If gonadal hormones are responsible for the female predominance (gender discrepancy, sexual dimorphism) that characterizes most autoimmune rheumatic diseases, pregnancy should be a particularly vulnerable period 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 common illnesses. Moreover, many illnesses pathogenetically similar to rheumatic diseases have the same hormonal background but are not characterized by sexual dimorphism. In nonrheumatic sexually dimorphic illnesses an environmental, behavioral, or genetic reason for gender discrepancy is usually present. To explain sexual dimorphism in the autoimmune rheumatic diseases, the fields of environmental, genetic, chromosomal, and in utero sex differentiation need further exploration.
