POTS and Ferritin Levels
POTS (Postural Orthostatic Tachycardia Syndrome) does not typically involve increased ferritin levels as part of its core pathophysiology. However, ferritin abnormalities may be found incidentally in POTS patients as part of broader metabolic or nutritional screening.
Core Pathophysiology of POTS
POTS is characterized by three primary pathophysiologic mechanisms, none of which directly cause elevated ferritin 1, 2:
- Partial autonomic neuropathy affecting lower body vasoconstriction 2
- Hypovolemia from reduced blood volume 1, 2
- Hyperadrenergic state with excessive sympathetic activity 1, 2
Nutritional Deficiencies in POTS
The documented nutritional abnormalities in POTS patients involve deficiencies, not elevations 3:
- Vitamin B12 deficiency has been observed with increased prevalence 3
- Vitamin D deficiency is more common in POTS patients 3
- Iron deficiency (not iron overload) has been documented 3
- Vitamin B1 deficiency occurs in approximately 6% of POTS patients 3
Ferritin Interpretation Context
If elevated ferritin is found in a POTS patient, consider alternative explanations unrelated to POTS itself 4:
- Inflammatory conditions cause ferritin elevation as an acute phase reactant 4
- Chronic inflammatory states including autoimmune conditions 4
- Liver disease (alcoholic liver disease, chronic hepatitis, nonalcoholic fatty liver disease) 4
- Lymphomas or other malignancies 4
Low ferritin with low transferrin saturation (<20%) would be more consistent with the iron deficiency pattern actually observed in POTS 3, rather than elevated ferritin.
Clinical Pitfall
Do not attribute elevated ferritin to POTS itself. If ferritin is elevated in a POTS patient, investigate for concurrent inflammatory, infectious, or hepatic conditions that are independent of the POTS diagnosis 4. The association between POTS and nutritional abnormalities specifically involves deficiencies requiring supplementation, not excess states 3.