Quick Search
  Home Journal Information Current Issue Past Issues Services Contact Us  
Low iron storage in children with tilt positive neurally mediated syncope 
Low iron storage in children with tilt positive neurally mediated syncope
  Baris Guven, Taliha Oner, Vedide Tavli, Murat Muhtar Yilmazer, Savas Demirpence, Timur Mese
 [Abstract] [Full Text] [PDF]   Pageviews: 10083 Times

Low iron storage in children with tilt positive neurally mediated syncope

Baris Guven, Taliha Oner, Vedide Tavli, Murat Muhtar Yilmazer, Savas Demirpence, Timur Mese

Izmir, Turkey

Author Affiliations: Department of Pediatric Cardiology, Izmir Dr Behcet Uz Children's Hospital, Izmir, Turkey (Guven B, Oner T, Tavli V, Yilmazer MM, Demirpence S, Mese T)

Corresponding Author: Baris Guven, M.D., Pediatric Cardiology, Izmir Dr Behcet Uz Children's Hospital,  Izmir, Turkey (Tel: +902324895656-2210; Fax: +902324892315; Email: drbarisguven@yahoo.com)

doi: 10.1007/s12519-012-0396-7

Background: The mechanisms under neurally mediated syncope (NMS) are not fully understood. This study aimed to assess the level of storage iron in children with different hemodynamic patterns in head-up tilt test.

Methods: Altogether 210 children (11.31¡À2.49 years) with syncope or pre-syncope treated between May 2008 and September 2010 were studied prospectively. Following history taking and physical examination, their levels of hemoglobin (Hb), hematocrit (Hct) and serum ferritin were measured.

Results: In the 210 children, 162 (77.1%) had NMS and 48 (22.9%) had syncope due to other causes. In the 162 children with NMS, 98 children were subjected to positive tilt test. The level of serum ferritin was significantly lower in the 98 children with NMS (P<0.001). The comparison of levels of Hb, Hct and mean cell volume (MCV) displayed no significant difference between the two groups. Reduced iron storage (serum ferritin <25 ng/mL) was found to be more prevalent in children with NMS (63% vs. 20%, P<0.001). Prevalence of iron deficiency was also significantly higher in children with NMS than in children with syncope due to other causes (27% vs. 6%, P=0.003).

Conclusions: In head-up tilt test positive children with NMS, the level of serum ferritin should be evaluated. Low storage iron may be one of the underlying mechanisms of NMS.

Key words: head-up tilt table test; neutrally mediated syncope; serum ferritin

World J Pediatr 2013;9(2):146-151


Syncope remains one of the most widespread, still annoying, sign-complexes in children, which are characterized by abrupt loss of consciousness and postural tone with complete recovery of symptoms. Syncope is a common problem in children and adolescents, with 15% to 25% of them experiencing at least one syncopal episode in early adulthood.[1] The most common form of syncope in children is neurally mediated syncope (NMS), frequently denoted as the simple faint, which comprises nearly 75% or more of patients.[2-4] Diagnosis of NMS is established by history, frequently verified by tilt testing.[5] The presentation of syncope possibly will be dramatic, and direct physicians to suspect a malignant cardiac situation.

Thus studies proposed that patients with NMS have a high prevalence of orthostatic intolerance and chronic fatigue syndrome.[6,7] There is also evidence from studies in adults that iron deficiency anemia may have a role in the pathogenesis of chronic fatigue.[8] Besides, investigations in patients with orthostatic hypotension have demonstrated a beneficial effect following the use of erythropoietin, commonly given with iron supplementation.[9] Moreover, there are reports suggesting that breath-holding spell, a brief period of loss of consciousness in infants and young children, shares similar pathophysiological mechanisms with NMS.[10] It has been shown that iron has a therapeutic effect on children with breath holding spell, even if they are non-anemic.[11]

We hypothesized that low iron may have a role in the pathogenesis of NMS. Therefore, we assessed the complete blood count and iron parameters in children, who had a history of recurrent syncope attacks.


