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TOTAL INVERSIÓN 80.752,

5.1.3 PRESUPUESTO DE COSTOS Y GASTOS

without POTS, in agreement with some (16) but not all previously reported studies (14). Several pathophysiological mechanisms have previously been described that could be responsible for the development of POTS. Such mechanisms include hypovolaemia (17, 36), increased sympathetic activity (37) and cardiovascular deconditioning (18), although it is not clear whether the latter is the cause of POTS or rather a consequence. However, given the fact that CFS patients are usually less active than healthy control subjects (22), we assumed deconditioning to be a contributing factor. Although maximum oxygen uptake during exercise is the gold standard to measure deconditioning, actometer scores give an indication of a patient’s activity pattern, and both of these methods have not been used previously in POTS-CFS patients. We did not find differences in the level of physical activity between POTS-CFS and non-POTS-CFS patients, which makes it less likely that deconditioning is the cause of POTS in these patients.

The influence of POTS on CFS treatment outcome has not been investigated previously. For adults, no differences could be found in the response to CBT. However, adolescents with POTS did have a higher fatigue score after treatment, although these patients did not report more POTS-related symptoms. Despite this significant difference, 58% of POTS-CFS adolescents were no longer severely fatigued after treatment, which indicates that treatment is still effective in the majority of patients. We propose the use of a stepped-care approach in adolescents, with evaluation for the presence of POTS in those who do not respond to CBT treatment or those who report vasovagal symptoms. Fortunately, treatment of POTS patients is remarkably successful, which means a combined approach could be effective (38). Treatment of POTS mainly includes lifestyle interventions, such as preventing dehydration and avoiding extreme heat; in addition, regular exercise should be promoted (13). There is limited evidence to support pharmacological treatment, for example using aldosterone analogues or beta-adrenergic blockers (36).

This study has several limitations. First, blood pressure measurement was resumed after a standing period of 5–8 min. This means that the reported values could be slightly underestimating the true prevalence of POTS. Nevertheless, patients with POTS had persistent tachycardia at least until 18 min in the standing position, which is consistent with the findings of others (39). In previous studies, POTS prevalence was most often based on heart rate after 2 min in the upright position, without taking into account the remaining 8 min. In that situation it should be realized that a transient tachycardia directly after standing is normal (40). Thus in daily practice, difficulties are encountered in differentiating those patients with a tachycardia upon standing from those with a normal physiological response, particularly among adolescents. Another limitation of the present study is the fact

that POTS-related symptoms were not recorded during the active standing test. However, these symptoms were recorded in the diary kept by all participants for 12 days.

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Conclusion

In conclusion, in adult CFS patients the prevalence of POTS was low and not different from that in the non-CFS fatigued population. In addition, POTS in adult CFS patients was not related to disease severity, physical activity or treatment outcome. POTS-CFS adolescent patients showed a smaller reduction in fatigue after CBT. However, as most patients still benefit from CBT, there is no reason to withhold such treatment. Based on the results of this study, evaluation for POTS appears to be of limited additional value for the diagnosis of CFS; our findings do not support the addition of POTS to a new CFS case definition as proposed by the IOM. With the new SEID criteria, we are concerned that a subset of patients will not be diagnosed with CFS, although they are not different from other patients with respect to fatigue severity or mental and physical disabilities. This eventually could lead to a delay in starting effective treatment, which is in contrast to the goal of the IOM to accelerate the diagnostic process.

Acknowledgements

We would like to thank Tiny Fasotti-Dumont, Carel Kruip and Liesbeth Nieboer for performing the blood pressure measurements. We would also like to thank Remco Oomen and Betty Roerink-Raaijmakers for their help with structuring the data.

References

1. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Redefining an Illness. The National Academies Collection: Reports funded by National Institutes of Health. Washington (DC)2015.

