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Biomedical subjects

T Y Chan

Publications and source records attributed to T Y Chan.

At least 73 records · Page 4Linked to original sources
PubMed1997

Drug-induced syndrome of inappropriate antidiuretic hormone secretion. Causes, diagnosis and management.

Hyponatraemia is common among the elderly, and may be caused by physiological changes, disease processes or drugs. About half of elderly patients with hyponatraemia have features typical of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). It is important to establish whether drugs are the cause, as this is easily remediable. The clinical manifestations of SIADH are predominantly attributable to hyponatraemia and serum hypo-osmolality. The severity of the signs and symptoms depends on the degree of hyponatraemia and the rapidity with which the syndrome develops. Although a growing number of drugs have been reported to produce SIADH, most published reports concern vasopressin and its analogues, thiazide and thiazide-like diuretics, chlorpropamide, carbamazepine, antipsychotics, antidepressants and nonsteroidal anti-inflammatory drugs. Old age is a risk factor for SIADH following the use of many of these drugs. The use of these drugs in combination, excessive fluid intake and other underlying conditions that limit free water excretion increase the risk. Drug-induced SIADH usually resolves following cessation of the offending agent(s). Additional measures are required in patients with symptomatic hyponatraemia, including fluid restriction and intravenous sodium chloride and/or furosemide (frusemide) therapy. Careful monitoring is essential, with particular attention paid to the rate and extent of correction of the hyponatraemia.

Aged↗
PubMed1997

Nitric oxide- and superoxide-mediated toxicity in cerebral endothelial cells.

Nitric oxide and superoxide are free radicals that appear to contribute to the pathogenesis of a number of brain disorders, and cerebral endothelial cells are a potential target of these agents. Because of the capacity for these two agents to combine, it has been suggested that nitric oxide might either enhance or inhibit the toxic effects of superoxide. To establish the effect of the generation of superoxide and nitric oxide alone and in combination, cerebral endothelial cells were exposed to sodium nitroprusside, a source of nitric oxide, and/or paraquat, a source of superoxide. Paraquat enhanced the toxicity of sodium nitroprusside, as did diethyldithiocarbamate, an inhibitor of superoxide dismutase, which supports the hypothesis that enhanced levels of superoxide can combine with nitric oxide to form a more toxic product. Also, the toxicity of paraquat could be partially inhibited by blocking endogenous nitric oxide synthesis using N(G)-monomethyl-L-arginine. When ascorbate was administered along with sodium nitroprusside to increase nitric oxide generation, as little as 5 microM sodium nitroprusside was toxic when superoxide dismutase was inhibited. Whereas concentrations of 50 to 500 microM sodium nitroprusside and 0.4 mM ascorbate caused approximately 100% toxicity, there was no measurable toxicity when these doses were accompanied by 2 mM glutathione or 50 U/ml of catalase; this suggests that peroxides may also contribute to nitric oxide toxicity. These results suggest that the simultaneous generation of nitric oxide and superoxide is synergistic, resulting in enhanced toxicity.

Animals↗
PubMed1997

Trends in hospitalizations and mortality due to medicinal or non-medicinal poisonings in Hong Kong.

Previous epidemiologic studies of poisonings in Hong Kong are regional hospital-or poison information center-based and have focused on either adults or children. This paper reports on the territory-wide hospitalization and mortality rates, comparing medicinal and non-medicinal poisonings in the general population. Between 1980 and 1995, the figures for hospitalizations and mortality due to medicinal (ICD codes 960-977) or non-medicinal (ICD codes 980-989) poisonings were obtained from the Annual Reports of the Department of Health, Hong Kong Government. Rates of medicinal poisonings increased between 1980/81 (57.3/100,000) and 1987/88 (80.9/100,000), but then declined (59.1/100,000) in 1993/94. Rates of non-medicinal poisonings were rather static (49-53/100,000) between 1980/81 and 1988/89, but then declined (22.0/100,000) in 1994/95. Between 1980/81 and 1988/89, rates of fatal medicinal poisonings (0.73-1.31/100,000) were similar to those of fatal non-medicinal poisonings (0.98-1.70/100,000). However, from 1989/90, there was an increase in the rates of fatal medicinal poisonings (1.94-2.80/100,000), although rates for non-medicinal poisonings remained much the same (0.80-1.38/100,000). Hospitalizations due to poisonings are now less common in Hong Kong than before, due largely to a greater decline in non-medicinal poisonings.

