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Biomedical subjects

F K Chan

Publications and source records attributed to F K Chan.

At least 73 records · Page 4Linked to original sources
PubMed1998

Diagnosis of Helicobacter pylori infection after gastric surgery for peptic ulcer: is the rapid urease test useful?

BACKGROUND: The usefulness of the rapid urease test (RUT) in diagnosing Helicobacter pylori infection after peptic ulcer surgery is unknown. METHODS: Patients who had undergone peptic ulcer surgery were offered endoscopic examination if they presented with dyspepsia or gastrointestinal bleeding. Biopsy specimens were taken for RUT and histology from the corpus and the stoma in patients who had undergone partial gastrectomy or from the corpus and the antrum in patients who had undergone vagotomy. Histologic examination using haematoxylin and eosin stain and Warthin-Starry stain were used as the gold standard. RESULTS: Ninety patients were studied (69 had partial gastrectomy and 21 had vagotomy). Forty-three patients (32 in the partial gastrectomy group and 11 in the vagotomy group) were positive for H. pylori by histology. The respective sensitivity of RUT was 59% (stoma) and 75% (corpus) in the partial gastrectomy group (P = 0.36) and 55% (antrum) and 73% (corpus) in the vagotomy group (P = 0.51). CONCLUSIONS: RUT is not sensitive for detecting H. pylori after acid reduction surgery.

Biopsy↗
PubMed1998

Ulcer recurrence after gastric surgery: is Helicobacter pylori the culprit?

OBJECTIVES: Helicobacter pylori is the most important cause of recurrent peptic ulcer disease. However, its role in ulcer recurrence after peptic ulcer surgery is unclear. We aimed at studying the prevalence and distribution of H. pylori in patients who had undergone peptic ulcer surgery, and any association between H. pylori infection and ulcer recurrence in these patients. METHODS: Patients with previous vagotomy or partial gastrectomy presenting with dyspepsia or ulcer bleeding were recruited. Ulcer recurrence was documented by endoscopy. Biopsy specimens were taken from the gastric remnant and gastroenteric anastomosis in patients with previous partial gastrectomy, or from the antrum and corpus in vagotomized patients. H. pylori infection was detected by either a positive rapid urease test or the presence of the bacteria on histology. RESULTS: Ninety-three patients were studied; 73 patients (78%) had partial gastrectomy and 20 (22%) had vagotomy with drainage. H. pylori infection was documented in 36 patients (49%) in the gastrectomy group and in 13 (65%) in the vagotomy group. Thirty-six patients in the gastrectomy group had recurrent ulcers and 15 (42%) of them had H. pylori infection. Twelve patients in the vagotomy group had recurrent ulcers and eight (67%) of them were H. pylori positive. The prevalence of H. pylori infection did not differ between patients with or without ulcer recurrence. CONCLUSION: H. pylori infection cannot account for ulcer recurrence after peptic ulcer surgery.

Adult↗
PubMed1998

False-negative biopsy urease test in bleeding ulcers caused by the buffering effects of blood.

OBJECTIVES: A false-negative biopsy urease test (BUT) is common in Helicobacter pylori-associated bleeding peptic ulcers. Although blood in the stomach is thought to interfere with the biopsy urease test, the underlying mechanism remains unknown. This in vitro experiment sought to identify the blood component(s) that interfere with the biopsy urease test, and delineate the mechanism of inhibition. METHODS: The modified Hazell's microtiter test was used to detect the urease activity of H. pylori. A positive result was indicated by a color change of the pH indicator, bromothymol blue, at 630 nm. Human whole blood, sera with and without anti-H. pylori antibody, electrolytes, and enzymes were incubated with H. pylori to identify the blood component(s) causing the inhibition of urease activity. In addition, any interference of the pH color indicator was tested by adding different concentrations of serum albumin to the urease reagent that contained a fixed quantity of ammonia in the absence of H. pylori. RESULTS: The color change of the microtiter urease test was significantly reduced by blood (p < 0.0001), regardless of the presence of anti-H. pylori antibody. Electrolytes and serum enzymes did not interfere with the urease test. The color change of the pH indicator was progressively suppressed by higher concentrations of serum albumin. CONCLUSIONS: Blood adversely affects the performance of the BUT. This is mediated by the buffering effect of serum albumin on the pH indicator, rather than by a direct inhibition on the urease activity.

