The effect of endogenous and exogenously administered oestrogens, androgens and progesterone on plasma and urinary uric acid and uric acid clearance was studied in a total of 65 healthy volunteers, including normal menstruating and post-menopausal women, girls with primary amenorrhoea and adult male subjects. A serial study throughout a full cycle in 3 women showed an inverse relationship between plasma uric acid levels and endogenous oestrogens. Administration of conjugated and synthetic oestrogens produced a fall in plasma uric acid concentration through a uricosuric effect in most subjects of both sexes. Testosterone propionate caused a definite increase in plasma uric acid levels in post-menopausal women while endogenous testosterone changes due to Leydig cell stimulation produced no definite effect in male subjects. Administration of a progesterone preparation produced an effect similar to that of oestrogens in post-menopausal women. The evidence presented here supports the view that sex steroids play a significant part in uric acid regulation in biological fluids of both sexes.It has been well established that uric acid (UA) concentration in the plasma of healthy subjects is related to age and sex and that in women of reproductive age plasma uric acid (PUA) levels are markedly lower than those of adult men of comparable age (Mikkelsen et al. 1965). The underlying cause for these

apparently in relation to the epithelial basement membrane, with thickening of this structure. The immunofluorescence in the choroid plexus was negative in all cases ofthe control group. Histopathological changes of the choroid plexus, with a pattern similar to that of the systemic hypertension group, were found in only two of the control group.Our results indicate that in about 25% of patients with systemic hypertension the choroid plexus is a site for the deposition of Ig and fractions of C. We suggest that these findings may be secondary to increased vascular permeability produced by hypertension, leading to the passage of plasma and retention of circulating immune complexes in the walls of the choroid plexus, perhaps in a manner analogous to that which occurs in the kidney.'3 A question unanswered by this work is the nature of antigens which stimulate the immune complexes formation and lead to their precipitation in the choroid plexus in some cases of systemic hypertension. Further research into the identification of these antigens as well as the demonstration of a pathogenetic association between immune complexes and histopathological changes in the choroid plexus is needed.

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