Displaying publications 1 - 20 of 49 in total

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  1. Sahathevan S, Khor BH, Ng HM, Gafor AHA, Mat Daud ZA, Mafra D, et al.
    Nutrients, 2020 Oct 15;12(10).
    PMID: 33076282 DOI: 10.3390/nu12103147
    Hemodialysis (HD) majorly represents the global treatment option for patients with chronic kidney disease stage 5, and, despite advances in dialysis technology, these patients face a high risk of morbidity and mortality from malnutrition. We aimed to provide a novel view that malnutrition susceptibility in the global HD community is either or both of iatrogenic and of non-iatrogenic origins. This categorization of malnutrition origin clearly describes the role of each factor in contributing to malnutrition. Low dialysis adequacy resulting in uremia and metabolic acidosis and dialysis membranes and techniques, which incur greater amino-acid losses, are identified modifiable iatrogenic factors of malnutrition. Dietary inadequacy as per suboptimal energy and protein intakes due to poor appetite status, low diet quality, high diet monotony index, and/or psychosocial and financial barriers are modifiable non-iatrogenic factors implicated in malnutrition in these patients. These factors should be included in a comprehensive nutritional assessment for malnutrition risk. Leveraging the point of origin of malnutrition in dialysis patients is crucial for healthcare practitioners to enable personalized patient care, as well as determine country-specific malnutrition treatment strategies.
    Matched MeSH terms: Acidosis
  2. Khositseth S, Bruce LJ, Walsh SB, Bawazir WM, Ogle GD, Unwin RJ, et al.
    QJM, 2012 Sep;105(9):861-77.
    PMID: 22919024 DOI: 10.1093/qjmed/hcs139
    Distal renal tubular acidosis (dRTA) caused by mutations of the SLC4A1 gene encoding the erythroid and kidney isoforms of anion exchanger 1 (AE1 or band 3) has a high prevalence in some tropical countries, particularly Thailand, Malaysia, the Philippines and Papua New Guinea (PNG). Here the disease is almost invariably recessive and can result from either homozygous or compound heterozygous SLC4A1 mutations.
    Matched MeSH terms: Acidosis, Renal Tubular/genetics*; Acidosis, Renal Tubular/epidemiology
  3. Arumugasamy N, Siqueira EB
    Med J Malaya, 1970 Dec;25(2):155-60.
    PMID: 4251137
    Matched MeSH terms: Acidosis/complications; Acidosis/etiology*; Diabetic Ketoacidosis
  4. Mazlan MZ, Mohd Zaini RH, Hassan SK, Ali S, Che Omar S, Wan Hassan WMN
    Respir Med Case Rep, 2017;21:129-131.
    PMID: 28487824 DOI: 10.1016/j.rmcr.2017.04.014
    INTRODUCTION: Closed suctioning is commonly used in the context of high-setting mechanical ventilation (MV), given its ability to prevent lung volume loss that otherwise accompanies open suctioning. However, closed suctioning systems (CSS) are not equivalent regarding components and capabilities, and thus this technique may be differentially effective to adequately clear patient secretions from an endotracheal tube (ETT), which is of paramount importance when the tube size makes the ETT particularly vulnerable to block by patient secretions.

    CASE PRESENTATION: A 25-year-old super morbidly obese female (body mass index = 55 kg/meter2) presented with worsening shortness of breath. For MV, pairing of a 6 mm (mm) diameter ETT to accommodate the patient's vocal cord edema, with a CSS not designed to maintain a clean catheter tip, precipitated ETT blockage and respiratory acidosis. Replacement of these devices with a 6.5 mm ETT and a CSS designed to keep the catheter tip clean resolved the complications. After use of the different ETT and CSS for approximately one week, the patient was discharged to home.

    DISCUSSION: The clean-tip catheter CSS enabled a more patent airway than its counterpart device that did not have this feature. Use of a clean-tip catheter CSS was an important care development for this patient, because this individual's super morbidly obese condition minimized tolerance for MV complications that would exacerbate her pre-existing tenuous respiratory health status.

    CONCLUSION: Special attention should be given to the choices of ETT size and CSS to manage super morbidly obese patients who have a history of difficult airway access.

