“…These three conditions are also states of increasing estrogen levels in the blood. Circumstantial evidence indicates a major role of estrogen in the induction of telangiectasias and in the stimulation of angiomas [Bean, 1958;N ewman, 1958;Smith, 1959;Newquist and Mayfield, 1960;Barter el al., 1963;Cunliffe el al., 1972;Wilkin, 1977], Thus, the unilateral dermatomal distribution of the superficial telangiectasia suggests a nevoid distribution of target end organs [Selmanowitz, 1970] sensitive to estrogens [Wilkin, 1977]. As for the onset of congenital UDST, one would only have to postulate a lower threshold to estrogen in the abnormal target end organs.…”