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ORIGINAL ARTICLE
Year : 2022  |  Volume : 49  |  Issue : 3  |  Page : 288-293

Iron and zinc deficiency in children with febrile convulsions aged 6‒60 months ‒ A 1-year hospital-based case‒control study


1 Department of Paediatrics, JNMC, KLE University, Belagavi, Karnataka, India
2 Department of Paediatric Neurology, JNMC, KLE University, Belagavi, Karnataka, India
3 Department of Community Medicine, JNMC, KLE University, Belagavi, Karnataka, India

Date of Submission18-Jun-2021
Date of Acceptance19-Apr-2022
Date of Web Publication27-Dec-2022

Correspondence Address:
Dr. Tanmaya Metgud
Department of Paediatrics, JNMC, KLE University, Belagavi, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jss.jss_83_21

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  Abstract 


Context: Febrile seizures are one of the most common seizures in childhood. Febrile seizures occur in 2%–5% of children who are younger than 5 years of age. Studies have shown that iron, zinc, selenium, copper, and magnesium play a significant role in febrile seizures. This study was intended to study the relationship between iron and zinc deficiency with febrile seizures. Aim: To find the association of febrile convulsions with iron and zinc deficiency. Methodology: This hospital-based casecontrol study was done in a tertiary care center in North Karnataka from January 2017 to December 2017. A total of 52 children fulfilling the inclusion criteria were included in case group. Control group contained 52 children who had fever without convulsions and matched for age, sex, and background disease with respective cases. Results: Both the groups were matched for age and gender. Majority of the children (76.92%) had a simple seizure. Cases had lower serum (Sr.) ferritin levels compared to controls with high odds ratio (OR) (25% vs. 1.92%; P < 0.001; OR = 17.00; P = 0.0075). Furthermore, cases had zinc deficiency compared to controls (84.62% vs. 25%; OR = 12.269; P < 0.001). The mean Sr. zinc levels (37.16 ± 22.07 vs. 75.75 ± 15.25 μg/dL; P < 0.001) were significantly low in cases. Conclusion and Interpretation: There was a significant association between febrile seizures with iron and zinc deficiency.

Keywords: Febrile seizures, iron deficiency, zinc deficiency


How to cite this article:
Mallela J, Metgud T, Kamate M, Kadeangadi DM. Iron and zinc deficiency in children with febrile convulsions aged 6‒60 months ‒ A 1-year hospital-based case‒control study. J Sci Soc 2022;49:288-93

How to cite this URL:
Mallela J, Metgud T, Kamate M, Kadeangadi DM. Iron and zinc deficiency in children with febrile convulsions aged 6‒60 months ‒ A 1-year hospital-based case‒control study. J Sci Soc [serial online] 2022 [cited 2023 Jan 31];49:288-93. Available from: https://www.jscisociety.com/text.asp?2022/49/3/288/365182




  Introduction Top


A seizure is caused by abnormal electrical discharge inside the brain, and it is a paroxysmal event.[1],[2] A simple febrile seizure is usually generalized, lasts for a short period and does not recur.[3],[4],[5] Febrile seizures occur in 2%‒5% of children who are younger than 5 years of age, with a peak incidence in the 2nd year of life, and they are the single most common seizure type.[5],[6] Febrile seizures account for 30% of all seizures types in children.[2],[7] This is a response of the immature brain to fever in children, which is age dependent,[2],[8] and it occurs in children who do not have evidence of metabolic disturbance, intracranial infection, or any history of afebrile seizures.[9] Between 6 months and 3 years of age, 80%–85% of febrile seizures occur, and the peak incidence is usually at 18 months.[6],[10]

The most important micronutrient which is used by almost all the cells in the human body is iron. Iron acts as a cofactor for the synthesis of several enzymes in the body and it also has a role in the production and functioning of neurotransmitters. It is also useful in deoxyribonucleic acid duplication and functioning of hormones.[11],[12] Maximum prevalence of iron-deficiency anemia (IDA) is between 1 and 2 years.[11],[13] Functioning of neurons is stimulated by iron deficiency (ID) and consequently, the risk of febrile seizures is increased.[13],[14] The exact relationship between febrile seizures and IDA is not known. According to some studies, IDA is considered a risk factor for the development of febrile seizures and no relation according to some studies.[11] IDA has a protective effect on the development of febrile seizures, according to some studies.[2] There was a controversy regarding the role of ID with febrile seizures.

