Search PubMed⌕ Search

Biomedical subjects

H L Chan

Publications and source records attributed to H L Chan.

At least 37 records · Page 2Linked to original sources

Lack of intravenous lidocaine effects on HRV changes of tracheal intubation during induction of general anesthesia.

BACKGROUND: Intravenous lidocaine has been widely used for suppressing the autonomic activation from tracheal intubation during induction of general anesthesia. Conventionally, researches of its effectiveness through assessment of heart rate and blood pressure changes obtained by common clinical methods result in the conclusions deduced of much controversy. Heart rate variability is a noninvasive measurement of autonomic regulation and is suitable for the study of this subject. METHODS: 36 ASA class I-II patients undergoing general anesthesia were divided into 3 groups. Besides induction agents, intravenous lidocaine was given 5 min before tracheal intubation in group A, 3 min before intubation in group B and nothing in group C. HRV spectral powers were measured at awake state, anesthetized state before tracheal intubation and anesthetized state after tracheal intubation by time frequency spectral analysis method and comparison was made between the three groups. RESULTS: The HRV spectral power in high frequency (HF) and mid-frequency (MF) power bands and their ratios (MF/HF) were not significantly different among the 3 groups during the 3 observation periods. CONCLUSIONS: There was no evidence to indicate the effectiveness of intravenous lidocaine on the autonomic regulation during tracheal intubation under the influence of induction agents used in general anesthesia.

Anesthesia, General↗

Sézary syndrome in a Malay--case report and literature review.

Sézary syndrome is a rare form of primary cutaneous T cell lymphoma. It is a distinct systemic variant of mycosis fungoides, marked by erythroderma, lymphadenopathy and circulating cerebriform lymphocytes in the peripheral blood. We report a case of Sézary syndrome in a 61-year-old Malay man with a five-year history of indurated plaques, ulcers and tumours on the head and trunk, with characteristic findings on physical examination, skin biopsy, electron microscopy, immunophenotyping and peripheral blood film. A literature review on Sézary syndrome is presented.

Biopsy↗

Association of pityriasis rosea with human herpesvirus-6 and human herpesvirus-7 in Taipei.

BACKGROUND AND PURPOSE: Pityriasis rosea (PR) is a common papulosquamous skin disease with unknown etiology. The possible relationship of PR with human herpesvirus infection (HHV) has been extensively studied. This study used the polymerase chain reaction (PCR) to investigate the presence of human herpesvirus 6 and 7 (HHV-6 and HHV-7) in 41 PR patients from two hospitals in Northern Taiwan. The epidemiologic features of PR in patients were also studied. METHODS: A total of 41 PR patients (11 males, 30 females) were enrolled in this study from April 1999 to March 2000. PCR of skin biopsy specimens from 24 PR patients was used to identify the existence of HHV-6 and HHV-7. Viral culture from PR biopsy specimens was also performed. Blood from these patients was sampled for Venereal Disease Research Laboratory tests. Skin biopsies from 20 age- and sex-matched controls with other skin diseases were also subjected to PCR study. RESULTS: The ages of the 41 PR patients ranged from 8 to 62 years. An increased incidence (17/41) of PR episodes was observed during the spring. Both HHV-6 and HHV-7 DNA was below the limit of detection in all biopsy specimens from patients and healthy controls. Viral culture for HHV was negative in all patients. CONCLUSION: The epidemiologic features of PR in this series are comparable to other studies except for an exaggerated female predominance (male:female ratio 1:2.7). Our data indicate a lack of association between HHV-6 and HHV-7 infection and PR.

Adolescent↗

Hepatitis B virus reactivation during cytotoxic chemotherapy-enhanced viral replication precedes overt hepatitis.

The diagnosis of HBV reactivation during cytotoxic chemotherapy is based on an abrupt rise in levels of serum HBV DNA in conjunction with a hepatitic picture and in the absence of other causes of hepatitis. However, several cases of "hepatitis" have been noted during chemotherapy in HBsAg-positive patients, for which no cause could be found and in which HBV DNA levels were negative. One possible explanation is that HBV reactivation may, indeed, have been the cause but that HBV DNA levels became negative by the time ALT levels peaked and the clinical diagnosis of hepatitis was made. During the course of a longitudinal study of HBsAg-seropositive cancer patients who were monitored during standard chemotherapy, the opportunity was available to test this hypothesis.

