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Genetic cause: Deletions or mutations in one or more of the four alpha globin genes on chromosome 16 (HBA1 and HBA2). Clinical features: Depending on the number of genes affected - silent carrier, mild anemia, HbH disease, or hydrops fetalis (with four gene deletions). Management: Transfusion for HbH disease, monitoring, genetic counseling.

Genetic cause: Compound heterozygous state for HbS and HbC mutations. Clinical features: Similar to sickle cell anemia but generally milder; includes hemolytic anemia, occasional pain crises, and retinopathy. Management: Similar to sickle cell anemia; monitoring, pain relief, and sometimes hydroxyurea.

Genetic cause: Mutation in the HBB gene causing a substitution of valine for glutamic acid at position 6 in the beta globin chain. Clinical features: Painful crises, anemia, splenomegaly, increased risk of infections, and vaso-occlusive complications. Management: Hydration, pain management, hydroxyurea, and prophylactic antibiotics.

Genetic cause: Mutations in the HBB gene that reduce or prevent the production of beta-globin chains. Clinical features: Microcytic anemia, bone deformities, splenomegaly, and iron overload. Management: Blood transfusions, iron chelation therapy, and bone marrow transplantation.

Genetic cause: Mutation in the HBB gene resulting in the substitution of lysine for glutamic acid at the sixth position of the beta-globin chain. Clinical features: Mild hemolytic anemia, splenomegaly, and rarely, vaso-occlusive crises. Management: Typically requires no treatment but folic acid supplementation can be helpful.