scholarly journals Iron deficiency anemia as a predictor of coronary artery abnormalities in Kawasaki disease

2019 ◽  
Vol 62 (8) ◽  
pp. 301-306 ◽  
Author(s):  
Sohyun Kim ◽  
Lucy Youngmin Eun
Keyword(s):  
Coronary Artery ◽  
Iron Deficiency ◽  
Kawasaki Disease ◽  
Iron Deficiency Anemia ◽  
Deficiency Anemia ◽  
Coronary Artery Abnormalities

P4641Are coronary artery abnormalities in Kawasaki disease associated with iron deficiency anemia?

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
L Eun ◽  
S K Kim ◽  
J K Kim
Keyword(s):  
Coronary Artery ◽  
Iron Deficiency ◽  
Kawasaki Disease ◽  
Iron Deficiency Anemia ◽  
Serum Iron ◽  
Deficiency Anemia ◽  
Coronary Artery Abnormalities ◽  
Iron Saturation ◽  
Group 2 ◽  
Group 1

Abstract Purpose Coronary artery abnormalities (CAA) are the most important complication of Kawasaki disease (KD). Iron deficiency anemia (IDA) is prevalent micronutrient deficiencies and its association with KD remains unknown. We hypothesized the presence of IDA could be a predictor of CAA. Methods This retrospective study included 173 KD patients, divided into two groups by absence (Group 1) and presence (Group 2) of CAA. The odds ratio (OR) with 95% confidence interval (CI) was calculated using a logistic regression model to estimate the association between CAA and other indicators. Due to the collinearity between the IDA indicators, each indicator was paired with anemia in 3 models. Results The 3 indicators of IDA, serum iron, iron saturation and ferritin, were all significantly higher in Group 1 than in Group 2. Three sets of models including anemia with iron indicators produced the odd ratio (OR) of CAA of 3.513, 3.171, and 2.256, respectively. The 3 indicators of IDA were negatively associated with CAA, by OR of 0.965, 0.914, and 0.944, respectively. The Area under the curve (AUC) of ferritin, iron saturation, serum iron, anemia, and Kobayashi score was 0.907 (95% CI, 0.851–0.963), 0.729 (95% CI, 0.648–0.810), 0.711 (95% CI, 0.629–0.793), 0.638 (95% CI, 0.545–0.731), and 0.563 (95% CI, 0.489–0.636) respectively. Figure 1 & 3 Conclusion The indicators of IDA, especially ferritin, were highly associated with CAA, so that they were stronger predictors compared to the Kobayashi score. The IDA indicators can be used to predict CAA development and suggest the need for early intervention. Acknowledgement/Funding None

Abstract 206: Coronary Artery Thrombosis in an Infant with Kawasaki Disease without Giant Coronary Aneurysm and Iron Deficiency Anemia: a Case Report

Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Rungrote Natesirinilkul ◽  
Pimlak Charoenkwan ◽  
Rekwan Sittiwangkul ◽  
Suchaya Silvilairat ◽  
Yupada Prongpot
Keyword(s):  
Coronary Artery ◽  
Iron Deficiency ◽  
Kawasaki Disease ◽  
Iron Deficiency Anemia ◽  
Coronary Aneurysm ◽  
Deficiency Anemia ◽  
Z Score ◽  
Cardiac Enzymes ◽  
Artery Thrombosis ◽  
Coronary Artery Thrombosis

