n=32 in each group). RESULTS: Initial haemostasis was not achieved in one patient in the adrenaline group, two in the gold probe group, and two in the injection gold probe group (p>0.1). Rebleeding episodes were fewer in the injection gold probe group (2/30, 6.7%) than in the gold probe group (9/30, 30%, p=0.04) and in the adrenaline group (11/31, 35.5%, p=0.01). Treatment failure (other therapy required) was rarer in the injection gold probe group (4/32, 12.5%) than in the adrenaline group (12/32, 37.5%, p=0.04). The volume of blood transfused after entry of the study was less in the injection gold probe group (mean 491 ml) than in the adrenaline group (1548 ml, p<0. 0001) and the gold probe group (1105 ml, p<0.01). Duration of hospital stay, numbers of patients requiring urgent surgery, and death rate were not statistically different among the three groups. CONCLUSIONS: For patients with peptic ulcer bleeding, combined adrenaline injection and gold probe treatment offers an advantage in preventing rebleeding and decreasing the need for blood transfusion.

Adolescent↗
PubMed1999

Influence of Helicobacter pylori on gastric secretion and gastrin release in normal Chinese subjects.

BACKGROUND: Controversy exists concerning the influence of Helicobacter pylori on gastric secretion. Hyper-, normo- and hyposecretion of gastric acid in normal subjects with H pylori infection have been reported, although there is no such report for Chinese subjects. The goal of this study was to identify the effect of H pylori on gastric secretion in normal Chinese subjects. METHODS: Twenty normal subjects with a normal upper gastrointestinal tract by endoscopy were recruited. H pylori status was assayed by a rapid urease test. Gastric secretion and gastrin release were also measured. RESULTS: Among the subjects studied, nine were infected with H pylori. All enrolled subjects were males. Age and body weight were similar between both groups. No significant difference was found in basal acid output, maximal acid output, basal pepsin output or maximal pepsin output between the H pylori-positive group (median, 1.1 mmol/hour, 95% confidence interval 0.2-3.6 mmol/hour; 8.0, 3.0-18.3 mmol/hour; 0, -1.3-11.2 mmol/hour; and 4.1, -4.2-59.3 mmol/hour, respectively) and the H pylori-negative group (2.5, -1.3-11.3 mmol/hour; 12.2, 8.7-26.9 mmol/hour; 4.3, 1.8-13.5 mmol/hour; and 14.8, -5.7-73.0 mmol/hour, respectively). Serum basal gastrin and pepsinogen I concentration were 63.5, 50.0-78.6 pg/ml and 75.1, 50.6-89.8 ng/ml in the H pylori-positive group, and 65.9, 50.2-79.8 pg/ml and 79.1, 59.5-120.1 ng/ml in the H pylori-negative group (p > 0.05). CONCLUSIONS: H pylori plays no role in the gastric secretion and gastrin release in normal Chinese subjects.

Aged↗
PubMed1999

Varicella arthritis diagnosed by polymerase chain reaction.

We report a 2-year-old girl who developed acute arthritis of the left knee 4 days after the onset of a typical varicella infection. She was first thought to have pyogenic arthritis caused by Staphylococcus aureus. Accordingly, oxacillin was administered upon hospitalization. On the third day after hospitalization, bacterial cultures of the synovial fluid and blood showed no growth and oxacillin was discontinued. Although a viral culture of the synovial fluid for varicella-zoster virus (VZV) was negative, varicella DNA was identified by means of polymerase chain reaction (PCR) with VZV-specific primers. The patient recovered spontaneously. To differentiate this condition from septic arthritis is important. PCR is a sensitive technique that can demonstrate the presence of VZV DNA in synovial fluid, even if viral cultures are negative.

Arthritis, Infectious↗
PubMed1998

HPV-associated cervical cancers show frequent allelic loss at 3p14 but no apparent aberration of FHIT mRNA.

