Possible interplay between vitamin C deficiency and prolactin in pregnant women with premature rupture of membranes: facts and hypothesis

The present hypothesis proposes that a decreased hypothalamic dopaminergic tone-and thus an increased synthesis/release of pituitary PRL - is induced by vitamin C deficiency below a critical threshold (<18 μg/108 leukocytes) and that both factors, in turn, would cause upregulation of the expression/activity of several MMP. The increased PRL concentrations (acting like a Th1-type cytokine) along with the overexpression of other proinflammatory cytokines would induce a premature switch from a favorable Th2-type immune response to a noxious Th1-type immune response in the intrauterine environment. This change, in conjunction with the upregulation of MMP-2 and MMP-9, would cause a premature imbalance between synthesis/degradation of collagen in chorioamniotic membranes (an “anticipation” of the normal parturition cascade?), which favors extracellular matrix degradation, proposed as the most relevant event in the genesis of PROM. This hypothesis represents a new dimension in the study of the etiology of PROM.