Synthesis of Gamma amino butyric acid (GABA) is regulated by zinc and has a regulatory effect on glutamic acid decarboxylase.[9],[15] Zinc is useful for proteins and cellular metabolism, enzymatic activity of different organs, hormone release, nerve impulse transmission, and neurological functions.[2],[16],[17] Different studies have mentioned about the possible role of zinc deficiency in provoking febrile seizures.[2],[9],[18],[19] It also modifies neurotransmitters affinity, and thus, excitatory neuronal discharge is prevented.[2],[7]

Although febrile seizures seem to be a benign condition which causes fear and anxiety among parents due to seizures, it is essential to evaluate modifiable risk factors of febrile seizures such as iron and zinc deficiency. Here are limited data which show the association of zinc deficiency[20],[21],[22] with febrile seizures. Similarly, few studies have been attempted to evaluate the relationship between ID and febrile seizures, but the results are controversial.[3],[11] Hence, the present study sought to find the association of febrile seizures with ID and zinc deficiency.


  Methodology Top


This present hospital-based case‒control study was undertaken at a tertiary care center situated in North Karnataka, India, for 1 year from January 2017 to December 2017. Based on the previous study, considering ID as 48% in children with febrile seizure as against 28% in controls, with odds ratio (OR) of 4.3 (P = 0.03),[23] the sample size was calculated using the formula as mentioned below.

n = 2 (Zα + Zβ)2 pq/(P1 – P2)2

=2 (1.95 + 0.84)2 × 14.65 × 85.35/(26.7)2

=47 + 10% = 51.7 ≈ 52 (taking Zα =1.95)

hence, groups of 52 were considered for the study.

Children presenting with febrile seizures (both simple and complex), aged between 6 and 60 months of age, temperature of >38°C (100.4°F) with no evidence of Central nervous system (CNS) infection/metabolic abnormalities, and no history of prior afebrile seizures were selected for the study. Children with structural brain damage, history of afebrile seizures, chronic systemic disease (cardiac, renal, metabolic, malignancy, and rheumatologic), and neurodevelopmental delay were excluded from the study. Febrile seizures were defined as[24] generalized, tonic‒clonic, associated with fever, lasting for a maximum of 15 min, and not recurrent within a 24-h period. Complex febrile seizures were defined as[24] more prolonged (>15 min), focal, and recurred within 24 h. Children of the control groups were selected using objective-based method matched with cases in terms of age, gender, and background disease. Before the commencement, the ethical clearance was obtained from the Institutional Ethical committee.

Parents or legal guardians or attendants of the children fulfilling the selection criteria were selected and their guardians were briefed about the nature of the study in their local language, and written informed consent was obtained. After obtaining written informed consent, parents were interviewed, and sociodemographic data, along with a detailed history of the child with specific reference to seizures and birth history were obtained. A detailed examination of the child was done.

Under aseptic precautions, 3 mL of venous blood (without any anticoagulant) was taken and centrifuged at 3000 cycles per minute over 10 min. The serum (Sr.) obtained was stored at 80°C, which was used for the estimation of iron and 1 mL was taken for the estimation of zinc. The venous blood was investigated for hemoglobin (Hb) level, peripheral smear, Sr. ferritin, erythrocyte sedimentation rate (ESR), red cell distribution width (RDW), and Sr. iron and Sr. zinc levels.

ID was defined as Sr. ferritin levels <12 ng/mL under normal ESR OR <30 ng/mL in the presence of raised ESR or Sr. iron levels <22 μg/dL.[25] Estimation of Sr. ferritin levels was done by electrochemiluminenscence immunoassay on Cobas analyzer.

The diagnosis of ID was mainly relied on Sr. ferritin levels due to the variation between subjects is at least as large and suggests that assessing iron status based on a single measurement of plasma iron concentration has a high risk of misclassifying iron status and may lead to an error in any estimate of prevalence.[25] IDA was defined as children having Hb <11 gm/dL, and peripheral smear showing microcytic hypochromic anemia along with RDW of >15%.[26] Sr. ferritin levels <12 ng/mL in patients with normal ESR OR <30 ng/mL in patients with raised ESR, or Sr. iron levels <22 μg/dL.[25]

Zinc levels were measured by flame atomic absorption spectroscopy using Atomic Absorption Spectrophotometer AA-7000 (Shimadzu, Japan), Department of Scientific and Industrial Research, Government of India approved. Normal range of zinc using the above technique was interpreted as 65 μg/dL.[23],[26]

Statistical analysis

Data were analyzed using the SPSS statistical software version 20.0. Categorical data were expressed as rates, ratios, and percentages. Continuous data were expressed as mean ± standard deviation. Chi-square test and/or Fisher's exact test were used to find the association between two variables. The risk stratification was determined by calculating OR for iron and zinc deficiency. A probability (P) value of ≤0.050 at a 95% confidence interval (CI) was considered statistically significant.


