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  1. Chua CT, Wang F
    Med J Malaysia, 1983 Sep;38(3):244-50.
    PMID: 6672569
    Study site: CAPD, University Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
    Matched MeSH terms: Potassium/blood
  2. Singh HJ, Mohammad NH, Nila A
    J Matern Fetal Med, 1999 May-Jun;8(3):95-100.
    PMID: 10338062
    To ascertain the calcium status in normal pregnant Malay women.
    Matched MeSH terms: Potassium/blood
  3. Hawkins RC
    Clin Chem Lab Med, 2010;48(1):105-8.
    PMID: 19929751 DOI: 10.1515/CCLM.2010.010
    It has been suggested that potassium concentrations may vary between different geographical regions, possibly reflecting ethnic differences in potassium status. This study compared the serum potassium concentrations of three Asian ethnicities in a single geographical location.
    Matched MeSH terms: Potassium/blood*
  4. Khan S, Khan SU
    J Clin Pharm Ther, 2020 Oct;45(5):927-936.
    PMID: 32672366 DOI: 10.1111/jcpt.13204
    WHAT IS KNOWN AND OBJECTIVE: The imbalance in serum potassium caused by laxatives can negatively affect the cardiovascular system, leading to life-threatening consequences. Our objective was to evaluate the reported evidence of adverse events related to the cardiac system due to laxative-induced hypokalaemia from case reports.

    METHODS: A systematic electronic literature search of PubMed, Embase, the Cochrane Library and Science Direct was conducted for the period 1995-2019. In these databases, search terms describing hypokalaemia and cardiotoxicity were combined with the term laxative use.

    RESULTS AND DISCUSSION: Over the 23 years, 27 incidents were identified in 12 countries. There were 19 female and eight male patients, with ages ranging from 1 month to 93 years. The frequency of reported cases according to severity was the following: severe hypokalaemia 48%, moderate hypokalaemia 44.4% and mild hypokalaemia 7.4%. In 70% of patients, the effect of laxative on the heart was typical hypokalaemic electrographic changes, 7.4% showed abnormal changes in cardiac rhythm, whereas in 18.5%, the cardiotoxicity observed was a very serious kind. Two patients died due to severe cardiac effects.

    WHAT IS NEW AND CONCLUSION: The laxatives-along with the involvement of some other contributing factors-caused mild-to-severe hypokalaemic cardiotoxicity. These factors were non-adherence of the patient to the recommended dosage, laxative abuse, drug-drug and drug-disease interactions, non-potassium electrolyte imbalances and the use of herbal laxatives. We recommend that laxatives and aggravating factors should be taken into account in the assessment of patients with suspected hypokalaemic cardiotoxicity.