Adult↗
PubMed1996

Protection of astrocytes by fructose 1,6-bisphosphate and citrate ameliorates neuronal injury under hypoxic conditions.

Fructose 1,6-bisphosphate (FBP) protects astrocytes from hypoxic injury in vitro. To determine whether FBP and citrate (inhibitors of phosphofructokinase) ameliorate hypoxia-induced injury to neurons and, if they do, whether the protective effects are a direct result of their actions on neurons or a consequence of their actions on astrocytes, we added FBP or citrate to the media of normoxic and hypoxic 'pure', mixed and co-culture systems. FBP (3.5 mM) and citrate (10 microM-2 mM) decreased release of LDH from astrocytes following 24 h of hypoxia. Eight hours of hypoxia killed pure neuronal cultures and neither FBP nor citrate prevented this death. However, in mixed and co-culture systems, FBP and citrate increased neuronal viability (as determined by the ratio of live-to-total cells), even after 47 h of hypoxia. In co-culture, following 24 h of hypoxia, both FBP and citrate reduced neuronal release of LDH and neuronal death. Fluorocitrate, a suicidal-inhibitor of aconitase, also protected astrocytes, but not neurons, from hypoxia in 'pure' culture, presumably by increasing intracellular citrate concentrations through inhibition of the catalysis of citrate to isocitrate We conclude that FBP and citrate attenuate hypoxic neuronal injury through their effects on astrocytes.

Animals↗
PubMed1996

Aminopyrine-induced blood dyscrasias--still a problem in many parts of the world.

The aminopyrines were introduced about a century ago as analgesics and antipyretics, but it was not until the 1930s that agranulocytosis, their major adverse reaction, was recognized. In patients receiving aminopyrines, although agranulocytosis is the most frequent blood dyscrasia, aplastic anaemia has also been reported. For these reasons, these drugs have been banned or withdrawn from the market in most industrialized countries. However, aminopyrines are still available in many parts of the world, including the Far East, Africa and Latin and South America and can be found as adulterants in some 'herbal' patent preparations. Their continuing availability in the Far East may have contributed in part to the higher incidence of aplastic anaemia, compared with the West.

Journal Article↗
PubMed1996

Oxygen deprivation but not a combination of oxygen, glucose, and serum deprivation induces DNA degradation in mouse cortical neurons in vitro: attenuation by transgenic overexpression of CuZn-superoxide dismutase.

The present work was designed to study the possible implication of apoptosis in ischemic neuronal death, a phenomenon that has been suggested to be involved in neurodegeneration following focal as well as global ischemia. In this study, mouse cortical neurons in primary culture were subjected to oxygen deprivation or oxygen, glucose, and serum deprivation to simulate hypoxia and "ischemia-like" conditions; also, cellular viability as well as DNA degradation were investigated. The results showed that DNA degradation occurred in neurons subjected to oxygen deprivation but not to oxygen and substrate deprivation together. This DNA degradation, resulting in a laddering by agarose gel electrophoresis, could be prevented by cycloheximide and actinomycin-D treatments, although these inhibitors were unable to reduce neuronal death. To investigate if DNA degradation could be elicited by an intracellular free radical generation during reoxygenation, transgenic neurons overexpressing copper-zinc superoxide dismutase were subjected to 9 h of oxygen deprivation and analyzed after 24 h of reoxygenation. The results showed a significant attenuation of DNA degradation in these cells and confirmed a possible relationship between reactive oxygen species and neuronal apoptosis. This study opens the way to further investigations regarding the involvement of an apoptotic process in necrotic neuronal death, and provides some new insights into the mechanisms underlying selective sensitivity of neuronal cells to oxygen and glucose deprivation.

Animals↗
PubMed1996

Factors determining the maintenance dose of warfarin in Chinese patients.

