Clinically significant endogenous circulating heparin-like anticoagulant activity has been associated with hematological malignancies, liver damage, and other pathological conditions. The source of high plasma concentrations of endogenous heparin-like anticoagulants is poorly understood. We report three cases of circulating heparin-like anticoagulants in three patients with hematological malignancies: CLL, multiple myeloma, and T-prolymphocytic leukemia. The severity of bleeding in our patients ranged from severe epistaxis and deep-site hematoma to bleeding of biopsy site and occasional ecchymosis.
Twenty-three hemodialysis patients exposed to an accidental aluminum overload, showed increased erythropoietin requirements and decreased erythrocyte mean corpuscular volume (MCV). At the peak of the intoxication, MCV and plasma aluminum levels changed from unrelated (r = 0.02) to strongly related (r = 0.425) variables. The molar proportion of plasma aluminum to plasma iron increased dramatically (from 1:13.8 to 1:2.4). This significant increment in the aluminum/iron ratio made higher the relative offer of aluminum with respect to iron to the erythroid precursor cells. Accordingly, in a subset of 13 randomly selected aluminum-intoxicated patients we found increased intraerythrocytic aluminum, which paralleled the increase in plasma aluminum. Furthermore, in the aluminum-intoxicated group, intraerythrocytic ferritin, a marker of iron content, and the ratio between erythrocyte and plasma ferritin were lower (P < 0.01 and < 0.001, respectively), than in the control group. These findings support the hypothesis that in some cases of aluminum-related microcytosis, a ferropenic mycrocitosis, as expression of erythroid ferropenia, may exist in spite of the presence of normal body iron stores.
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