Study population

The study was approved by the ethical committee of Izmir Behcet Uz Children's Hospital, and followed the Declaration of Helsinki. Informed consents were obtained from parents of each child. Between May 2008 and August 2010, 210 children (aged 11.31¡À2.49 years) with syncope or pre-syncope were prospectively evaluated for eligibility to participate in the study. Syncope was defined as loss of consciousness or loss of posture. Presence of any premonitory signs of an imminent syncope was described as pre-syncope. Patients with structural heart disease, congenital long QT syndrome, Brugada syndrome, chronic illnesses (diabetes mellitus, renal or liver disease), acute systemic illness or those on medication recognized to alter heart rate or to cause orthostatic hypotension were excluded. The inclusion criteria were as follows: (1) age younger than 18 years; (2) history of NMS; (3) less than 6 months between index episode of syncope, pre-syncope and first assessment; and (4) no history of infection at the time of blood sampling. Physical examination, 12-lead electrocardiography and transthoracic echocardiography were normal in all subjects who were recruited in the study.

Head-up test protocol

All children were tested in the morning after fasting for 8 hours. Studies were carried out in silent, dimly lit room at a comfortable ambient temperature (20¡ãC-24¡ãC). Heart rate was monitored continuously, and blood pressure was recorded every 2 minutes using an automatic sphygmomanometer. The children were then kept in a supine position for 10 minutes. Subsequently, they were tilted to a head-up position at 85¡ã for 20 minutes. Previous reports showed that this protocol was associated with optimal and adequate sensitivity rates.[12,13] Positive response was defined as the occurrence of syncope or pre-syncope during the head-up tilt test, accompanied by at least one of the following signs:[14] (1) bradycardia, characterized by heart rate <75 bpm in children of 4 to 6 years old, heart rate <65 bpm in children of 7 to 8 years old, heart rate <60 bpm in children of more than 8 years old, sinus arrest, degree II or greater atrioventricular block and asystole for 3 seconds; (2) hypotension defined as ¡Ü80 mmHg in systolic blood pressure or drop of >15 mmHg or/and diastolic blood pressure <50 mmHg; and (3) junctional rhythm together with escaped rhythm and accelerated idioventricular rhythm. Cardioinhibitory response was defined as an abrupt decrease in heart rate. Vasodepressor response was defined as a decrease in blood pressure. The mixed pattern was characterized by a decrease in both heart rate and blood pressure.[15] Postural orthostatic tachycardia syndrome (POTS) was diagnosed on the basis of a heart rate increase >30 bpm or the maximum heart rate >120 bpm in the absence of profound hypotension but reproducing light headedness, fatigue, pre-syncope and dizziness.[16]

Study design

The history of first event was taken from the child, the parents, and other witnesses if possible. Afterwards, all the children were re-evaluated, and symptoms were ordered into two sets. Children who fit the inclusion criteria were assigned to the NMS group. The criteria applied to classify the attack of loss of consciousness as revealing sign of NMS have been described previously in detail.[17,18] The inclusion criteria for NMS were as follows: a short period of attack, syncope characterized by the existence of triggering factors (e.g., strong fear, pain, medical procedure, heat), syncope with POTS or autonomic dysfunction. We excluded children who had negative tilt test. Children, who did not meet any condition of the inclusion criteria for NMS, formed the other syncope group. The other syncope group comprised children with uncertain, metabolic and neurological causes of syncope. The children with tilt positive were divided into two groups according to the tilt response pattern as POTS group and vasovagal syncope (VVS) group.

Analytical methods

Blood samples were obtained for analysis of serum ferritin, hemoglobin (Hb), hematocrit (Hct) and mean cell volume (MCV). The samples were collected after an 8-hour fasting in the morning. Iron deficiency was defined with a ferritin level of less than 15 ng/mL.[19] Low iron level was considered if it was lower than 25 ng/mL.[20,21] Iron deficiency anemia was defined as iron deficiency plus low hemoglobin values.[22]

Statistical analysis

The results of descriptive analysis were expressed as mean ¡À SD for numerical variables. The normality of distribution was examined by the Kolmogorov-Smirnov test. Only one parameter, serum ferritin, was not normally distributed. The mean values of normally distributed variables were compared between the groups using Student's t test; if not normally distributed using the Mann-Whitney U test. The Kruskal-Wallis test was used to determine statistical significance between continuous variables. If the overall P value was significant, the Mann-Whitney U test was conducted to evaluate the differences among the groups. The Chi-square test was performed for each categorical variable.


The demographic and clinical characteristics of our study are shown in Table 1. Among the 210 children with syncope, 162 (77.1%) had NMS and 48 (22.9 %) had syncope due to other causes. In the 162 children with NMS, 98 had a positive tilt test. No significant difference was found in mean age and sex distribution between the two groups (P=0.545 and P=0.409, respectively). The prevalence of palm sweat was higher in the NMS group than in the other causes group (P<0.001). However, there was no significant difference in headache and pale frequency between the two groups (P=0.26 and P=0.26, respectively).

