Yet Hoi Hong

Medication Errors in the Southeast Asian Countries: A Systematic Review.

Background Medication error (ME) is a worldwide issue, but most studies on ME have been undertaken in developed countries and very little is known about ME in Southeast Asian countries. This study aimed systematically to identify and review research done on ME in Southeast Asian countries in order to identify common types of ME and estimate its prevalence in this region. Methods The literature relating to MEs in Southeast Asian countries was systematically reviewed in December 2014 by using; Embase, Medline, Pubmed, ProQuest Central and the CINAHL. Inclusion criteria were studies (in any languages) that investigated the incidence and the contributing factors of ME in patients of all ages. Results The 17 included studies reported data from six of the eleven Southeast Asian countries: five studies in Singapore, four in Malaysia, three in Thailand, three in Vietnam, one in the Philippines and one in Indonesia. There was no data on MEs in Brunei, Laos, Cambodia, Myanmar and Timor. Of the seventeen included studies, eleven measured administration errors, four focused on prescribing errors, three were done on preparation errors, three on dispensing errors and two on transcribing errors. There was only one study of reconciliation error. Three studies were interventional. Discussion The most frequently reported types of administration error were incorrect time, omission error and incorrect dose. Staff shortages, and hence heavy workload for nurses, doctor/nurse distraction, and misinterpretation of the prescription/medication chart, were identified as contributing factors of ME. There is a serious lack of studies on this topic in this region which needs to be addressed if the issue of ME is to be fully understood and addressed.

Role of nitric oxide in skeletal muscle glucose uptake during exercise

What is the topic of this review? Is nitric oxide (NO) important in mediating skeletal muscle glucose uptake during contraction/exercise? What advances does it highlight? Nitric oxide appears essential for skeletal muscle glucose uptake during contraction/exercise.

Glucose uptake during contraction in isolated skeletal muscles from neuronal nitric oxide synthase μ knockout mice

Inhibition of nitric oxide synthase (NOS) significantly attenuates the increase in skeletal muscle glucose uptake during contraction/exercise, and a greater attenuation is observed in individuals with Type 2 diabetes compared with healthy individuals. Therefore, NO appears to play an important role in mediating muscle glucose uptake during contraction. In this study, we investigated the involvement of neuronal NOSμ (nNOSμ), the main NOS isoform activated during contraction, on skeletal muscle glucose uptake during ex vivo contraction. Extensor digitorum longus muscles were isolated from nNOSμ(-/-) and nNOSμ(+/+) mice. Muscles were contracted ex vivo in a temperature-controlled (30°C) organ bath with or without the presence of the NOS inhibitor N(G)-monomethyl-l-arginine (L-NMMA) and the NOS substrate L-arginine. Glucose uptake was determined by radioactive tracers. Skeletal muscle glucose uptake increased approximately fourfold during contraction in muscles from both nNOSμ(-/-) and nNOSμ(+/+) mice. L-NMMA significantly attenuated the increase in muscle glucose uptake during contraction in both genotypes. This attenuation was reversed by L-arginine, suggesting that L-NMMA attenuated the increase in muscle glucose uptake during contraction by inhibiting NOS and not via a nonspecific effect of the inhibitor. Low levels of NOS activity (~4%) were detected in muscles from nNOSμ(-/-) mice, and there was no evidence of compensation from other NOS isoform or AMP-activated protein kinase which is also involved in mediating muscle glucose uptake during contraction. These results indicate that NO regulates skeletal muscle glucose uptake during ex vivo contraction independently of nNOSμ.

No effect of NOS inhibition on skeletal muscle glucose uptake during in situ hindlimb contraction in healthy and diabetic Sprague-Dawley rats.

Nitric oxide (NO) has been shown to be involved in skeletal muscle glucose uptake during contraction/exercise, especially in individuals with Type 2 diabetes (T2D). To examine the potential mechanisms, we examined the effect of local NO synthase (NOS) inhibition on muscle glucose uptake and muscle capillary blood flow during contraction in healthy and T2D rats. T2D was induced in Sprague-Dawley rats using a combined high-fat diet (23% fat wt/wt for 4 wk) and low-dose streptozotocin injections (35 mg/kg). Anesthetized animals had one hindlimb stimulated to contract in situ for 30 min (2 Hz, 0.1 ms, 35 V) with the contralateral hindlimb rested. After 10 min, the NOS inhibitor, N(G)-nitro-l-arginine methyl ester (l-NAME; 5 μM) or saline was continuously infused into the femoral artery of the contracting hindlimb until the end of contraction. Surprisingly, there was no increase in skeletal muscle NOS activity during contraction in either group. Local NOS inhibition had no effect on systemic blood pressure or muscle contraction force, but it did cause a significant attenuation of the increase in femoral artery blood flow in control and T2D rats. However, NOS inhibition did not attenuate the increase in muscle capillary recruitment during contraction in these rats. Muscle glucose uptake during contraction was significantly higher in T2D rats compared with controls but, unlike our previous findings in hooded Wistar rats, NOS inhibition had no effect on glucose uptake during contraction. In conclusion, NOS inhibition did not affect muscle glucose uptake during contraction in control or T2D Sprague-Dawley rats, and this may have been because there was no increase in NOS activity during contraction.