    Matched MeSH terms: Potassium/blood
  5. Reddy SV, Sein K
    Singapore Med J, 1991 Feb;32(1):29-30.
    PMID: 2017701
    Sixty patients who received massive blood transfusion intraoperatively and/or in the immediate post-operative period were analysed. Six patients had hypokalemia and two had hyperkalemia. The multifactorial changes leading to electrolyte disturbances especially involving potassium are discussed in relation to hypotension, hypothermia, acidosis, pH, and release of catecholamine. Potassium changes in relation to anaesthesia are discussed. The danger of routine administration of calcium during massive blood transfusion is stressed.
    Matched MeSH terms: Potassium/blood*
  6. Zyoud SH, Awang R, Sulaiman SA, Al-Jabi SW
    Pharmacoepidemiol Drug Saf, 2011 Feb;20(2):203-8.
    PMID: 21254292 DOI: 10.1002/pds.2060
    Acetaminophen overdose may be accompanied by electrolyte disturbances. The basis for electrolyte change appears to be due to increased fractional urinary electrolyte excretion.
    Matched MeSH terms: Potassium/blood*
  7. Asmah BJ, Wan Nazaimoon WM, Norazmi K, Tan TT, Khalid BA
    Horm. Metab. Res., 1997 Nov;29(11):580-3.
    PMID: 9479560 DOI: 10.1055/s-2007-979105
    The effect of thyroid hormones on the renin-angiotensin-aldosterone system has not been fully resolved. Highly specific immunoassays for measurement of renin, aldosterone, free T4 (fT4), free T3 (fT3) and ultrasensitive TSH enables a direct and more accurate measurement of these hormones. We investigated the relationship between plasma renin, aldosterone and thyroid hormones in the basal state and after intravenous frusemide. This is a cross-sectional study involving 37 patients with thyrotoxicosis, 42 rendered euthyroid with normal fT4, fT3 and TSH levels, 17 with euthyroid levels of fT4 and fT3 but suppressed TSH, and 11 with hypothyroidism. Basal plasma renin was significantly higher in thyrotoxicosis (63.4 +/- 9.8 microU/ml, mean +/- SEM) compared to euthyroid (32.7 +/- 4.4 microU/ml) and hypothyroid (26.7 +/- 9.8 microU/ml). Basal plasma renin for euthyroid with suppressed TSH (41.0 +/- 7.4 microU/ml) was significantly higher than hypothyroid (p = 0.02). Basal plasma aldosterones were not significantly different except for suppressed TSH (157.7 +/- 13 pg/ml), which was higher than normal (109.9 +/- 10.4 pg/ml; p = 0.04). Following frusemide, plasma renin and aldosterone were significantly increased in all groups. Plasma renin was highly correlated to fT3 (r = 0.405, p < 0.001), total T3 (r = 0.359, p < 0.001), fT4 (r = 0.331, p < 0.001) and TSH (r = 0.300, p < 0.001) in the basal state, but less to total T4 (r = 0.248, p < 0.01). Plasma renin correlated poorly to serum aldosterone (r = 0.212, p < 0.03). This study clearly showed that regulation of renin was mainly influenced by fT3, and that aldosterone response to frusemide was blunted in thyrotoxicosis despite normal electrolytes.
    Matched MeSH terms: Potassium/blood
  8. Reid HA
    Lancet, 1975 Mar 15;1(7907):622-3.
    PMID: 47960
    Among a series of 101 patients bitten by sea-snakes in Malaya in the years 1957-64, 80% were fishermen. Bathers and divers are occasionally bitten. Before sea-snake antivenom became available the mortality-rate (despite the high toxicity of sea-snake venom) was only 10%; however, of 11 with serious poisoning, 6 died. Subsequently 10 patients with serious poisoning received specific sea-snake antivenom; 2 patients, admitted moribund, temporarily improved but died, and 8 patients recovered dramatically. In serious poisoning the suitable dosage of intravenous sea-snake antivenom is 3000-10,000 units; in mild poisoning 1000-2000 units should suffice.
    Matched MeSH terms: Potassium/blood
  9. Ruszymah BH, Nabishah BM, Aminuddin S, Khalid BA
    Clin Exp Hypertens, 1995 Apr;17(3):575-91.
    PMID: 7613529
    Glycyrrhizic acid (GCA) the active component of liquorice acts by inhibiting 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) which catalyses the reversible conversion of cortisol to cortisone. The aim of this study was to examine the effect of GCA on pulmonary arterial pressure. Male Sprague-Dawley rats (200g) received drinking water containing 0.1 mg/ml and 1.0 mg/ml GCA for 12 weeks. Tail blood pressure (BP) was recorded every three weeks and serum Na+ and K+ were measured at the beginning and the end of the experiment. Right atrial pressure (RAP) were measured at the end of 12 weeks just before the animals were sacrificed. Lung tissues were taken for histological examination using the elastic-van Gieson (EVG) staining method. There was a significant increase in tail BP in GCA treated rats compared to controls, for both dosages used. This was associated with an increase in serum Na+ and a decrease in K+ level. The mean RAP increased significantly from 2.69 +/- 0.23 mmHg to 4.47 +/- 0.32 mmHg (P < 0.001) in 0.1 mg/ml GCA treated rats and 6.86 +/- 0.54 mmHg (P < 0.0001) in rats receiving 1.0 mg/ml GCA in their drinking water. Histological examination showed increased thickness of pulmonary arterial wall (P < 0.0001). In conclusion GCA caused an increase in right atrial pressure as well as thickening of the pulmonary vessels suggesting pulmonary hypertension.
    Matched MeSH terms: Potassium/blood
  10. Sasongko TH, Nagalla S, Ballas SK
    PMID: 26041152 DOI: 10.1002/14651858.CD009191.pub3
    BACKGROUND: Sickle cell disease is a group of disorders characterized by deformation of erythrocytes. Renal damage is a frequent complication in sickle cell disease as a result of long-standing anemia and disturbed circulation through the renal medullary capillaries. Due to the improvement in life expectancy of people with sickle cell disease, there has been a corresponding significant increase in the incidence of renal complications. Microalbuminuria and proteinuria are noted to be a strong predictor of subsequent renal failure. There is extensive experience and evidence with angiotensin-converting enzyme (ACE) inhibitors over many years in a variety of clinical situations for patients who do not have sickle cell disease, but their effect in people with this disease is unknown. It is common practice to administer ACE inhibitors for sickle nephropathy due to their renoprotective properties; however, little is known about their effectiveness and safety in this setting. This is an update of a Cochrane Review first published in 2013.