During the head-up tilt table test, vasodepressor response was seen in 16 of the 98 children in the NMS group, cardioinhibitory response in 13, mixed pattern response in 21, and POTS pattern in 48.

Clinical and laboratory studies in the 48 children with syncope other than NMS revealed that 22 children had neurological problems (epilepsy, hyperventilation syndrome, and head injury), 7 had atypical syncope (conversion), and 2 had cardiac problems (aortic stenosis, arrhythmia). No definite cause was found in 17 patients. Hematological parameters and ferritin levels in both groups are shown in Table 2. The ferritin level was found to be significantly lower in children in the NMS group than in those in the other causes group (P<0.001). On the other hand, the comparison of Hb, Hct and MCV levels showed no significant difference between the two groups. Reduced iron storage (serum ferritin <25 ng/mL), pointing to either probable inadequate or almost totally depleted iron stores, was found to be more prevalent among children with NMS (63% vs. 20%, P<0.001). Iron deficiency was observed more often in children with NMS than those with syncope due to other causes (27% vs. 6%, P=0.003). Iron deficiency was observed in 27 of the 98 children in the NMS group and in 48 children in the other causes group. In the 98 children with NMS, 50 (34.2%) demonstrated VVS pattern and 48 (32.9%) POTS pattern. When the Kruskal-Wallis test was used to evaluate the significance of differences in the levels of ferritin among the above-mentioned groups, it was demonstrated that children with vasovagal syncope patterns and POTS patterns had significantly lower serum ferritin levels than the other causes group (24.50¡À14.37 ng/mL, 24.20¡À17.24 ng/mL, 39.25¡À18.45 ng/mL, respectively, P<0.001, Fig.). Furthermore, there was no significant difference in iron and hematological indices between children with vasovagal syncope and those with POTS (Table 3).


We investigated the relationship between serum ferritin and NMS as well as the relationship between ferritin and types of NMS. We also investigated hemoglobin, hematocrit and MCV in children with NMS. To our knowledge, this is the first study to evaluate iron deficiency in different types of NMS which is confirmed by tilt table test although some aspects have been covered previously.[23] The determination of serum ferritin as a simple laboratory method for assessing the amount of the body iron store was performed in the 1970s.[24] Although the level of serum ferritin is a distinctive marker for the initial stage of iron deficiency, the limitation of serum ferritin is the boost in iron levels that occurs independently in children with inflammation, malignancy or liver disease.[25] Further commonly used laboratory tests such as serum iron, total iron binding capacity, mean corpuscular volume and transferrin saturation are of less diagnostic significance over ferritin.[26] Decreased iron storage or serum ferritin <25 ng/mL was 2.5 times more prevalent in 56.1% of children with NMS than in healthy children. However, no difference was observed in prevalence of low iron storage among subsets of NMS. Depleted iron store and reduced transport iron (as measured by transferrin saturation) occur in children with iron deficient erythropoiesis, which is the second stage of iron deficiency.[21] Jarjour and Jarjour[23] found that low transferrin saturation as an indicator for iron deficient erythropoiesis was present in 23% of children with NMS. The last stage of iron deficiency is anemia. According to Hallberg,[26] in patients with nutritional deficiency, in whom anemia is usually insignificant, a great number of children with iron deficiency would not be recognized via measurements of hemoglobin, because of the overlapping of normal and pathological findings. In the present study, no significant differences in hemoglobin and hematocrit were found between children with NMS and those with syncope due to other causes. However, anemia was more prevalent in the NMS group than in the other causes group. 

The mechanisms underlying syncopal episodes have been the topic of clinical-investigative interest during the last decade. There are various reports suggesting that sympathoneural and adrenomedullary hormonal systems play crucial roles in several expression of cardiovascular stress response.[27] Epinephrine and norepinephrine may circulate for 1 to 3 minutes to preserve a somewhat prolonged symphathoexcitatory effect.[28] A clinical study demonstrated that there is a common dissociation between sympathoneural and adrenomedullary catecholamine release during the syncope episode.[29] Kikushima et al[30] found that epinephrine surge possibly will activate NMS. Evidence from several animal studies suggested that epinephrine can increase the activity of ventricular mechanoreceptors and provoke the Bezold-Jarisch reflex through dynamic contraction.[31,32] Moreover, high plasma norepinephrine levels are found in children with postural orthostatic tachycardia syndrome.[33] Some reports suggested that iron deficiency may be linked to alterations in catecholamine metabolism. This finding is supported by the evidence that monoamine oxidase activity is reduced in iron-deficiency rats.[34] In vivo studies also suggested that platelets of patients with iron deficiency include decreased monoamine oxidase activity.[35] It is known that catecholamines such as epinephrine and norepinephrine are metabolized by monoamine oxidase. Urinary norepinephrine was found to be higher in children with iron deficiency than in normal children and the high level of urinary norepinephrine was reversed after one week of iron therapy.[36] We found that the prevalence of palm sweat was greater in children with NMS than in those with syncope due to other causes. It was found that sympathetic nervous hyperactivity may lead to palmar hyperhidrosis.[37] The result of our study confirmed the role of the sympathetic nervous system in the pathogenesis of NMS.

