The epidemiology of molar pregnancy and choriocarcinoma.

The available evidence suggests quite strongly that a hydatidiform mole arises as a consequence of production of a defective ovum. That the defect is maternal is implied by the risk associated with increasing maternal (but not paternal) age, by the recurrence in some women of multiple moles (even in one instance by different husbands), and by reports of familial aggregation of hydatidiform moles among sisters. The absence of maternal genetic material in most complete hydatidiform moles and the dispermic fertilization of some complete and most partial moles further suggests that the ovum is defective. The causes of defective or "blighted" ova are not known. The dramatic increase in risk with age, the smaller increase in young women, and the high incidence in women in parts of Asia must all be important clues. Consanguinity, malnutrition, racial (genetic) predisposition, oral contraceptives, and viral infections have been advanced as causative or contributory factors. Disorders of ovulation, with prolongation of the follicular phase or an inadequate luteal phase, may produce a suboptimum ovum. At some time after ovulation, when the viability of the ovum has become borderline, abnormal (e.g., dispermic) fertilization may become more likely. These and other speculations are being investigated in the detailed case-control studies of trophoblastic disease epidemiology, currently in progress.