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Biomedical subjects

H L Tan

Publications and source records attributed to H L Tan.

At least 55 records · Page 3Linked to original sources
PubMed1999

Long-term (subacute) potassium treatment in congenital HERG-related long QT syndrome (LQTS2).

INTRODUCTION: Congenital long QT syndrome (LQTS) is subdivided according to the underlying gene defect. In LQTS2, an aberrant HERG gene that encodes the potassium channel IKr leads to insufficient IKr activity and delayed repolarization, causing ECG abnormalities and torsades de pointes (TdP). Increasing serum potassium levels by potassium infusion normalizes the ECG in LQTS2 because IKr activity varies with serum potassium levels. METHODS AND RESULTS: In an LQTS2 patient who presented with TdP, we attempted to achieve a long-term (subacute) elevation of serum potassium by increased potassium intake and potassium-sparing drugs. However, due to renal potassium homeostasis, it was impossible to achieve a long-lasting rise of serum potassium above 4.0 mmol/L. CONCLUSION: Although raising serum potassium reverses the ECG abnormalities in LQTS2, a long-lasting rise of serum potassium is only partially achievable because in the presence of normal renal function, potassium homeostasis limits the amount of serum potassium increase.

Adult↗
PubMed1999

Comparison of the diagnostic utility of CK, CK-MB (activity and mass), troponin T and troponin I in patients with suspected acute myocardial infarction.

OBJECTIVE: The aim of the study was to investigate the clinical performance of serum creatine kinase (CK), CKMB (mass and activity), Troponin T (TnT) and Troponin I (TnI) in the diagnosis of acute myocardial infarction (AMI) in patients admitted to the Coronary Care Unit at Tan Tock Seng Hospital between June and July 1998. METHODS: Routine blood samples sent to the laboratory for cardiac enzyme determination (CK, CKMB activity) were stored at -20 degrees C for later determination of CKMB mass (Abbott Axsym, Ortho Clinical Diagnostics (OCD) ECi and Roche Elecsys), Troponin I (Abbott Axsym) and Troponin T (Roche Elecsys). For CKMB mass measurements, the relative index (RI = CKMB mass/CK) was calculated. The diagnosis of acute myocardial infarction was obtained from inspection of clinical notes and/or discharge diagnosis for each patient. RESULTS: Forty-four of fifty-nine specimens were from AMI patients. Area under Receiver Operating Curve values were: CK 0.56, CKMB activity 0.72, percentage of CKMB activity 0.73, CKMB mass (Abbott) 0.76, CKMB mass (Roche) 0.77, CKMB mass (OCD) 0.78, RI (Roche) 0.83, RI (Abbott) 0.86, RI (OCD) 0.87, TnT 0.94, TnI 0.95. Sensitivity: TnI 88%, TnT 93%; specificity TnI 100%, TnT 92%. There was no significant difference in performance between Troponin T and Troponin I assays or between any of the CKMB mass measurements. CONCLUSION: Troponin T and I are superior to CKMB (mass or activity) and CK in the identification of patients with AMI. Combining multiple sampling of the percentage of CKMB with single confirmatory troponin testing may provide a cost-effective testing protocol for suspected AMI patients.

Adult↗
PubMed1998

osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification.

Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG-/- mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.

Animals↗
PubMed1998

Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation.

The ligand for osteoprotegerin has been identified, and it is a TNF-related cytokine that replaces the requirement for stromal cells, vitamin D3, and glucocorticoids in the coculture model of in vitro osteoclastogenesis. OPG ligand (OPGL) binds to a unique hematopoeitic progenitor cell that is committed to the osteoclast lineage and stimulates the rapid induction of genes that typify osteoclast development. OPGL directly activates isolated mature osteoclasts in vitro, and short-term administration into normal adult mice results in osteoclast activation associated with systemic hypercalcemia. These data suggest that OPGL is an osteoclast differentiation and activation factor. The effects of OPGL are blocked in vitro and in vivo by OPG, suggesting that OPGL and OPG are key extracellular regulators of osteoclast development.

