25 HYDROXYVITAMIN D – SERUM

Overview

25-Hydroxyvitamin D (25(OH)D), also called Calcidiol or the Sunshine Vitamin, is the major circulating form of vitamin D and the most reliable indicator of an individual’s vitamin D status. It is a fat-soluble vitamin synthesized in the liver by hydroxylation of vitamin D. Vitamin D3 (cholecalciferol) is produced in the skin’s Malpighian layer when UVB radiation (290–320 nm) converts 7-dehydrocholesterol into vitamin D3, while vitamin D2 (ergocalciferol) is derived from plants and diet. After conversion to 25(OH)D in the liver, it is metabolized in the kidney to 1,25(OH)2D (Calcitriol), the biologically active form. This active form regulates calcium absorption, bone mineralization, kidney reabsorption of calcium and phosphorus, and supports immune and cardiovascular health. Testing serum 25(OH)D helps in diagnosing deficiency, insufficiency, toxicity, rickets, osteomalacia, and monitoring replacement therapy.

Symptoms

(Clinical features suggesting the need for serum 25(OH)D estimation)

1. In children: delayed growth, skeletal deformities, bone pain, bowing of legs, and rickets (hypophosphatemic, vitamin D–resistant, renal, or end-organ refractoriness).
2. In adults: osteoporosis, osteomalacia, generalized bone pain, and fractures.
3. Systemic effects: muscle weakness, fatigue, susceptibility to infections, and reduced immunity.
4. Pregnancy-related conditions: gestational diabetes mellitus and pre-eclampsia.
5. Severe deficiency: hypocalcemia, leading to tetany and convulsions.
6. Excessive levels: vitamin D intoxication causing calcinosis (metastatic calcification).

Causes

(Factors contributing to altered 25(OH)D levels)

1. Decreased levels:
   1. Limited sun exposure.
   1. Poor dietary intake.
   1. High phytate content in diet reducing calcium absorption.
   1. Malabsorption syndromes (steatorrhea, obstructive jaundice).
   1. Celiac disease and inflammatory bowel disease.
   1. Liver or kidney disorders affecting vitamin D activation.
2. Increased levels:
   1. Excessive supplementation leading to vitamin D intoxication.
   1. Resulting in calcinosis due to metastatic calcium deposition.

Risk factors

(Populations at higher risk of deficiency or abnormal levels)

1. Older adults: reduced skin synthesis and poor nutrient intake.
2. Individuals with dark skin: higher melanin reduces UVB-mediated synthesis.
3. People with limited sunlight exposure: due to indoor lifestyle, sunscreen use, or living at high latitudes.
4. Patients with chronic liver or kidney disease: impaired conversion to active forms.
5. Pregnant women: increased demand for calcium and vitamin D.
6. Children: especially in areas with poor nutrition or inadequate sun exposure.
7. People with malabsorption syndromes: celiac disease, IBD, obstructive jaundice.
8. Individuals consuming diets low in vitamin D sources: fish liver oil, eggs, milk.

Prevention

(Strategies to maintain adequate vitamin D levels and optimize testing accuracy)

1. Sunlight exposure: regular, safe exposure to morning sunlight to stimulate natural vitamin D3 production.
2. Balanced diet: include vitamin D–rich foods such as fish liver oil, eggs, and milk.
3. Supplementation: oral vitamin D2 or D3 supplementation under medical supervision to correct deficiencies.
4. Regular testing: monitor serum 25(OH)D levels, particularly in at-risk groups, to prevent deficiency or toxicity.
5. Sample collection protocols:
   1. Collect 2–3 mL venous blood in plain or gel tubes.
   1. Store samples at 2–8 °C for reliable results.
6. Reliable estimation methods: CLIA, ELISA, RIA, HPLC, or LC-MS ensure accurate detection of vitamin D status.
7. Maintain reference levels:
   1. Deficiency: <10 ng/mL
   1. Insufficiency: 10–30 ng/mL
   1. Sufficiency: 30–100 ng/mL
   1. Toxicity: >100 ng/mL
8. Awareness of variations: consider seasonal changes, age, latitude, and lifestyle factors when interpreting results.
9. Public health measures: educate communities about safe sunlight exposure, nutrition, and supplementation.