    Matched MeSH terms: Acidosis, Respiratory
  5. Faridah Hanim Zam Zam, Nazimah Idris, Tham, Seng Woh
    MyJurnal
    Background: Fetal surveillance in labour is performed mostly to identify fetuses at risk of hypoxia in order to reduce neonatal morbidity and mortality by initiating timely intervention. While normal and abnormal fetal heart rate (FHR) patterns have been well recognised and characterized for the first stage of labour, FHR patterns during the second stage of labour commonly showed some forms of abnormalities leading to problems in interpretation, particularly in predicting fetal hypoxia and acidosis. This study aims to identify patterns of FHR tracing during the second stage of labour associated with neonatal acidosis. Methods: A prospective cross sectional study was conducted in the Labour Ward of a state referral hospital. The study population were patients with low-risk
    singleton pregnancies between 37 to 42 weeks gestation who had normal cardiotocograph (CTG) tracing in the first stage of labour. CTG was recorded during the second stage of labour and neonatal umbilical cord blood was obtained for acid-base analysis immediately after birth prior to the delivery of placenta. FHR patterns were grouped according to modified Melchior and Barnard’s
    classification and matched with neonatal acid-base status. Patients with normal FHR pattern in the second stage acted as control. Results: A total of 111 matched pairs were analysed. Ninety nine (89.2%) second stage FHR tracings showed abnormal features when compared to control. There were significantly more neonatal acidosis and hypercapnia in type 1b, type 2a, type 2b and type 3 CTG patterns compared to control, in increasing order of severity. In addition, types 2b and 3 showed significant difference in the base excess. Conclusion: Certain second stage fetal heart rate
    patterns were found to be associated with neonatal acidosis.
    Matched MeSH terms: Acidosis
  6. Shariffuddin II, Rai V, Chan YK, Muniandy RK
    BMJ Case Rep, 2014;2014.
    PMID: 24862427 DOI: 10.1136/bcr-2014-205135
    Care of an acutely ill parturient is particularly difficult when we have to balance the needs of both mother and the fetus to survive. The literature suggests there should be emphasis on stabilising the mother's condition. In dealing with metabolic acidosis, however, we believe delivering the baby early might not only relieve the threat of the acidosis on the mother, it may be the only way to deliver a live baby. We report two parturient women with severe metabolic acidosis which was considerably reduced very soon after the delivery and how our timely delivery resulted in the birth of two neurologically intact babies.
    Matched MeSH terms: Acidosis/etiology; Acidosis/therapy; Diabetic Ketoacidosis/therapy*
  7. 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: Acidosis, Renal Tubular/complications*; Acidosis, Renal Tubular/physiopathology
  8. Choo KE, Nicoli TK, Bruce LJ, Tanner MJ, Ruiz-Linares A, Wrong OM
    Pediatr Nephrol, 2006 Feb;21(2):212-7.
    PMID: 16252102
    Mutations of the AE1 (SLC4A1, Anion-Exchanger 1) gene that codes for band 3, the renal and red cell anion exchanger, are responsible for many cases of familial distal renal tubular acidosis (dRTA). In Southeast Asia this disease is usually recessive, caused either by homozygosity of a single AE1 mutation or by compound heterozygosity of two different AE1 mutations. We describe two unrelated boys in Sarawak with dRTA associated with compound heterozygosity of AE1 mutations. Both had Southeast Asian ovalocytosis (SAO), a morphological abnormality of red cells caused by a deletion of band 3 residues 400-408. In addition, one boy had a DNA sequence abnormality of band 3 residue (G701D), which has been reported from elsewhere in Southeast Asia. The other boy had the novel sequence abnormality of band 3 (Q759H) and profound hemolytic anemia.
    Matched MeSH terms: Acidosis, Renal Tubular/genetics*
  9. Usman A, Shaikh MF, Dujaili JA, Mustafa N, Gan SH
    Diabetes Metab Syndr, 2021 Mar 05;15(2):573-580.
    PMID: 33706189 DOI: 10.1016/j.dsx.2021.03.001
    BACKGROUND AND AIMS: Diabetic ketoacidosis (DKA) treatment guidelines recommend to initiate potassium-replacement when serum potassium (SK) drops within normal range, and to withhold insulin if SK is below normal. Despite strict recommendations, hypokalemia is frequently observed in DKA.

    METHODS: Scientific literature was thoroughly searched to find 1) DKA treatment guidelines, 2) studies reporting hypokalemia in DKA, 3) and literature elaborating mechanisms involved in hypokalemia.