Urinary metabolic evaluation of stone formers-a Malaysian perspective

OBJECTIVE To investigate the urinary metabolic excretion pattern among local stone formers given the great differences in the intrinsic and extrinsic risk factors as well as the urinary metabolic excretions compared with other populations. METHODS Thirty urinary stone formers out of an initial 62 recruited provided a complete 24-hour urine sample for metabolic evaluation. Students t-test and Pearson correlation test were used for the statistical analysis. RESULTS Urinary volume (1719 ± 712 vs 1215 ± 575, P < .05) and oxalate excretion (0.386 ± 0.111 vs 0.306 ± 0.104, P < .05) were significantly higher among stone formers than controls. Other commonly studied urinary parameters and urinary melamine did not differ significantly between the 2 groups. Similarly, the calcium/citrate ratio was unable to discriminate the stone formers from their controls. Hypocitraturia was the most prevalent urinary abnormality found in stone formers and low urinary citrate excretion was a general phenomenon in both stone formers and controls. Comparing within the stone formers cohort, the recurrent stone formers had a significantly higher urinary saturation and calcium excretion than their first-time stone former counterparts. CONCLUSION Elevated urinary oxalate level was the most important urinary risk factor among the local stone formers. A low urinary citrate excretion appeared to be a general phenomenon among the studied cohorts.

Glucose-6-phosphate dehydrogenase contributes to the regulation of glucose uptake in skeletal muscle

Objective The development of skeletal muscle insulin resistance is an early physiological defect, yet the intracellular mechanisms accounting for this metabolic defect remained unresolved. Here, we have examined the role of glucose-6-phosphate dehydrogenase (G6PDH) activity in the pathogenesis of insulin resistance in skeletal muscle. Methods Multiple mouse disease states exhibiting insulin resistance and glucose intolerance, as well as obese humans defined as insulin-sensitive, insulin-resistant, or pre-diabetic, were examined. Results We identified increased glucose-6-phosphate dehydrogenase (G6PDH) activity as a common intracellular adaptation that occurs in parallel with the induction of insulin resistance in skeletal muscle and is present across animal and human disease states with an underlying pathology of insulin resistance and glucose intolerance. We observed an inverse association between G6PDH activity and nitric oxide synthase (NOS) activity and show that increasing NOS activity via the skeletal muscle specific neuronal (n)NOSμ partially suppresses G6PDH activity in skeletal muscle cells. Furthermore, attenuation of G6PDH activity in skeletal muscle cells via (a) increased nNOSμ/NOS activity, (b) pharmacological G6PDH inhibition, or (c) genetic G6PDH inhibition increases insulin-independent glucose uptake. Conclusions We have identified a novel, previously unrecognized role for G6PDH in the regulation of skeletal muscle glucose metabolism.

Skeletal muscle glucose uptake during treadmill exercise in neuronal nitric oxide synthase-μ knockout mice

Nitric oxide influences intramuscular signaling that affects skeletal muscle glucose uptake during exercise. The role of the main NO-producing enzyme isoform activated during skeletal muscle contraction, neuronal nitric oxide synthase-μ (nNOSμ), in modulating glucose uptake has not been investigated in a physiological exercise model. In this study, conscious and unrestrained chronically catheterized nNOSμ(+/+) and nNOSμ(-/-) mice either remained at rest or ran on a treadmill at 17 m/min for 30 min. Both groups of mice demonstrated similar exercise capacity during a maximal exercise test to exhaustion (17.7 ± 0.6 vs. 15.9 ± 0.9 min for nNOSμ(+/+) and nNOSμ(-/-), respectively, P > 0.05). Resting and exercise blood glucose levels were comparable between the genotypes. Very low levels of NOS activity were detected in skeletal muscle from nNOSμ(-/-) mice, and exercise increased NOS activity only in nNOSμ(+/+) mice (4.4 ± 0.3 to 5.2 ± 0.4 pmol·mg(-1)·min(-1), P < 0.05). Exercise significantly increased glucose uptake in gastrocnemius muscle (5- to 7-fold) and, surprisingly, more so in nNOSμ(-/-) than in nNOSμ(+/+) mice (P < 0.05). This is in parallel with a greater increase in AMPK phosphorylation during exercise in nNOSμ(-/-) mice. In conclusion, nNOSμ is not essential for skeletal muscle glucose uptake during exercise, and the higher skeletal muscle glucose uptake during exercise in nNOSμ(-/-) mice may be due to compensatory increases in AMPK activation.

