Vitamin D (also called calciferol) is a vital dietary component. Several forms of vitamin D can be distinguished, most notably vitamin D2 (ergocalciferol) and D3 (synonyms: calcitriol; 1,25-Di-OH-cholecalciferol; 1α-25-OH-vit. D3). Coming from food intake, cholecalciferol is converted in the liver to 25-OH-vitamin D (synonyms: calcifediol, 25-OH-D3, 25-OH-vitamin D). In the kidney, it is further converted to 1,25-dihydroxyvitamin D (synonyms: calcitriol, 1α-25-OH-D3 ), the biologically active form of vitamin D. Endogenously, 1,25-di-OH-cholecalciferol (vitamin D3) is formed from 7-dehydroxycholesterol under UV light action (sunlight). By determining the 25-OH vitamin D, the vitamin D content of the body can be determined. The starting substance for the endogenous synthesis of vitamin D3 is 7-dehydrocholesterol. This provitamin is absorbed through food and subsequently converted into the active vitamin D3 under the influence of UV-B light (photoisomerization) and simultaneous exposure to heat (thermoisomerization). Vitamin D is considered a hormone (D-hormone) and is fat-soluble. It can be stored in hormone-producing organs such as the adrenal cortex, and these stores then have reserves for a few weeks. Vitamin D acts similarly to steroid hormones by binding to a nuclear receptor. Vitamin D has essential functions for calcium and phosphate balance – furthermore, vitamin D is an antiproliferative and differentiation-inducing substance. The following diseases may occur in vitamin D deficiency:
- Rickets – in the child occurring form of bone softening.
- Osteomalacia – form of bone softening occurring in adults.
- Secondary hyperparathyroidism (parathyroid hyperfunction).
The following conditions/symptoms may indicate vitamin D deficiency:
- Bone pain
- Myalgia (muscle pain)
- Fatigue and weakness
- Depression
The following diseases/symptoms may occur with vitamin D overdose:
- Anorexia nervosa (anorexia).
- Hyperacidemia – too much nitrogen in the blood.
- Hypercalcemia (excess calcium)
- Hypophosphatemia (phosphate deficiency)
- Nausea (nausea)/vomiting
- Nephrocalcinosis – calcifications in the kidneys.
- Constipation (constipation)
- Calcifications in the area of the epiphyseal joints – joint end on a long bone responsible for growth.
The procedure
Material needed
- Blood serum
Preparation of the patient
- Not necessary
Disruptive factors
- For the measurement of 25-hydroxy vitamin D, the blood sample must be stored away from light
Standard values
| Parameter | Value (adult) | Value (children) |
| 25-Hydroxy vitamin D (depending on the season). | 10-120 μg/l Optimal 30-70 µg/l | 12-144 μg/l |
| Winter: 10-50 μg/l | 12-60 μg/l | |
| Summer: 20-120 μg/l | 24-144 μg/l | |
| In dialysis patients: Target > 30 µg/l [= 75 nmol/l] (K/DOQI guidelines). | ||
| 1,25-Dihydroxy vitamin D | 16-70 ng/l | 20-84 ng/l |
1 µg/l = 1 ng/ml
Indications
- Suspected vitamin D deficiency
- Low calcium excretion and low serum calcium and serum phosphate levels.
- Increased parathyroid hormone level
- Increased alkaline phosphatase
- Other indications include:
- Patients with dark skin color (Afro or Latin American).
- Patients with older age who have already fallen, or have suffered fractures
- Patients in pregnancy or breastfeeding
- Patients with malabsorption syndromes (group of diseases caused by impaired absorption of substrates from the intestine).
- Diseases of the skeletal system
- Chronic renal failure (process leading to a slowly progressive reduction in kidney function).
- Granuloma-forming diseases (berylliosis, histoplasmosis, coccidiomycosis, sarcoidosis, tuberculosis).
- Liver failure
Interpretation
25-hydroxyvitamin D
Interpretation of elevated 25-hydroxyvitamin D levels (synonyms: calcifediol, 25 (OH)-vitamin D).