Since the early 1980s, studies have focused on the association of iron and cardiovascular diseases.[38-42] It was found that iron deficiency can lead to ventricular hypertrophy in developing rats.[38,39,41] Although the exact pathogenesis of ventricular hypertrophy in iron deficiency is not clear, the underlying mechanisms are supposed to be changes of blood volume, chronic elevation of sympathetic nervous activity, and alterations of alpha and beta receptor expressions in the heart.[43,44] Moreover, changes in distensibility of the abdominal aorta were observed in rats.[41] Turner et al[41] found that iron deficiency hypertrophic hearts demonstrated altered cardiovascular response to intravenous epinephrine, and the abdominal aorta of iron deficiency rats displayed significantly increased distensibility. Reduced peripheral vascular resistance in anemic patients is another theory describing the association of iron deficiency and NMS.[45] Furuland et al[45] reported that normalization of hemoglobin after erythropoietin therapy elevated blood viscosity and peripheral vascular resistance in predialysis patients. In the present study, although hemoglobin levels were slightly lower in children with NMS, they were not significantly different from those in children with syncope due to other causes. We also did not find any significant difference in the prevalence of iron deficiency anemia between children with NMS and those with syncope due to other causes. Clinical studies suggested that decreased erythrocyte mass may play a role in the pathogenesis of patients with orthostatic hypotension and chronic fatigue.[9,46] Erythropoietin therapy might be effective to such patients.[46] Similar findings have also been observed in patients with POTS. Raj et al[47] reported that patients with POTS have a deficit in red blood cell volume. In the mentioned studies, however, hemoglobin levels and iron indices were not determined.

In this study, limitations include the possible bias caused by excluding hematological parameters of patients who had negative tilt test and lack of data on iron indices and hematological parameters in Turkish children and adolescents. Therefore, reference values reported by others[20,22] were used. In conclusion, the present study shows that low serum ferritin may cause NMS. Serum ferritin should be measured in children with NMS. Further investigations for a large group of patients are needed to elucidate the role of low iron storage in the pathogenesis of NMS.

Funding: None.

Ethical approval: Our study was conducted according to the proper standards and ethics, and approved by the Izmir Dr Behcet Uz Children's Hospital Ethical Committee.

Competing interest: None to declare.

Contributors: Guven B was the responsible investigator. Oner T contributed to collection of data and manuscript editing. Tavli V was the head of the study. Yilmazer MM contributed to collection of data. Demirpence S contributed to data analysis. Mese T contributed to collection of data and data analysis.


1   Day SC, Cook EF, Funkenstein H, Goldman L. Evaluation and outcome of emergency room patients with transient loss of consciousness. Am J Med 1982;73:15-23.

2   Steinberg LA, Knilans TK. Syncope in children: diagnostic tests have a high cost and low yield. J Pediatr 2005;146:355-358.

3   McHarg ML, Shinnar S, Rascoff H, Walsh CA. Syncope in childhood. Pediatr Cardiol 1997;18:367-371.

4   Massin MM, Bourguignont A, Coremans C, Comt¨¦ L, Lepage P, G¨¦rard P. Syncope in pediatric patients presenting to an emergency department. J Pediatr 2004;145:223-228.

5   Benditt DG, Ferguson DW, Grub BP, Kapoor WN, Kugler J, Lerman BB, et al. Tilt table testing for assessing syncope. American College of Cardiology. J Am Coll Cardiol 1996;28:263-275.

6   Stewart JM, Gewitz MH, Weldon A, Munoz J. Patterns of orthostatic intolerance: the orthostatic tachycardia syndrome and adolescent chronic fatigue. J Pediatr 1999;135(2 Pt 1):218-225.