Biopsy↗
PubMed1998

Comparison of two rapid whole-blood tests for Helicobacter pylori infection in Chinese patients.

Consecutive Chinese patients undergoing endoscopy for dyspepsia were tested for Helicobacter pylori infection by two rapid whole-blood tests: FlexPack HP (Abbott Laboratories) and Helisal One-Step (Cortecs Diagnostics). Biopsy-based tests (rapid urease test and histology) and the [13C]urea breath test were used as the "gold standard." One hundred sixty-one consecutive patients were studied, and 88 (54.7%) were confirmed to have H. pylori infection. The sensitivities, specificities, and positive and negative predictive values were 81.8%, 83.6% (P = 0.008), 85.7% (P = 0.04), and 79.2% for FlexPack HP and 84.1%, 63.0% (P = 0.008), 73.3% (P = 0.047), and 76.7% for Helisal One-Step, respectively.

Adult↗
PubMed1998

Normal growth hormone secretory reserve in men with idiopathic osteoporosis and reduced circulating levels of insulin-like growth factor-I.

Many men with idiopathic osteoporosis have reduced circulating insulin-like growth factor-I (IGF-I) levels. The major source of circulating IGF-I is GH-mediated production by the liver. The known anabolic effects of GH on the skeleton raised the possibility of GH deficiency in these men. We sought to test this hypothesis in this study. Fourteen men (mean age, 52.1 +/- 3.2 yr, range 31-68) with idiopathic osteoporosis were studied. Mean lumbar spine bone mineral density (BMD) was 0.723 g/cm2, T score -3.5; femoral neck BMD was 0.642 g/cm2, T score, -3.07; distal (1/3) radius BMD was 0.708 g/cm2, T score, -2.05. Eleven of 14 (79%) had frank reductions in serum IGF-I levels compared with age and sex-matched values (158.5 +/- 50 SD vs. 180 +/- 45 SD). GH secretion was stimulated by iv arginine infusion (30 g) over 30 min followed 1 h later by oral L-dopa (500 mg). Serum GH was measured at time (t) = -15, 0, 30, 45, 60, 90, 120, 150, and 180 min. All patients responded to at least one stimulus with the majority (n = 9) responding to both. Five patients responded either to arginine or to L-dopa but not to both. Baseline GH for the entire group was 0.77 + 0.08 ng/mL (SEM). Peak GH following arginine (t = 45-60 min) was 14.0 +/- 2.8 ng/mL, a 17.7 +/- 2.8-fold rise. Peak GH following L-dopa (t = 120-180 min) was 5.7 +/- 1.0 ng/mL, a 9.2 +/- 2.2-fold rise. No difference in maximal secretion was observed between those with low or normal IGF-I levels. Neither IGF-I nor IGF binding protein-3 concentrations changed significantly during the short period of GH stimulation. These data suggest that men with osteoporosis and reduced IGF-I levels do not appear to have a deficiency in the GH axis. Other hormonal or local factors may be important in regulating IGF-I expression. Deficiencies of IGF-I production at skeletal sites may be important in the pathogenesis of this syndrome.

Adult↗
PubMed1997

Randomised trial of eradication of Helicobacter pylori before non-steroidal anti-inflammatory drug therapy to prevent peptic ulcers.

