Essence of the disease and classification
According to the Global Consensus (2016), nutritional rickets is defined as a pathology in which chondrocyte differentiation is disrupted, and the mineralization of osteoid and growth plates suffers. The leading etiological factor is recognized as vitamin D deficiency combined with calcium deficiency (or an isolated deficiency of either nutrient).
In ICD-10, the disease is classified under Chapter IV (Endocrine, nutritional and metabolic diseases). The following subcategories are distinguished:
- E55 — Vitamin D deficiency;
- E55.0 — Active phase of rickets;
- E64.3 — Sequelae and late effects of rickets.
The main prerequisite for the development of the disease in infants is the colossal rate of physical development and active bone tissue remodeling. An infant requires 50–55 mg of calcium per 1 kg of body weight per day. Due to the physiological immaturity of transport systems, minerals are poorly integrated into the bone, leading to insufficient mineralization of the bone matrix. Anatomically, this process manifests primarily in the metaphyseal zones.
Physiology of bone mass formation
Bone tissue accumulation occurs unevenly, but the overwhelming part (more than 80%) of an adult's bone mass is formed precisely during childhood and puberty. The level of mineralization is genetically determined by approximately 50%. The remaining half depends on environmental factors such as nutrition, sun exposure, and physical activity.
In pediatrics, three critical windows are distinguished when the programmed peak bone mass is established:
- Antenatal (intrauterine) period;
- Early childhood (first 3 years of life);
- Pubertal period (adolescence).
The maximum peak bone mass accumulated in childhood is the main protective factor against age-related resorption. X-ray densitometry data confirm that bone density deficiency in children directly correlates with the risk of osteoporotic fractures (particularly of the femoral neck) in older age.
Vitamin D and its metabolism
The main form of the vitamin is the fat-soluble vitamin D3 (cholecalciferol). It can be obtained exogenously (dietary sources include fatty sea fish and cod liver) or synthesized endogenously in the epidermis under the influence of ultraviolet radiation.
To acquire biological activity, vitamin D undergoes two stages of enzymatic hydroxylation. The initial substance binds to the D-binding protein, interacts with albumin, and is transported to the liver.
- First stage (liver): the first hydroxyl group is attached. 25-hydroxycholecalciferol—25(OH)D—is formed. This is the circulating transport form in the blood, the level of which is maintained stably through a feedback mechanism. It is 25(OH)D that serves as the main laboratory criterion for the body's vitamin stores.
- Second stage (kidneys): the second hydroxyl group is attached, converting the transport form into the biologically active hormone—calcitriol, or 1,25(OH)2D.
Causes of deficiency in modern conditions
Adequate mineralization processes are controlled by three hormones: parathyroid hormone (produced by the parathyroid glands), thyrocalcitonin (synthesized by C-cells of the thyroid gland), and renal calcitriol. For the system to function, a sufficient supply of nutrients is required, which is often compromised in modern realities.
Risk factors for deficiency development:
- Dietary factor: breastfeeding cannot fully cover an infant's needs. Human milk contains only about 70 IU/L of vitamin D, and cow's milk contains about 20 IU/L.
- Limited sun exposure: sun exposure is no longer considered the primary and reliable source of the vitamin. In the Russian Federation, this is explained by its geographical location with low insolation. Furthermore, optimal UV synthesis occurs only during a short window (from 11:00 AM to 2:00 PM), and atmospheric pollution in cities creates an additional barrier to the rays.
That is why today the primary method of rickets prevention is recognized as the additional intake of oral vitamin D supplements.
Hormones of phosphorus-calcium metabolism: the PTK rule — Parathyroid hormone, Thyrocalcitonin, Calcitriol.
Class and exam questions
Which blood test indicates vitamin D deficiency?
The main laboratory criterion for the body's vitamin D sufficiency is the level of 25(OH)D, which is produced in the liver.
Does a child get enough vitamin D if they are exclusively breastfed?
No, breast milk does not cover the high demands of an intensively growing organism, as it contains only about 70 IU/L of vitamin D.
Can vitamin D deficiency be corrected solely by sun exposure?
In modern conditions, especially in middle latitudes, sun exposure is not a sufficient source. Adequate UV radiation intensity occurs for only about 3 hours a day, which is also hindered by air pollution in megacities.
What else to study on this topic
- Clinical manifestations of rickets at different stages
- Radiological signs of metaphyseal demineralization
- Specific therapy: dosages of oral vitamin D
- Differential diagnosis with genetic rickets-like diseases
- Detailed mechanisms of action of parathyroid hormone and thyrocalcitonin
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Other topics in "Chapter 3. Adaptation, Early Childhood Nutrition, Rickets"
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