https://doi.org/10.53453/ms.2024.9.10
Vitamin D deficiency: literature review of a growing pandemic
Evelina Gailiešaitė
1
1
Lithuanian University of Health Sciences, Academy of Medicine, Faculty of Medicine, Lithuania
Abstract
Background. Many regions of the world have high rates of clinical vitamin D insufficiency, which can lead to
rickets and osteomalacia. In Europe and Australasia, rickets is also becoming more common in children from
ethnic minority groups. The measurement of 25OHD in plasma is a valuable indicator of clinical vitamin D
insufficiency risk.
Aim. To conduct a literature research and review vitamin D deficiency symptoms, diagnostic methods and
treatment options.
Methods. A literature review was performed using a computer bibliographic medical database PubMed. A search
was performed using search keywords "vitamin D", "vitamin D deficiency", "vitamin D insufficiency", "vitamin
D hypovitaminosis".
Results. A 25(OH)D concentration of less than 50 nmol/L, or 20 ng/mL, is generally accepted to be indicative of
a vitamin D deficiency. Vitamin D deficiency manifests as painful bones, muscle weakness, cramps and spasms,
slowed growth and development in children. Adults experience osteopenia, osteoporosis, and an increased risk of
fracture.
Conclusion. Both skeletal and non-skeletal health depend on vitamin D. It is generally known that a large number
of individuals do not get as much vitamin D as is currently advised for good health. The main symptoms of vitamin
D are muscle weakness, cramps, slow growth and development in children. Adults can experience osteoporosis,
increased risk of fracture, muscle weakness. It is widely acknowledged that a 25(OH)D concentration of less than
50 nmol/L, or 20 ng/mL, indicates a vitamin D deficit. Vitamin D supplements should be taken as a precaution.
Keywords: vitamin D, deficiency, avitaminosis, hypovitaminosis.
Journal of Medical Sciences. 24 Sep, 2024 - Volume 12 | Issue 4. Electronic - ISSN: 2345-0592
Medical Sciences 2024 Vol. 12 (4), p. 80-84, https://doi.org/10.53453/ms.2024.9.10
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1. Introduction
Metabolites of vitamin D (alphacaldidol, calcitriol,
calcifediol) and cholecalciferol (vitamin D3).
Cholecalciferol is the natural form of vitamin D that
humans have received throughout the evolution
period, clear details of its metabolism, regulation,
storage are known processes – it is easily absorbed
by the body and converted into an active form or
stored in fatty tissue and released according to the
need.
Cholecalciferol is the drug of first choice and the
main one for the prevention and treatment of
deficiency in the everyday patient (for children and
adults) [1,2]. Alfacalcidol and calcifediol are
second-line agents suitable for specific patients
(alfacalcidol for those with kidney failure,
calcifediol for those with liver and intestinal
disorders (malabsorption), but when prescribing
second-choice preparations, attention should be paid
to safety measures: periodically monitor calcium
and phosphorus levels in the serum, alkaline
phosphatase activity, and despite a possible faster
effect [3] they are also associated with more
frequent hypercalcemia and in cases of overdose.
2. Methodology
A literature review was performed using a computer
bibliographic medical database PubMed. A search
was performed using search keywords "Vitamin D",
"vitamin D deficiency", "vitamin D insufficiency",
"vitamin D hypovitaminosis".
Publications, not older than 10 years, written in
English were analysed. A total of 49 publications
were reviewed, of which 25 publications were
included based on the inclusion/exclusion criteria.
3. Results
3.1 Sources of Vitamin D
For the majority of people, exposure to sunlight is
the primary source of vitamin D [4,5,6,7]. The two
primary forms of vitamin D are D3 (cholecalciferol)
and D2 (ergocalciferol). Apart from the D3 and D2
forms of vitamin D, 25-hydroxy vitamin D also
makes a substantial contribution to the amount of
vitamin D that is consumed by food. It is present in
a lot of goods derived from animals. Dietary
supplements may include 25-hydroxy vitamin D, a
metabolite of vitamin D, or vitamin D3 or D2 forms.
Vitamin D (D refers to D3 and/or D2) is contained
in relatively few foods (> 4 μg/100 g). Examples of
such foods include a variety of fish (5–25 μg/100 g),
some mushrooms (21.1–58.7 μg/100 g), Reindeer
lichen (87 μg/100 g), and fish liver oils (250 μg/100
g) [7,8]. Vitamin D supplements are typically
advised since it is difficult to meet the European
Food Safety Authority's recommended daily intake
of 15 μg of vitamin D by diet alone.