BACKGROUND: Helicobacter pylori infection is common in patients with peptic ulcers caused by the use of non-steroidal anti-inflammatory drugs (NSAIDs). But the pathogenic role of H pylori in this disease is controversial. We studied the efficacy of eradication of H pylori in the prevention of NSAID-induced peptic ulcers. METHODS: We recruited patients with musculoskeletal pain who required NSAID treatment. None of the patients had previous exposure to NSAID therapy. Patients who had H pylori infection but no pre-existing ulcers on endoscopy were randomly allocated naproxen alone (750 mg daily) for 8 weeks or a 1-week course of triple therapy (bismuth subcitrate 120 mg, tetracycline 500 mg, metronidazole 400 mg, each given orally four times daily) before administration of naproxen (750 mg daily). Endoscopy was repeated after 8 weeks of naproxen treatment or when naproxen treatment was stopped early because of bleeding or intractable dyspepsia. All endoscopic examinations were done by one endoscopist who was unaware of treatment assignment. The primary endpoint was the cumulative rate of gastric and duodenal ulcers. FINDINGS: 202 patients underwent endoscopic screening for enrolment in the trial, and 100 eligible patients were randomly assigned treatment. 92 patients completed the trial (47 in the naproxen group, 45 in the triple-therapy group). At 8 weeks, H pylori had been eradicated from no patients in the naproxen group and 40 (89%) in the triple-therapy group (p < 0.001). 12 (26%) naproxen-group patients developed ulcers: five had ulcer pain and one developed ulcer bleeding. Only three (7%) patients on triple therapy had ulcers, and two of these patients had failure of H pylori eradication (p = 0.01). Thus, 12 (26%) patients with persistent H pylori infection but only one (3%) with successful H pylori eradication developed ulcers with naproxen (p = 0.002). INTERPRETATION: Eradication of H pylori before NSAID therapy reduces the occurrence of NSAID-induced peptic ulcers.

Anti-Bacterial Agents↗
PubMed1997

Cholestatic effects of cyclosporine in the rat.

BACKGROUND: Previous studies of cyclosporine-induced cholestasis were flawed by confounders encountered in human studies and discrepancies in acute animal experiments. Even the cyclosporine vehicle, polyoxyethylated castor oil (Cremophor EL), had been implicated in cholestasis. The purpose of this study was to investigate how cyclosporine affects bile salt kinetics and biliary lipid secretion in a rat model under steady state conditions. METHODS: Three groups of male Lewis rats (n=10) were given daily subcutaneous injections of either cyclosporine (CsA; 10 mg/kg body weight), Cremophor, or NaCl (control) for 1 week. Twenty-four-hour bile collection was performed 18 hr after the last injection. The first hour's output measured bile flow and organic bile solute secretion rates. Bile salt pool size and basal synthesis were determined with the washout technique. RESULTS: CsA significantly reduced basal bile flow and bile salt secretion by 25%. Bile salt synthesis was suppressed 45% (CsA: 3.50+/-0.8 micromol/g liver/24 hr vs. control: 6.31+/-1.17 micromol/g liver/24 hr; P<0.05), which resulted in a 28% reduction in the bile salt pool size (CsA: 16.9+/-1.9 micromol/g liver vs. control: 23.6+/-2.0 micromol/g liver; P<0.05). Bile salt-independent flow was significantly suppressed (29%), whereas bile salt-dependent flow was only modestly reduced. Biliary phospholipid output decreased 23% (CsA: 11.7+/-0.8 nmol/min/g liver vs. control 15.2+/-1.1 nmol/min/g liver; P<0.05), but cholesterol secretion was unaltered, resulting in a 29% increase in the cholesterol saturation index (CsA: 0.40+/-0.03 vs. control 0.31+/-0.02; P<0.05). Cremophor had no significant effects on bile secretion or bile salt kinetics. CONCLUSIONS: CsA induces cholestasis by decreasing both bile flow and bile salt secretion. Its suppression of bile salt synthesis reduces the bile salt pool size. The drug inhibits bile salt and phospholipid secretion without a corresponding change in cholesterol secretion and thus elevates cholesterol saturation in bile, a potential risk for gallstone formation.

