ABSTRACT
Platelet rich plasma (PRP) is a novel method of using plasma concentrated with platelets for wound healing and tissue regeneration. Platelet rich plasma is prepared from the venous blood using a differential centrifugation technique. It involves a separation spin and a concentration spin, yielding platelet rich plasma. PRP products have been classified into 4 types depending upon major cell constituent and fibrin density upon activation. These are as follows: Pure PRP, Leukocyte and PRP, Pure PRF, Leukocyte and PRF. PRF differs from PRP in that it is rich in a high density fibrin network after activation. PRP is abundant in a variety of growth factors such as VEGF, PDGF, TGF, EGF, and Interleukin-1. Literature consists of reports by different authors about the platelet yield of PRP centrifuged by different systems. A number of factors have also been quoted to influence the platelet concentration in platelet rich plasma. Hence, the aim of this review is to discuss the platelet concentration in PRP centrifuged by different systems and to observe for variations if any
ABSTRACT
BACKGROUND: The three direct factors that could lead cancer patients to anemia, apart from therapy are iron deficiency, inflammatory cytokines surge and decreased erythropoietin (Epo). Our aim was to quantify biochemical and hematologic markers serum Epo, ferritin (Fe) and tumor necrosis factor‑alpha (TNF‑α) along with hemoglobin (Hb) to understand the associations between these factors, patient characteristics and anemia. MATERIALS AND METHODS: The study group consisted of 100 anemic cancer patients and 80 controls. Biochemical marker levels were determined by the enzyme linked immunosorbent assay on an autoanalyser. Univarient analysis, t‑test, ANOVA, Bonferroni test, linear regression was performed to find correlations and associations among various factors. RESULTS: The baseline serum Epo (153.07 ± 173.88 vs. 23.607 ± 36.462) and Fe levels (233.53 ± 257.12 vs. 23.06 ± 20.04) were adequately high in cases compared with that controls (P ≤ 0.001). Considerable raise in TNF‑α levels was also observed (16.26 ± 13.44 vs. 11.2375 ± 4.84) (P = 0.001). TNF‑α correlated positively (P = 0.022) with Epo and Fe (P = 0.000), which was also evident from large effect size of Epo (r2 = 0.414), TNF‑α (r2 = 0.369), Hb (r2 = 0.226). Epo and Hb were negatively correlated (β = −0.375, P = 0.001) and Epo production was found to be appropriate for the degree of anemia (O/P ratio of 3.51 ± 1.26 vs. 1.43 ± 0.47). A strong association was seen between Hb, Epo and TNF‑α in hematological and gynecological malignancies for different grades of anemia. Men were more prone to life‑threatening anemia (13%) than women (9%). CONCLUSION: Anemia in cancers was not because of inadequate Epo or Fe levels, but because of improper Epo response. Further studies on molecular analysis of Epo, biochemical and molecular interplay between Epo and TNF‑α could explain a rationale for anemia in cancers.