Displaying all 10 publications

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  1. Yong SM, Aik S
    Med J Malaysia, 2000 Sep;55 Suppl C:101-4.
    PMID: 11200035
    We report two cases of x-linked dominant hypophosphatemic rickets involving a man and his daughter. The family tree consists of 44 members with 13 of them having short stature and bowing of the lower limbs. The study of this family tree strongly suggests an x-linked dominant inheritance.
    Matched MeSH terms: Hypophosphatemia, Familial/genetics*; Hypophosphatemia, Familial/pathology; Hypophosphatemia, Familial/radiography*; Hypophosphatemia, Familial/surgery
  2. Hisham AN, Aina EN, Zanariah H
    Med J Malaysia, 2000 Mar;55(1):132-4.
    PMID: 11072498
    Hungry bone syndrome (HBS) following successful parathyroid surgery is a well described phenomenon. However, few studies have clearly addressed this syndrome or looked at the outcome of perioperative management. We report a case of HBS following successful parathyroid surgery. The perioperative management is discussed and literature pertaining to this interesting case is reviewed.
    Matched MeSH terms: Hypophosphatemia/therapy*
  3. Vijay, A.P., Tan, A.T.B., Suhaida, A.M., Chan, S.P.
    JUMMEC, 2010;13(1):63-68.
    MyJurnal
    Tumour-induced or oncogenic osteomalacia (OOM) is a rare paraneoplastic syndrome characterized by bone pain and muscle weakness. A biochemical profile consisting of normocalcaemia, hypophosphataemia, phosphaturia, increased serum alkaline phosphatase and inappropriately low serum levels of 1, 25-dihydroxyvitamin-D is diagnostic. OOM is usually caused by an osseous or soft-tissue tumour of mesenchymal origin that secretes phosphaturic substances leading to increased urinary phosphate wasting. These tumours are small and slow growing. The diagnosis continues to be easily missed and when eventually made, localization of the tumour can be difficult. We describe the case of a young man who presented with severe generalized pain associated with muscle weakness. He was extensively investigated and eventually diagnosed to have OOM 3 years after initial presentation. Specialized investigations were necessary to localize the offending tumour.
    Matched MeSH terms: Hypophosphatemia, Familial; Hypophosphatemia
  4. 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*
  5. 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/blood; Hypophosphatemia/diagnosis; Hypophosphatemia/etiology; Hypophosphatemia/therapy*
  6. Poh F, Sing WH, Mohan PC
    Med J Malaysia, 2015 Feb;70(1):38-41.
    PMID: 26032529
    We present a case of a 53-year-old woman who developed multifocal insufficiency fractures associated with adefovir dipivoxil (ADV) induced osteomalacia, including recurring metatarsal insufficiency fractures and a subtrochanteric femoral insufficiency fracture requiring surgical fixation. She had received low-dose ADV treatment for 59 months for chronic hepatitis B viral infection at the time of presentation with subtrochanteric fracture. Imaging evidence of multifocal insufficiency fractures and metabolic disease on background of hypophosphatemia is attributed to hypophosphatemic osteomalacia from adefovir-induced renal proximal tubular dysfunction. Radiologists and clinicians should be aware of the possibility of insufficiency fractures in patients receiving ADV therapy to avoid delayed diagnosis and progression of high-risk proximal femoral fractures.
    Matched MeSH terms: Hypophosphatemia
  7. Hanizah Ngadiron, Razrim Rahim, Firdaus Hayati, Nornazirah Azizan, Affirul Chairil Ariffin
    MyJurnal
    Hypophosphataemia occurs in an abnormally low serum phosphate level. Three main mechanisms are postulated: decreased intestinal absorption, increased renal excretion, and extracellular shifts to intracellular compartments. It is potentially a fatal disease if not intervene. The management is merely treating the underlying disorder, giving phosphate supplement and requiring close biochemical monitoring. The incidence of symptomatic isolated hypophosphataemia is extremely rare. In this case report, a 33-year-old man presented with three days history of dysphagia, inability to complete sentences and generalized muscle weakness. He developed blurred vision especially upon exposure to bright light. He had a history of single parathyroidectomy for parathyroid adenoma 2 years ago. Physical examinations were unremarkable. Laboratory investigations were normal except for phosphate level of 0.30 mmol/L. Intravenous KH2PO4 with a dosage of 10 mmol was administered in slow bolus in 3 hours. His symptoms resolved slowly after correction. Although isolated hypophosphataemia is rare but need to recognize the symptoms and signs of hypophosphataemia and treat accordingly.
    Matched MeSH terms: Hypophosphatemia
  8. Nagaratnam S, Karupiah M, Mustafa N
    J ASEAN Fed Endocr Soc, 2020;35(1):105-108.
    PMID: 33442176 DOI: 10.15605/jafes.035.01.17
    Hypophosphatemic osteomalacia is a rare form of metabolic bone disorder in neurofibromatosis type 1 (NF1). The exact disease mechanism of this disorder in NF1 is yet to be established. We present a 44-year-old female known to have NF1, who presents with debilitating bone pain, weakness and multiple fractures. Laboratory investigations showed persistent hypophosphatemia with renal phosphate wasting suggestive of hypophosphatemic osteomalacia. She also had concomitant vitamin D deficiency which contributed to the disease severity. Medical therapy with oral phosphate and vitamin D improved her symptoms without significant changes in fracture healing or phosphate levels.
    Matched MeSH terms: Hypophosphatemia
  9. 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*
  10. Basri, M.N., Janattul, A.J., Azrina, M.R., Abdul Hadi, M.
    MyJurnal
    Introduction: Our objectives are to identify the incidence of hypophosphatemia and the associated risk factors. We also want to establish intravenous replacement therapy that is effective for ICU patients. Methods: A prospective observational study assessing adults admitted to ICU in between March and May 2009. All patients without baseline phosphate level and renal failure were excluded. They were evaluated for the occurrence of common risk factors. Association with independent variables that includes age, gender and BMI were verified. Evaluation of IV replacement therapy was done in the treated patients. Results: From 50 patients that were reviewed, nine were excluded. There were 66% male and 34% female with mean age 46.88±17.89. The mean ICU stay was 8.00±6.41 days. The incidence of hypophosphatemia was 29% (n=12/41). Gender and
    creatinine clearance was found to be significantly different between normophosphatemia and
    hypophosphatemia patients. There was no significant association for each potential risk factor and the number of risk factors (≥3) with the incidence of hypophosphatemia. Multi-linear regression analysis showed that lactate, creatinine clearance and pH were significant predictors to the serum levels. A significant difference of mean serum phosphate was seen after repletion by total dose of 10, 20 and 40 mmols in the treatment subgroups. Conclusions: The incidence of hypophosphatemia in our ICU was high and comparable to previous studies. None of the commonly reported risk factors is associated with hypophosphatemia in this studied population. Among all significant correlated variables, only pH was found to be a significant predictor for serum phosphate. Baseline phosphate level may guide the initial replacement dose to prevent delay in normalization of serum levels.
    Matched MeSH terms: Hypophosphatemia
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