Open Access 01-11-2018 | What's New in Intensive Care
Vitamin therapy in critically ill patients: focus on thiamine, vitamin C, and vitamin D
Published in: Intensive Care Medicine | Issue 11/2018
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Recent hypothesis-generating studies have sparked new interest in an old concept: adjuvant vitamin therapy in critical illness or “metabolic resuscitation”. In this mini-review, we report on the most promising players in this setting: thiamine (vitamin B1), vitamin C, and vitamin D. Their main characteristics are summarized in Table 1 (see also electronic supplementary material, ESM).
Thiamine
|
Vitamin C
|
Vitamin D
|
|
---|---|---|---|
Other names
|
Vitamin B1
|
Ascorbic acid
|
Native forms
D3: cholecalciferol
D2: ergocalciferol
Active form
Calcitriol
|
Molecular characteristics
|
Water-soluble
|
Water-soluble
|
Fat-soluble
|
Formula
|
C12H17N4OS
|
C6H8O6
|
D3: C27H44O
|
Molar mass (g/mol)
|
265.35
|
176.12
|
D3: 384.64
|
Source
|
Diet (seeds, legumes, rice, cereals, corns, pork, spinach)
|
Diet [fruits and vegetables (lost by long cooking)]; supplements
|
Mainly from skin: synthesis from cholesterol elicited by sun exposure (UVB radiation); diet (fatty fish); supplements
|
Excretion
|
Renal
Daily loss with CRRT ± 4-5 mg/day
|
Renal
Daily loss with CRRT ± 70 mg/day
|
Bile/feces and renal
Catabolizing enzymes
Daily loss with CRRT unknown
|
Risk of deficiency
|
Poor diet
Alcoholism
Hypermetabolism
Increased loss (CRRT)
|
Poor diet
Oxidative stress: sepsis, ischemia–reperfusion, trauma, burns, CRRT
Increased loss (CRRT)
|
Low sun exposure
Comedication
Obesity
Dark skin
Chronic disease
Malnutrition
|
Stores and time to deficiency
|
Half-life of 18 days. Stores are rapidly depleted when metabolic demands are high
|
In otherwise healthy persons, scurvy develops in 4–8 weeks. Stores are rapidly depleted if oxidative stress is high
|
Half-life of 2–3 weeks
Metabolism in acute illness unknown
|
Functions
|
Coenzyme for glucose metabolism, Krebs cycle, generation of ATP, pentose phosphate pathway, NADPH production
|
Donation of electrons Cofactor/co-substrate
Anti-oxidant
Anti-inflammatory and immune-promoting actions
|
Classic: regulation of intestinal calcium absorption
Nonclassic: cell-specific regulation of transcriptional activity, inhibition of PTH secretion, promotion of insulin secretion, regulatory action on adaptive and innate immunity, inhibition of cell proliferation, stimulation of differentiation
|
Clinical consequences of deficiency
|
Lactic acidosis
Wet beriberi: high-output cardiac failure
Dry beriberi: polyneuropathy, muscle weakness, confusion, ataxia, nystagmus
Wernicke–Korsakoff encephalopathy
|
Scurvy
Poor wound healing
Lassitude, depression
Hypotension
Capillary leakage
Bleeding
Infections
|
Rickets (children)
Osteomalacia (adults)
Unspecific or absent symptoms
Musculoskeletal pain in some cases
|
Side effects, toxicity
|
Unknown
|
Oxalate nephropathy (ESM) in susceptible persons
|
Hypercalcemia
Acute renal failure
Nephrocalcinosis
|
Recommended dosea
|
Healthy persons: 1.5 mg/day
Acute critical illness: 100–300 mg/day
CRRT: 100 mg/day of therapy to safely compensate effluent losses
|
Healthy persons: 200 mg/day
Acute critical illness: 2–3 g/day iv to correct deficiency (ESM)
Chronic critical illness: 0.2–1 g/day?
Dialysis/hemofiltration: 0.5–1 g/day
Burns: 0.5–1 g/day
|
Native vitamin D3 or D2
Healthy persons: 600–800 IU/day
Risk groups: 1500–2000 IU/day
Safe dose: up to 10 000 IU/day
Acute critical illness: unknown
Dialysis/CRRT: unknown
|