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  1. Zakaria NH, Sthaneshwar P, Shanmugam H
    Malays J Pathol, 2017 Dec;39(3):317-320.
    PMID: 29279597 MyJurnal
    Hypophosphataemia is a metabolic disorder that is commonly encountered in critically ill patients. Phosphate has many roles in physiological functions, thus the depletion of serum phosphate could lead to impairment in multiple organ systems, which include the respiratory, cardiovascular, neurological and muscular systems and haematological and metabolic functions. Hypophosphataemia is defined as plasma phosphate level below 0.80 mmol per litre (mmol/L) and can be further divided into subgroups of mild (plasma phosphate of 0.66 to 0.79 mmol/L), moderate (plasma phosphate of 0.32 to 0.65 mmol/L) and severe (plasma phosphate of less than 0.32 mmol/L). The causes of hypophosphataemia include inadequate phosphate intake, decreased intestinal absorption, gastrointestinal or renal phosphate loss, and redistribution of phosphate into cells. Symptomatic hypophosphataemia associated with haematological malignancies has been reported infrequently. We report here a case of asymptomatic severe hypophosphataemia in a child with acute T-cell lymphoblastic leukaemia. A 14-year-old Chinese boy was diagnosed to have acute T cell lymphoblastic leukaemia (ALL). His serum biochemistry results were normal except inorganic phosphate and lactate dehydrogenase levels. The serum inorganic phosphate level was 0.1mmol/L and the level was low on repeated analysis. The child had no symptoms related to low phosphate levels. The possible causes of low phosphate were ruled out and urine Tmp/GFR was normal. Chemotherapy regime was started and the serum phosphate levels started to increase. Hypophosphataemia in leukaemia was attributed to shift of phosphorus into leukemic cells and excessive cellular phosphate consumption by rapidly proliferating cells. Several reports of symptomatic hypophosphataemia in myelogenous and lymphoblastic leukaemia in adults have been reported. To our knowledge this is the first case of severe asymptomatic hypophosphataemia in a child with ALL.
    Matched MeSH terms: Hypophosphatemia/etiology*
  2. Md Ralib A, Mat Nor MB
    Asia Pac J Clin Nutr, 2018 2 1;27(2):329-335.
    PMID: 29384319 DOI: 10.6133/apjcn.062017.09
    BACKGROUND AND OBJECTIVES: Refeeding hypophosphataemia (RH) is characterized by an acute electrolyte derangement following nutrition therapy. Complications associated include heart failure, respiratory failure, paraesthesia, seizure and death. We aim to assess its incidence, risk factors, and outcome in our local intensive care unit (ICU).

    METHODS AND STUDY DESIGN: A prospective observational cohort study was conducted at the mixed medical- surgical of a tertiary ICU in Kuantan, Malaysia. The study was registered under the National Medical Research Register (NMRR-14-803-19813) and has received ethical approval. Inclusion criteria include adult admission longer than 48 hours who were started on enteral feeding. Chronic renal failure patients and those receiving dialysis were excluded. RH was defined as plasma phosphate less than 0.65 mmol/L and a drop of more than 0.16 mmol/L following feeding.

    RESULTS: A total of 109 patients were recruited, of which 44 (42.6%) had RH. Patients with RH had higher SOFA score compared to those without (p=0.04). There were no differences in the APACHE II and NUTRIC scores. Serum albumin was lower in those with RH (p=0.04). After refeeding, patients with RH had lower serum phosphate, magnesium and albumin, and higher supplementation of phosphate, potassium and calcium. There were no differences in mortality, length of hospital or ICU stay.

    CONCLUSIONS: Refeeding hypophosphataemia occurs in almost half of ICU admission. Risk factors for refeeding include high organ failure score and low albumin. Refeeding was associated with imbalances in phosphate, magnesium, potassium and calcium. Future larger study may further investigate these risk factors and long-term outcomes.

    Matched MeSH terms: Hypophosphatemia/etiology*
  3. Mohamed Koya SNM
    Saudi J Kidney Dis Transpl, 2019 6 30;30(3):670-677.
    PMID: 31249232 DOI: 10.4103/1319-2442.261343
    Studies have shown that the mean or median phosphate levels were related to certain factors although applying this finding into the clinical setting is challenging. In this study, we attempted to determine treatment characteristics for patients with end-stage renal disease (ESRD) on maintenance hemodialysis (MHD) having hyperphosphatemia or hypophosphatemia in comparison with those with normal phosphate level. This was a cross-sectional survey conducted at HD units of Central Pahang Cluster Hospitals, Malaysia, in April 2017 involving 110 ESRD patients on MHD. About 40% of the study patients had normo-or hyperphosphatemia. As many as 84.5% (n = 93) of our patients were prescribed calcium carbonate (CC); the phosphate level was not affected by phosphate binder (PB) adherence. None of our patients received more than one type of PBs. Although there were no significant differences in any factors between normo- and hyperphosphatemic patients, 64% (n = 28) of the hyperphosphatemic patients did not receive the recommended maximum PB dose. In addition, 42% (n = 30) of patients with normo- and hyperphosphatemia prescribed CC received more than the recommended daily elemental calcium. On the other hand, our hypophosphatemic patients tended to be significantly older and had lower HD duration compared to normophosphatemic patients. No other significant differences were found in medication factors between normo- and hypophos-phatemic patients. There is potential to maximize phosphate control in hyperphosphatemic patients in Malaysia by maximizing PB therapy. On the other hand, proactive supervision is required in caring and prescribing for hypophosphatemic patients, especially the older patients.
    Matched MeSH terms: Hypophosphatemia/etiology
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