The major complication of Kawasaki disease is coronary aneurysm which can cause acute coronary disease in early adulthood. There are some reports of coronary artery thrombosis during the period of active Kawasaki disease in infants with giant coronary aneurysm. This report demonstrated a 5-month-old male infant who presented high-grade fever for 7 days. He was treated as urinary tract infection for 6 days before referral. At admission, he had fever, red lips and swelling of both feet, then was diagnosed Kawasaki disease. His EKG showed ST elevation at lead II, III and AVF. His initial echocardiogram revealed coronary dilatation with perivascular brightness; RCA 2.7 mm (Z-score 4.38), LMCA 2.88 mm (Z-score 2.83) and LAD 2.7 mm (Z-score 5.79). There was a clot 2.5 X 2.5 mm in LAD. However, his LV systolic function was normal (EF 76%). His blood test showed low hemoglobin as 8.9 g/dL and MCV as 61.9 fL, high white cell count 20,400/mm3 and platelet count as 606,000/mm3. His initial ESR and CRP elevated at 91 mm/hr and 52 mg/L, respectively. The cardiac enzymes were normal; CKMBmass 2.9 ng/mL (0-3) and troponin-T 0.004 ng/mL (< 0.4). He received IVIG 2.3 g/kg and aspirin 79 mg/kg/day and was closely monitored the vital signs and cardiac enzymes. His fever completely disappeared within 24 hours after treatment, then aspirin was decreased to 6 mg/kg/day. Also, he received intravenous heparin for 4 days, and then was switched to Enoxaparin. He was discharged uneventfully on day 22 of admission. Further blood test confirmed the diagnosis of iron deficiency anemia as follow; serum iron 30 [[Unable to Display Character: &#613;]]g/dL, transferrin-iron binding capacity 446 [[Unable to Display Character: &#613;]]g/dL and transferrin saturation 6.7% (< 16). He received iron supplement for 4 months. The clot in coronary artery gradually decreased in size and finally disappeared in seven months after diagnosis. So, the Enoxaparin was discontinued. He received low-dose aspirin for total course 15 months. His thrombophilia work up was unremarkable. Anemia which is one of the supplementary criteria for atypical Kawasaki disease should be properly evaluated for the cause. The study to find the association between iron deficiency anemia, which was reported as a risk for thromboembolic events, and severity of Kawasaki disease should be further investigated.

scholarly journals Effect of Hepcidin and Iron Deficiency  Anemia on Clinical Outcome in patients  with Kawasaki Disease

2019 ◽  
Author(s):  
Hyun Jung Kim ◽  
Eun Hye Choi ◽  
Hong Ryang Kil
Keyword(s):  
Iron Deficiency ◽  
Kawasaki Disease ◽  
Iron Deficiency Anemia ◽  
Ivig Therapy ◽  
Acute Stage ◽  
Deficiency Anemia ◽  
Ivig Treatment ◽  
Enzyme Linked Immunosorbent Assay ◽  
Subacute Phase

Abstract Background: The role of iron in children with Kawasaki disease (KD) and the importance of iron deficiency anemia (IDA) in children with KD are not fully known. We aimed to evaluate the effects of IDA on clinical outcomes of KD patients and the role of inflammation-induced hepcidin and leptin in the development of anemia in patients with KD. Methods: A total of 50 children with KD and 47 age-matched children with controls were enrolled. Hepcidin, leptin, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were measured by an enzyme-linked immunosorbent assay and IDA work-up was performed before and after IVIG therapy, and in the convalescent phase in patients with KD and control patients. Results: (1) Pre-IVIG iron and transferrin saturations in KD children were significantly lower than those in controls ( P =0.001). (2) Pre-IVIG hemoglobin and iron levels were positively correlated with leptin levels ( P =0.018 and P =0.021, respectively). (3) Serum hepcidin levels were significantly elevated after IVIG treatment in patients with KD (1.53 ± 1.36 ng/ml in the acute stage vs 3.09 ± 4.22 ng/mL in the subacute phase, P = 0.001). (4) There was no difference in parameters of IDA, leptin, and hepcidin levels between KD patients with and without coronary artery lesion (CAL). Conclusion: Serum iron and transferrin saturations were lowest in the acute phase, while hepcidin levels were highest in the subacute phase of KD. Although the presence of iron deficiency in the acute stage of KD did not predict CAL, further studies are necessary to clarify the association of hepcidin on the pathogenesis of anemia in KD.

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