Methods: A 16yo caucasian girl presented with scoliosis and fatigue and daytime sleepiness. Her symptoms began gradually 2–3 months after the menarche, worsening to the point that she began having functional difficulties with her normal tasks. She denied changes in weight, new stressors, difficulty falling asleep or anxiety. All was normal apart from cholesterol (249 mh/dl) a light anemia and vit D (9.29).

Results: VitD supply was initiated with cholecalciferol 500-1.000 UI/die with few benefits (vitD raised to 10.5). After 6 months the vitD supply was implemented to 2k-3k/die and fructose was added to the diet in suspicious of mitochondrial disease which would also explain the cholesterol not to be converted into vitD. She reported improvement of his fatigue and daytime sleepiness within 2 weeks of start of vitD supplementation and resolution of the most of her symptoms within 3 months of vitD+fructose initiation.

Discussion: To summarize, there are several observational studies showing an association between vitamin D deficiency and different pain conditions, but a causal relationship is not obvious. Importantly, patients with sufficient 25-OHD levels from the beginning do not benefit from treatment. The suppression of inflammation in general and of PGE2 especially exhibits credible mechanistic explanations for the effect of vitamin D in pain. Vitamin D supplementation has not shown adverse effects in any studies reviewed here and is also easy to administer. Today, the evidence is too weak for making general recommendations for vitamin D in pain management and more randomized and placebo-controlled studies are needed before any firm conclusions can be drawn. However, current knowledge allows us to conclude that patients with deficient levels, defined here as 25-OHD <30 nmol/L, are most likely to benefit from supplementation, while individuals with 25-OHD levels >50 nmol/L probably have little benefit from supplementation. Vitamin D might therefore be offered as independent therapy to vitamin D-deficient patients with chronic pain. Further clinical studies in this field should focus on patients with 25-OHD <30 nmol/L at baseline, and offer intervention that raises the individual’s 25-OHD levels to >50 nmol/L.

Conclusion: vitD deficiency might be an easily reversible etiology of fatigue. Although a causal relationship cannot be confirmed by this case alone, the temporal relationship as well as biological plausibility makes this a possibility. Serum vitD levels in patients who present with daytime sleepiness/fatigue, nonspecific musculoskeletal pain, and risk factors for vitD deficiency should be checked as a routine.