Adult↗

Hepatitis B e antigen-negative chronic hepatitis B in Hong Kong.

Hepatitis B e antigen-negative chronic hepatitis B (e-CHB) has been reported in Asia but its prevalence and clinical significance have not been determined. The aims of this study were to determine the prevalence of e-CHB in Hong Kong and the frequency of precore and core promoter mutations in these patients. A cross-sectional study was performed in 350 consecutive Chinese patients (230 men and 120 women; mean age +/-SD, 42 +/- 13 years) with chronic hepatitis B virus infection. A total of 243 (69%) patients were hepatitis B e antigen (HBeAg)-negative of whom 15% had clinical cirrhosis. In the remaining 85% of patients, 63% had normal and 22% had elevated transaminases. Serum hepatitis B virus (HBV) DNA was detectable using branched DNA assay in 46% of HBeAg-negative patients with clinical cirrhosis/elevated transaminases. Forty-five percent of the patients with e-CHB had the precore stop codon mutation, and an additional 41% had core promoter changes. There was no correlation between the presence of precore/core promoter mutations and liver disease or HBV-DNA levels. Overall, 17% of HBeAg-negative patients were viremic and had evidence of chronic liver disease (e-CHB) with mean HBV-DNA levels comparable with that in HBeAg-positive patients. In summary, we found that e-CHB may be present in up to 17% of HBeAg-negative patients seen in a tertiary referral center in Hong Kong. e-CHB may be a heterogeneous condition and is not invariably associated with the precore HBV mutant. Population studies are needed to determine the true prevalence of e-CHB in Asia and to assess its natural course and response to treatment.

Adolescent↗

Dermatofibroma is a clonal proliferative disease.

Benign fibrous histiocytoma of the skin or dermatofibroma (DF) has been regarded as a fibrohistiocytic tumor. Whether DF is a neoplastic growth or a reactive process has not been settled. Since a neoplastic process is clonal in nature, clonal analysis of DF was conducted to see if DF is a clonal disease. Fresh specimens of 13 DFs and 2 hypertrophic scars obtained from female patients were studied. The adjacent nonlesional skin tissues served as controls. The clonal analysis was based on the methylation pattern of the polymorphic X-chromosome linked androgen-receptor gene (HUMARA). Eight DFs and 1 hypertrophic scar were heterozygous at the androgen receptor gene and could be analyzed. All 8 informative DFs showed a significant reduction in one of the allelic bands compared with the corresponding bands of the nonlesional tissue after Hha I digestion. Therefore, DF is a clonal proliferative disease. In contrast, 1 hypertrophic scar showed a polyclonal pattern of X-chromosome inactivation. We conclude that DF is a clonal disease favoring a neoplastic process.

Alleles↗

Toxic epidermal necrolysis following combination of methotrexate and trimethoprim-sulfamethoxazole.

