Syndrome of inappropriate anti‐diuretic hormone in Kawasaki disease

Mori, Jiro; Miura, Masaru; Shiro, Hiroyuki; Fujioka, Kenichiro; Kohri, Takeo; Hasegawa, Tomonobu

doi:10.1111/j.1442-200x.2010.03264.x

Cited by 15 publications

(19 citation statements)

References 15 publications

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“…17 The development of hyponatremia during the acute stage can be caused by the syndrome of inappropriate secretion of anti-diuretic hormone (SIADH), and the inappropriate ADH secretion is induced by interleukin (IL)-6 or IL-1b. 13,15,18,19 Several cytokines, including IL-6 and IL-1b, are involved in the development of KD and their levels increase during the acute stage. Furthermore, they are strongly associated with the pathogenesis of acute KD, the development of coronary aneurysms, IVIG resistance, and the severity of KD.…”

Section: Hyponatremia In Acute Kdmentioning

confidence: 99%

Indicators of unresponsiveness after initial i.v. immunoglobulin treatment in acute Kawasaki disease

Hashimoto

2019

Pediatrics International

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Background The aim of this study was to identify the indicators of unresponsiveness to initial i.v. immunoglobulin (IVIG) treatment for Kawasaki disease (KD). Methods One hundred and forty‐five patients with KD, who had received initial treatment consisting of a single IVIG dose (1 g/kg or 2 g/kg) and oral aspirin (30 mg/kg), were studied. Laboratory parameters, including C‐reactive protein (CRP) and serum sodium (Na), were measured before and after IVIG treatment, and during the convalescent phase, and the laboratory data compared with regards to IVIG response. Multiple logistic regression models, which included laboratory data obtained immediately after the IVIG treatment, were constructed to determine the indicators of IVIG unresponsiveness immediately after the completion of the initial treatment. Results On logistic regression analysis, serum Na after IVIG treatment was the only independent factor related to initial IVIG unresponsiveness (β = 0.53, P < 0.01; OR, 1.69; 95%CI: 1.15–2.49). On receiver operating characteristic curve analysis, the optimal serum Na cut‐off immediately after IVIG treatment was 135.5 mEq/L with a sensitivity of 0.75, and a specificity of 0.79. Conclusions Prolonged hyponatremia after completion of the initial IVIG therapy was an indicator of the need for subsequent IVIG therapy. Treatment plans should be established for patients with acute KD that pay particular attention to prolonged hyponatremia.

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Section: Hyponatremia In Acute Kdmentioning

confidence: 99%

Indicators of unresponsiveness after initial i.v. immunoglobulin treatment in acute Kawasaki disease

Hashimoto

2019

Pediatrics International

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“…Hyponatremia is reported in 45% to 69% of KS patients53)54) and is associated with the formation of coronary artery lesions and giant coronary artery aneurysms 55)56). ADH levels are elevated in KS, which increases water retention and peripheral vascular resistance, hence, increasing blood pressure.…”

Section: Sodiummentioning

confidence: 99%

“…At higher levels, ADH provokes hyponatremia due to the increased volume of water circulating in the blood. Syndrome of inappropriate antidiuretic hormone (SIADH) resulting from increased ADH levels are observed in KS and associated with hyponatremia 54)57)58). Levels of NT-proBNP were found to be higher in KS patients with hyponatremia, although NT-proBNP levels were lower in patients with SIADH,57) which is likely the result of BNP suppressing the release of vasoconstrictors including ADH.…”

Section: Sodiummentioning

confidence: 99%

Mercury Promotes Catecholamines Which Potentiate Mercurial Autoimmunity and Vasodilation: Implications for Inositol 1,4,5-Triphosphate 3-Kinase C Susceptibility in Kawasaki Syndrome