Amino Acid Sequence↗
PubMed1998

Suppression of torsades de pointes by atropine.

A 67 year old woman with a history of chronic atrial fibrillation presented with asthma cardiale. She took no medication and there was no family history of long QT syndrome. She was treated with furosemide, nitroprusside, acenocoumarol, and digoxin. Two days later excessively prolonged RR intervals, which were terminated by escape beats with a right bundle branch block morphology, suggested impending total AV block. There was also severe QT (0.48 s) and QTc (0.56) interval prolongation with bizarre inverted TU waves and multifocal premature ventricular complexes within the U waves. The patient experienced angina pectoris followed by episodes of torsades de pointes, which were interpreted as the result of bradycardia, and the bradycardia as the result of high grade AV block induced by increased vagal tone caused by ischaemia in the presence of digoxin intoxication (serum digoxin was 2.5 micrograms/l). Subsequent atropine infusion sped up the ventricular rate and shortened the QT (0.39) and QTc (0.51) intervals. Digoxin was replaced by metoprolol to control ventricular rate and angina pectoris. Within days, QT and QTc intervals became normal and the U waves disappeared. Neither torsades de pointes nor angina pectoris recurred. Based on a review of the literature, it is suggested that the electrophysiological mechanism of this effect is not only an increase of the heart rate, but also a direct action of muscarinic receptor antagonism on Purkinje cells and ventricular refractoriness.

Aged↗
PubMed1998

T wave alternans after sotalol: evidence for increased sensitivity to sotalol after conversion from atrial fibrillation to sinus rhythm.

A 64 year old woman with an 11 year history of paroxysmal atrial fibrillation presented to the emergency room because of palpitations that had started two weeks previously. She had used sotalol 80 mg once daily for three years without any episodes of proarrhythmia or other adverse effects. However, she developed pronounced T wave alternans with giant inverted T waves and excessive QT prolongation following sotalol administration one day after conversion from atrial fibrillation to sinus rhythm. This case demonstrates bizarre T wave changes, T wave alternans, and extreme QT prolongation following sotalol administration shortly after conversion from atrial fibrillation to sinus rhythm. In this situation, sotalol administration may be proarrhythmic, because it enhances repolarisation inhomogeneities based on a spatially inhomogeneous distribution of repolarisation controlling ion channels to induce repolarisation abnormalities that may lead to torsade de pointes.

Adrenergic beta-Antagonists↗
PubMed1997

Osteoprotegerin: a novel secreted protein involved in the regulation of bone density.

A novel secreted glycoprotein that regulates bone resorption has been identified. The protein, termed Osteoprotegerin (OPG), is a novel member of the TNF receptor superfamily. In vivo, hepatic expression of OPG in transgenic mice results in a profound yet nonlethal osteopetrosis, coincident with a decrease in later stages of osteoclast differentiation. These same effects are observed upon administration of recombinant OPG into normal mice. In vitro, osteoclast differentiation from precursor cells is blocked in a dose-dependent manner by recombinant OPG. Furthermore, OPG blocks ovariectomy-associated bone loss in rats. These data show that OPG can act as a soluble factor in the regulation of bone mass and imply a utility for OPG in the treatment of osteoporosis associated with increased osteoclast activity.

Amino Acid Sequence↗
PubMed1996

Electrophysiologic and extracellular ionic changes during acute ischemia in failing and normal rabbit myocardium.