7   Kenny RA, Graham LA. Chronic fatigue symptoms are common in patients with vasovagal syncope. Am J Med 2001;110:242-243.

8   Beutler E, Larsh SE, Gurney CW. Iron therapy in chronically fatigued, nonanemic women: a double-blind study. Ann Intern Med 1960;52:378-394.

9   Hoeldtke RD, Streeten DH. Treatment of orthostatic hypotension with erythropoietin. N Engl J Med 1993;329:611-615.

10 Bridge EM, Livingston S, Tietz C. Breath holding spells: their relationship to syncope, convulsions, and other phenomena. J Pediatr 1943;23:539-561.

11 Daoud AS, Batieha A, al-Sheyyab M, Abuekteish F, Hijazi S. Effectiveness of iron therapy on breath holding spells. J Pediatr 1997;130:547-550.

12 Grubb BP, Temesy-Armos P, Moore J, Wolfe D, Hahn H, Elliott L. The use of head-upright tilt table testing in the evaluation and management of syncope in children and adolescents. Pacing Clin Electrophysiol 1992;15:742-748.

13 Strieper MJ, Auld DO, Hulse JE, Campbell RM. Evaluation of recurrent pediatric syncope: role of tilt table testing. Pediatrics 1994;93:660-662.

14 Qingyou Z, Junbao D, Jianjun C, Wanzhen L. Association of clinical characteristics of unexplained syncope with the outcome of head-up tilt tests in children. Pediatr Cardiol 2004;25:360-364.

15 Brignole M, Menozzi C, Del Rosso A, Costa S, Gaggioli G, Bottoni N, et al. New classification of hemodynamics of vasovagal syncope: beyond the VASIS classification. Analysis of the pre-syncopal phase of the tilt test without and with nitroglycerin challenge. Vasovagal Syncope International Study. Europace 2000;2:66-76.

16 Grubb BP, Kosinski DJ, Boehm K, Kip K. The postural orthostatic tachycardia syndrome: a neurocardiogenic variant identified during head-up tilt table testing. Pacing Clin Electrophysiol 1997;20(9 Pt 1):2205-2212.

17 Willis J. Syncope. Pediatr Rev 2000;21:201-204.

18 Sheldon R, Rose S, Connolly S, Ritchie D, Koshman ML, Frenneaux M. Diagnostic criteria for vasovagal syncope based on a quantitative history. Eur Heart J 2006;27:344-350.

19 Hallberg L, Bengtsson C, Lapidus L, Lindstedt G, Lundberg PA, Hult¨¦n L. Screening for iron deficiency: an analysis based on bone-marrow examinations and serum ferritin determinations in a population sample of women. Br J Haematol 1993;85:787-798.

20 Milman N, Ulrik CS, Graudal N, Jordal R. Iron status in young Danes: evaluation by serum ferritin and haemoglobin in a population of 634 individuals aged 14-23 yr. Eur J Haematol 1997;58:160-166.

21 Centers for Disease Control and Prevention. Recommendations to prevent and control iron deficiency in the United States. MMWR Recomm Rep 1998;47:1-29.

22 Looker AC, Dallman PR, Carroll MD, Gunter EW, Johnson CL. Prevalence of iron deficiency in the United States. JAMA 1997;277:973-976.

23 Jarjour IT, Jarjour LK. Low iron storage in children and adolescents with neurally mediated syncope. J Pediatr 2008;153:40-44.

24 Addison GM, Beamish MR, Hales CN, Hodgkins M, Jacobs A, Llewellin P. An immunoradiometric assay for ferritin in the serum of normal subjects and patients with iron deficiency and iron overload. J Clin Pathol 1972;25:326-329.

25 Cook JD. Defining optimal body iron. Proc Nutr Soc 1999;58:489-495.

26 Hallberg L. Perspectives on nutritional iron deficiency. Annu Rev Nutr 2001;21:1-21.

27 Goldstein DS. Clinical assessment of catecholaminergic function. In: Goldstein DS, eds. Stress, Catecholamines, and Cardiovascular Disease. New York: Oxford University Press, 1995: 234-286.

28 Quan KJ, Carlson MD, Thames MD. Mechanisms of heart rate and arterial blood pressure control: implications for the pathophysiology of neurocardiogenic syncope. Pacing Clin Electrophysiol 1997;20:764-774.

29 Robertson D, Johnson GA, Robertson RM, Nies AS, Shand DG, Oates JA. Comparative assessment of stimuli that release neuronal and adrenomedullary catecholamines in man. Circulation 1979;59:637-643.

