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Serum salicylic acid levels in children with Kawasaki disease

BMC Pediatrics volume 24, Article number: 613 (2024) Cite this article

Abstract

Background

This study aimed to clarify serum salicylic acid (SA) levels in patients with Kawasaki disease (KD) after the administration of moderate-dose acetylsalicylic acid (ASA) and their relationship with the therapeutic effect.

Methods

We retrospectively analyzed the clinical data of 142 children with KD. We measured serum SA trough levels during the acute and recovery periods and determined their relationship with clinical and laboratory parameters.

Results

The median age of patients was 2.4 years. Thirty-one patients had incomplete KD, 29 were intravenous immunoglobulin (IVIG) non-responders, and one patient had coronary artery lesions. The median ASA dose was 49.7 mg/kg/day. The median serum SA level was 22 µg/mL in the acute period and 15 µg/mL in the recovery period, with 45 (33%) in the acute period and 60 (44%) in the recovery period below the limit of measurement (< 10 µg/mL). Serum SA levels during the recovery period were significantly lower in patients who received steroids. There were no significant differences in IVIG responsiveness based on serum SA levels.

Conclusions

Serum SA trough levels in KD patients treated with moderate-dose ASA were highly variable and did not reach sufficient levels. Serum SA levels were not associated with IVIG responsiveness.

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Background

Kawasaki disease (KD) is an acute childhood vasculitis that can causes coronary artery lesions (CALs). The first-line treatment for KD is a combination of intravenous immunoglobulin (IVIG) and acetylsalicylic acid (ASA), as supported by clinical trials [1, 2]. The efficacy of IVIG is well established [3,4,5].

ASA was used in children with KD before IVIG administration became widespread. Although ASA is presumed to exert anti-inflammatory, antipyretic, and antiplatelet effects, it does not appear to lower the frequency of coronary abnormalities [6]. The high doses (80–100 mg/kg/day) of ASA recommended in the United States are associated with a high risk of hepatic dysfunction in Japanese children. Thus, moderate doses (30–50 mg/kg/day) of ASA are usually administered to children with KD to suppress inflammation during the febrile phase in Japan [1, 2]. However, there are some reports that ASA absorption is poor during the acute phase of KD and that serum ASA levels may not be sufficient for anti-inflammatory effects [7,8,9,10]. In recent years, some authors have suggested that ASA can be used at low doses from an early stage, as ASA is much less effective than IVIG [11,12,13,14].

This study aimed to clarify the relationship between the therapeutic effect of ASA and serum levels of salicylic acid (SA), as ASA is hydrolyzed to SA in vivo. We measured the serum trough levels of SA in children with KD during the acute and recovery periods, and explored their relationship with various clinical parameters.

Methods

The participants of this study were children with KD who were hospitalized in the Department of Pediatrics of Aichi Medical University Hospital between April 2019 and April 2024. KD was diagnosed in accordance with the Japanese guidelines [15] after the exclusion of other diseases, including various viral and bacterial infections, cervical lymphadenitis, and toxic shock syndrome. Complete KD (cKD) was diagnosed when a child exhibited five or more of the six major symptoms or four major symptoms and CALs. A diagnosis of incomplete KD (iKD) was made when a child had three major symptoms and CALs or four major symptoms without CALs [1, 2].

In our hospital, children with KD are treated with ASA and IVIG (2 g/kg) immediately after the diagnosis. ASA was administered orally at a dose of 30–50 mg/kg/day (50 mg/kg/day, in principle). Until March 2021, flurbiprofen (3–5 mg/kg/day) was administered to children with hepatic dysfunction with aspartate aminotransferase (AST) ≥ 200 IU/L and/or alanine aminotransferase (ALT) ≥ 200 IU/L, instead of ASA. Thereafter, ASA was administered to all the children with KD. Steroids were administered to patients who were expected to be unresponsive to IVIG based on their refractoriness prediction scores (Kobayashi [16], Egami [17], and Sano scores [18]). Steroids were used in combination with ASA and IVIG when one or more of these scores indicated IVIG refractoriness (Kobayashi score ≥ 5, Egami score ≥ 3, or Sano score ≥ 2).

