MATERIALS AND METHODS: A total of 3,175 adult University Malaya Medical Centre (UMMC) patients deemed free of any calcium metabolism disorders were selected and divided into two groups for derivation and validation. Simple linear regression associating total calcium and albumin was constructed from the data in the derivation group. The new albumin-adjusted calcium equation was validated in the validation group. Differences in calcium status classification following adjustments based on existing and new albumin-adjusted calcium equation was compared in a 469 hypoalbuminaemic patients.
RESULT: The new albumin adjusted calcium equation was: total calcium + 0.014 x (39-albumin). Of the 469 hypoalbuminemic patients, 78 were classified differently based on new equation. Based on the new equation, 55 normocalcemic patients were classified as hypocalcemic and 22 were classified as normocalcemic instead of hyperclacaemic.
CONCLUSION: Based on the newly derived albuminadjusted calcium equation 17% of patients had different adjusted calcium classifications. This could potentially impact in the management. It is recommended that laboratories derive equations specific to their calcium/albumin methods and analytical platforms.
OBJECTIVES: (1) Evaluate the four published equations' performance in estimating ionised calcium; (2) Determine the accuracy of calculated ionised and adjusted total calcium in classifying patients according to calcium states; and (3) Identify factors associated with hypocalcaemia in the critically ill population.
MATERIALS AND METHODS: This is a cross-sectional study involving 281 critically ill patients aged 18-80 years of both genders in a Malaysian tertiary intensive care unit. Performance of the four equations was analysed using Bland-Altman difference plot and Passing Bablok regression analysis. Crosstabulation was conducted to assess classification accuracy. Mann-Whitney U or Pearson Chi-Square tests were performed to identify variables associated with hypocalcaemia.
RESULTS: Calculated ionised calcium using all four equations significantly overestimated ionised calcium. Calculated ionised and adjusted total calcium had poor accuracies in classifying hypocalcaemic patients. pH was significantly higher in hypocalcaemics.
CONCLUSION: Calculated ionised and adjusted total calcium significantly overestimate ionised calcium in the critically ill. In this specific population, calcium status should only be confirmed with ionised calcium measured by direct ion-selective electrode (ISE).
EVIDENCE ACQUISITION: We conducted a meta-analysis to evaluate the relationship between primary aldosteronism (PA) with bone biochemical markers and to assess bone mineral density in patients with primary aldosteronism.
EVIDENCE SYNTHESIS: A total of 939 subjects were examined (37.5% with PA). Patients with PA had significantly higher serum parathyroid hormone, lower serum calcium, higher urine calcium excretion and higher serum alkaline phosphatase compared to patients without PA, with no significant difference in serum vitamin D between both groups. Bone mineral density of lumbar spine, femoral neck and total neck of femur were similar between two groups. With PA treatment, there was a significant increment in serum calcium and reduction in serum parathyroid hormone.
CONCLUSIONS: PA is associated with hypercalciuria with subsequent secondary hyperparathyroidism. This potentially affects bone health. We recommend this to be part of complication screening among patients with PA.
DESIGN: Serum intact parathormone (PTH) concentrations were measured on samples taken before and during a variable-rate tri-sodium citrate infusion designed to 'clamp' the whole blood ionised calcium concentration 0.20 mmol L-1 below baseline for 120 min.
SUBJECTS: Six Malaysian patients aged 17-42 years with acute malaria, four of whom were restudied in convalescence, and 12 healthy controls aged 19-36 years.
MAIN OUTCOME MEASURES: Whole-blood ionised calcium and serum intact PTH concentrations.
RESULTS: The mean (SD baseline ionised calcium was lower in the malaria patients than in controls (1.09 +/- 0.06 vs. 1.18 +/- 0.03 mmol L-1, respectively; P = 0.01) but PTH concentrations were similar (3.0 +/- 1.8 vs. 3.3 +/- 1.3 pmol L(-1); P = 0.33). Target whole-blood ionised calcium concentrations were achieved more rapidly in the controls than the patients (within 15 vs. 30 min) despite significantly more citrate being required in the patients (area under the citrate infusion-time curve 0.95 (0.25 vs. 0.57 +/- 0.09 mmol kg-1; P < 0.01). The ratio of the change in serum PTH to that in ionised calcium (delta PTH/ delta Ca2+), calculated to adjust for differences in initial rate of fall of ionised calcium, was similar during the first 5 min of the clamp (132 +/- 75 x 10(-6) vs. 131 +/- 43 x 10(-6) in patients and controls, respectively, P > 0.05), as were steady-state serum PTH levels during the second hour (7.0 +/- 2.2 pmol L-1 in each case). Convalescent patients had normal basal ionised calcium levels but the lowest serum intact PTH levels before and during the clamp, consistent with an increase in skeletal PTH sensitivity after treatment.
CONCLUSIONS: There is a decreased ionised calcium 'set point' for basal PTH secretion but a normal PTH response to acute hypocalcaemia in malaria. Skeletal resistance may attenuate the effects of the PTH response but patients with malaria appear relatively resistant to the calcium chelating effects of citrated blood products.