30 Kikushima S, Kobayashi Y, Nakagawa H, Katagiri T. Triggering mechanism for neurally mediated syncope induced by head-up tilt test: role of catecholamines and response to propranolol. J Am Coll Cardiol 1999;33:350-357.

31 Oberg B, Thor¨¦n P. Increased activity in left ventricular receptors during hemorrhage or occlusion of caval veins in the cat: a possible cause of the vasovagal action. Acta Physiol Scand 1972;85:164-173.

32 Barron KV, Bishop VS. Influence of vagal afferents on the left ventricular contractile performance in response to intracoronary administration of catecholamines in the conscious dog. Circ Res 1981;49:159-169.

33 Vincent S, Robertson D. The broader view: catecholamine abnormalities. Clin Auton Res 2002;12 Suppl 1:I44-49.

34 Symes AL, Missala K, Sourkes TL. Iron and riboflavin-dependent metabolism of a monoamine in the rat in vivo. Science 1971;174:153-155.

35 Callender S, Grahame-Smith DG, Woods HF, Youdim MB. Reduction of platelet monoamine oxidase activity in iron deficiency anaemia. Br J Pharmacol 1974;52:447P-448P.

36 Voorhess ML, Stuart MJ, Stockman JA, Oski FA. Iron deficiency anemia and increased urinary norepinephrine excretion. J Pediatr 1975;86:542-547.

37 Kazemi B, Yahyaii L, Salmanpour R, Hadianfard MJ, Shirzi ZR. Comparison of sympathetic skin response between palmar hyperhidrotic and normal subjects. Electromyogr Clin Neurophysiol 2004;44:51-55.

38 Rossi MA, Carillo SV. Pathogenesis of cardiac hypertrophy in iron deficiency anaemia: the role of noradrenaline. Br J Exp Pathol 1982;63:269-277.

39 Rossi MA, Carillo SV, Oliveira JS. The effect of iron deficiency anemia in the rat on catecholamine levels and heart morphology. Cardiovas Res 1981;15:313-319.

40 Tanne Z, Coleman R, Nahir M, Shomrat D, Finberg JP, Youdim MB. Ultrastructural and cytochemical changes in the heart of iron-deficient rats. Biochem Pharmacol 1994;47:1759-1766.

41 Turner LR, Premo DA, Gibbs BJ, Hearthway ML, Motsko M, Sappington A, et al. Adaptations to iron deficiency: cardiac functional responsiveness to norepinephrine, arterial remodeling, and the effect of beta-blockade on cardiac hypertrophy. BMC Physiol 2002;2:1.

42 Medeiros DM, Beard JL. Dietary iron deficiency results in cardiac eccentric hypertrophy in rats. Proc Soc Exp Biol Med 1998;218:370-375.

43 Whittaker P, Mahoney AW, Hendricks DG. Effect of iron-deficiency anemia on percent blood volume in growing rats. J Nutr 1984;114:1137-1142.

44 Beard JL, Tobin B, Smith SM. Norepinephrine turnover in iron deficiency, at three environmental temperatures. Am J Physiol 1988;255:R90-96.

45 Furuland H, Linde T, Sandhagen B, Andr¨¦n B, Wikström B, Danielson BG. Hemorheological and hemodynamic changes in predialysis patients after normalization of hemoglobin with epoetin-alpha. Scand J Urol Nephrol 2005;39:399-404.

46 Streeten DH, Thomas D, Bell DS. The roles of orthostatic hypotension, orthostatic tachycardia, and subnormal erythrocyte volume in the pathogenesis of the chronic fatigue syndrome. Am J Med Sci 2000;320:1-8.

47 Raj SR, Biaggioni I, Yamhure PC, Black BK, Paranjape SY, Byrne DW, et al. Renin-aldosterone paradox and perturbed blood volume regulation underlying postural tachycardia syndrome. Circulation 2005;111:1574-1582.

Received July 5, 2011 Accepted after revision September 29, 2011


  [Articles Comment]

  title Author The End Revert Time Revert / Count

  Comment Title: 


World Journal of Pediatric Surgery

roger vivier bags 美女 美女

Home  |  Journal Information  |  Current Issue  |  Past Issues  |  Journal Information  |  Contact Us
Children's Hospital, Zhejiang University School of Medicine, China
Copyright 2007  www.wjpch.com  All Rights Reserved Designed by eb