A 15-year-old boy with T-cell acute lymphoblastic leukemia (ALL) (FAB L1), diagnosed in 1995, received combination chemotherapy consisting of 6 weeks of induction (vincristine, epirubicin, L-asparaginase, prednisolone) and 2 weeks of consolidation (cytosine arabinosides, etoposide). After achieving remission, for further maintenance of remission, he was treated with 14 cycles of intensive chemotherapy consisting of 6-MP, 10 mg/kg orally on the first 4 days, and cyclophosphamide, 1200 mg/m2, vincristine, 1.5 mg/m2, epirubicin, 15 mg/m2, and cytosine arabinoside, 40 mg/m2, intravenously on days 4, 11, 39, and 40, respectively. On day 18 of each cycle, he received intravenous methotrexate (MTX) infusion in a total dose of 150 mg/m2 plus oral leucovorin (30 mg/m2 ) rescue 36 h after starting MTX therapy. In addition, oral trimethoprim-sulfamethoxazole was given regularly to prevent Pneumocystis carinii infection. The patient achieved remission during the first course of treatment, but 8 months later the disease relapsed. He then received four doses of MTX (800 mg intravenously) plus leucovorin rescue in the following 4 months. During the last MTX therapy, small hemorrhagic bullae were found on the lateral side of the right ankle, but subsided after a few days. Due to partial remission of the disease, he was admitted again in January 1999 for high-dose MTX therapy. An initial hemogram on admission revealed hemoglobin 7.2 g/dL, white cell count 15,200/mm3, platelet count 153/mm3, blood creatinine 0.5 mg/dL, and alanine leucine aminotransferase (ALT) 20 U/L. He received 8500 mg of MTX (5000 mg/m2 ) as a continuous intravenous infusion for 24 h. Thirty-six hours after the start of MTX infusion, leucovorin (30 mg, intravenous) rescue was initiated every 6 h for 3 days. Another preventive measure to cover MTX toxicity included aggressive intravenous fluid replacement (4 L/m2 /day) and the addition of 25 meq/L sodium bicarbonate to the intravenous fluid to alkalinize the urine. Concurrent medication included 6-MP (50 mg) once daily and trimethoprim-sulfamethoxazole (120 mg, 600 mg) twice daily every other day. Plasma MTX levels were 52.36 micromol/L 24 h after MTX infusion, 1.87 micromol/L after 48 h, 0.57 micromol/L after 72 h, and 0.41 micromol/L after 96 h. These indicated delayed MTX plasma clearance. The blood creatinine level was mildly elevated from 0.5 mg/dL to 0.7 mg/dL. Thirty-six hours after the administration of MTX, the patient developed an erythematous painful swelling on the right middle finger. The erythema, with subsequent large bulla formation, progressed to all the fingers, toes, palms, and the soles of the feet. Some erythematous to hemorrhagic papules also appeared on the bilateral elbows. Subsequently, diffuse tender erythema with extensive erosions and focal tiny pustules developed on the back, abdomen, proximal extremities, and face (Fig. 1a,b). A positive Nikolsky's sign was also present. A biopsy specimen of the right dorsal hand lesion revealed parakeratosis, detached acanthotic epidermis with scattered necrotic keratinocytes, dyskeratotic cells and nuclear atypia, neutrophilic exocytosis, and many neutrophils in the papillary dermis (Fig. 2). The skin condition deteriorated rapidly. Toxic epidermal necrolysis-like lesions involved 90% of the total body surface on the fifth day after MTX infusion. Mucositis, diarrhea, involuntary tremor, fever, and chills were noted. The patient was then sent to the burn unit for intensive skin care. Ten days after MTX therapy, profound agranulocytosis and thrombocytopenia (white cell count 100/mm3, platelets 14,000/mm3, and hemoglobin 5.6 g/dL) were found. The patient was then started on granulocyte colony stimulation factor (G-CSF, 5 microg/kg/day), but his general condition deteriorated rapidly and he died 6 days later due to septic shock and multiple organ failure.

Adolescent↗

Decreased autonomic nervous system activity as assessed by heart rate variability in patients with chronic tetraplegia.

OBJECTIVES: To assess the alterations of autonomic nervous functions and sympathovagal balance of the subjects with spinal cord injuries (SCIs) in different levels by heart rate variability analysis. DESIGN: Prospective, observational study. SETTING: All participants were recruited from the outpatient clinic from National Taiwan University Hospital, which is a tertiary referral center. PARTICIPANTS: Thirty-one patients with traumatic chronic complete SCI (more than 6 months): 14 with paraplegia (Group A), and 17 with tetraplegia (Group B). MAIN OUTCOME MEASURES: Heart rate variability assessed by 24-hour Holter monitoring. RESULTS: Two patients in Group A and 1 in Group B were excluded from final data analysis because of poor recording data. Two time domain variables, the standard deviation (SD) of all normal RR intervals (SDNN) and the mean of the SDs of all normal RR intervals for all 5-minute intervals (SDNNi), over 24 hours were decreased in Group B. All time domain variables, SDNN, SDNNi, root mean square of the successive normal RR interval difference (rMSSD), and the percentage of RR intervals differing >50msec from the preceding one (pNN50), were decreased during the nighttime recordings (all p < .05) in Group B. The very-low-frequency, low-frequency (LF), and high-frequency (HF) components of the power spectrum of the RR intervals were also decreased in Group B (p < .05), irrespective of the daytime and nighttime recordings. The LF-to-HF ratio did not differ significantly in these two groups, indicating the maintained sympathovagal balance in the chronic SCI patients. CONCLUSION: These findings suggested that the autonomic nervous system activity was depressed in the patients with chronic tetraplegia, but the autonomic nervous system still maintained homeostasis.

