Serum HO-1 is useful to make differential diagnosis of secondary hemophagocytic syndrome from other similar hematological conditions View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2010-01-22

AUTHORS

Takuya Miyazaki, Yohei Kirino, Mitsuhiro Takeno, Maasa Hama, Ayumi Ushihama, Reina Watanabe, Kaoru Takase, Takayoshi Tachibana, Kenji Matsumoto, Masatsugu Tanaka, Satoshi Yamaji, Haruko Ideguchi, Naoto Tomita, Hiroyuki Fujita, Shigeru Ohno, Atsuhisa Ueda, Yoshiaki Ishigatsubo

ABSTRACT

Heme oxygenase (HO)-1, a heme-degrading enzyme inducible by various stimuli, plays a key role in the regulation of inflammatory response in monocytes/macrophages. The serum HO-1 level is remarkably increased in patients with secondary hemophagocytic syndrome (HPS) or adult-onset Still’s disease. We measured serum HO-1 levels in patients with a variety of hematological diseases, including secondary HPS, by means of ELISA. Serum HO-1 levels were significantly higher in 22 patients with HPS (134.7 ± 116.2 ng/mL, P < 0.0001) at diagnosis than in 80 patients with other hematological diseases. The most effective cutoff point between HPS and other conditions was 14.5 ng/mL, with 100.0% sensitivity and 96.3% specificity. In HPS patients, the serum HO-1 levels showed the highest correlation with serum ferritin (r = 0.682, P = 0.0005), which reflects the disease activity of HPS. Moreover, both HO-1 and ferritin levels were reduced in parallel after successful treatment in patients with HPS, irrespective of underlying diseases. However, HO-1 levels were not elevated in patients with other causes of hyperferritinemia. These data demonstrate that serum HO-1 can distinguish secondary HPS from other hematological diseases, including those associated with hyperferritinemia. More... »

PAGES

229-237

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s12185-010-0495-y

DOI

http://dx.doi.org/10.1007/s12185-010-0495-y

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009572107

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/20091384


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