Yeter¹,

Deth

Kuo

2013

Korean Circ J

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Previously, we reviewed biological evidence that mercury could induce autoimmunity and coronary arterial wall relaxation as observed in Kawasaki syndrome (KS) through its effects on calcium signaling, and that inositol 1,4,5-triphosphate 3-kinase C (ITPKC) susceptibility in KS would predispose patients to mercury by increasing Ca2+ release. Hg2+ sensitizes inositol 1,4,5-triphosphate (IP3) receptors at low doses, which release Ca2+ from intracellular stores in the sarcoplasmic reticulum, resulting in delayed, repetitive calcium influx. ITPKC prevents IP3 from triggering IP3 receptors to release calcium by converting IP3 to inositol 1,3,4,5-tetrakisphosphate. Defective IP3 phosphorylation resulting from reduced genetic expressions of ITPKC in KS would promote IP3, which increases Ca2+ release. Hg2+ increases catecholamine levels through the inhibition of S-adenosylmethionine and subsequently catechol-O-methyltransferase (COMT), while a single nucleotide polymorphism of the COMT gene (rs769224) was recently found to be significantly associated with the development of coronary artery lesions in KS. Accumulation of norepinephrine or epinephrine would potentiate Hg2+-induced calcium influx by increasing IP3 production and increasing the permeability of cardiac sarcolemma to Ca2+. Norepinephrine and epinephrine also promote the secretion of atrial natriuretic peptide, a potent vasodilator that suppresses the release of vasoconstrictors. Elevated catecholamine levels can induce hypertension and tachycardia, while increased arterial pressure and a rapid heart rate would promote arterial vasodilation and subsequent fatal thromboses, particularly in tandem. Genetic risk factors may explain why only a susceptible subset of children develops KS although mercury exposure from methylmercury in fish or thimerosal in pediatric vaccines is nearly ubiquitous. During the infantile acrodynia epidemic, only 1 in 500 children developed acrodynia whereas mercury exposure was very common due to the use of teething powders. This hypothesis mirrors the leading theory for KS in which a widespread infection only induces KS in susceptible children. Acrodynia can mimic the clinical picture of KS, leading to its inclusion in the differential diagnosis for KS. Catecholamine levels are often elevated in acrodynia and may also play a role in KS. We conclude that KS may be the acute febrile form of acrodynia.

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“…Hyponatremia is a common manifestation of Kawasaki disease (KD) and is reported to occur in 26–69% of patients . Hyponatremia is a known risk factor for unresponsiveness to intravenous immunoglobulin (IVIG) and giant coronary aneurysms .…”

Section: Introductionmentioning

confidence: 99%

“…Hyponatremia is a known risk factor for unresponsiveness to intravenous immunoglobulin (IVIG) and giant coronary aneurysms . Previously reported mechanisms of hyponatremia in KD include hypotonic dehydration and the “syndrome of inappropriate secretion of antidiuretic hormone” (SIADH), as well as ingestion of fluid that is hypo‐osmolar relative to fluid loss . However, the diagnoses in these reports were not based on an assessment of total body water by daily measurement of body weight, which is the first step for evaluation of hypotonic hyponatremia, and / or plasma arginine vasopressin (ADH) levels.…”

Section: Introductionmentioning

confidence: 99%

Nonosmotic secretion of arginine vasopressin and salt loss in hyponatremia in Kawasaki disease

Miura

Harita

Takahashi

et al. 2020

Pediatrics International

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Background The precise mechanism of hyponatremia in Kawasaki disease (KD) remains elusive because assessment of volume status based on serial changes in body weight is lacking in previous reports. Methods Seventeen patients who were diagnosed with KD and hyponatremia (serum sodium levels <135 mmol/L) were analyzed. Volume status was assessed based on serial changes in body weight. Plasma arginine vasopressin (ADH), urine electrolytes, and serum cytokine levels were measured on diagnosis of hyponatremia. An increase in body weight by >3% was defined as hypervolemia and a decrease in body weight by >3% was defined as hypovolemia. Results The volume status was hypervolemic in three patients (18%), euvolemic in 14 (82%), and hypovolemic in none (0%). Five (29%) patients were diagnosed with “syndrome of inappropriate secretion of antidiuretic hormone” (SIADH) and no patients were diagnosed with hypotonic dehydration. The contribution of decreased total exchangeable cations (salt loss) to hyponatremia (5.9% [interquartile range, 4.3%, 6.7%]) was significantly larger than that of increased total body water (−0.7% [−1.8%, 3.1%]) (P = 0.004). Serum interleukin‐6 levels were elevated in all of the nine patients who were evaluated. Among the 12 (71%) patients who did not meet the criteria of SIADH and hypotonic dehydration, plasma ADH levels were inappropriately high in ten patients. These patients were also characterized by euvolemic or hypervolemic hyponatremia and salt loss, which might be compatible with a diagnosis of SIADH. Conclusions Our study shows that hyponatremia in KD is euvolemic or hypervolemic and is associated with nonosmotic secretion of ADH and salt loss in the majority of patients.

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Syndrome of inappropriate anti‐diuretic hormone in Kawasaki disease

Cited by 15 publications

References 15 publications

Indicators of unresponsiveness after initial i.v. immunoglobulin treatment in acute Kawasaki disease

Indicators of unresponsiveness after initial i.v. immunoglobulin treatment in acute Kawasaki disease

Mercury Promotes Catecholamines Which Potentiate Mercurial Autoimmunity and Vasodilation: Implications for Inositol 1,4,5-Triphosphate 3-Kinase C Susceptibility in Kawasaki Syndrome

Nonosmotic secretion of arginine vasopressin and salt loss in hyponatremia in Kawasaki disease

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