This study has demonstrated that prophylactic RBCX during pregnancy is a feasible and safe procedure for prevention of complications. Given the decrease in the risks of transfusion, RBCX warrants further study.

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Increased thrombocyte activation leads to a higher likelihood of coagulation in sickle-cell disease. On the other hand, chronic inflammation and endothelial cell activation promote vaso-occlusion. The effect of circulating microparticles derived from erythrocytes, monocytes, thrombocytes, and endothelial cells on the vaso-occlusive process is unclear. This study aims to analyze the relationship between sickle-cell disease and miscellaneous organ complications by defining the circulating microparticles during the steady-state and painful crisis periods in 45 patients with sickle-cell disease. Microparticle analysis was conducted using an eight-parameter flow cytometric method, using CD61 PERCP, CD142PE, CD106 FITC, CD14 APC-H7, CD235a FITC, and Annexin-V APC monoclonal antibodies. Microparticle levels of sickle-cell patients were found to be significantly higher during both painful crisis and steady-state situations compared with the control group (for all, p < 0.001). Among these microparticles, levels of erythrocyte microparticles (eMPs) were significantly higher during crisis than in the steady-state period (eMP steady state vs. painful crisis: 7.59 ± 12.24 vs. 7.59 ± 12.24, respectively; p < 0.01). Microparticles, including eMPs, were not affected by hydroxyurea treatment. Their level did not reflect the high frequency of crisis (>3 times/year). Thrombocyte microparticle levels were found to be higher in patients with nephropathia than in those without (48.05 ± 40.23 vs. 7.67 ± 6.75, respectively; p < 0.049). Circulating microparticles seem to be involved in the pathogenesis of sickle-cell disease. eMPs may help with the management of crisis. Thrombocyte microparticles might predict renal damage induced by vaso-occlusion.

Background/purpose: Sickle cell disease (SCD) is a chronic, hereditary, autosomal recessive disorder. The pathophysiology of SCD is thought to result from polymerization of hemoglobin S in red blood cells under hypoxic conditions, which results in vaso-occlusion. The aim of this study was to determine the periodontal and dental health status of patients with SCD. Materials and methods: Fifty-five SCD patients and 41 healthy individuals were evaluated. Detailed medical and dental histories were taken, and a record made of dental status (missing teeth, restorations, impacted teeth, root canal treatment), periodontal status [plaque index (PI), gingival index (GI), probing depth (PD), bleeding on probing (BOP)], alveolar bone level (ABL), mandibular cortex index, and bone quality index. Results: Two hundred and six teeth were missing, and a total of 195 teeth had restorations. Between-group differences existed for the PI, GI, and BOP; these variables were higher in patients than in the healthy individuals (P < 0.0001). No between-group differences existed for PD. In patients, there was a positive correlation between PD and BOP (P < 0.0001; r Z 0.657), PD and GI (P Z 0.02; r Z 0.299), PD and PI (P Z 0.01; r Z 0.343); BOP and GI (P < 0.0001; r Z 0.503), BOP and PI (P < 0.0001; r Z 0.496); and GI and PI (P Z 0.003; r Z 0.388). The ABL in patients was found to be similar to that of the general population with an unknown periodontal condition.

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