Serum levels of dehydroepiandrosterone sulfate (DHEAS) in ocular toxoplasmosis

Abstract

Ocular toxoplasmosis is the most common infectious cause of retinochoroidal inflammation in immunocompetent individuals and is one of the most important causes of visual damage in some countries.1 Thus, in Colombia, it is estimated that 6% of the population has retinochoroidal scars after a non congenital infection and 20% of these persons have reduced visual capacity.2 Recurrent retinochoroiditis is a typical characteristic of ocular toxoplasmosis and the factors related to this remain to be discovered.3 In a field study in Brazil, a relation between puberty, gender and apparition of new lesions in ocular toxoplasmosis was described.4 A hormonal factor triggering recurrences has been evocated but the precise hormones linked to these events have not been studied. In recent years there has been strong speculation that puberty-related hormones, dehydroepiandrosterone (DHEA) in particular, might play some role in inducing resistance during Schistosoma, HIV and malaria infections.5, 6, 7 DHEA is one of the steroid hormones produced by the adrenal cortex and is found mostly in its sulfate form, DHEA sulfate (DHEAS); it is converted to DHEA by DHEA sulfatase.8 The secretion of DHEAS is high just before birth and again at puberty, and the maximum concentration is reached at around 20 to 30 years of age, followed by a progressive decline with age. DHEAS is implicated in age-related changes in the immune system and has been associated with disease susceptibility.9 To our knowledge, no report has been made of the DHEAS levels during human toxoplasmosis.