Vitamin D Deficiency Is Highly Prevalent in Critically Ill Patients and a Risk Factor for Mortality: A Prospective Observational Study Comparing Noncirrhotic Patients and Patients With Cirrhosis
Journal of Intensive Care Medicine, https://doi.org/10.1177/0885066618803844
Ulrich Mayr, MD, Leonie Fahrenkrog-Petersen, MD, Gonzalo Batres-Baires, MD
- Alcoholic liver cirrhosis treated by 1,000 IU of vitamin D – July 2018
- Cirrhosis in hospital 2.9 X less likely to get need ICU when supplemented with Vitamin K – Nov 2015
- Cirrhosis infection and death both associated with low vitamin D – June 2015
- Advanced liver cirrhosis death 6.3X more likely if extremely low vitamin D – Jan 2013
- Search for CIRRHOSIS in VitaminDWiki 361 items July 2018
Overview Liver and vitamin D contains the following summary
- Fact: A properly functioning liver is needed for the efficient activation of vitamin D in the body
- Fact: Liver diseases often result in lower levels of vitamin D
- Fact: Various pain relievers damage the liver function
- Fact: Lower levels of vitamin D result in osteoporosis and many other diseases
- Options with a poorly functioning liver appear to be:
- Increased vitamin D (example: 2X more vitamin D if Liver is 1/2 as efficient)
- Increase the response you get from vitamin D
- Increase sunshine / UVB,
- Get the response you get from the sun/UVB
- Consider supplementing with Iron - a patented Iron supplement appears to work very well
- Get prescription for active form of vitamin D (Calcitriol) which does not need the liver or kidney to get the benefits of vitamin D in the body
- Get Calcidiol which does not need the liver
PDF is available free at Sci-Hub 10.1177/0885066618803844
A 25-hydroxyvitamin D, 25(OH)D, deficiency is common among critically ill patients and correlated with increased mortality. Furthermore, deficiency is associated with advanced liver disease. However, there are no studies available comparing the dimensions and consequences of a 25(OH)D deficiency between patients with and without liver cirrhosis in the setting of intensive care units (ICUs). This study focuses on differences in 25(OH)D status between critically ill noncirrhosis patients and patients with cirrhosis (primary end point), hypothesizing that deficiency and its impact on mortality risk are even more pronounced in patients with cirrhosis.
We performed a prospective observational study of 176 patients (noncirrhosis patients, N = 114; patients with cirrhosis, N = 62) with a laboratory assessment of 25(OH)D on ICU admission and survival analyses after 180 days.
On admission, 55% of patients showed a severe deficiency, 25(OH)D <10 ng/mL, and a further 23% moderate deficiency (10-19 ng/mL). The overall median level of 25(OH)D was 8.0 (5.0-18.0) ng/mL (10.5 [6.0-21.3] in noncirrhosis patients vs 7.0 [4.8-10.0] in patients with cirrhosis; P < .001). We found extremely low levels particularly in patients without prior vitamin D supplementation (6.0 [4.0-7.5] in patients with cirrhosis vs 8.0 [5.0-12.0] ng/mL in noncirrhosis patients; P = .004).
Vitamin D status correlated inversely with the
- sequential organ failure assessment,
- acute and physiology chronic health evaluation,
- model of end-stage liver disease, and
- Child-Pugh scores.
Survival analyses categorized 25(OH)D levels <10 ng/mL as a high-risk factor for mortality 180 days after admission (hazard ratio [HR]: 2.45, 95% confidence interval [CI] = 1.60-3.70; P < .001). In patients with cirrhosis, a severe deficiency (<10 ng/mL) involved a significantly higher mortality risk than in noncirrhosis patients (HR: 2.30, 95% CI = 1.39-3.82; P = .001). In cases of admission levels ≥10 ng/mL, however, mortality risk was similar between patients with cirrhosis and noncirrhosis patients (HR: 1.08, 95% CI = 0.43-2.73; P = .873).
Hypovitaminosis D is a highly frequent disorder in critically ill patients admitted to ICU. A severe deficiency with levels <10 ng/mL is a high risk factor for increased mortality, especially in patients with cirrhosis.