Soluble transferrin receptor as an indicator of iron deficiency and febrile seizures

Main Article Content

Salma Salma
Rita Arifin
Erial Bahar
Rini Purnamasari


Background Iron deficiency (ID) has a high incidence in
Indonesia, and is a risk factor for febrile seizures. The most suitable
assay to detect iron deficiency in the presence of inflammation
has not yet been defined. An indicator of ID unaffected by
inflammation is needed, soluble transferrin receptor (sTfR) may
be such an indicator.
Objective To evaluate ID as a risk factor for febrile seizures in
children with inflammation by sTfR measurements.
Method We conducted an age-matched, case-control study,
focused on children experiencing on acute illnesses at the time.
Subjects were 80 children matched by age (40 in the case group
with febrile seizures, and 40 in the control group who were febrile
without seizures) aged 3 months to 5 years in Mohammad Hoesin
Hospital, Palembang from February to August 2013. Subjects’
clinical data and sTfR levels were recorded. Risk factors were
analyzed with odd ratios and 95% confident intervals. The
sTfR level cut-off point as a predictor of febrile seizures was also
defined. Other risk factors were analyzed with multivariate logistic
regression test.
Results Mean sTfR levels were 41.36 (SD 2.04) nmol/L in the
case group and 33.09 (SD 1.02) nmol/L in the control group.
Multivariate analysis revealed ID and iron deficient anemia
(IDA), as measured by sTfR levels, to be risk factors for febrile
seizures (adjusted OR=3.9; 95%CI 1.41 to 10.8; P=0.007 and
OR 3.27; 95%CI 1.21 to 8.84; P=0.017, respectively). The sTfR
level cut-off point that could be used as a predictor of febrile
seizures was 37nmol/L.
Conclusion Iron deficiency as measured by increased sTfR is
a risk factor for febrile seizures in children.

Article Details

How to Cite
Salma S, Arifin R, Bahar E, Purnamasari R. Soluble transferrin receptor as an indicator of iron deficiency and febrile seizures. PI [Internet]. 30Apr.2015 [cited 23Sep.2020];55(2):95-00. Available from:
Received 2016-06-29
Accepted 2016-06-29
Published 2015-04-30


1. Soetomenggolo TS. Kejang demam. In: Soetomenggolo TS, Ismael S, editors. Buku ajar neurologi anak. 1st ed. Jakarta: BP IDAI; 1999. p. 244-51.
2. Pusponegoro HD. Kejang demam patofisiologi dan penatalaksanaannya. In: Kustiowati E, editor. Kumpulan makalah pertemuan nasional – I epilepsi. Semarang: Penerbit UNDIP; 2004. p. 149-55.
3. Hartfield DS, Tan J, Yager JY, Rosychuk RJ, Spady D, Haines C, et al. The association between iron deficiency and febrile seizures in childhood. Clin Pediatr. 2009;48:420–6.
4. Raspati H, Reniarti L, Susanah S. Anemia defisiensi besi. In: Permono B, Sutaryo, editors. Buku ajar hematology-onkologi anak. Jakarta: BP IDAI; 2005. p. 30-42.
5. Depkes RI. Hasil riset kesehatan dasar (Riskesdas) kota Palembang tahun 2007. Available from:
6. Pisacane A, Sansone R, Impagliazzo N, Coppolo A, Rolando P, D’Apuzzo A, et al. Iron deficiency anemia and febrile convulsions: a case-control study in children under 2 years. BMJ. 1996;313:343.
7. Afifah R. Anemia defisiensi besi dan defisiensi besi sebagai faktor resiko terjadinya kejang demam. [thesis]. [Palembang]: Sriwijaya University; 2007.
8. Ahluwalia N. Diagnostic utility of serum transferrin receptors measurement in assessing iron status. Nutr Rev. 1998;56:133-41.
9. Mittal RD, Pandey A, Mittal B, Agarwal KN. Effect of latent iron deficiency on GABA and glutamate neuroreceptors in rat brain. Indian J Clin Biochem. 2003;18:111–6.
10. Testa U. Soluble transferrin receptor. In: Testa U, editor. Proteins of iron metabolism. Informa Health Care : CBC press; 2001. p. 371-80.
11. Berg AT, Shinnar S, Shapiro ED, Salomon ME, Crain EF, Hauser WA. Risk f actors for a first febrile seizure: a matched case-control study. Epilepsia. 1995;36:334–41.
12. Beard J. Iron deficiency alters brain development and functioning. J Nutr. 2003;133:1468-72.
13. Khanis. Defisiensi besi sebagai faktor risiko bangkitan kejang demam. [thesis]. [Semarang]: Universitas Diponegoro; 2010.