{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T21:01:23Z","timestamp":1791320483870,"version":"4.3.1"},"reference-count":37,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2004,11,18]],"date-time":"2004-11-18T00:00:00Z","timestamp":1100736000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2004,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The aim of our study was to assess the cytokine profile of sickle cell disease (SCD) patients in steady state and in vaso\u2010occlusive crisis (VOC). VOC has a complex nature, involving interactions between sickle red blood cells (RBC), the endothelium, and leucocytes. Endothelial damage due to recurrent adhesion of sickle RBCs may disrupt endothelial function, leading to altered cytokine release. It is therefore pertinent to study the cytokine profile of SCD patients in steady state and in crisis prior to exploring its contribution to vaso\u2010occlusive manifestations, since it is believed that an altered balance of proinflammatory and anti\u2010inflammatory cytokines plays an important role in painful crisis. Cytokines including IL\u20101\u03b2, IL\u20102, IL\u20104, IL\u20106, IL\u20108, TNF\u2010\u03b1, and IFN\u2010\u03b3 were measured by commercially available ELISA kits in SCD patients (<jats:italic>n<\/jats:italic> = 60); in steady state (<jats:italic>n<\/jats:italic> = 26) and in painful crisis (<jats:italic>n<\/jats:italic> = 34) and compared with nonanemic age\u2010 and sex\u2010matched normal Omani controls (<jats:italic>n<\/jats:italic> = 20). SCD patients in crisis showed elevated levels of TNF\u2010\u03b1 (<jats:italic>P<\/jats:italic> &lt; 0.092) and IL\u20106 (<jats:italic>P<\/jats:italic> &lt; 0.024) when compared with steady state. It was also observed that SCD patients in steady state showed a significant elevation in IL\u20101\u03b2 (<jats:italic>P<\/jats:italic> &lt; 0.04), IL\u20106 (<jats:italic>P<\/jats:italic> &lt; 0.0001), and IFN\u2010\u03b3 (<jats:italic>P<\/jats:italic> &lt; 0.02) as compared to normal subjects. It is thus evident that both type I and type II cytokines are significantly altered in SCD patients. In steady state, type II proinflammatory cytokines are elevated, whereas in crisis, an additional augmentation of type I cytokines occurs, with persistent elevation of type II cytokines, emphasizing the role of perturbed endothelium and activated monocytes in the pathophysiology of vaso\u2010occlusion in sickle cell crisis. Am. J. Hematol. 77:323\u2013328, 2004 \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ajh.20196","type":"journal-article","created":{"date-parts":[[2004,11,18]],"date-time":"2004-11-18T21:52:24Z","timestamp":1100814744000},"page":"323-328","source":"Crossref","is-referenced-by-count":126,"title":["Cytokine profile of sickle cell disease in Oman"],"prefix":"10.1002","volume":"77","author":[{"given":"Anil","family":"Pathare","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Salam","family":"Al Kindi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adel 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