The incidence of ventricular arrhythmias is higher in failing hearts than in control hearts, especially during acute ischemia. Electrophysiological and extracellular ionic changes during acute ischemia in normal and failing rabbit myocardium were assessed. Heart failure was induced in rabbits by combined volume and pressure overload. In perfused papillary muscles, the onset of electrical uncoupling and changes in action potential duration and conduction velocity during acute ischemia were determined. In Langendorff-perfused rabbit hearts the changes in extracellular potassium concentration ([K+]o) and pH during acute global ischemia were studied. In perfused papillary muscles, during the first 10 min of ischemia, action potential duration at 80% of repolarization decreased more in preparations from failing than from control hearts (from 174 to 104 ms and from 156 to 119 ms respectively (P < 0.001)). Conduction velocity was significantly lower in failing hearts during ischemia (P < 0.005). The onset of electrical uncoupling was similar in failing and control hearts (mean +/- S.E.M., 17 +/- 1 and 15 +/- 1 min respectively, n.s.). Langendorff-perfused hearts [K+]o, after 10 min of ischemia, was 11.0 +/- 0.4 mM in failing and 9.5 +/- 0.3 mM in control hearts (P < 0.01), while the change in pH was the same. After pretreatment with glibenclamide, an ATP sensitive K+ channel blocker, [K+]o reached lower values after 10 min of ischemia in both failing (8.8 +/- 0.5 mM) and control hearts (7.2 +/- 0.4 mM). During ischemia, action potential duration shortening is more pronounced and conduction velocity is lower in failing myocardium than in control myocardium. [K+]o reaches higher values during acute ischemia in failing compared with normal myocardium. These changes are not caused by an earlier activation of IK.ATP. Increased spatial dispersion in electrophysiological parameters and [K+]o over the ischemic border in failing hearts may explain the higher propensity for reentrant arrhythmias during acute regional ischemia in failing hearts.

Action Potentials↗
PubMed1996

Laparoscopic dismembered pyeloplasty in children: preliminary results.

OBJECTIVES: To investigate the technique of laparoscopic pyeloplasty in children with pelvi-ureteric junction (PUJ) obstruction. PATIENTS AND METHODS: Six children, aged between 2.5 and 15 years, were treated by laparoscopic pyeloplasty in a prospective study. The outcome was assessed by post-operative isotopic renography. Four of the children underwent a Y/V plasty of the PUJ structure and one a Hynes-Anderson dismembered pyeloplasty. RESULTS: One case (the first in this series) was converted to open pyeloplasty due to adhesions around the PUJ from previous surgery. One patient developed an abdominal haematoma at the trocar site, which resolved without treatment. All anastomoses were completed without complication. Five of the children had normal or significantly improved drainage times on post-operative renography. In one patient, the drainage time deteriorated post-operatively, although differential function of the operated kidney improved. CONCLUSIONS: These early results suggest that laparoscopic pyeloplasty in children is feasible, safe and effective; a longer term follow-up is awaited.

Adolescent↗
PubMed1995

Electrophysiologic mechanisms of the long QT interval syndromes and torsade de pointes.

PURPOSE: To review the current understanding of the mechanisms and treatment of the long QT interval syndromes and torsade de pointes. DATA SOURCES: Personal databases of the authors and a search of the MEDLINE database from 1966 to 1994. STUDY SELECTION: Experimental and clinical studies and topical reviews on the electrophysiologic mechanisms and treatment of torsade de pointes were analyzed. RESULTS: The long QT interval syndromes have been classified into acquired and hereditary forms, both of which are associated with a characteristic type of life-threatening polymorphic ventricular tachycardia called torsade de pointes. The acquired form is caused by various agents and conditions that reduce the magnitude of outward repolarizing K+ currents, enhance inward depolarizing Na+ or Ca2+ currents, or both, thereby triggering the development of early afterdepolarizations that initiate the tachyarrhythmia. The hereditary form appears to result from an abnormal response to adrenergic or sympathetic nervous system stimulation. At least some cases of the hereditary long QT interval syndromes may result from a single gene defect that alters the intracellular regulatory proteins responsible for the modulation of K+ channel function. Treatment of the acquired form is primarily directed at identifying and withdrawing the offending agent, although emergent therapy using maneuvers and agents that favorably modulate transmembrane ion currents can be lifesaving. In torsade de pointes associated with the hereditary long QT interval syndromes, early diagnosis leading to treatments designed to both shorten the QT interval and block the beta-adrenergic-induced instability of the QT interval is essential. CONCLUSIONS: The long QT interval syndromes and torsade de pointes are potentially life-threatening conditions caused by various agents, conditions, and genetic defects. The mechanisms responsible for these conditions and available treatment options for them are reviewed.