  Results Top


The boy-to-girl ratio in this both groups was 2.25:1 (P = 1.000). In cases and controls, 51.92% of the children were aged between 1–2 years (P = 1.000). Lower respiratory tract infection and gastroenteritis were noted in 55.77% and 30.77% of the children each, respectively, in cases and controls (P = 1.000). The family history of febrile seizures was significantly high in cases (21.15%) compared to controls (5.77%) (P = 0.041). Natal history revealed a significantly higher number of children with low birth weight in cases and controls (13.46% vs. 5.77%; P = 0.607). Significantly higher number of the children in cases had RDW of ≥15 compared to controls (71.15% vs. 44.23%; P = 0.010) and microcytic hypochromic picture on peripheral smear compared to controls (67.3% vs. 19.23%; P < 0.001) [Table 1]. The seizure profile (type of seizure of the children, the time gap between fever and seizure and history of similar episodes in the past) is shown in [Table 2].
Table 1: Demographic, clinical characteristics, and clinical profile of the children

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Table 2: Seizure profile in cases

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Significantly higher number of children in cases had lower Sr. ferritin levels compared to control (25% vs. 1.92% P < 0.001). The OR of low Sr. ferritin levels in children with febrile seizures was 17.00 (95% CI 2.131–135.570; z = 2.675; P = 0.0075) [Graph 1]. Similarly, significantly higher number of children in cases had IDA compared to controls (73.08% vs. 46.15%). The OR of IDA in children with febrile seizures was 3.166 (95% CI = 1.394–7.191; P = 0.005) [Graph 2]. Further, significantly higher number of children in cases had zinc deficiency compared to controls (84.62% vs. 25%). The OR of zinc deficiency in cases was 12.269 (95% CI = 4.523–33.275; P < 0.001) [Graph 3].




  Discussion Top


In this study, majority of the children were boys in cases as well as controls (69.23% of boys and 30.77% of girls in each group) with boy-to-girl ratio of 2.25:1 (P = 1.000), suggesting male preponderance. These findings were consistent with a study by Sharif et al.[27] reported febrile seizures in 62% of the boys and 38% of the girls. The distribution of children according to the age, gender, and background disease in cases and controls was matched.

In the present study, a significantly higher number of cases reported positive family history of febrile seizures (21.15% vs. 5.77%; P = 0.041). History of febrile seizures can be seen in multiple family members, and there is evidence of genetic and environmental causes.[26]

No significant difference was noted in mean iron levels (51.59 ± 43.98 vs. 62.40 ± 43.54; P = 0.211). Sr. iron substantial day-to-day variation within subjects is approximately 15%, assessing iron status based on a single measurement of plasma iron concentration has a high risk of misclassifying iron status and may lead to an error in any estimate of prevalence. Hence, in this study, the utility of Sr. ferritin was emphasized as an indicator of iron status.[23],[25]

In this study, a significantly higher number of children in cases had lower Sr. ferritin levels compared to controls (25% vs. 1.92%; P < 0.001). The OR of low Sr. ferritin levels in children with febrile seizures was 17.00 (95% CI = 2.131–135.570; z = 2.675; P = 0.0075) [Table 3]. The mean Sr. ferritin levels were almost twice in controls as that in cases (44.45 ± 43.29 vs. 92.49 ± 70.19 ng/mL; P < 0.001). The lower Sr. ferritin levels observed in the present study were consistent with the study by Fallah et al.[28] who reported that Sr. ferritin levels were lower than those of the healthy children group (38.52 ± 11.38 vs. 54.32 ± 13.46; P = 0.001). A systemic review and meta-analysis by Kwak et al.[29] (2017) indicated that IDA diagnosed on the basis of plasma ferritin (OR = 3.78;95% CI = 1.80–7.94;P < 0.001) was modestly associated with febrile seizures. However, a study by Ghasemi et al.[30] also reported that the mean plasma ferritin concentration in the healthy group was lower than that in the two groups of febrile seizure and febrile without seizure, but there was no significant difference between the two latter groups. In studies by Daoud et al.,[31] Naveed-ur-Rehman and Billoo,[32] and Momen et al,[33] the mean plasma ferritin level in the febrile seizure group was significantly lower than the control group, which led them to the conclusion that it can demonstrate the role of ID in the incidence of febrile seizure.
Table 3: Comparison of mean hemoglobin, serum ferritin, serum zinc, and iron levels in cases and control group

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In this study, a significant number of children with febrile seizures had IDA compared to controls (73.08% vs. 46.15%). The OR of IDA in children with febrile seizures was 3.166 (95% CI = 1.394–7.191; P = 0.005) [Table 3]. Mean Hb levels were significantly low among cases compared to controls (9.17 ± 1.29 vs. 11.09 ± 1.59 gm%; P < 0.001). Significant number of the children in cases (71.15%) had RDW of ≥15 compared to controls (44.23%) (P = 0.010), while peripheral smear studies revealed microcytic hypochromic picture in cases are high as compared to controls (67.3% vs. 19.23%; P < 0.001).