2. Reyes M, Nisenbaum R, Hoaglin DC, Unger ER, Emmons C, Randall B, et al. Prevalence and incidence of chronic fatigue syndrome in Wichita, Kansas. Archives of internal medicine. 2003;163(13):1530-6. 3. Viner R, Hotopf M. Childhood predictors

of self reported chronic fatigue syndrome/ myalgic encephalomyelitis in adults: national birth cohort study. Bmj. 2004;329(7472):941. 4. Lindal E, Stefansson JG, Bergmann S. The

prevalence of chronic fatigue syndrome in Iceland - a national comparison by gender drawing on four different criteria. Nordic journal of psychiatry. 2002;56(4):273-7. 5. Fukuda K, Straus SE, Hickie I, Sharpe

MC, Dobbins JG, Komaroff A. The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med. 1994;121(12):953-9. 6. Reeves WC, Lloyd A, Vernon SD, Klimas N,

Jason LA, Bleijenberg G, et al. Identification of ambiguities in the 1994 chronic fatigue syndrome research case definition and recommendations for resolution. BMC health services research. 2003;3(1):25.

7. Carruthers BM, van de Sande MI, De Meirleir KL, Klimas NG, Broderick G, Mitchell T, et al. Myalgic encephalomyelitis: International Consensus Criteria. Journal of internal medicine. 2011;270(4):327-38. 8. Holmes GP, Kaplan JE, Gantz NM,

Komaroff AL, Schonberger LB, Straus SE, et al. Chronic fatigue syndrome: a working case definition. Annals of internal medicine. 1988;108(3):387-9.

9. Haney E, Smith ME, McDonagh M, Pappas M, Daeges M, Wasson N, et al. Diagnostic Methods for Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome: A Systematic Review for a National Institutes of Health Pathways to Prevention Workshop. Annals of internal medicine. 2015;162(12):834-40. 10. Freeman R, Wieling W, Axelrod FB,

Benditt DG, Benarroch E, Biaggioni I, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clinical autonomic research : official journal of the Clinical Autonomic Research Society. 2011;21(2):69-72. 11. Task Force for the D, Management of S,

European Society of C, European Heart Rhythm A, Heart Failure A, Heart Rhythm S, et al. Guidelines for the diagnosis and management of syncope (version 2009). European heart journal. 2009;30(21):2631-71. 12. Lambert E, Lambert GW. Sympathetic

dysfunction in vasovagal syncope and the postural orthostatic tachycardia syndrome. Frontiers in physiology. 2014;5:280. 13. Raj SR. Postural tachycardia syndrome

(POTS). Circulation. 2013;127(23):2336-42. 14. Reynolds GK, Lewis DP, Richardson AM,

Lidbury BA. Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort. Journal of internal medicine. 2014;275(4):409-17.

15. Lewis I, Pairman J, Spickett G, Newton JL. Clinical characteristics of a novel subgroup of chronic fatigue syndrome patients with postural orthostatic tachycardia syndrome. Journal of internal medicine. 2013;273(5):501-10. 16. Hoad A, Spickett G, Elliott J, Newton J.

Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome. QJM : monthly journal of the Association of Physicians. 2008;101(12):961-5.

9

17. Thieben MJ, Sandroni P, Sletten DM, Benrud- Larson LM, Fealey RD, Vernino S, et al. Postural orthostatic tachycardia syndrome: the Mayo clinic experience. Mayo Clinic proceedings. 2007;82(3):308-13. 18. Parsaik A, Allison TG, Singer W, Sletten

DM, Joyner MJ, Benarroch EE, et al. Deconditioning in patients with orthostatic intolerance. Neurology. 2012;79(14):1435-9. 19. Jones JF, Nicholson A, Nisenbaum R,

Papanicolaou DA, Solomon L, Boneva R, et al. Orthostatic instability in a population- based study of chronic fatigue syndrome. The American journal of medicine. 2005;118(12):1415.

20. Prins JB, Bleijenberg G, Bazelmans E, Elving LD, de Boo TM, Severens JL, et al. Cognitive behaviour therapy for chronic fatigue syndrome: a multicentre randomised controlled trial. Lancet. 2001;357(9259):841-7.

21. Castell BD, Kazantzis N, Moss-Morris RE. Cognitive Behavioral Therapy and Graded Exercise for Chronic Fatigue Syndrome: A Meta-Analysis. Clin Psychol-Sci Pr. 2011;18(4):311-24.

