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Factor XIII (FXIII) deficiency is a rare autosomal recessive disorder that can result in life-threatening bleeding and early fetal loss. FXIII not only is responsible for cross-linking fibrinogen to stabilize and strengthen clot formation but also facilitates wound healing and angiogenesis and plays an important role in fetal vitality. Modern therapeutics allow for prophylactic treatment that can prevent most major bleeding and increasing fetal viability. Early diagnosis is paramount due to the high risk of intracranial bleeding.

Splenosis describes ectopic splenic tissue found in patients after rupture of the spleen. These implants are commonly located on the omentum but can be scattered throughout the body in varying number and size. Although splenosis was first documented over a century ago, the precise mechanism for its development remains unknown. The degree of immunoprotection offered by this tissue remains unclear. Much of the human data is in the form of case reports documenting failure of splenotic tissue to protect against septicemia. Even accessory spleens may not offer complete protection once the primary spleen is removed. This review of the literature demonstrates that no amount of splenosis should be considered protective against overwhelming post-splenectomy infection.

Excerpt To the editor: The occurrence of hypokalemia with the blast crisis of acute myeloid leukemia has been described by Mir and co-workers (1a), and accounts of hypokalemia in other leukemic sta...