If gonadal hormones are responsible for the female predominance (gende
r discrepancy, sexual dimorphism) that characterizes most autoimmune r
heumatic diseases, pregnancy should be a particularly vulnerable perio
d for onset of new disease as well as for exacerbation of established
disease. Currently available data support neither the contention: that
pregnancy increases incidence nor that it worsens severity of the com
mon illnesses. Moreover, many illnesses pathogenetically similar to rh
eumatic diseases have the same hormonal background but are not charact
erized by sexual dimorphism. In nonrheumatic sexually dimorphic illnes
ses an environmental, behavioral, or genetic reason for gender discrep
ancy is usually present. To explain sexual dimorphism in the autoimmun
e rheumatic diseases, the fields of environmental, genetic, chromosoma
l, and in utero sex differentiation need further exploration.