Looking at OR, it may be hypothesized that there is a significant strong association between IDA and febrile seizures, and there is a high risk (1.5 times) of developing febrile seizures in children with IDA. These observations were consistent with several other studies in the literature. The study of Pisacane et al.[34] reported significantly higher anemia in the cases (30%) than in control (14%) and healthy groups (12%). In the study of Vaswani et al.[35] also, 68% of cases were iron deficient compared to 30% of the controls. A study by Naveed-ur-Rehman and Billoo[32] on 30 children with febrile seizures and 30 children with other febrile diseases indicated that IDA in the cases was significantly more common than in the control group. More recently, Sharif et al.[27] (2015) suggested that a considerable percentage of children having febrile seizure suffer from IDA. The presence of anemia can serve as a reinforcing factor for febrile seizure in children.

In the study of Sadeghzadeh et al.,[36] (2012) although anemia was not common among febrile seizure patients, ID was more frequent in these patients. In the study of Hartfield et al.,[13] ID was found to be 9%‒5% in the children of two groups of febrile seizure and febrile without seizure, respectively; and IDA was found to be 6%‒4% in the former and latter groups, respectively.

In contrast to the observations of the present study and several other studies,[27],[28],[32],[34],[35],[37] Bidabadi and Mashouf[38] stated that ID in the febrile seizures group (44%) was less than in the control group (48%), with no significant difference. This disparity may be attributed to not considering the effect of age during the interpretation of tests for the diagnosis of ID, the difference in the age and number of samples, and difference in the diagnostic criteria of IDA. Furthermore, age, nutritional habit, geographic area, sample size, and the control group may have resulted in these differences.

In this study, a significantly higher number of children in cases had zinc deficiency compared to control (84.62% vs. 25%). The OR of febrile seizure in children with zinc deficiency was 12.269 (95% CI = 4.523–33.275; P < 0.001) [Table 3]. Furthermore, the mean Sr. zinc levels were significantly low in cases (37.16 ± 22.07 μg/dL) compared to controls (75.75 ± 15.25 μg/dL) (P < 0.001). The mean Sr. zinc levels were two-fold higher in controls compared to cases. These findings indicate a significant strong association between zinc deficiency with febrile seizure (3.38 times risk of febrile seizure in children with zinc deficiency). Despite methodological differences, the observations in the present study were in agreement with other studies in the literature. A case‒control study by Mahyar[17] in Iran reported that the mean Sr. zinc levels in the patient group as 62.84 ± 18.40 μg/dL and in the control group as 85.7 ± 16.76 μg/dL (P < 0.05) indicating that hypozincemia predisposes to febrile seizures.[39] Another case‒control study by Ganesh and Janakiraman[18] reported that the mean Sr. zinc levels in cases and controls as 32 μg/dL and 87.6 μg/dL, respectively (P < 0.001), and concluded that Indian children with febrile seizures had low Sr. zinc levels. Another study by Mollah et al.[19] reported that the mean Zn concentration in both Sr. and Cerebro spinal fluid (CSF) was less in febrile seizure children than in their matched nonseizure febrile peers (P < 0.001). Kumar et al.[39] in a case‒control study found that the mean Sr. zinc level was significantly lower in cases as compared to control (P < 0.05) in children having a febrile seizure. Waqar Rabbani et al.[2] reported that zinc deficiency could be a potential risk factor for febrile seizures in children. Recently, Imran et al.[23] showed that the presence of biochemical hypozincemia, associated with other risk factors for simple febrile seizures may enhance the occurrence of febrile seizures; thus, a possible correlation exists between the mean Sr. zinc level and simple febrile seizures. In contrast to the findings of the present study, Garty et al.[22] did not support the hypothesis that febrile seizures are related to the reduced zinc concentration.


  Conclusion Top


There is a high risk (1.5 times) of developing febrile seizures in children with IDA (OR = 3.166). Children with zinc deficiency had 3.38 times high risk of developing febrile seizures (OR = 12.269). The OR of low Sr. ferritin levels in children with febrile seizures was 17.00. There was a significant association between febrile seizures with IDA, ID (ferritin), and zinc deficiency, and the risk is more pronounced with zinc deficiency.

Acknowledgment

We thank the head of the department and principal for allowing us to carry out the study in the institute. We thank the parents and children who had consented and participated in the study. We thank Dr. Sanjay Mishra, Scientist, KAHER'S, Dr. Prabhakar Kore Basic Science Research Center, Belagavi, for helping us in the assessment of Sr. zinc levels in BSRC.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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