Background and Aims

Orthostatic intolerance (OI) is defined by multiple symtpoms resulting from upright position, that are usually alleviated by recumbency. Postural tachycardia syndrome (POTS) and orthostatic hypotension (OH) are the most prevalent forms of OI.
Evidence suggest that many patients develop OH or POTS after experiencing febrile, predominantly viral ilness, which has lead to hypothesis of an autoimmune mediated cause of orthostatic intolerance. Several studies demonstrated the presence of autoantibodies against adrenergic receptors, particularly β1, β2 and α1 in majority of patients with POTS. Similar results have been observed in demonstration of the presence of antibodies to cholinergic receptors.
Moreover patients with POTS were found to have significantly higher prevalence of other non organ specific autoantibodies, especially antinuclear antibodies (ANA), antophospholipid antibodies (aPL) and also various co-morbid autoimmune disorders. Hashimoto thyroiditis was the most common associated autoimmune disease (p < 0.001), followed by rheumatoid arthritis ( p < 0.01) and SLE (p < 0.001), respectively. Recent studies have focused on the role of renin-angiotensin system in the pathogenesis of OI showing that most patients with POTS harbor antibodies against angiotensin 1 receptor (AT1R). Less is known about the role of adrenal cortex in the manifestation of POTS or OH symptoms.
Autoimmune etiology of some forms of OI is also supported by few reports demonstrating that immunomodulation therapy resulted in a significant improvement of orthostatic symptoms. Studies on larger groups of patients are required.

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