It was concluded that mild and transient valvular regurgitation, which cannot be detected by

auscultation, may occur in some patients in the acute stage of Kawasaki disease. These may be caused
by acute inflammation of the valve related to coronary artery lesions.

The proposed mechanism of hepcidin-induced transient anemia and coronary artery lesions in patients
with Kawasaki disease. While the exact etiology of Kawasaki disease (KD) remains uncertain, we have
reported that KD stimulates the extraordinary upregulation of most TLRs that upregulate hepcidin
expression. After hepcidin interacts with ferroportin, ferroportin becomes internalized and degraded,
ultimately leading to intracellular iron sequestration and decreased iron absorption from duodenum.
Hepcidin not only controls iron absorption, but also has a direct inhibitory effect on erythropoiesis,
which leads to transient hyposideremia and anemia in KD patients. Following intravenous
immunoglobulin (IVIG) treatment, hepcidin levels decrease significantly. Notably, the changes of
hepcidin levels after IVIG administration are related to IVIG treatment resistance and coronary artery
lesions formation. Macrophage iron homeostasis is correlated with the functional polarization and
plasticity of these cells. Doing so makes M1-macrophages a major iron storage site under inflammatory
conditions. However, little is known about whether iron homeostasis influences the ability of the
macrophage polarization program and molecular machinery involved in KD processes.
source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412404/figure/ijms-18-00820-f001/

Anemias

Iron-deficiency anemia is mainly caused by blood loss, such as may occur during menses or
gastrointestinal hemorrhage. This often results in a depapilled, atrophic glossitis, giving the tongue a
bald and shiny appearance, along with pallor (paleness) of the lips and other mucous membranes a
tendency towards recurrent oral ulceration,[5] and cheilosis (swelling of the lips).[6] The appearance of
the tongue in iron deficiency anemia has been described as diffuse or patchy atrophy with tenderness or
burning.[7] One cause of iron deficiency anemia is sideropenic dysphagia (Plummer–Vinson or Paterson–
Brown–Kelly syndrome) which is also characterized by esophageal webbing and dysphagia.[5]

Pernicious anemia is usually caused by autoimmune destruction of gastric parietal cells. Parietal cells
secrete intrinsic factor which is required for the absorption of vitamin B12. Vitamin B12 deficiency
results in megaloblastic anemia and may present as glossitis. The appearance of the tongue in vitamin
B12 deficiency is described as "beefy" or "fiery red and sore".[5] There may be linear or patchy red
lesions.[1]

Other Sources

https://emedicine.medscape.com/article/965367-overview#a3

https://www.frontiersin.org/articles/10.3389/fped.2018.00198/full

https://europepmc.org/abstract/med/29461753

https://emedicine.medscape.com/article/965367-treatment