    OBJECTIVES: To determine the effectiveness of ACE inhibitor administration in people with sickle cell disease for decreasing intraglomerular pressure, microalbuminuria and proteinuria and to to assess the safety of ACE inhibitors as pertains to their adverse effects.

    SEARCH METHODS: The authors searched the Cochrane Cystic Fibrosis and Genetic Disorders Group's Hameoglobinopathies Trials Register comprising references identified from comprehensive electronic database searches and handsearches of relevant journals and abstract books of conference proceedings.Date of the most recent search: 03 June 2015.

    SELECTION CRITERIA: Randomized or quasi-randomized controlled trials of ACE inhibitors designed to reduce microalbuminuria and proteinuria in people with sickle cell disease compared to either placebo or standard treatment regimen.

    DATA COLLECTION AND ANALYSIS: Three authors independently applied the inclusion criteria in order to select studies for inclusion in the review. Two authors assessed the risk of bias of studies and extracted data and the third author verified these assessments.

    MAIN RESULTS: Five studies were identified through the searches, only one met our inclusion criteria. The included study randomized 22 participants (seven males and 15 females) having proteinuria or microalbuminuria with sickle cell disease and treated the participants for six months (median length of follow up of three months) with captopril or placebo. The overall quality of the outcomes reported was high, since most aspects that may contribute to bias were regarded to be of low risk, although allocation concealment was not reported. At six months, the study reported no significant difference in urinary albumin excretion between the captopril group and the placebo group, although the mean urinary albumin excretion in the captopril group was lower by a mean difference of -49.00 (95% confidence interval -124.10 to 26.10) compared to that of placebo. However, our analysis on the absolute change score showed significant changes between the two groups by a mean difference of -63.00 (95% confidence interval -93.78 to -32.22). At six months albumin excretion in the captopril group was noted to decrease from baseline by a mean of 45 ± 23 mg/day and the placebo group was noted to increase by 18 ± 45 mg/day. Serum creatinine and potassium levels were reported constant throughout the study. The potential for inducing hypotension should be highlighted; the study reported a decrease of 8 mmHg in systolic pressure and 5 mmHg in diastolic and mean blood pressure.

    AUTHORS' CONCLUSIONS: There is not enough evidence to show that the administration of ACE inhibitors is associated with a reduction of microalbuminuria and proteinuria in people with sickle cell disease, although a potential for this was seen. More long-term studies involving multiple centers and larger cohorts using a randomized-controlled design are warranted, especially among the pediatric age group. Detailed reporting of each outcome measure is necessary to allow a clear cut interpretation in a systematic review. One of the difficulties encountered in this review was the lack of detailed data reported in the included study.