Serum SA levels were measured at two time points: acute and recovery periods. The day after the first IVIG administration was defined as the acute period, and the period after the acute symptoms had recovered and just before the ASA dose was reduced was defined as the recovery period. Serum SA levels were measured trough levels as previously reported [7]. To determine trough SA levels, ASA was administered orally at night, and a blood sample was collected the next morning before breakfast. Serum SA levels were measured using an enzymatic assay (Cobas 6000; Roche Diagnostics, Basel, Switzerland), with a lower measurement limit of 10 µg/mL.

We collected clinical information from the medical records regarding age, sex, body weight, duration of KD at the initiation of IVIG, ASA dose, presence or absence of CALs, duration of hospitalization, and treatment-related adverse events. We also retrieved the following laboratory data: white blood cell count (WBC), neutrophil ratio, platelet count (PLT), and levels of total bilirubin (T-Bil), albumin (Alb), AST, ALT, sodium (Na), C-reactive protein (CRP), and brain natriuretic peptide (BNP). These data were selected because several studies have supported their utility in predicting unresponsiveness to IVIG [16,17,18] and/or diagnosis of KD [19]. In this study, a patient was defined as an IVIG responder when pyrexia was not observed after IVIG administration. A non-responder was defined as a child who had persistent or recurrent pyrexia within 24–36 h after IVIG administration and required second-line treatment.

We compared serum SA levels during the acute and recovery periods. Wilcoxon signed-rank sum test was used to compare continuous variables between the two corresponding groups. We also investigated the association of serum SA levels with KD type (cKD vs. iKD), steroid use (with vs. without steroid use), and IVIG responsiveness (IVIG responder vs. non-responder). Mann-Whitney U test was used to compare continuous variables between the two independent groups. In addition, we divided serum SA levels into three groups: low (< 10 µg/mL), medium (≥ 10 µg/mL, < 50 µg/mL), and high (≥ 50 µg/mL), and compared demographic and laboratory data among the three groups. Because the effective blood concentration of ASA in KD is unknown, we divided it into three levels and conducted a preliminary analysis. Fisher’s exact probability test and Kruskal-Wallis test were used to compare categorical and continuous variables among the three groups, respectively. For multiple comparison of categorical variables among the three groups, we adjusted using Bonferroni method when Fisher’s exact probability test showed a p value of < 0.05. For multiple comparison of continuous variables among the three groups, Steel-Dwass test was used when Kruskal-Wallis test showed a p value of < 0.05. A p value < 0.05 was considered to indicate statistical significance. All statistical analyses were performed using the EZR software program, version 1.61 (available at http://www.jichi.ac.jp/saitama-sct/SaitamaHP.files/statmed.html) [20].

Results

One hundred and eighty-six children with KD were hospitalized during the study period. Among them, we excluded 27 children for whom serum SA levels were not measured and 17 children who received flurbiprofen because of markedly elevated AST and/or ALT levels. Finally, 142 children with KD were included in the analysis.

Table 1 presents the demographic characteristics of study participants. 141 children (99.3%) were Japanese (the remaining one was Chinese). The median age was 2.4 years; eighty-eight patients were male and 54 were female. Thirty-one patients were diagnosed with iKD. The median duration of illness at IVIG initiation was 5 days, and the median ASA dose was 49.7 mg/kg/day. Thirty-six patients received steroids with IVIG (35 with prednisolone and 1 with methylprednisolone pulse). There were 29 IVIG non-responders, and second-line treatment consisted of additional IVIG in 25 patients, IVIG + prednisolone in 2 patients, and IVIG + methylprednisolone pulse in 2 patients. Only one patient developed CALs, and two other patients had transient coronary artery dilation. No adverse events related to ASA were observed.

Table 1 Patient demographic data (n = 142)
Full size table

Serum SA levels during the acute and recovery periods are shown in Fig. 1. The median serum SA level was 22 µg/mL in the acute period and 15 µg/mL in the recovery period, with 45 (33%) in the acute period and 60 (44%) in the recovery period below the limit of measurement (< 10 µg/mL). No patient reached serum SA levels (≥ 150 µg/mL) that would be expected to exert an anti-inflammatory effect [21]. There were no significant differences in serum SA levels between the acute and recovery periods.