    RESULTS: Acidosis affects SK and its regulators including insulin, catecholamines and aldosterone. Current conceptual framework is an argument to gauge the degree of hypokalemia before it strikes DKA patients utilizing SK level after adjusting it with pH. Suggested approach will reduce hypokalemia risk and its associated complications. The nomogram calculates pH-adjusted potassium and expected potassium loss. It also ranks hypokalemia associated risk, and proposes the potassium-replacement rate over given time period. The differences between current DKA treatment guidelines and proposed strategy are also discussed. Moreover, reasons and risk of hyperkalemia due to early initiation of potassium replacement and remedial actions are debated.

    CONCLUSION: In light of proposed strategy, utilizing the nomogram ensures reduced incidence of hypokalemia in DKA resulting in improved clinical and patient outcomes. Pharmacoeconomic benefits can also be expected when avoiding hypokalemia ensures early discharge.

    Matched MeSH terms: Acidosis; Diabetic Ketoacidosis
  10. Firdaus Hayati, Nornazirah Azizan, Nik Amin Sahid, Hilal Zahabi Abdul Fattah, Rohamini Sibin, Andee Dzulkarnaen Zakaria
    MyJurnal
    Necrotizing fasciitis (NF) is a deadly soft tissue infection causing a significant morbidity and mortality. Abdominal and chest wall NF are unusual. We describe a 49-year-old male with anterior abdominal wall NF secondary to per- forated gastric ulcer (PGU). He was admitted in septic shock presenting an abdominal wall NF with severe metabolic acidosis requiring dialysis and admission to the intensive care unit. There was a patch of gangrene with surrounding skin discoloration at lower quadrant of the abdominal wall. Local debridement was done without a preoperative computed tomography that was performed after surgery. Adequate source control was not achieved after the second surgery and the patient had worsened resulting to death. We describe this rare presentation of NF and discuss the issues learnt from this unfortunate event.
    Matched MeSH terms: Acidosis
  11. Campion KL, McCormick WD, Warwicker J, Khayat ME, Atkinson-Dell R, Steward MC, et al.
    J Am Soc Nephrol, 2015 Sep;26(9):2163-71.
    PMID: 25556167 DOI: 10.1681/ASN.2014070653
    The calcium-sensing receptor (CaR) modulates renal calcium reabsorption and parathyroid hormone (PTH) secretion and is involved in the etiology of secondary hyperparathyroidism in CKD. Supraphysiologic changes in extracellular pH (pHo) modulate CaR responsiveness in HEK-293 (CaR-HEK) cells. Therefore, because acidosis and alkalosis are associated with altered PTH secretion in vivo, we examined whether pathophysiologic changes in pHo can significantly alter CaR responsiveness in both heterologous and endogenous expression systems and whether this affects PTH secretion. In both CaR-HEK and isolated bovine parathyroid cells, decreasing pHo from 7.4 to 7.2 rapidly inhibited CaR-induced intracellular calcium (Ca(2+)i) mobilization, whereas raising pHo to 7.6 potentiated responsiveness to extracellular calcium (Ca(2+)o). Similar pHo effects were observed for Ca(2+)o-induced extracellular signal-regulated kinase phosphorylation and actin polymerization and for L-Phe-induced Ca(2+)i mobilization. Intracellular pH was unaffected by acute 0.4-unit pHo changes, and the presence of physiologic albumin concentrations failed to attenuate the pHo-mediated effects. None of the individual point mutations created at histidine or cysteine residues in the extracellular domain of CaR attenuated pHo sensitivity. Finally, pathophysiologic pHo elevation reversibly suppressed PTH secretion from perifused human parathyroid cells, and acidosis transiently increased PTH secretion. Therefore, pathophysiologic pHo changes can modulate CaR responsiveness in HEK-293 and parathyroid cells independently of extracellular histidine residues. Specifically, pathophysiologic acidification inhibits CaR activity, thus permitting PTH secretion, whereas alkalinization potentiates CaR activity to suppress PTH secretion. These findings suggest that acid-base disturbances may affect the CaR-mediated control of parathyroid function and calcium metabolism in vivo.
    Matched MeSH terms: Acidosis/metabolism
  12. Lew YS
    Singapore Med J, 2000 Aug;41(8):398-400.
    PMID: 11256348
    One lung anaesthesia in paediatric patients may not always be achievable by bronchial blockade or double lumen tube intubation due to inadequate experiences or facilities. We attempted to isolate right lung by selectively intubating the left bronchus with single lumen tube on a 10 kg child. Optimal surgical condition and satisfactory oxygenation achieved but complicated with severe respiratory acidosis. The possible causes for hypercapnea in this child were discussed.
    Matched MeSH terms: Acidosis, Respiratory/blood; Acidosis, Respiratory/etiology*
  13. Lee WS, Sokol RJ
    J Pediatr, 2013 Oct;163(4):942-8.
    PMID: 23810725 DOI: 10.1016/j.jpeds.2013.05.036
    Matched MeSH terms: Acidosis, Lactic/genetics
  14. Muhammad Adil ZA, Nur Zawani J, Hazariah AH, Rao G, Zailiza S, Mohd Nasir H
    Med J Malaysia, 2019 Oct;74(5):413-417.
    PMID: 31649218
    INTRODUCTION: A methanol outbreak occurred in the district of Hulu Langat on 16 September 2018. The Hulu Langat District Health Office received 25 notifications of a suspected methanol poisoning from Kajang and Ampang Hospital. An outbreak investigation was done to determine the source followed by a preventive and control measure.