    Matched MeSH terms: Potassium/blood
  11. Hanip MR, Cheong IK, Chin GL, Khalid BA
    Singapore Med J, 1990 Apr;31(2):159-61.
    PMID: 2371581
    Two cases of hypokalaemia with serum potassium levels of 1.4 mmol/L and 1.9 mmol/L causing severe periodic paralysis since childhood are presented. There were associated with muscular aches and markedly raised muscle enzymes suggesting massive rhabdomyolysis. These abnormalities were due to renal tubular acidosis with markedly acidic arterial pH. The hypokalaemia and rhabdomyolysis responded to potassium and bicarbonate replacement. We postulate these patients had sporadic distal type of renal tubular acidosis and that the hypokalaemia and acidosis had caused the rhabdomyolysis.
    Matched MeSH terms: Potassium/blood
  12. Loh KC, Koay ES, Khaw MC, Emmanuel SC, Young WF
    J Clin Endocrinol Metab, 2000 Aug;85(8):2854-9.
    PMID: 10946893
    Recent studies using the ratio of plasma aldosterone concentration (PAC) to PRA as the screening test for primary aldosteronism in hypertensive populations suggested that the prevalence may be as high as 5-15%, with well over half of the subjects having normal serum potassium concentrations. Despite an increasing clinical awareness of this entity, many clinicians are reluctant to consider routine screening for primary aldosteronism in essential hypertensive patients because there are few community-based prevalence studies of primary aldosteronism in different populations. Furthermore, genetic and environmental differences may affect the prevalence and presentation of primary aldosteronism in distinct populations. This study was designed to determine the prevalence of primary aldosteronism in the predominantly Chinese population in Singapore. Three hundred and fifty unselected adult hypertensive patients attending two primary care clinics had random ambulatory measurements for PAC (nanograms per dL) and PRA (nanograms per mL/h). Serum urea, creatinine, and electrolyte measurements were obtained simultaneously. Subjects with renal insufficiency (serum creatinine, >140 micromol/L) and those treated with glucocorticoids or spironolactone were excluded. Screening was considered positive if the PAC: PRA ratio was more than 20 and the PAC was more than 15 ng/dL (>416 pmol/L). Primary aldosteronism was confirmed with the determination of PAC after 2 L saline administered iv over 4 h. Adrenal computed tomographic (CT) scans were performed in biochemically confirmed cases of primary aldosteronism. Further localization with adrenal vein sampling was carried out in selected patients with equivocal findings on adrenal CT scan. Sixty-three (18%) of the 350 hypertensive patients (215 women and 135 men; age range, 23-75 yr) were screened positive for primary aldosteronism. Only 13 of these 63 subjects (21%) were hypokalemic (serum potassium, <3.5 mmol/L). Confirmatory studies were carried out in 56 (89%) of the subjects with a positive PAC:PRA ratio. Using a PAC above 10 ng/dL (>277 pmol/L) after saline infusion as the diagnostic cut-off, 16 of the 56 patients had biochemically confirmed primary aldosteronism. Hypokalemia was found in 6 of the 16 patients (37.5%) with primary aldosteronism. Subtype evaluation with adrenal CT scan and adrenal vein sampling indicated that half of the patients with primary aldosteronism may have had potentially curable unilateral adrenal adenoma. Our data suggest that primary aldosteronism occurs in at least 5% of the adult Asian hypertensive population, and approximately half of these individuals may have potentially curable, unilateral, aldosterone-producing adrenal adenoma. Our findings also confirm the poor predictive value of hypokalemia in both the diagnosis and the exclusion of primary aldosteronism.
    Matched MeSH terms: Potassium/blood
  13. Ling LL, Chan YM, Mat Daud Z'
    Asia Pac J Clin Nutr, 2019;28(2):401-410.
    PMID: 31192570 DOI: 10.6133/apjcn.201906_28(2).0023
    BACKGROUND AND OBJECTIVES: Poor sleep quality is prevalent among hemodialysis (HD) patients and leads to adverse health outcomes. This study investigated the association of nutritional parameters with sleep quality among Malaysian HD patients.

    METHODS AND STUDY DESIGN: A cross-sectional study was conducted among 184 Malaysian HD patients. Anthropometric measurements and handgrip strength (HGS) were obtained using standardized protocols. Relevant biochemical indicators were retrieved from patients' medical records. Nutritional status was assessed using the dialysis malnutrition score. The sleep quality of patients was determined using the Pittsburgh Sleep Quality Index questionnaire on both dialysis and non-dialysis days.