3.2 Presentation of Vitamin D insufficiency
There is a lot of disagreement on what constitutes a
vitamin D deficit. A 25(OH)D concentration of less
than 50 nmol/L, or 20 ng/mL, is generally accepted
to be indicative of vitamin D deficiency; a value of
51–74 nmol/L, or 21–29 ng/mL, is thought to
suggest insufficiency; amounts greater than 30
ng/mL are seen to be sufficient [9,10,11].
Children who are deficient in vitamin D will
experience growth retardation [13] as well as the
typical rickets symptoms [6,13,14] such as painful
bones, muscle weakness, cramps and spasms,
slowed growth and development.
Adults with low vitamin D levels will experience
osteopenia, osteoporosis, and an increased risk of
fracture [15,16]. Vitamin D insufficiency has long
been linked to muscle weakness. Skeletal muscle
contains a vitamin D receptor [17]. A lack of vitamin
D has been linked to proximal muscle weakening, an
increase in body sway, and a higher risk of falling
[18,19].
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3.3 Vitamin D intoxication
It normally takes 25(OH)D values of >375 nmol/L,
or 150 ng/mL, to cause vitamin D intoxication [12].
The initial indication of excessive vitamin D intake
is hypercalciuria, which is followed over time by
hypercalcemia, which is linked to severe and
protracted morbidity [8].
Patients with Vitamin D intoxication typically have
high serum 25OHD, low serum parathyroid
hormone (PTH), hypercalcemia, normal or high
serum phosphorus levels, normal or low levels of
alkaline phosphatase (ALP), and high urine
calcium/creatinine [20].
The correction of hypercalcemia is the primary
objective of treatment for vitamin D intoxication.
Emergency action is required when the calcium
concentration is more than 14 mg/dl due to the
negative effects of hypercalcemia on the heart,
central nervous system, kidneys, and
gastrointestinal tract. Even if the external supply of
vitamin D is removed, the consequences of toxicity
may persist for months because vitamin D is
retained in fat tissues. The following are some of the
treatments for VDI: stopping the medication, eating
a diet low in calcium and phosphorus, intravenous
saline hydration, loop diuretics, glucocorticoids,
calcitonin, and bisphosphonates [20,21].
3.4 Vitamin D deficiency correction
The American Academy of Pediatrics and the
Institute of Medicine recommended that adults and
children under the age of 50 should consume 200 IU
of vitamin D per day, while people over the age of
70 and those over the age of 51 should have 400 and
600 IU of vitamin D per day [22]. As of late, the
National Osteoporosis Foundation advised all
postmenopausal women to consume 800–1000 IU of
vitamin D per day [23].
Many specialists now concur that adults and
children of all ages require 800–1000 IU of vitamin
D per day in the absence of sufficient sun exposure
[23,24,25]. Pludowski et al suggests daily dosage of
800–2000 IU of vitamin D for adults who wish to
guarantee adequate vitamin D status; for some
groups, such as patients with obesity and
malabsorption syndromes, as well as those with dark
skin pigmentation, the recommended daily dosage
may be as high as 4000 IU [26].
4. Conclusions
Both skeletal and non-skeletal health depend on
vitamin D. It is now generally known that a large
number of individuals do not get as much vitamin D
as is currently advised for good health. The two
main ways that people get vitamin D in the world are
by sun exposure (UVB radiation) and cutaneous
vitamin D production.
Even in nations with plenty of sunshine, primary
insufficiency is very common when skin exposure to
UVB radiation is restricted due to lifestyle choices
and other factors. In populations with very low
calcium intakes or other circumstances, such as
underlying disease, that may raise the biological
requirement for vitamin D, secondary insufficiency
may also be common.
Despite limitations brought about by a lack of
methodological uniformity, plasma 25OHD at
concentrations <25 nmol/L (10 ng/mL) is an
effective indication of the risk of clinical deficiency.
The symptoms of the insufficiency can vary from
muscle weakness and cramps to growth deficiency
in children, and increased fracture risk or
osteoporosis in adults.
When vitamin D deficiency is found treatments
should be prescribed. Crrection doses range from
800 IU to 4000 IU per day. The dose depends on the
severity of the deficiency and on the underlying
conditions the patient has.
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