Animals↗
PubMed1997

Randomised comparison between adrenaline injection alone and adrenaline injection plus heat probe treatment for actively bleeding ulcers.

OBJECTIVE: To compare endoscopic adrenaline injection alone and adrenaline injection plus heat probe for the treatment of actively bleeding peptic ulcers. DESIGN: Randomised prospective study of patients admitted with actively bleeding peptic ulcers. SETTING: One university hospital. SUBJECTS: 276 patients with actively bleeding ulcers detected by endoscopy within 24 hours of admission: 136 patients were randomised to endoscopic adrenaline injection alone and 140 to adrenaline injection plus heat probe treatment. MAIN OUTCOME MEASURES: Initial endoscopic haemostasis; clinical rebleeding; requirement for operation; requirement for blood transfusion; hospital stay, ulcer healing at four weeks; and mortality in hospital. RESULTS: Initial haemostasis was achieved in 131/134 patients (98%) who received adrenaline injection alone and 135/136 patients (99%) who received additional heat probe treatment (P = 0.33). Outcome as measured by clinical rebleeding (12 v 5), requirement for emergency operation (14 v 8), blood transfusion (2 v 3 units), hospital stay (4 v 4 days), ulcer healing at four weeks (79.1% v 74%), and in hospital mortality (7 v 8) were not significantly different in the two groups. In the subgroup of patients with spurting haemorrhage 8/27 (29.6%; 14.5% to 50.3%) patients from the adrenaline injection alone group and 2/31 (6.5%; 1.1% to 22.9%) patients from the dual treatment group required operative intervention. The relative risk of this was lower in the dual treatment group (0.17; 0.03 to 0.87). Hospital stay was significantly shorter in the dual treatment group than the adrenaline injection alone group (4 v 6 days, P = 0.01). CONCLUSION: The addition of heat probe treatment after endoscopic adrenaline injection confers an advantage in ulcers with spurting haemorrhage.

Adult↗
PubMed1997

Functional redundancy of the Nur77 and Nor-1 orphan steroid receptors in T-cell apoptosis.

The transcription factor Nur77 (NGFI-B), a member of the steroid nuclear receptor superfamily, is induced to a high level during T-cell receptor (TCR)-mediated apoptosis. A transgenic dominant-negative Nur77 protein can inhibit the apoptotic process accompanying negative selection in thymocytes, while constitutive expression of Nur77 leads to massive cell death. Nur77-deficient mice, however, have no phenotype, suggesting the possible existence of a protein with redundant function to Nur77. To explore this possibility, we have characterized the role of two Nur77 family members, Nurr1 and Nor-1, in TCR-induced apoptosis. We found that Nor-1 and Nurr1 can transactivate through the same DNA element as Nur77, and that their transactivation activities can be blocked by a Nur77 dominant-negative protein. In thymocytes, Nor-1 protein is induced to a very high level upon TCR stimulation and has similar kinetics to Nur77. In contrast, Nurr1 is undetectable in stimulated thymocytes. Furthermore, constitutive expression of Nor-1 in thymocytes leads to massive apoptosis and up-regulation of CD25, suggesting a functional redundancy between Nur77 and Nor-1 gene products. As in the case of our Nur77-FL mice, FasL is not detectable in the thymocytes of Nor-1 transgenic mice. Constitutive expression of Nur77 in gld/gld mice rescues the lymphoproliferative phenotype of the FasL mutant mice. Thus, Nor-1 and Nur77 demonstrate functional redundancy in an apparently Fas-independent apoptosis.