    RESULTS: Slightly more than half of the HD patients were poor sleepers, with approximately two-third of them having a sleep duration of <7 hours per day. Sleep latency (1.5±1.2) had the highest sleep component score, whereas sleep medicine use (0.1±0.6) had the lowest score. Significantly longer sleep latency and shorter sleep duration were observed in the poor sleepers, regardless of whether it was a dialysis day or not (p<0.001). Poor sleep quality was associated with male sex, old age, small triceps skinfold, hypoproteinemia, hyperkalemia, hyperphosphatemia, and poorer nutritional status. In a multivariate analysis model, serum potassium (β=1.41, p=0.010), male sex (β=2.15, p=0.003), and HGS (β=-0.088, p=0.021) were found as independent predictors of sleep quality.

    CONCLUSIONS: Poor sleep quality was evident among the HD patients in Malaysia. The sleep quality of the HD patients was associated with nutritional parameters. Routine assessment of sleep quality and nutritional parameters indicated that poor sleepers have a risk of malnutrition and may benefit from appropriate interventions.

    Matched MeSH terms: Potassium/blood*
  14. Iqbal MO, Yahya EB
    Tissue Cell, 2021 Oct;72:101525.
    PMID: 33780659 DOI: 10.1016/j.tice.2021.101525
    Aminoglycoside antibiotics are widely employed clinically due to their powerful bactericidal activities, less bacterial resistance compared to beta lactam group and low cost. However, their use has been limited in recent years due to their potential induction of nephrotoxicity. Here we investigate the possibility of reversing nephrotoxicity caused by gentamicin in rat models by using ethanolic crude extract of the medicinal plant Jatropha Mollissima. Nephrotoxic male Wistar rats was obtained by gentamicin antibiotic, which then treated with two doses of J. mollissima crude extract for 3 weeks with monitoring their parameter in weekly base. Our results indicate that J. mollissima crude extract at both doses has strong protection ability against gentamicin nephrotoxicity, most of tested parameters backed to normal values after few days from the administration of the crude extract, which could be due to the antagonized the biochemical action of gentamicin on the proximal tubules of the kidney. The results of histopathologic analysis showed observable improvement in J. mollissima treated groups compared with untreated groups. Our findings suggests the J. mollissima has exceptional nephron protection potentials able to reverse the nephrotoxicity caused by gentamicin antibiotic.
    Matched MeSH terms: Potassium/blood
  15. Kamarul T, Krishnamurithy G, Salih ND, Ibrahim NS, Raghavendran HR, Suhaeb AR, et al.
    ScientificWorldJournal, 2014;2014:905103.
    PMID: 25298970 DOI: 10.1155/2014/905103
    The in vivo biocompatibility and toxicity of PVA/NOCC scaffold were tested by comparing them with those of a biocompatible inert material HAM in a rat model. On Day 5, changes in the blood parameters of the PVA/NOCC-implanted rats were significantly higher than those of the control. The levels of potassium, creatinine, total protein, A/G, hemoglobulin, erythrocytes, WBC, and platelets were not significantly altered in the HAM-implanted rats, when compared with those in the control. On Day 10, an increase in potassium, urea, and GGT levels and a decrease in ALP, platelet, and eosinophil levels were noted in the PVA/NOCC-implanted rats, when compared with control. These changes were almost similar to those noted in the HAM-implanted rats, except for the unaltered potassium and increased neutrophil levels. On Day 15, the total protein, A/G, lymphocyte, monocyte, and eosinophil levels remained unaltered in the PVA/NOCC-implanted rats, whereas urea, A/G, WBC, lymphocyte, and monocyte levels remained unchanged in the HAM-implanted rats. Histology and immunohistochemistry analyses revealed inflammatory infiltration in the PVA/NOCC-implanted rats, but not in the HAM-implanted rats. Although a low toxic tissue response was observed in the PVA/NOCC-implanted rats, further studies are necessary to justify the use of this material in tissue engineering applications.