- Very strong sunlight
- Vitamin D substitution
Interpretation of decreased 25-hydroxy vitamin D levels.
- Alimentary (dietary)
- Unbalanced diet, etc.
- Malnutrition / malnutrition
- Vegetarian
- Malabsorption (disorder of absorption)
- Due to chronic intestinal diseases – for example, in celiac disease (leading symptoms: Weight loss, meteorism (flatulence) and diarrhea – diarrhea) etc.
- Digestive insufficiency
- Maldigestion (disorder of digestion).
- Due to chronic intestinal diseases
- Diseases
- Hepatitis (inflammation of the liver)
- Liver cirrhosis (liver shrinkage; in this process, liver tissue is destroyed and permanently transformed into scar tissue and connective tissue)
- Renal insufficiency (kidney weakness)
- Women with postmenopausal osteoporosis (bone loss after menopause).
- Medication
- Taking antiepileptic drugs (medications that act against seizures) – such as phenytoin and diphenylhydantoin, and barbiturates.
- Increased need
- Growth/children
- Pregnancy/breastfeeding phase
- Older women respectively men (≥ 65 years)
- Insufficient UV-B exposure (winter months, people who are bedridden for long periods of time or spend little time outdoors or have a lack of sunlight or use sunscreens extensively).
- Colored
25-Hydroxy vitamin D (25-OH vitamin D) and health status
| nmol/l2 | μg/l | Health status |
| < 30 | < 12 | Vitamin D deficiency, causes rickets in infants and children and osteomalacia (softening of bones) in adults |
| 30-50 | 12-20 | Generally considered inadequate with respect to bone health in healthy individuals |
| ≥ 50 | ≥ 20 | Generally considered sufficient with respect to bone health in healthy individuals |
| > 125 | > 50 | Potential adverse effect, especially from > 150 nmol/l (> 60 µg/l) |
2 1 nmol/l = 0.4 µg/l = 0.4 ng/mlDesirable target value of 25-OH-vitamin D: > 75 nmol/l or > 30 ng/ml or > 30 µg/l, respectively.
1,25-dihydroxy-vitamin D
Interpretation of elevated 1,25-dihydroxyvitamin D levels (synonyms: vitamin D3, 1,25-di-OH-cholecalciferol, 1α-25-OH-vit. D3; calcitriol).
- Acromegaly – enlargement of hands, feet, nose, and ears after completion of growth due to excessive production of growth hormones.
- Hyperparathyroidism, primary (parathyroid hyperfunction).
- Hypothyroidism (hypothyroidism)
- Lymphomas – malignant neoplasms originating from the lymphatic system.
- Rickets (type 2; vitamin D receptor defect) – form of bone softening occurring in childhood.
- Sarcoidosis – inflammatory systemic disease affecting mainly the lungs, lymph nodes and skin.
- Tuberculosis (consumption)
- Vitamin D
- Moderate vitamin D deficiency (compensatory)
- Vit D-dependent rickets type 2 (vitamin D receptor defect).
- Vitamin D substitution of calcitriol, e.g. Rocatrol.
- Growth
- Condition after kidney transplantation
Interpretation of decreased 1,25-dihydroxy vitamin D levels.
- Hypercalcemia (calcium excess) due to dihydrotachysterol.
- Hyperthyroidism (hyperthyroidism)
- Hypoparathyroidism (parathyroid hypofunction).
- Hypophosphatemia (phosphate deficiency), autosomal-dominant/X-chormosomal (= vitamin D-resistant rickets).
- Intoxication with cadmium
- Renal insufficiency (kidney weakness)
- Vitamin D
- Severe vitamin D deficiency
- Vitamin D-dependent rickets type 1 (1α-hydroxylase deficiency) – childhood-onset form of bone softening.
Other indications
- The normal requirement for vitamin D in children, adolescents and adults is 20 µg/d (= 800 IU).
- Vitamin D is found mainly in fish (liver oil), eggs, butter, milk, as well as in animal tissues.
Attention. Note on the state of supply (National Consumption Study II 2008) 100% of children, adolescents and adults do not reach the recommended daily intake of vitamin D.
