The role of new biochemical markers associated with osteoporosis in patients with sickle cell anemia in diagnosis

Autosomal recessive inherited sickle cell anemia (SCA), originates from the single point mutation in the gene encoding the β-globin chain. This mutation, which causes the load balance of hemoglobin to change, causes HbS to polymerize in environments with insufficient oxygen. As a result, the biceps of the red blood cells change the shape and take the form of a sickle. Osteoporosis, which is a bone disease, may develop due to the low bone mass density caused by bone deformities occurred by depending on remaining the tissues and organs without oxygen. In this study, we aimed to investigate the relationship between sickle cell anemia and osteoporosis in sickle cell patients by measuring serum levels of bone turnover markers. For this purpose, in this study, 33 adult patients with SCA (30 patients with HbSS/3 patients with HbSβ) compared with a sex- and age-matched control group. Blood of all patients and healthy individuals were collected and the collected blood samples were centrifuged at 3500 rpm for 10 minutes, then the blood serum of those was separated and stored at -80°C for biochemical analysis. Working day in serum samples; bone formation markers of bone turnover; PINP, PICP, BALP and Osteocalcin, bone resorption markers of bone turnover; CTX, Hydroxyproline, and Pridinoline were studied by ELISA and 25(OH)D levels measured spectrophotometrically by Immunoassay (EIA). The data were evaluated statistically, and the results were discussed. As a result, there was no statistically significant difference between sickle cell anemia study group and control group in PINP (p=0,345), PICP (p=0,071) and BALP (p=0,607) levels. However, the OT level was significantly higher in the study group (p=0,016). In addition, no statistically significant difference was found between CTX (p=0,763), Hyp (p=0,546) and PYD (p=0,890) levels when compared with the control group. Finally, 25(OH)D sickle cells were significantly lower in the study group compared to the control group (p=0,01). In conclusion, when the results of the study were evaluated according to osteocalcin which is a marker of bone formation, it can be said that osteoblastic activity and thus bone turnover increased in patients with sickle cell anemia. Increased osteocalcin level and low 25(OH)D result of patient group support the pathology of osteoporosis but are not sufficient for diagnosis. In conclusion, to understand the effect of sickle cell anemia on bone metabolism, biochemical markers need to be further investigated by supporting BMD and increasing the sample size of patients.