PMID- 19680167
OWN - NLM
STAT- MEDLINE
DCOM- 20100112
LR  - 20161125
IS  - 1530-0447 (Electronic)
IS  - 0031-3998 (Linking)
VI  - 66
IP  - 5
DP  - 2009 Nov
TI  - Clinical score and transcript abundance patterns identify Kawasaki disease 
      patients who may benefit from addition of methylprednisolone.
PG  - 577-84
LID - 10.1203/PDR.0b013e3181baa3c2 [doi]
AB  - Intravenous immunoglobulin (IVIG) treatment-resistant patients are high risk of 
      developing coronary artery lesions with Kawasaki disease. The IVIG-responsive 
      (Group A; n = 6) and IVIG-resistant patients (Group B) were predicted before 
      starting the initial treatment using the Egami scoring system and randomly 
      allocated as a single-IVIG treatment group (group B1; n = 6) or as a 
      IVIG-plus-methylprednisolone (IVMP) combined therapy group (group B2; n = 5). We 
      investigated the transcript abundance in the leukocytes of those patients using a 
      microarray analysis. Five patients in group A and one patient in group B1 
      responded to initial IVIG treatment. All group B2 patients responded to 
      IVIG-plus-IVMP combined therapy. Before performing these treatments, those 
      transcripts related to IVIG resistance and to the development of coronary artery 
      lesions, such as IL1R, IL18R, oncostatin M, suppressor of cytokine signaling-3, 
      S100A12 protein, carcinoembryonic antigen-related cell adhesion molecule-1, 
      matrix metallopeptidase-9, and polycythemia rubra vera-1, were more abundant in 
      group B patients in comparison with group A patients. Moreover, those transcripts 
      in group B2 patients were more profoundly and broadly suppressed than group B1 
      patients after treatment. This study elucidated the molecular mechanism of the 
      effectiveness of IVIG-plus-IVMP combined therapy.
FAU - Ogata, Shohei
AU  - Ogata S
AD  - Department of Pediatrics, Kitasato University School of Medicine, Sagamihara, 
      Kanagawa, Japan.
FAU - Ogihara, Yoshihito
AU  - Ogihara Y
FAU - Nomoto, Keiko
AU  - Nomoto K
FAU - Akiyama, Kazumasa
AU  - Akiyama K
FAU - Nakahata, Yayoi
AU  - Nakahata Y
FAU - Sato, Kayoko
AU  - Sato K
FAU - Minoura, Katsunori
AU  - Minoura K
FAU - Kokubo, Kenichi
AU  - Kokubo K
FAU - Kobayashi, Hirosuke
AU  - Kobayashi H
FAU - Ishii, Masahiro
AU  - Ishii M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Pediatr Res
JT  - Pediatric research
JID - 0100714
RN  - 0 (Glucocorticoids)
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (Receptors, Interleukin-18)
RN  - 0 (S100 Proteins)
RN  - 0 (S100A12 Protein)
RN  - 0 (S100A12 protein, human)
RN  - 0 (SOCS3 protein, human)
RN  - 0 (Suppressor of Cytokine Signaling 3 Protein)
RN  - 0 (Suppressor of Cytokine Signaling Proteins)
RN  - 106956-32-5 (Oncostatin M)
RN  - X4W7ZR7023 (Methylprednisolone)
SB  - IM
MH  - Coronary Vessels/pathology
MH  - Female
MH  - Glucocorticoids/therapeutic use
MH  - Humans
MH  - Immunoglobulins, Intravenous/therapeutic use
MH  - Infant
MH  - Male
MH  - Methylprednisolone/*therapeutic use
MH  - Mucocutaneous Lymph Node Syndrome/*drug therapy/*metabolism
MH  - Oligonucleotide Array Sequence Analysis
MH  - Oncostatin M/metabolism
MH  - RNA, Messenger/*metabolism
MH  - Receptors, Interleukin-1/metabolism
MH  - Receptors, Interleukin-18/metabolism
MH  - S100 Proteins/metabolism
MH  - S100A12 Protein
MH  - Suppressor of Cytokine Signaling 3 Protein
MH  - Suppressor of Cytokine Signaling Proteins/metabolism
MH  - Treatment Outcome
EDAT- 2009/08/15 09:00
MHDA- 2010/01/13 06:00
CRDT- 2009/08/15 09:00
PHST- 2009/08/15 09:00 [entrez]
PHST- 2009/08/15 09:00 [pubmed]
PHST- 2010/01/13 06:00 [medline]
AID - 10.1203/PDR.0b013e3181baa3c2 [doi]
PST - ppublish
SO  - Pediatr Res. 2009 Nov;66(5):577-84. doi: 10.1203/PDR.0b013e3181baa3c2.