BackgroundPosterior reversible encephalopathy syndrome is a neurotoxic condition that occurs as a result of the failure of posterior circulatory autoregulation in response to acute changes in blood pressure. Overperfusion with resultant disruption of the blood-brain barrier results in vasogenic edema, but not infarction. Posterior reversible encephalopathy syndrome can be the presenting feature of postinfectious glomerulonephritis, which has been reported in approximately 5% of hospitalized children, and it has been reported in very few cases of adult patients with sickle cell anemia. We report a very rare case of posterior reversible encephalopathy syndrome that occurred in a child with sickle cell anemia. This presentation should be differentiated from other neurologic manifestations that occur in patients with sickle cell anemia, because management is totally different.Case presentationWe report what is to our knowledge the first reported case of a 9-year-old Saudi girl with sickle cell anemia who developed posterior reversible encephalopathy syndrome secondary to asymptomatic poststreptococcal glomerulonephritis. This occurred after full recovery from acute chest syndrome and severe vaso-occlusive crisis.ConclusionsThe purpose of this report is to emphasize that all efforts should be made to explore the causes of different neurologic manifestations that occur in patients with sickle cell anemia, because this will require different pathways of management.
Higher levels of plasma substance P and sP-selectin were observed in thalassemic patients versus the controls. Both substance P and sP-selectin were significantly higher in the splenectomized group of patients. Conclusions: Substance P and sP-selectin might have a role in platelet activation and subsequent hypercoagulability in thalassemic patients.
Introduction: Evans syndrome is the occurrence of immune-mediated thrombocytopenia in the conjunction with autoimmune hemolytic anemia (AIHA). On the other hand, autoimmune thyroiditis is the presence of antibodies directed to thyroid peroxidase, thyroglobulin and thyroid stimulating hormone receptor. The association of Evans syndrome with hypothyroidism or autoimmune thyroiditis is extremely rare. Case: We present an 8-year-old boy as the first such case in pediatric population diagnosed with Evans syndrome and neutropenia associated with autoimmune hypothyroidism. Conclusion: As autoimmune diseases can occur simultaneously, we emphasize the need to perform appropriate investigations in patients with autoimmune cytopenias.
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