Adult↗

Toxicity and DNA binding of dextran-doxorubicin conjugates in multidrug-resistant KB-V1 cells: optimization of dextran size.

We previously showed that conjugating doxorubicin to very large 70-500 kDa dextran decreased its removal rate from P-glycoprotein (P-gp) over-expressing, multidrug-resistant KB-V1 cells. Furthermore these conjugates could act synergistically with other cancer drugs. In the drug-sensitive 3-1 clone, but not in the V1 subclone which was 300-fold more resistant to free doxorubicin, conjugation led to a size-related decrease in toxicity. Here we identified the optimal size of dextran for avoiding P-gp-mediated efflux and yet preserving as much as possible doxorubicin toxicity. Chemically reduced, intracellularly stable 3.4-10 kDa conjugates were prepared. Confocal microscopy and fluorescence quenching experiments showed that these conjugates entered nuclei and interacted with DNA. In 3-1 cells, but not in V1 cells, cytotoxicity of conjugates decreased 14- to 45-fold linearly related to log size of the carrier (r=0.95). In V1 cells toxicity of the 10 kDa conjugate exceeded that of free doxorubicin. After conjugation the equilibrium binding constant of the DNA-drug complex (KA) decreased only by up to 3-fold. In 3-1 cells, but not in VI cells, DNA binding kinetics was an important factor and toxicity could be linearly correlated to 1/KA of conjugate (r=0.94). Drug accumulation decreased with an increase in dextran size but drug removal was decreased only in V1 cells. It appeared that drug uptake was also sensitive to dextran conjugation. In Vl cells drug removal was sensitive to the P-gp inhibitor verapamil or energy starvation. Ratios of V1/3-1 toxicity, drug accumulation and drug removal correlated linearly with log dextran size. When these ratios equaled 1, dextran sizes were estimated to be 32, 103 and 21 kDa, respectively.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Risk factors for active liver disease in HBeAg-negative chronic hepatitis B virus-infected patients.

OBJECTIVES: HBeAg-negative patients constitute approximately 70% of all chronic hepatitis B virus (HBV) infections in Southeast Asia, and some of these patients continue to suffer from active disease. We aimed to study the risk of hepatitis relapse in chronic HBV-infected patients with negative HBeAg and the predictor(s) of relapses. METHODS: This was a retrospective analysis of patients carrying HBsAg but lacking HBeAg. Patients recruited were required to have been followed for > or = 12 months with a minimum of three blood samples available for analysis. Patient demographic data, liver biochemistry, and HBV serology were analyzed in relation to relapses of hepatitis. Relapse was defined as an abrupt elevation of ALT > 200 IU/L or > 3-fold previous levels, whichever was higher. RESULTS: In a period of 3 months, 317 patients seen at the Hepatitis Clinic at the Prince of Wales Hospital in Hong Kong were recruited. The median duration of follow-up was 34 months. On initial consultation, 111 (35.0%) patients had elevated ALT (>60 IU/L). Overall, 57 (18.0%) patients developed at least one relapse, including 37 (33.3%) patients with elevated ALT and 20 (9.7%) patients with normal ALT at the first visit. Multiple logistic regression analysis showed that elevated ALT level at first presentation (odds ratio 4.17, 95% confidence interval 2.24-7.75) and male gender (odds ratio 2.83, 95% confidence interval 1.23-6.49) were the two independent factors associated with a higher risk of hepatitis relapse. The sensitivity, specificity, and positive and negative predictive values of a single ALT test for hepatitis relapse were 64.9%, 71.5%, 33.3%, and 90.3%, respectively. CONCLUSIONS: HBeAg-negative HBV carriers with normal ALT levels have a low risk of hepatitis relapse.

Adult↗

Comparison of three different sensitive assays for hepatitis B virus DNA in monitoring of responses to antiviral therapy.