Fig. 1
figure 1

Distribution of serum salicylic acid levels during the acute and recovery periods. SA: salicylic acid, NS: not significant

Full size image

We compared serum SA levels between patients with cKD and those with iKD (Fig. 2a). Serum SA levels were not significantly different between the two groups. We also compared serum SA levels between the patients with and without steroid use (Fig. 2b). Serum SA levels in the acute period were not significantly different between the two groups; however, serum SA levels in the recovery period were significantly lower in patients who received steroids. Serum SA levels were also compared between IVIG responders and non-responders (Fig. 2c). Serum SA levels were not significantly different between the two groups.

Fig. 2
figure 2

Distribution of serum salicylic acid levels according to disease type of KD (a), steroid use (b), and IVIG responsiveness (c). The left column shows the acute period and the right column shows the recovery period. KD: Kawasaki disease, SA: salicylic acid, cKD: complete KD, iKD: incomplete KD, IVIG: intravenous immunoglobulin, NS: not significant

Full size image

Table 2 shows the demographic and laboratory data for low (< 10 µg/mL), medium (≥ 10 µg/mL, < 50 µg/mL), and high (≥ 50 µg/mL) serum SA levels. In the acute period, there were no significant differences in ASA dose, steroid use, IVIG responsiveness, or other parameters among the three groups. In the recovery period, IVIG responsiveness was not also significantly different among the three groups, but patients with low levels of serum SA were significantly more likely to use steroids than those with medium levels. In addition, patients with low levels of serum SA received significantly lower doses of ASA and had significantly lower serum sodium levels than those with medium levels. In both the acute and recovery periods, there was no significant difference in serum albumin levels between serum SA levels, and no correlation was observed. The serum SA level in one patient with CALs was 21 µg/mL in the acute period and 22 µg/mL in the recovery period.

Table 2 Demographic and laboratory data at diagnosis between serum SA levels
Full size table

Discussion

We measured serum SA trough levels in KD patients receiving moderate doses of ASA. Serum SA levels in the acute period were below the limit of measurement in approximately one-third of the patients. Even in the recovery period, when serum SA levels were presumed to have reached a steady state, nearly half of the patients were below the limit of measurement. No patient reached serum SA levels expected to exert an anti-inflammatory effect. There was no correlation between serum SA levels and IVIG response. Even patients with serum SA levels below the limit of measurement did not exhibit any sequelae, including CALs.

There are few reports on serum SA levels in patients with KD, but there have been previous reports that serum SA levels are difficult to increase during the acute phase of KD [7,8,9,10]. Koren et al. evaluated serum SA levels in 49 KD patients and reported that no patient reached effective therapeutic levels (> 200 µg/mL) when the ASA dose was < 80 mg/kg/day, and 55% were below the effective therapeutic levels even when the ASA dose was 100–110 mg/kg/day [7]. Decreased absorption from the intestinal tract and decreased protein binding of SA have been reported as reasons why serum SA levels are difficult to increase during the acute phase of KD [8, 9]. During the acute phase of KD, free (non-albumin-bound) SA may increase with a decrease in the albumin concentration. This causes increased excretion of SA in urine, suggesting a faster decrease in its blood concentration [10, 22]. However, no correlation was observed between serum albumin and SA levels in the present study. Changes in the plasma pH affect the saturation of protein-binding sites [22]. In the present study, the plasma pH was measured in only a few patients and could not be examined. Serum SA levels during the recovery period were significantly lower in patients who received steroids. Corticosteroids have been reported to increase SA clearance, which may account for decreased serum SA levels [23, 24]. Additionally, serum sodium levels were significantly lower in patients with low serum SA levels during the recovery period. Patients with lower serum sodium levels were more likely to be using steroids and therefore may have had lower serum SA levels (median sodium levels for steroid users and non-users were 133 and 135 mmol/L, respectively; p < 0.001).