    Matched MeSH terms: Potassium/blood
  16. Zyoud SH, Awang R, Syed Sulaiman SA, Al-jabi SW
    Hum Exp Toxicol, 2010 Sep;29(9):773-8.
    PMID: 20144962 DOI: 10.1177/0960327110361759
    Hypokalemia is not an isolated disease but an associated finding in a number of different diseases. It is also a commonly neglected condition among patients with acute acetaminophen overdose.
    Matched MeSH terms: Potassium/blood
  17. Zyoud SH, Awang R, Sulaiman SA, Al-Jabi SW
    Pharmacoepidemiol Drug Saf, 2010 May;19(5):511-7.
    PMID: 20333776 DOI: 10.1002/pds.1940
    Acetaminophen poisoning is a common clinical problem, and early identification of patients with more severe poisoning is key to improving outcomes.
    Matched MeSH terms: Potassium/blood
  18. Sattar MA, Yusof AP, Gan EK, Sam TW, Johns EJ
    J Auton Pharmacol, 2001 5 15;20(5-6):297-304.
    PMID: 11350495
    1. This study compared the effect of a non-peptide angiotensin II receptor antagonist and a series of clonidine analogues on blood pressure and renal function in a two-kidney two-clip Goldblatt rat model of hypertension subjected to 2 weeks of dietary sodium deprivation. 2. Animals received either vehicle, the angiotensin II antagonist, ZD7155 or structural analogues derived from clonidine (AL-11, AL-12 and CN-10) at 10 mg kg-1 day-1 for 4 days. 3. All groups of rats had systolic blood pressure in the hypertensive range (160-180 mmHg). ZD7155 caused a 33-mmHg fall in blood pressure (P < 0.05) and raised plasma urea and creatinine four- to six-fold. 4. AL-12 decreased blood pressure by 30 mmHg (P < 0.05), but had no effect on water intake, urine flow or plasma urea and creatinine. AL-11 and CN-10 had minimal effects on blood pressure and water intake and while CN-10 decreased urine flow on the third treatment day, AL-11 markedly reduced urine flow by some 70%. 5. These data show that in this sodium deficient renovascular model of hypertension, blockade of angiotensin II receptors normalizes blood pressure but causes renal failure, whereas the vasodepressor action of the clonidine analogue AL-12 occurs without detriment to renal function. These findings imply that angiotensin II receptor antagonists could lead to renal failure if used as antihypertensive agents in renovascular hypertension whereas this would be avoided with the use of clonidine-like analogues.
    Matched MeSH terms: Potassium/blood
  19. Fernando HA, Chandramouli C, Rosli D, Lam YL, Yong ST, Yaw HP, et al.
    Nutrients, 2014 Nov 04;6(11):4856-71.
    PMID: 25375630 DOI: 10.3390/nu6114856
    Glycyrrhizic acid (GA) ameliorates many components of the metabolic syndrome, but its potential therapeutic use is marred by edema caused by inhibition of renal 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2). We assessed whether 100 mg/kg per day GA administered orally could promote metabolic benefits without causing edema in rats fed on a high-sucrose diet. Groups of eight male rats were fed on one of three diets for 28 days: normal diet, a high-sucrose diet, or a high-sucrose diet supplemented with GA. Rats were then culled and renal 11β-HSD2 activity, as well as serum sodium, potassium, angiotensin II and leptin levels were determined. Histological analyses were performed to assess changes in adipocyte size in visceral and subcutaneous depots, as well as hepatic and renal tissue morphology. This dosing paradigm of GA attenuated the increases in serum leptin levels and visceral, but not subcutaneous adipocyte size caused by the high-sucrose diet. Although GA decreased renal 11β-HSD2 activity, it did not affect serum electrolyte or angiotensin II levels, indicating no onset of edema. Furthermore, there were no apparent morphological changes in the liver or kidney, indicating no toxicity. In conclusion, it is possible to reap metabolic benefits of GA without edema using the current dosage and treatment time.
    Matched MeSH terms: Potassium/blood
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