Electrophysiology↗
PubMed1995

Laparoscopic bipolar strip-tease appendicectomy. A new endosurgical technique.

Since its conception, several techniques have been described for laparoscopic appendicectomy. We describe a technique which utilizes a 5-mm bipolar forceps designed to coagulate and cut tissues at the same time; 50 pediatric patients underwent laparoscopic appendicectomy for acute appendicitis using this "stripping and teasing" technique. No bleeding complications occurred. There were only two postoperative abscesses in the series. We believe that the bipolar laparoscopic striptease appendicectomy technique as developed by the senior author is safe, quick, and effective, even for severe appendicitis.

Abdominal Abscess↗
PubMed1995

Intravenous sotalol for the termination of supraventricular tachycardia and atrial fibrillation and flutter: a multicenter, randomized, double-blind, placebo-controlled study. Sotalol Multicenter Study Group.

Sotalol is an antiarrhythmic agent with combined beta-blocking and class III antiarrhythmic properties. This study was designed to assess the safety and efficacy of sotalol in terminating supraventricular tachycardia (SVT), atrial fibrillation (AFib), and atrial flutter (AFl). Ninety-three patients with spontaneous or induced SVT (n = 45) or AF (AFib or AFl; n = 48) with a ventricular rate of > or = 120 beats/min were studied. In the first phase, the double-blind phase, patients were randomly assigned to receive placebo or intravenous (i.v.) sotalol, 1.0 or 1.5 mg/kg. If SVT or AF did not convert to sinus rhythm or if the ventricular rate did not slow to < 100 beats/min within 30 minutes, patients then entered the second phase, the open-label phase, which also lasted 30 minutes, and were given 1.5 mg/kg iv sotalol. In the SVT group, during the double-blind phase conversion to sinus rhythm occurred in 2 (14%) of 14 of patients who received placebo, 10 (67%) of 15 who received sotalol, 1.0 mg/kg (p < 0.05 vs placebo), and 10 (67%) of 15 who received 1.5 mg/kg sotalol (p < 0.05 vs placebo); during the open-label phase, 1.5 mg/kg i.v. sotalol converted 7 (41%) of 17 of patients. In the AF group, during the double-blind phase conversion to sinus rhythm occurred in 2 (14%) of 14 of patients who received placebo, 2 (11%) of 18 who received 1.0 mg/kg sotalol (p not significant [NS] vs placebo), and 2 (13%) of 16 who received 1.5 mg/kg sotalol (p = NS vs placebo); in these groups, a > 20% reduction of ventricular rate without conversion to sinus rhythm occurred in 0 (0%) of 14, 13 (72%) of 18 (p < 0.05 vs placebo), and 12 (75%) of 16 of patients (p < 0.05 vs placebo), respectively; during the open-label phase, 1.5 mg/kg i.v. sotalol converted 7 (30%) of 23 of patients. The most common adverse events were hypotension and dyspnea. During the double-blind phase they occurred in 10% of patients who received placebo, 9% of those who received 1.0 mg/kg i.v. sotalol (p = NS vs placebo), and 10% of those who received 1.5 mg/kg i.v. sotalol (p = NS vs placebo). Most of these events were mild to moderate, but all were transient and clinically manageable.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

Early experience with laparoscopic pyloromyotomy for infantile hypertrophic pyloric stenosis.

The authors report on 37 infants with infantile hypertrophic pyloric stenosis who underwent successful laparoscopic pyloromyotomy. The average age was 6 weeks and average weight was 4.5 kg. Three 4-mm ports were used in each procedure. The average operating time was 29 minutes (range, 7 to 60 minutes). Feeding was begun an average of 5.2 hours (range, 3 to 12 hours) postoperatively, and the average time of discharge was 28 hours (range, 16 to 52 hours) postoperatively. There were no technical failures. One patient had minor surgical emphysema, which resolved spontaneously. Laparoscopic pyloromyotomy can be safe and successful in infants with hypertrophic pyloric stenosis.