In the present study, serum SA levels were not correlated with IVIG responsiveness. There have been some reports that there is no association between ASA dose and IVIG responsiveness or CALs incidence [25,26,27,28,29,30,31,32,33]. Jia X et al. reported that there were no differences in IVIG resistance (relative risk (RR): 1.26; 95% CI: 0.55, 2.92; p = 0.59) or CALs incidence (RR: 1.15; 95% CI: 0.93, 1.43; p = 0.19) between high-dose and low-dose ASA in a meta-analysis of 12,176 KD patients [27]. Zheng X et al. reported that there were no differences in IVIG resistance (RR: 1.39; 95%CI: 1.00, 1.93; p = 0.05) or CALs incidence (RR: 0.85; 95%CI: 0.63, 1.14; p = 0.28) between low-dose (3-5 mg/kg/day) and high-dose ASA(≥ 30 mg/kg/day) in a meta-analysis of 11,103 KD patients [28]. Chiang M et al. reported that there was no difference in IVIG resistance (odds ratio (OR): 1.35, 95% CI: 0.91, 1.98) between low-dose/no-ASA group and high-dose ASA (≥ 30 mg/kg/day) group in a meta-analysis of 12,182 KD patients [29]. Wang J et al. reported in a retrospective study of 2,359 KD patients that aspirin at a dose of 20–29 mg/kg/day did not increase IVIG resistance or CALs incidence compared to a dose of 30–50 mg/kg/day [30]. These results indicate that the influence of serum SA levels on the outcome of patients with KD is not significant. Therefore, we consider that it will not be necessary to further increase the dose of ASA to enhance its anti-inflammatory effect. However, there was only one patient with CALs in the present study, so further large-scale studies including patients with CALs are needed to clarify the influence of serum SA levels.

This study had some limitations. First, this was a single-center retrospective study with a small number of patients. Therefore, these results should be verified in larger patient cohorts. Second, serum SA levels were not measured in some patients. It is possible that severe cases were present in these children, which may have affected the results. Third, we excluded children who received flurbiprofen instead of ASA. Most of these children had markedly elevated AST and/or ALT levels, which likely excluded those who were predicted to be unresponsive to IVIG. Fourth, serial monitoring of SA levels was not performed. Therefore, pharmacokinetic parameters such as Cmax and half-life were not determined. Fifth, as most of the patients were Japanese children, it was not possible to verify any differences based on race. Finally, as only one child developed CALs during the study period, the effect of SA levels on the occurrence of CALs could not be examined.

Conclusions

Serum SA trough levels in KD patients treated with moderate doses (30–50 mg/kg/day) of ASA were highly variable and did not reach sufficient levels. Serum SA levels were not related to IVIG responsiveness. To clarify the influence of serum SA levels on KD patients in detail, it is necessary to conduct prospective studies examining the pharmacokinetics of SA in a large population, including patients with CALs.

Data availability

The datasets used and/or analyzed in this study are available from the corresponding author upon reasonable request.

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Acknowledgements

We would like to thank the staff of the Department of Pediatrics, Aichi Medical University for their cooperation in this study.

Funding

The authors did not receive support from any organization for the submitted work.

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Authors and Affiliations

  1. Department of Pediatrics, Aichi Medical University, 1-1 Yazako Karimata, Nagakute, 480-1195, Aichi, Japan

    Hitoshi Honma, Sae Takahashi, Jun Sada, Hiroaki Somiya, Hiromitsu Mori, Taichiro Muto, Yoshinori Ito & Akihisa Okumura

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  1. Hitoshi Honma
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Contributions

HH, JS, TM, and AO conceived the study, collected the data, performed the analysis, and drafted the manuscript. ST, HS, HM, and YI collected the data and assisted with interpretation. All authors approved the final version of the manuscript and agreed to be accountable for all aspects of this work.

Corresponding author

Correspondence to Hitoshi Honma.

Ethics declarations

Ethics approval and consent to participate

This study was approved by the Ethics Committee of Aichi Medical University School of Medicine (approval no. 2024-098). This study adhered to the tenets of the Declaration of Helsinki. Informed consent was obtained from all participants and/or their caregivers.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Abbreviations

KD, Kawasaki disease.

CALs, Coronary artery lesions.

IVIG, Intravenous immunoglobulin.

ASA, Acetylsalicylic acid.

SA, Salicylic acid.

AST, Aspartate aminotransferase.

ALT, Alanine aminotransferase.

WBC, White blood cell.

PLT, Platelet.

T-Bil, Total bilirubin.

Alb, Albumin.

Na, Sodium.

CRP, C-reactive protein.

BNP, Brain natriuretic peptide.

cKD, Complete Kawasaki disease.

iKD, Incomplete Kawasaki disease.

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Honma, H., Takahashi, S., Sada, J. et al. Serum salicylic acid levels in children with Kawasaki disease. BMC Pediatr 24, 613 (2024). https://doi.org/10.1186/s12887-024-05100-7

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BMC Pediatrics

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