Animals↗
PubMed1997

NMR structural characterization of the CDK inhibitor p19INK4d.

p19INK4d is a 165 amino acid protein that belongs to the INK4 family of CDK4 and CDK6 inhibitors. Assignments of 1H, 15N and 13C resonances have enabled the determination of the secondary structure of the protein which is largely alpha-helical (residues 14-18, 21-29, 54-62, 77-83, 87-95, 110-116, 120-128, 142-148 and 152-160). The protein comprises five 32-amino acid ankyrin-like repeats; each ankyrin repeat contains a helix-beta-turn-helix core. The exception is the second ankyrin repeat, which lacks the first helix. All beta-turns have a central glycine residue flanked by two residues in beta-conformations. There is also a high conservation of Ala at position 8 in the first helix and Leu-Leu(Val) at positions 17-18 of the second helix in all ankyrin repeats of p19. The location of the helix-turn-helix segments found in p19 should be general for all other members of the INK4 family, including, for example, a homologous tumor suppressor p16INK4a. 1H-15N heteronuclear steady-state NOE measurements on p19 indicate that most of the backbone of p19INK4d exists in a well defined structure of limited conformational flexibility on the nano- to picosecond time scale.

Amino Acid Sequence↗
PubMed1997

One-week antibiotics versus maintenance acid suppression therapy for Helicobacter pylori-associated peptic ulcer bleeding.

Bleeding peptic ulcer is the most important cause of upper gastrointestinal bleeding. Our aim was to compare the effect of anti-Helicobacter therapy with maintenance treatment of H2-receptor antagonist in the prevention of relapses of ulcer and bleeding. Patients with bleeding duodenal or gastric ulcers and H. pylori infection were randomized to receive either a one-week course of triple therapy with bismuth subcitrate, metronidazole, and tetracycline plus ranitidine or a six-week course of ranitidine 300 mg/day. After the ulcers healed, the antibiotic-treated patients were not given any medication, whereas the ranitidine-treated patients continued to receive a maintenance dose of 150 mg/day. One hundred twenty-six patients were randomized to receive anti-Helicobacter therapy and 124 patients to receive long-term ranitidine. H. pylori eradication was achieved in 98.2% in those who received triple therapy and 6.1% in those who received ranitidine (P < 0.0001). At the six-week follow-up, ulcer healing was documented in 88.2% in those who received triple therapy and 86.1% in those who received ranitidine (P = 0.639). Recurrent ulcer developed in nine of the ranitidine-treated patients and three of them presented with recurrent upper gastrointestinal bleeding. One patient in the antibiotic group developed recurrent ulcer without rebleeding (P = 0.01). It is concluded that eradication of H. pylori is sufficient for the prevention of recurrent bleeding ulcers.

Adult↗
PubMed1997

Does smoking predispose to peptic ulcer relapse after eradication of Helicobacter pylori?

OBJECTIVES: To investigate whether smoking would increase ulcer recurrence after eradication of Helicobacter pylori (H. pylori) without maintenance acid-suppression therapy. METHODS: A total of 287 patients, 256 patients with duodenal ulcers and 31 patients with gastric ulcers, were followed-up for up to 18 months after ulcer healing and successful eradication of H. pylori. There were 83 smokers (defined as smoking > or = 10 cigarettes/day) and 204 patients who never smoked or stopped smoking after the diagnosis of peptic ulcer disease. None were taking nonsteroidal anti-inflammatory drugs or receiving maintenance acid suppression therapy. Endoscopy was repeated either at the end of the follow-up period or when ulcer symptoms recurred. RESULTS: Of the 83 smokers, 3 (3.6%) had ulcer recurrence, which included two duodenal ulcers and one gastric ulcer. Of the 204 nonsmokers, 4 (2.0%) had ulcer relapse, and all being recurrent duodenal ulcers. Four smokers (4.8%) and nine nonsmokers (4.4%) had recurrence of H. pylori infection after 10-18 months. There was no significant difference in ulcer relapse or recurrence of H. pylori infection between smokers and nonsmokers. CONCLUSIONS: Cigarette smoking did not increase the recurrence of peptic ulcers after eradication of H. pylori.