22. Vercoulen JH, Bazelmans E, Swanink CM, Fennis JF, Galama JM, Jongen PJ, et al. Physical activity in chronic fatigue syndrome: assessment and its role in fatigue. Journal of psychiatric research. 1997;31(6):661-73. 23. van der Werf SP, Prins JB, Vercoulen JH,

van der Meer JW, Bleijenberg G. Identifying physical activity patterns in chronic fatigue syndrome using actigraphic assessment. Journal of psychosomatic research. 2000;49(5):373-9. 24. Stulemeijer M, Vos PE, Bleijenberg G, van

der Werf SP. Cognitive complaints after mild traumatic brain injury: things are not always what they seem. Journal of psychosomatic research. 2007;63(6):637-45.

25. Vercoulen JH, Swanink CM, Fennis JF, Galama JM, van der Meer JW, Bleijenberg G. Dimensional assessment of chronic fatigue syndrome. J Psychosom Res. 1994;38(5):383- 92.

26. Wiborg JF, van Bussel J, van Dijk A, Bleijenberg G, Knoop H. Randomised controlled trial of cognitive behaviour therapy delivered in groups of patients with chronic fatigue syndrome. Psychotherapy and psychosomatics. 2015;84(6):368-76. 27. Jacobs HM, Luttik A, Touw-Otten FW, de Melker RA. [The sickness impact profile; results of an evaluation study of the Dutch version]. Nederlands tijdschrift voor geneeskunde. 1990;134(40):1950-4.

28. Beck AT, Guth D, Steer RA, Ball R. Screening for major depression disorders in medical inpatients with the Beck Depression Inventory for Primary Care. Behaviour research and therapy. 1997;35(8):785-91.

29. Knoop H, Bleijenberg G, Gielissen MF, van der Meer JW, White PD. Is a full recovery possible after cognitive behavioural therapy for chronic fatigue syndrome? Psychotherapy and psychosomatics. 2007;76(3):171-6. 30. Naschitz JE, Sabo E, Naschitz S, Rosner

I, Rozenbaum M, Fields M, et al. Hemodynamics instability score in chronic fatigue syndrome and in non-chronic fatigue syndrome. Seminars in arthritis and rheumatism. 2002;32(3):141-8.

31. Galland BC, Jackson PM, Sayers RM, Taylor BJ. A matched case control study of orthostatic intolerance in children/adolescents with chronic fatigue syndrome. Pediatric research. 2008;63(2):196-202.

32. de Jong-de Vos van Steenwijk CC, Wieling W, Johannes JM, Harms MP, Kuis W, Wesseling KH. Incidence and hemodynamic characteristics of near-fainting in healthy 6- to 16-year old subjects. Journal of the American College of Cardiology. 1995;25(7):1615-21. 33. Singer W, Sletten DM, Opfer-Gehrking TL,

Brands CK, Fischer PR, Low PA. Postural tachycardia in children and adolescents: what is abnormal? The Journal of pediatrics. 2012;160(2):222-6.

34. Brurberg KG, Fonhus MS, Larun L, Flottorp S, Malterud K. Case definitions for chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME): a systematic review. BMJ open. 2014;4(2):e003973.

35. Timmers HJ, Wieling W, Soetekouw PM, Bleijenberg G, Van Der Meer JW, Lenders JW. Hemodynamic and neurohumoral responses to head-up tilt in patients with chronic fatigue syndrome. Clinical autonomic research : official journal of the Clinical Autonomic Research Society. 2002;12(4):273-80.

36. Jacob G, Shannon JR, Black B, Biaggioni I, Mosqueda-Garcia R, Robertson RM, et al. Effects of volume loading and pressor agents in idiopathic orthostatic tachycardia. Circulation. 1997;96(2):575-80.

37. Garland EM, Raj SR, Black BK, Harris PA, Robertson D. The hemodynamic and neurohumoral phenotype of postural tachycardia syndrome. Neurology. 2007;69(8):790-8.

38. Sousa A, Lebreiro A, Freitas J, Maciel MJ. Long-term follow-up of patients with postural tachycardia syndrome. Clinical autonomic research : official journal of the Clinical Autonomic Research Society. 2012;22(3):151-3.

39. Carew S, Cooke J, O’Connor M, Donnelly T, Costelloe A, Sheehy C, . What is the optimal duration of tilt testing for the assessment of patients with suspected postural tachycardia syndrome? Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2009;11(5):635-7.

40. Raj SR. The Postural Tachycardia Syndrome (POTS): pathophysiology, diagnosis & management. Indian pacing and electrophysiology journal. 2006;6(2):84-99.

Chapter 10

Summary and future

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