PubMed · 8315737
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K B Miller, D P Schenkein. 1993-07-14. Hematology.. https://pubmed.ncbi.nlm.nih.gov/8315737/
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Elevated levels of serum cobalamin may be a sign of a serious, even life-threatening, disease. Diseases such as chronic myeloid leukaemia, promyelocytic leukaemia, polycythaemia vera and hypereosinophilic syndrome are often accompanied by markedly elevated levels of cobalamin in the blood. A rise in the serum cobalamin concentration is one of the diagnostic criteria for polycythaemia vera and hypereosinophilic syndrome. In haematological disorders, the increase in circulating cobalamin levels is predominantly caused by enhanced production of haptocorrin. Several liver diseases such as acute hepatitis, cirrhosis of the liver, hepatocellular carcinoma and metastatic liver disease can also be accompanied by an increase in circulating cobalamin. In liver diseases, the increase in cobalamin is predominantly caused by cobalamin release during hepatic cytolysis and/or through decreased clearance of circulating cobalamin by the affected liver. Liver disorders are not an indication for determining the serum cobalamin concentration. However, a coincidentally observed elevated serum cobalamin concentration is reason for further investigation.
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Our understanding of the hemostatic abnormalities in acute promyelocytic leukemia (APL) has undergone remarkable changes over the past three decades. Hemorrhagic complications lead to significant morbidity and mortality in patients with APL. Up to 30% of early deaths are due to hemorrhagic complications. Our concept of the coagulation changes in APL have evolved from a simple belief that the bleeding was due to disseminated intravascular coagulation (DIC) from underlying infection, to a knowledge that the APL cells themselves are responsible for the bleeding. We have observed that apoptotic APL cells have increased generation of thrombin and therefore contribute to the hypercoagulability and DIC. In addition, excessive fibrinolysis has been recognized to play an important role. The advent of a new therapeutic approach with all-trans-retinoic acid has improved overall survival and has greatly shortened the hemorrhagic phase of the disease, but only to produce a new complication, the retinoic acid syndrome. Its pathogenesis and management still remain to be the challenge for the present.