The genetic aberration involved in the loss of heterozygosity (LOH) at 3p14 has recently been attributed to the disruption of the FHIT gene in many cancers. This study analyzed HPV DNA and allelic status of 5 microsatellite markers spaning 3p13-3p25 in 57 cases of cervical cancer. With no homozygous deletion found in any case, a 39% overall frequency of LOH was noted. The presence of tumorigenic HPV DNA (91%) did not correlate with the allelic loss at any marker, including THRB (3p22-24) and D3S1228 (3p14) which were found with high LOH rates of 43% (12/28) and 37% (11/30), respectively. Further analysis of FHIT mRNA in 29 cancers by reverse transcription (RT)-PCR showed a full-length transcript in all cases. However, additional minor transcripts were occasionally observed in cancer tissues (9/29) as well as in normal tissues (12/31) by nested PCR of the RT products. Sequence analysis of these transcripts showed exclusive internal exon deletions, suggesting a source of minor splicing variants. No apparent mutation of the mRNA sequences was found in 8 transcripts examined, except for a silent polymorphism and a site of alternative splicing. The results suggest that, although frequently reported to be abrogated in several cancers, the mRNA of FHIT remains intact in cervical cancer. Other genes closely linked to FHIT may be responsible for frequent LOH at 3p14 observed in cervical cancer.

Acid Anhydride Hydrolases↗
PubMed1998

A prospective randomized comparative trial showing that omeprazole prevents rebleeding in patients with bleeding peptic ulcer after successful endoscopic therapy.

BACKGROUND: A blood clot in a peptic ulcer is unstable in a low pH environment. The use of omeprazole may prevent rebleeding by elevating intragastric pH in patients with bleeding peptic ulcer after hemostasis has been achieved. OBJECTIVES: To assess the influence of using omeprazole and cimetidine on 24-hour intragastric pH and to determine their ability to prevent rebleeding after having achieved initial hemostasis in patients with active bleeding or nonbleeding visible vessels. METHODS: One hundred patients with bleeding peptic ulcers who had obtained initial hemostasis were enrolled in this randomized comparative trial. In the cimetidine group (n = 50), a 300-mg intravenous bolus of cimetidine was given, followed by a 1200-mg continuous infusion daily for 3 days. Thereafter, 400 mg of cimetidine was given orally twice daily for 2 months. In the omeprazole group (n = 50), a 40-mg intravenous bolus of omeprazole was given, followed by 160 mg of continuous infusion daily for 3 days. Thereafter, 20 mg of omeprazole was given orally once daily for 2 months. A pH meter was inserted in each patient's fundus under fluoroscopic guidance after the intravenous bolus of cimetidine or omeprazole had been administered. RESULTS: The stigmata of recent hemorrhage before endoscopic therapy in the omeprazole and cimetidine groups were, respectively, spurting (9 vs 12), oozing (4 vs 9), and nonbleeding visible vessel (37 vs 29) (P > .05). The duration of intragastric pH higher than 6.0 was longer in the omeprazole group (mean [+/- SD], 84.4% +/- 22.9%) than that of the cimetidine group (mean [+/- SD], 53.5% +/- 32.3%) (P < .001). Rebleeding occurred in 2 patients (4%) in the omeprazole group and in 12 patients (24%) in the cimetidine group by day 14 after enrollment (P = .004). There was a tendency for patients in the omeprazole group to require less blood transfusion (median, 0 mL; range, 0-2500 mL) than those in the cimetidine group (median, 0 mL; range, 0-5000 mL) (P = .08). The hospital stay and number of operations and mortality rate were similar between both groups. CONCLUSIONS: The use of omeprazole is more effective than cimetidine in increasing intragastric pH and reducing rebleeding episodes in patients with bleeding peptic ulcers after successful endoscopic therapy. This suggests that omeprazole should be used routinely after successful endoscopic therapy.

Adolescent↗
PubMed1998

The effect of galE gene inactivation on lipopolysaccharide profile of Helicobacter pylori.

The galE gene product, UDP-galactose 4-epimerase, mediates the incorporation of galactose in extracellular polysaccharide materials such as the O-side chain of lipopolysaccharide (LPS). The O-side chain in H. pylori LPS has been shown to cross-react with Lewis x and/or y blood group antigens, suggesting its potential involvement in H. pylori-linked autoimmune disease. To study its role in H. pylori LPS biosynthesis, the galE gene was cloned, sequenced, and a galE-knockout H. pylori strain was constructed. The H. pylori galE gene encoded a protein of 344 amino acids with a molecular weight of 39K. The LPS profile from the galE-knockout H. pylori strain showed a lower molecular weight than that of the parental strain, indicating the involvement of the galE gene in LPS biosynthesis of H. pylori.

Amino Acid Sequence↗