3. Etiology and Contributing Factors

← PREVIOUS: [[2.3. Diagnostic approaches and biomarkers]] | NEXT: [[3.1. Genetic factors and familial patterns]] → -------- ##### Summary >[!Summary] >**Hypothesis** >- aetiology of POTS largely unknown[[#^1]] >- three main hypotheses: autoimmune disorder, abnormally increased sympathetic activity, catecholamine excess, sympathetic denervation[[#^1]] >- POTS can have multiple variants resulting from these multiple etiologies (partial dysautonomia, centrally mediated hyperadrenergic stimulation, norepinephrine transporter dysfunction, autoimmune anti body against cholinesterase receptors, POTS associated with deconditioning, hypovolumia, autonomic cardiac neuropathy) [[#^6]] > >**Onset** > >- frequently reported that symptoms began following acute stressors (pregnancy, major surgery, presumed viral illness)[[#^2]][[#^6]] >- in other cases symptoms develop more insidiously[[#^2]] >- a substantial number of patients do not report any triggering event and experience rather slowly progressing or even stationary symptoms over a long period of time[[#^4]] >- most talked about a preceding event that caused a sudden exacerbation or triggering of full-blown POTS symptoms, although many had already experienced some symptoms prior to that[[#^5]] -------- >*“The aetiology of POTS is largely unknown and three main hypotheses include an autoimmune disorder, abnormally increased sympathetic activity and catecholamine excess, and sympathetic denervation leading to central hypovolaemia and reflex tachycardia.” *([[Fedorowski-2019]], [p. 1](zotero://open-pdf/library/items/BZ35QDLR?page=1&annotation=24927VAU))^1 >*“Patients frequently report that their symptoms began following acute stressors such as pregnancy, major surgery, or a presumed viral illness, but in others cases, symptoms develop more insidiously.” *([[Raj-2013]], [p. 2](zotero://open-pdf/library/items/CCJLQKRB?page=2&annotation=LEIFQ6SC)) ^2 >*“The onset of POTS may be precipitated by typical immunological stressors such as viral infection, frequently of the upper respiratory or gastrointestinal tract, vaccination, trauma, pregnancy, surgery or even a period of intensive psychosocial stress [17, 21, 23–29]. The antecedent history of suspected viral infection is reported by between 20% and 50% of all patients [23, 26]. However, a substantial number of POTS patients do not report any triggering event and experience rather slowly progressing or even stationary symptoms over a long period of time [21].” *([[Fedorowski-2019]], [p. 3](zotero://open-pdf/library/items/BZ35QDLR?page=3&annotation=VM36S36S))^4 >*“In relation to participants’ understanding of the causes of POTS, most talked about a preceding event that caused a sudden exacerbation or triggering of full-blown POTS symptoms, although many had already experienced some symptoms prior to that.”* ([[Knoop-2023]], [p. 7](zotero://open-pdf/library/items/P2VFKVHY?page=7&annotation=VIP4WZPV))^5 >*“Recent research has shown that this syndrome may have multiple etiologies, and we now know that POTS can have multiple variants resulting from these multiple etiologies including partial dysautonomia [3] centrally mediated hyperadrenergic stimulation [8], norepinephrine transporter dysfunction [16], autoimmune anti body against cholinesterase receptors [21], POTS associated with deconditioning [22] and hypovolumia [23]. A recently published study reported that POTS may be a manifestation of autonomic cardiac neuropathy [24]. POTS has been reported after traumata [25] and infections [26] as well.”* ([[Kanjwal-2011]], [p. 4](zotero://open-pdf/library/items/R4GMHSS7?page=4&annotation=9LJBXQTQ))^6 >*“The circumstances surrounding symptom onset may provide useful information, with some patients developing symptoms following a period of rapid growth while others recall a traumatic or immunologic trigger such as vaccination or Epstein–Barr virus infection.”* ([[Wells-2017]], [p. 3](zotero://open-pdf/library/items/HLELIN7I?page=3&annotation=AFAQQK9I)) #new