    METHOD: Active case detection was done on cases living quarters and workplaces. Patients were interviewed, and their blood and urine samples were sent for methanol analysis. Samples of suspected alcoholic beverages were also sent for analysis. A suspected case was defined as any person presented with clinical symptoms with a history of consuming alcoholic beverages within five days before symptoms and high anion gap metabolic acidosis. A confirmed case was defined as a suspected case with positive blood and urine methanol.

    RESULTS: In total, there were 25 suspected cases, of which 12 cases were confirmed. The calculated attack rate was 48%. There were six mortalities (50%) secondary to severe metabolic acidosis. The most common presenting symptom was vomiting (75%) and abdominal pain (41.7%). These cases were linked to consumption of illicitly produced alcohol. Samples of the alcoholic drinks were positive containing high level of methanol.

    CONCLUSION: The methanol outbreak in the Hulu Langat was successfully managed. Appropriate control and prevention measures were taken, including health promotion and joint enforcement activities. Steps were taken successfully through collaborations with multiple agencies and cooperation with Selangor Health Departments and the Ministry of Health. Continuous surveillance on the product of liquor, and health promotion are essential to prevent a similar outbreak from happening again in future.

    Matched MeSH terms: Acidosis
  15. Johnson RO, Johnson BH, Raman A, Lee EL, Lam KL
    Aust Paediatr J, 1979 Jun;15(2):101-6.
    PMID: 485988
    Matched MeSH terms: Acidosis/etiology*; Acidosis/metabolism
  16. Ngen CC, Cheong IK
    Med J Malaysia, 1989 Sep;44(3):199-203.
    PMID: 2626134
    Ten patients on long term lithium therapy (mean four years, range 1-10.5 years) were subjected to various renal, thyroid, haematological, cardiac and endocrine tests. There was impaired urinary concentrating ability in seven subjects, which was not responsive to vasopressin stimulation, suggesting a partial nephrogenic diabetes insipidus. Nine subjects had metabolic acidosis with higher urinary pH than expected suggesting presence of acidification defect in the kidney. No significant change in renal function, thyroid function, ECG or haematological parameters were detected. Our findings concur with previous reports from the West regarding the safety of lithium administration.
    Matched MeSH terms: Acidosis/chemically induced
  17. Chow YW, Leong CL, Chow HL, Hooi LS
    Med J Malaysia, 2007 Mar;62(1):78-80.
    PMID: 17682581
    Exposure to highly active antiretroviral therapy (HAART) may lead to adverse effects related to mitochondrial toxicity such as lactic acidosis. We describe two cases of severe lactic acidosis in HIV-positive patients to illustrate the clinical symptoms and abnormal laboratory results associated with this condition. There is a lack of awareness about the risk factors for developing severe lactic acidosis and recognition of its onset with dire consequences.
    Matched MeSH terms: Acidosis, Lactic/chemically induced*; Acidosis, Lactic/physiopathology
  18. Huan, Nai Chien, Wan Awatif Wan Mohd Zohdi
    MyJurnal
    High anion gap metabolic acidosis (HAGMA) is a hallmark of Diabetic Ketoacidosis (DKA). Occasionally, a Normal Anion Gap Metabolic Acidosis (NAGMA) can be seen, especially during the treatment phase. In this case report, a 55-year-old lady with diabetes mellitus who presented with a 2-day history of fever, lethargy and multiple episodes of vomiting and diarrhoea. Initial laboratory investigations revealed: capillary blood glucose as 27 mmol/L, urine ketone as 3+, blood ketone as 3.5 mmol/L, serum bicarbonate as 14 mmol/L, and serum chloride as 95 mmol/L. She was treated with intravenous normal saline fluid resuscitation and constant rate insulin infusion which was fortunately accompanied by stabilization of blood glucose and normalization of blood ketone to 0.2 mmol/L. However, despite normalization of her anion gap (25 to 14), she remained unwell with acidotic breathing due to refractory hyperchloraemic NAGMA with bicarbonate at 11 mol/L and chloride of 112 mmol/L. It was then decided to administer 100 mL of 8.4% Sodium Bicarbonate solution. The next day, she was no longer tachypneic as her bicarbonate and carbon dioxide improved to 21 mmol/L and 32 mmHg respectively. The presence of NAGMA in DKA should prompt clinicians to conduct a thorough search for possible underlying causes, such as gastrointestinal fluid loss, sepsis and chloride load from aggressive fluid resuscitation with normal saline. Sodium bicarbonate should only be considered in intractable cases to correct a NAGMA and not routinely used in the treatment of DKA.
    Matched MeSH terms: Acidosis; Diabetic Ketoacidosis
  19. Sheikh IA, Malik A, AlBasri SFM, Beg MA
    Life Sci, 2018 Jan 01;192:246-252.
    PMID: 29138116 DOI: 10.1016/j.lfs.2017.11.014
    AIMS: Chronic metabolic acidosis (CMA) refers to increased plasma acidity due to disturbed acid-base equilibrium in human body. CMA leads to many dysfunctions including disorders of intestinal metabolism and barrier functions. The human body responds to these intestinal dysfunctions by creating a compensatory mechanism at genomic level in intestinal epithelial cells. This study was to identify the molecular pathways involved in metabolic dysfunction and compensatory adaptations in intestinal epithelium during CMA.