Chinese patients are reportedly more sensitive than Caucasians to the anticoagulant effect of warfarin. We examined warfarin dose requirements and their determinants in 151 Chinese out-patients on stable maintenance dose of warfarin with international normalized ratio of 2 to 2.5. Mean daily warfarin requirement was 3.3 +/- 1.4 mg, much lower than reported doses in Caucasian patients. The most important determinant was age (r = -0.43, p < 0.001), with progressively lower warfarin requirement with increasing age (p = 0.0001). There was a weaker association with body weight (r = 0.20, p = 0.01). Patients with chronic rheumatic heart disease tended to require a smaller dose than those with heart valve replacements (2.94 +/- 1.24 vs. 3.69 +/- 1.42 mg, p < 0.01). We confirm that Chinese patients require a smaller dose of warfarin for the same degree of anticoagulation. Age is the most important factor affecting dose requirement, although body weight and underlying disease also play a role.

Adult↗
PubMed1996

The needs and sources of drug information among pharmacists in Hong Kong.

The objective of this study was to determine the drug information needs of pharmacists in Hong Kong, the sources of drug information available and the constraints limiting their ability to fulfil drug information needs at practice sites. A questionnaire survey was carried out in January 1995 of community (230 retail pharmacies, 10 outpatient clinics) and 44 hospital pharmacists working in Hong Kong. The information sought included: place of practice, availability of reference texts, journals or periodicals at practice sites, types of clinical pharmacy services provided, frequency and types of drug information questions received, sources of drug information used, needs for a drug information service, and constraints limiting their ability to fulfil drug information needs at practice sites. Ninety-four pharmacists (hospital 68.2%, community 26.6%) responded. Hospital pharmacists generally had more reference texts and journals/periodicals at practice sites than community pharmacists. The majority of pharmacists in this survey were involved in a variety of clinical pharmacy services, including the delivery of drug information to other health-care professionals and the general public. Community pharmacists were most often asked questions about over-the-counter drugs, drug dosage and drug identification. Hospital pharmacists were most often asked questions about drug identification and availability of drugs. The most important drug information sources for both the community and hospital pharmacists were their own knowledge and work-place reference texts. Few pharmacists frequently used the service provided by the national Drug and Poisons Information Bureau (DPIB). The scarcity of drug information sources was perceived as an important constraint by both community and hospital pharmacists when fulfilling drug information needs at practice sites. Lack of time was considered an equally important constraint by the hospital pharmacists. A national drug information service was generally felt to be necessary. In conclusion, inadequacy in drug information sources was perceived to be a very important constraint limiting the pharmacists surveyed in fulfilling drug information needs at their individual practice sites. However, many were unaware that the drug information requested was already available. Regular attempts to publicize this territory-wide DPIB are obviously needed.

Community Pharmacy Services↗
PubMed1996

Urinary dopamine and noradrenaline outputs during oral salt loading in healthy Chinese subjects with a family history of hypertension.

1. Increased salt sensitivity has been reported in first-degree relatives of hypertensive patients. To determine if the enhanced effect of oral salt intake on blood pressure in such individuals is related to abnormal renal dopamine (DA) or sympathetic nervous system responses, we studied the effects of two different sodium intakes (20 mmol/day followed by 220 mmol/day each given for 5 days) on mean arterial pressure (MAP) and urinary excretion of sodium, free DA and noradrenaline (NA) in seven normotensive Chinese subjects with a family history of hypertension. We compared these results with those we have reported previously for normotensive subjects without a family history of hypertension. 2. There was a seven- to ten-fold increase in sodium excretion (P < 0.02). MAP increased from 80.1 +/- 2.5 to 83.1 +/- 2.1 mmHg (P < 0.05). A 23% increase in urine DA (P < 0.02) was seen on day 1. From day 2 to day 5, the increase in urine DA (12-15%) became attenuated and reached statistical significance only on days 2 and 5. There was no significant change in urinary NA output. 3. As in healthy Chinese subjects without a family history of hypertension, those with a family history showed an early but unsustained rise in urine DA during oral sodium loading. Such an increase was rather small compared to the increase in urine sodium, suggesting that renal DA only contributes partly to the natriuretic response. Unlike those with no family history, subjects with a family history showed an increase in blood pressure after oral salt loading, possibly because of inadequate suppression of sympathetic nervous system activity.

Adult↗