Acute exercise increases insulin sensitivity in adult sheep: a new preclinical model

In healthy humans and rodents, chronic and acute exercise improves subsequent insulin sensitivity of skeletal muscle. A large animal species with similar metabolic responses to exercise would permit longitudinal studies, including repeated biopsies of muscle and other tissues not possible in rodents, and enable study of interactions with insulin-resistant physiological states not feasible in humans. Therefore, we examined whether acute exercise increases insulin sensitivity in adult sheep. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp (HEC) in mature female sheep (n = 7). Sheep were familiarized to treadmill walking and then performed an acute exercise bout (30 min, 8% slope, up to 4.4 km/h). A second HEC was conducted ∼18 h after the acute exercise. Musculus semimembranosus biopsies were obtained before and after each HEC. Glucose infusion rate during the HEC increased 40% (P = 0.003) and insulin sensitivity (glucose infusion rate/plasma insulin concentration) increased 32% (P = 0.028) after acute exercise. Activation of proximal insulin signaling in skeletal muscle after the HEC, measured as Ser(473) phosphorylation of Akt, increased approximately five-fold in response to insulin (P < 0.001) and was unaltered by acute exercise performed 18 h earlier. PGC1α and GLUT4 protein, glycogen content and citrate synthase activity in skeletal muscle did not change in response to insulin or exercise. In conclusion, improved insulin sensitivity and unchanged proximal insulin signaling on the day after acute exercise in sheep are consistent with responses in humans and rodents, suggesting that the sheep is an appropriate large-animal model in which to study responses to exercise.

Self-Care and Self-Management Among Adolescent T2DM Patients: A Review

Uncontrolled hyperglycaemia can lead to macro- and microvascular complications. Adolescents with T2DM develop similar complications as in adults, including cardiovascular disease, stroke, myocardial infarction, renal insufficiency, and chronic renal failure. Although regular medical follow-up is essential to avoid long-term complications, patients with diabetes mellitus need to perform holistic self-care activities such as opting for a healthy diet, physical activity, self-monitoring, and proper medication. To the best of our knowledge, only a limited number of studies have focused on self-care activities and self-management, including self-care practices, supportive networks, and self-care education programs in adolescent with T2DM. Some of the studies focused on the appreciation of self-care in adolescents with T2DM. This review aimed to analyse self-care and self-management among adolescents with T2DM, and discuss the impact of self-care and self-management on glycaemic control. The difficulties faced by adolescents in self-managing their disease are also highlighted. Such information is essential for healthcare providers in promoting self-care practices among adolescents with T2DM. A thorough search of the literature was performed using three databases: Medline, Google Scholar, and Scopus. The articles focused on self-care and self-management of adolescents patients with T2DM aged between 12 and 19 years old were included. Findings from this review reveal that healthy food adaptation, adequate physical activity, proper medication practices, and regular glucose monitoring are the most common self-care practices. Parental involvement and clinician encouragement also contribute toward the practice of self-care and self-management among the adolescents with T2DM. In conclusion, independent self-management regimens and supportive networks for appropriate administration are vital factors to enhance clinical outcomes of adolescents with T2DM.

Knowledge on Alzheimer's disease among public hospitals and health clinics pharmacists in the State of Selangor, Malaysia

The prevalence of Alzheimers disease (AD) has increased with the fast growing of aging population, thereby posing great challenges to provision of care for AD patients. Pharmacists play a vital role in the management of AD; this includes recognizing early symptoms of AD, providing medication counseling to AD patients and their caretakers, and identifying potential adverse drug reactions. A comprehensive understanding of the disease progression, as well as the pharmacological therapy, is essential to provide effective care to AD patients. The level of knowledge about AD among the pharmacists, however, remains unknown. Hence, this study aimed to assess the knowledge on AD among the pharmacists in public hospitals and health clinics and its correlates. A clear picture of the characteristics associated with different levels of knowledge could facilitate the targeted re-training of pharmacists. The 30-item validated Alzheimer disease knowledge scale (ADKS) tool was pilot-tested and used in this cross-sectional study. All pharmacists, from nine public hospitals and seven public health clinics in the State of Selangor, Malaysia, were invited to participate in this cross-sectional survey. The ADKS score was computed and compared across demographics characteristics. A total of 445 pharmacists responded to the survey. These pharmacists had a moderate overall score in ADKS; nevertheless, high scores were recorded in the domains of treatment management and care giving. No difference in AD knowledge was found among pharmacists worked in public hospitals and health clinics, except for the domain of care giving (p = 0.033). Ethnicity and age group were independent predictors of ADKS score in the current study. The pharmacists in the current study had moderate AD knowledge. On-going education and training programme on AD, in particular the domains other than treatment management and care giving, should be provided to the pharmacists to ensure delivery of quality care to AD patients.