Adolescent↗
PubMed1997

The medical care of patients with gastrointestinal bleeding after endoscopy.

After endoscopic hemostasis, eradication therapy should be given to those who are infected by H. pylori to prevent ulcer relapse and recurrent bleeding. Maintenance acid suppression is not required after successful eradication of H. pylori. Proton pump inhibitor is preferred for the healing of NSAID-induced ulcers. Use of the lowest possible dose, or discontinuation of NSAIDs, is recommended for those with history of ulcer disease. High risk patients who require long-term NSAID therapy should be put on maintenance misoprostal.

Anti-Bacterial Agents↗
PubMed1996

Bile secretory function of the arterialized versus nonarterialized rat liver allograft.

Arterialized and nonarterialized rat models of orthotopic liver transplantation are widely used for studying various aspects of graft function. Although bile duct damage has been implicated in graft nonarterialization, any impact on graft secretory function is unknown. This study sought to investigate whether nonarterialized orthotopic liver transplantation (NOLT) is a valid model for studying bile formation after the animal has fully recovered from the perioperative period. Twenty-four-hour bile collections were performed on eight arterialized and eight nonarterialized rats 4 weeks after transplantation to avoid the confounding effects of preservation-reperfusion injury and perioperative stress. Eight unoperated rats were used as control. There was no difference in mortality or biliary complications between the two transplant groups. The nonarterialized rats exhibited a higher serum aminotransferase level, but serum bilirubin was normal. NOLT resulted in more portal lymphocytic infiltration and bile ductular proliferation. Despite these histologic changes, bile duct epithelial cells remained intact, and spontaneous graft rearterialization was evident in the NOLT group. Bile salt secretion, pool size, and synthesis in both transplant groups did not differ from unoperated rats. NOLT did not adversely affect either bile acid-dependent or bile acid-independent flow. Biliary cholesterol secretion was markedly reduced in both transplant groups, resulting in a more favorable cholesterol saturation index. In conclusion, hepatic allograft secretory function is well maintained at 4 weeks even in the absence of hepatic arterial reanastomosis. Compensatory mechanisms possibly prevent irreversible hepatobiliary damage in NOLT. The NOLT model is quite reasonable to study bile formation after transplantation.

Alanine Transaminase↗
PubMed1995

Effects of liver transplantation on bile formation and biliary lipid secretion in the Sprague-Dawley rat.

Altered hepatic secretory function after orthotopic liver transplantation constitutes a major perioperative clinical problem. Cholestasis and cholesterol gallstone formation are among the most frequent complications reported. Such changes in the allograft secretory function can be secondary to many factors like graft injury due to preservation and marked rejection, surgical complications, immunosuppressive therapy, and sepsis. The effects of liver transplantation per se on bile formation and biliary lipid secretion are unknown. The rat model of orthotopic liver transplantation was used to characterize better the true effect of transplantation without the influence of these confounding variables. Twenty-four-hour bile collections were performed on nine transplanted versus nine liver-denervated (sham) rats 4 weeks after surgery, and nine normal Sprague-Dawley rats. The liver allografts showed mild lymphocytic infiltration in portal tracts and the serum alanine transaminase levels were not significantly elevated. Bile flow and the secretion of bile salts and bilirubin under basal conditions were unchanged. Bile salt pool size, synthesis rate, and bile acid composition did not differ among the three groups. However, cholesterol secretion was dramatically reduced (50%) in the transplanted rats and decreased 31% in the liver-denervated rats (P < .001 and .01, respectively), resulting in a more favorable cholesterol saturation index (CSI = 0.29 for transplanted and 0.32 for sham versus 0.45 for normal controls; P < .01). Thus, liver transplantation with its attendant denervation did not impair hepatic secretory function, but rather improved biliary lipid composition despite mild rejection.

Alanine Transaminase↗