The aim of our study was to compare the performances of two new hepatitis B virus (HBV) DNA assays, a cross-linking assay (NAXCOR) and a hybrid-capture amplification assay (Digene), versus the widely used branched-DNA (bDNA) assay (Chiron) in the monitoring of HBV DNA levels during antiviral treatment. Serial serum samples from 12 chronically HBV infected patients undergoing a phase II trial of an antiviral drug, 2',3'-dideoxy-5-fluoro-3'-thiacytidine (FTC), were studied. A total of 96 serum samples were tested for HBV DNA using the cross-linking, hybrid-capture amplification, and bDNA assays. In the comparison of the cross-linking and bDNA assays, concordant results were found in 77 (80.3%) samples, no significant difference was found between the median log(10) HBV DNA levels (6.66 versus 7. 17 meq/ml), and the results of the two assays were closely correlated (r = 0.95). In the comparison of the hybrid-capture amplification and bDNA assays, concordant results were found in 79 (82.3%) samples, no significant difference was found between the median log(10) HBV DNA levels (6.98 versus 6.99 meq/ml), and the results of the two assays were closely correlated (r = 0.99). Six (6. 3%) samples by the cross-linking assay and 10 (10.4%) samples by the bDNA assay required retesting because of unacceptably high within-run coefficients of variance. No sample required retesting in the hybrid-capture amplification assay according to the internal validation. In conclusion, the cross-linking and hybrid-capture amplification assays were as sensitive as the bDNA assay for HBV DNA detection and can be recommended for monitoring of HBV DNA levels during antiviral treatment.

Antiviral Agents↗

Generalized granuloma annulare associated with granulomatous mycosis fungoides.

We describe a 68-year-old man with plaque stage mycosis fungoides (MF) for 8 years. He developed tumorous lesions of granulomatous MF (GrMF) and generalized granuloma annulare (GA) after a previously indolent clinical course. Since then, the clinical course was aggressive with involvement of the bone marrow and lymph nodes, and leukemic change occurred. Systemic chemotherapy was given, but the patient died 9 months later due to neutropenic fever and septic shock. GA in malignant lymphoma has been reported most frequently in association with Hodgkin's disease. To the best of our knowledge, GA associated with GrMF has never been reported in the English language literature. The prognostic significance of the association of granulomatous inflammation and malignancy is reviewed.

Aged↗

An unusual case of cutaneous vasculitis.

INTRODUCTION: We report an unusual case of a patient with clinical and histological features of cutaneous vasculitis. CASE PICTURE: A middle-aged Chinese male presented with livedo reticularis and digital gangrene without visceral involvement. Skin biopsy showed features suggestive of cutaneous vasculitis. Repeated testing for anticardiolipin antibody was negative. TREATMENT: He was treated with two courses of intravenous prostacyclin and pulsed with one course of intravenous methylprednisolone. He was also put on oral prednisolone, pentoxifylline, aspirin, nifedipine and colchicine in addition to symptomatic therapy. OUTCOME: There was gradual improvement of his toe discolouration and relief of pain. CONCLUSIONS: This is an interesting case of cutaneous vasculitis, which has features of polyarteritis nodosa and the antiphospholipid syndrome, who responded well to intravenous prostacyclin, steroids, pentoxifylline, aspirin, nifedipine and colchicine.

Biopsy, Needle↗

Hexokinase type II: a novel tumor-specific promoter for gene-targeted therapy differentially expressed and regulated in human cancer cells.

