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Case report describes severe acyclic menstrual bleeding linked to erythrocytosis in congenital heart disease, highlighting bleeding risks from hypoxia-driven hematopoiesis.
EXCESSIVE acyclic menstrual bleeding associated with polycythemia is a relatively rare occurrence. It is the purpose of this paper to report such a case, secondary to congenital heart disease, and to discuss the possible mechanisms at work. Polycythemia may occur either in response to some known stimulus, in which case it is termed erythrocytosis, or it may be of unknown etiology and then it is called erythremia (1). Both erythrocytosis and erythremia may be complicated by thromboses and hemorrhage. The latter is commonly seen in the form of epistaxis, cerebral hemorrhage, hematemesis, melena, hemoptysis and purpura. In the course of congenital heart disease in which the contents of the right side of the heart mix with arterial blood, an increase in hematopoiesis is apt to occur. Such a situation arises in the Eisenmenger complex, the latter being characterized by (a) a membranous interventricular septal defect, (b) origin of the aorta either from both ventricles above the defect or entirely from the right ventricle, (c) right ventricular hypertrophy, and (d) absence of pulmonary or subpulmonary stenosis (2, 3). Arterial oxygen saturation is reduced in such cases and it is assumed that this low oxygen tension is a stimulus to the hematopoietic system (4).
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Green et al. (1955) studied this question.
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