Acute phase proteins and interleukins in steady state sickle cell disease

Abstract

To identify a possible acute phase response during the steady state of sickle cell disease, we estimated the serum alterations of acute phase proteins, β2‐microglobulin (β2M), κ and λ light chains, interleukins (ILs) and tumor necrosis factor‐α (TNFα) in 21 patients. Increased concentrations of C‐reactive protein (CRP) were found in 5 patients, alpha‐1‐acid‐glycoprotein (AGP) in 3, alpha‐1‐antitrypsin (AAT) in 8, ceruloplasmin (CER) in 2, alpha‐2‐macrogiobulin (AMG) in 14 and decreased haptoglobin (HPT) and transferrin (TFR) in 11 and 9, respectively. Increased β2M was found in 10 patients and κ and λ light chains in 11. IL‐1β, IL‐2, IL‐4, IL‐10 and TNFα were not detected in any of the patients. However, significantly increased values of IL‐6 and sIL‐2r were found. This study has demonstrated increased serum levels of some of the acute phase proteins in patients during the steady state of sickle cell disease. This may be a result of a subclinical vaso‐occlusion which in turn leads to a covert inflammatory response. Cytokines, and in particular IL‐6, produced after this response, seem to be responsible for the high levels of acute phase proteins in the steady state of this disease.

Sickle Trait in African-American Hemodialysis Patients and Higher Erythropoiesis-Stimulating Agent Dose

“…Inflammation is a feature of overt sickle cell diseases, and in ESRD it contributes to ESA resistance by blunting iron use and erythropoiesis. [27][28][29][30][31] If inflammation in ESRD is modified or augmented by sickle cell trait, it could explain the observed need for increased ESA.…”

Sickle Cell Disease and Renal Disease

“…Glycosylated protein, auto-oxidation, reduced superoxide dismutase enzyme and ascorbic acid and lack of reduced glutathione are other causes for oxidative stress. Sickle cell anaemia patients in both steady state and renal impairments undergo constant inflammatory process which may in turn leads to inflammatory response (Bourantas et al,1998;Emokpae et al, 2010d). Haemoglobin S containing red blood cells auto-oxidize faster thereby generating more superoxide, hydrogen peroxide, hydroxyl radicals and lipid peroxides than HbAA.…”

C-Reactive Protein Polymorphism and Serum Levels as an Independent Risk Factor in Sickle Cell Disease

“…Inflammation and abnormal adhesion of sickled cells are thought to contribute to vascular occlusions that lead to chronic organ dysfunction [5,10,21,24]. CRP induced inflammation is an acute phase response to vascular damage.…”

“…CRP induced inflammation is an acute phase response to vascular damage. Serum CRP levels are a newly recognized serum biomarker for vascular damage [19,25,26] but little literature addresses the utilization of CRP levels in assessing potential end-organ dysfunction in SCD patients [21].…”

“…One of these risk factors may be an abnormal response of hs-CRP to sub-clinical vascular inflammation from micro-occlusions that is seen in other inflammatory diseases [20]. One study showed CRP levels were more frequently elevated in baseline SCD patients and the alteration might be provoked by a low-grade inflammatory process [21].…”