    MAIN METHODS: In silico approaches were utilized to characterize a set of 88 differentially expressed genes (DEGs) from intestinal cells of rat CMA model. Interaction networks were constructed for DEGs by GeneMANIA and hub genes as well as enriched clusters in the network were screened using GLay. Gene Ontology (GO) was used for enriching functions in each cluster.

    KEY FINDINGS: Four gene hubs, i.e., trefoil factor 1, 5-hydroxytryptamine (serotonin) receptor 5a, solute carrier family 6 (neurotransmitter transporter), member 11, and glutamate receptor, ionotropic, n-methyl d-aspartate 2b, exhibiting the highest node degree were predicted. Six biologically related gene clusters were also predicted. Functional enrichment of GO terms predicted neurological processes such as neurological system process regulation and nerve impulse transmission which are related to negative and positive regulation of digestive system processes., intestinal motility and absorption and maintenance of gastrointestinal epithelium.

    SIGNIFICANCE: The study predicted several important genomic pathways that potentially play significant roles in metabolic disruptions or compensatory adaptations of intestinal epithelium induced by CMA. The results provide a further insight into underlying molecular mechanisms associated with CMA.

    Matched MeSH terms: Acidosis/genetics*
  20. Yusoff NM, Van Rostenberghe H, Shirakawa T, Nishiyama K, Amin N, Darus Z, et al.
    J Hum Genet, 2003;48(12):650-653.
    PMID: 14618420 DOI: 10.1007/s10038-003-0095-2
    Southeast Asian ovalocytosis (SAO) is a red blood cell abnormality common in malaria-endemic regions and caused by a 27 nt deletion of the band 3 protein gene. Since band 3 protein, also known as anion exchanger 1, is expressed in renal distal tubules, the incidence of SAO was examined in distal renal tubular acidosis (dRTA) in Malays in Kelantan, Malaysia. Twenty-two patients with dRTA and 50 healthy volunteers were examined for complication of SAO by both morphological and genetic analyses. SAO was identified in 18 of the 22 dRTA patients (81.8%), but only two of the 50 controls (4%). The incidence of SAO was significantly high in those with dRTA (p<0.001), indicating a dysfunctional role for band 3 protein/anion exchanger 1 in the development of dRTA.
    Matched MeSH terms: Acidosis, Renal Tubular/complications; Acidosis, Renal Tubular/genetics*
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