Crit Care Med. 2015 Jul 16.[Epub ahead of print]
- Note: 40% of the high-dose group was having Renal Replacement Therapy,
which indicates that 40% were probably not able to process Vitamin D
Vitamin D is not the appropriate form to give to those patients,
they needed Calcitriol injection - which does not require kidney processing
- They did not check for adverse reaction to a small dose before giving 300,000 IU injection
Overall, there was no statistially significant difference in mortality between the 150,000 and 300,000 groups
Strangely. the PDF fails to say the number of people who did not change PTH, nor the number of deaths.
- Reasons for low response to vitamin D
Wonder why the response to the bigger dose was not initially higher than smaller dose
Nair P1, Venkatesh B, Lee P, Kerr S, Hoechter DJ, Dimeski G, Grice J, Myburgh J, Center JR.
1Intensive Care Unit, St. Vincent's Hospital, Sydney, NSW, Australia. 2Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia. 3Bone Biology Division, Garvan Institute for Medical Research, Sydney, NSW, Australia. 4Critical Care and Trauma Division, George Institute for Global Health, Sydney, NSW, Australia. 5Intensive Care Unit, Princess Alexandra Hospital, Brisbane, QLD, Australia. 6Intensive Care Unit, Wesley Hospital, Brisbane, QLD, Australia. 7University of Queensland, Brisbane, QLD, Australia. 8Departement of Anesthesiology, LMU, Munich, Germany. 9Intensive Care Unit, St. George Hospital, Sydney, NSW, Australia.
OBJECTIVES: To determine the effect of two doses of intramuscular cholecalciferol on serial serum 25-hydroxy-vitamin-D levels and on pharmacodynamics endpoints: calcium, phosphate, parathyroid hormone, C-reactive protein, interleukin-6, and cathelicidin in critically ill adults.
DESIGN: Prospective randomized interventional study.
SETTING: Tertiary, academic adult ICU.
PATIENTS: Fifty critically ill adults with the systemic inflammatory response syndrome.
INTERVENTION: Patients were randomly allocated to receive a single intramuscular dose of either 150,000 IU (0.15 mU) or 300,000 IU (0.3 mU) cholecalciferol.
MEASUREMENTS AND MAIN RESULTS: Pharmacokinetic, pharmacodynamic parameters, and outcome measures were collected over a 14-day period or until ICU discharge, whichever was earlier. Prior to randomization, 28 of 50 patients (56%) were classified as vitamin D deficient. By day 7 after randomization, 15 of 23 (65%) and 14 of 21 patients (67%) normalized vitamin D levels with 0.15 and 0.3 mU, respectively (p = 0.01) and by day 14, 8 of 10 (80%) and 10 of 12 patients (83%) (p = 0.004), respectively. Secondary hyperparathyroidism was manifested in 28% of patients at baseline. Parathyroid hormone levels decreased over the study period with patients achieving vitamin D sufficiency at day 7 having significantly lower parathyroid hormone levels (p < 0.01). Inflammatory markers (C-reactive protein and interleukin-6) fell significantly over the study period. Greater increments in 25-hydroxy-vitamin-D were significantly associated with greater increments in cathelicidin at days 1 and 3 (p = 0.04 and 0.004, respectively).
Although in-hospital mortality rate did not differ between the groups, patients who did not mount a parathyroid hormone response to vitamin D deficiency had a higher mortality (35% vs 12%; p = 0.05). No significant adverse effects were observed.
CONCLUSIONS: A single dose of either dose of intramuscular cholecalciferol corrected vitamin D deficiency in the majority of critically ill patients. Greater vitamin D increments were associated with early greater cathelicidin increases, suggesting a possible mechanism of vitamin D supplementation in inducing bactericidal pleiotropic effects.