Similar to the literature, this study found a sensitivity of 97% and a specificity of 41% for CRP in the diagnosis of acute appendicitis. Among the assessed parameters, CRP had the highest sensitivity and the lowest specificity. RDW is commonly used to discriminate between selleck compound microcytic anemia’s due to iron deficiency and those due to thalassemia or hemoglobinopathies [7]. Increased RDW levels are related to impaired erythropoiesis or erythrocyte degradation [7]. The typical reference range spans between 11.6 and 15.5%. Recent studies have demonstrated that higher RDW levels, even within the normal reference range, were associated with

unfavorable clinical outcomes in patients with heart failure, coronary artery disease, pulmonary hypertension,

diabetes mellitus, and stroke independent of hemoglobin values [8–10, 18, 19]. Furthermore RDW has been studied as a surrogate marker in many pathological conditions such as rheumatoid arthritis, inflammatory bowel disease, colon cancer, and celiac disease [6, 20, 21]. Although the exact pathophysiological basis of this relationship is unclear, chronic inflammation, aging, malnutrition, and anemia are proposed underlying factors in this topic [10, 22]. In a patient with acute pancreatitis, RDW level at the presentation has been reported to be an independent risk factor for mortality [12]. Similarly, RDW level has also been found to be a predictor for mortality in bacteremia and septic shock [11, 13]. An increased RDW level has been reported in these inflammatory and infectious pathologies. Elevated C646 purchase RDW can result from any disease process that causes the premature release of reticulocytes into the circulation. Elevations in RDW have been shown to be associated with elevated inflammatory markers, such as CRP, erythrocyte sedimentation rate, and interleukin 6 [13, 23, 24]. Proinflammatory cytokines of sepsis (tumor necrosis

factor A, interleukin Adenosine triphosphate 6, and interleukin 1b) have been shown to directly and negatively affect the Caspase activation survival of red blood cells in the circulation, promote deformability of the red blood cell membrane, and suppress erythrocyte maturation. These inflammatory mediators of sepsis can thus lead to newer, larger reticulocytes to enter the peripheral circulation, and thus increase RDW [13]. Unlike the above-mentioned studies, we found a significantly lower, albeit within normal limits, RDW level in patients with acute appendicitis compared with subjects in the control group. This finding may be the result of greater RDW level in chronic inflammatory diseases compared to that in acute conditions. A strong correlation of RDW with inflammatory markers, CRP and sedimentation rate has also been observed [13, 23, 24]. In our study, on the other hand, RDW was not correlated with CRP and leukocyte count. In conclusion, RDW level was lower in patients with acute appendicitis.