The use of tissue- or tumor-selective promoters in targeted gene therapy for cancer depends on strong and selective activity. Hexokinase type II (HK II) catalyzes the first committed step of glycolysis and is overexpressed in tumors, where it is no longer responsive to normal physiological inhibitors, e.g., glucagon. We show, in a reporter gene assay, activation of HK II in non-small cell lung carcinomas NCI-H661 and NCI-H460 at 61 and 40%, respectively, relative to the activation observed with a constitutive promoter, while it was only 0.9% in different preparations of primary normal human bronchial epithelial cells (NHBECs). Similar results were observed in a variety of normal and tumor cells. Moreover, treatment of the transfectants with glucagon did not inhibit promoter activation in the transformed H661 cells, while endogenous HK II in NHBECs is suppressed by glucagon. H460 and H661 cells infected with a recombinant adenovirus carrying an HK II/LacZ expression cassette, AdHexLacZ, demonstrated beta-galactosidase activity that correlated with the level of HK II promoter activation in these cells. Under similar conditions, no enzyme activity was observed in NHBECs. Cells were then infected with AdHexTk and treated with GCV. Our results demonstrate selectivity in toxicity, with a 10- to 100-fold increase in IC50 between lung cancer cell lines H661 and H460, respectively, and NHBECs. There was also a 100-fold increase in IC50 in NHMECs relative to breast carcinoma cell line MCF-7. In HepG2 cells, an IC50 of 1 microg/ml was observed, comparable to that of other tumor cell lines. This represents a novel use of the hexokinase type II as a selective promoter in cancer gene therapy.

Adenoviridae↗

Different hepatitis B virus genotypes are associated with different mutations in the core promoter and precore regions during hepatitis B e antigen seroconversion.

Mutations in the core promoter and precore regions are frequently found in hepatitis B e antigen (HBeAg)-negative patients, but precore stop codon mutation is restricted to hepatitis B virus (HBV) genotypes that have T at nucleotide 1858. The aims of this study were to determine the role of core promoter and/or precore mutations in HBeAg seroconversion and their impact on the subsequent course of liver disease, and to determine if core promoter mutations are more frequently selected in patients with HBV genotypes that preclude the development of precore stop codon mutation. Serial sera from 45 patients with chronic HBV infection were polymerase chain reaction (PCR)-amplified, and the HBV core promoter and precore regions were sequenced. Ninety-two percent of patients had core promoter or precore mutations after HBeAg seroconversion: 42% had core promoter changes only, 38% had precore stop codon mutations only, and 12% had changes in both regions. Seventy-three percent of the patients had persistently normal aminotransferases, and only 8% had multiple flares in aminotransferases after HBeAg seroconversion. Core promoter changes were significantly more common in patients infected with HBV who have C at nucleotide 1858 (91% vs. 27%; P <.01), while precore stop codon changes were exclusively found in patients infected with HBV who have T at nucleotide 1858 (87% vs. 0; P <.01). The vast majority of our patients had core promoter and/or precore mutations after HBeAg seroconversion. Nevertheless, most patients had sustained remission of liver disease. Our data suggest that core promoter changes are preferentially selected in patients infected with HBV genotypes that preclude the development of precore stop codon mutation.

Adolescent↗

Long-term beta-blocker therapy improves autonomic nervous regulation in advanced congestive heart failure: a longitudinal heart rate variability study.

BACKGROUND: beta-Blocker therapy is believed to modulate the detrimental effect of overcompensating neurohormonal activation in chronic heart failure. However, clinical doubts remain, particularly the physiologic sympathovagal balance. METHODS: To respond to clinical concern about worsening autonomic nervous perturbation in beta-blocker therapy of advanced congestive heart failure, 15 consecutive patients were longitudinally studied to elucidate the evolution of cardiac function versus 24-hour heart rate variability (HRV) before and after 1, 3, and 6 to 9 months of atenolol-combined therapy. RESULTS: Two patients died prematurely within 1 month. All 13 surviving patients showed improvement in New York Heart Association functional class, with decrease in left ventricular end-systolic and end-diastolic dimensions and increase in fraction shortening and ejection fraction by echocardiography after at least 3 months of atenolol use. The retarded therapeutic effect was accompanied by a general rise of total, very low, low-, and high-frequency components (9.0 +/- 0.5, 8.8 +/- 0.5, 6.2 +/- 0.6, and 6.1 +/- 0.5 vs 10.9 +/- 0.3, 10.7 +/- 0.4, 8.6 +/- 0.3, and 7.8 +/- 0.3; all P <.02) of daily HRV. This implied recovery of parasympathetic and baroreceptor function. Return of sympathovagal interaction was further supported by the suppression of Cheyne-Stokes type HRV as detected by Wigner-Ville distribution. CONCLUSIONS: Long-term beta-blocker therapy for advanced congestive heart failure upwardly regulates the autonomic nervous interaction in synchrony with the evolution of cardiac function performance.

Adrenergic beta-Antagonists↗