Female↗
PubMed1995

Retrograde balloon dilation of ureteropelvic obstructions in infants and children: early results.

OBJECTIVES: Although balloon dilation is a successful and widely accepted minimally invasive method of treating vascular, esophageal, and colonic strictures, it has not been reported in the management of ureteropelvic junction (UPJ) obstruction in infants. We investigated the role of retrograde balloon dilation as the primary treatment of UPJ obstruction in infants, and we report the technique and early results. METHODS: Prospective study of infants and young children undergoing retrograde balloon dilation of primary UPJ obstruction using a 3.8 F, 8 atmosphere radial balloon dilator. RESULTS: Ten infants and children with a median age of 16 months (range, 3 months to 9 years 6 months) underwent retrograde balloon dilation for proven UPJ obstruction with successful outcome in 7 patients following one dilation. CONCLUSIONS: The minimally invasive nature of this technique and our encouraging early results lead us to conclude that this technique warrants further clinical evaluation.

Catheterization↗
PubMed1995

Pyloromyotomy: comparison between laparoscopic and open surgical techniques.

Several reports have appeared in the literature recently describing various techniques of performing pyloromyotomy laparoscopically. Although there is no doubt that this is now technically feasible, there are unanswered questions with regard to its safety, efficacy, and potential benefits or otherwise to the patient. In an attempt to resolve some of these issues, we compared the results in 37 infants who underwent open pyloromyotomy with 26 who underwent laparoscopic pyloromyotomy. The two groups were similar in terms of sex, age, weight, and presenting pH, although they could not be randomized. The time from feeding to discharge was less for the laparoscopic group (1.4 days) compared with the open group (1.8 days) (p = 0.04). Postoperative vomiting was not significantly different between the two groups. The operating time was identical for groups, 29 min vs 27 min. There were 3 complications in the open surgical group and 1 in the laparoscopic group. On the criteria measured, our results suggests that laparoscopic pyloromyotomy is at least as good as conventional surgery, and offers the potential benefits of shortened hospital stay and minimal cosmetic deformity.

Female↗
PubMed1995

Interleukin 4, interferon-gamma, and prostaglandin E impact the osteoclastic cell-forming potential of murine bone marrow macrophages.

Interleukin 4 (IL-4) is an immune cytokine that inhibits bone resorption in mice and suppresses osteoclastic cell formation in vitro through an undefined mechanism. In this report, we have established the cellular identity of the IL-4 target cell using a variety of bone marrow/stromal cell coculture methods. Initially, we found that the majority of IL-4's inhibition of osteoclastic cell formation was due to its effect on bone marrow cells, not stromal cells. Consequently, bone marrow macrophages were used as osteoclastic cell progenitors after they had been transiently exposed to IL-4 (48 h), before the addition of stromal cells, 1,25-dihydroxyvitamin D3, and dexamethasone. In this circumstance, IL-4 impaired subsequent osteoclastic cell formation, suggesting that the macrophage may be potentially targeted by many factors known to influence osteoclast formation. Consequently, we discovered that interferon-gamma (IFN gamma), prostaglandin E (PGE), and cell-permeant cAMP analogs also impacted osteoclastic cell formation when used to selectively treat bone marrow macrophages. IFN gamma suppressed osteoclastic cell formation, whereas PGE and cAMP analog treatment led to the formation of significantly enlarged osteoclastic cells. Importantly, PGE antagonized the inhibitory effects of both IL-4 and IFN gamma on the osteoclastic cell-forming potential of bone marrow macrophages. Collectively, these findings establish bone marrow macrophages as osteoclastic cell precursors with the degree of their commitment to the osteoclast pathway sensitive to the effects of soluble mediators, including IL-4, IFN gamma, and PGE.

Animals↗