Prolactin and calcitropic hormones in preterm premature rupture of membranes

AbstractObjectives: To investigate the role of prolactin and calcitropic hormones in preterm premature rupture of membranes (PPROM) with intrauterine infection. Methods: Amniotic fluid was retrieved by transabdominal amniocentesis from 40 patients with PPROM and 36 normal pregnant women of matched gestational age. Microbial state of amniotic cavity included culture for aerobic and anaerobic bacteria, mycoplasmas and ureaplasma. Maternal serum and fetal serum prolactin, parathyroid hormone mid‐molecule PTH‐M, 1,25‐dihydroxyvitamin D3 and calcitonin were determined by the corresponding radioimmunoassay Maternal serum and fetal serum electrolytes were determined by ion‐selective electrodes. Chlorides were assayed colorimetrically and osmolality was determined by osmometry. Results: Microbiological evaluation of amniotic fluid PPROM revealed aerobic, anaerobic or mixed aerobic anaerobic infections PPROM was associated with significant elevation of both fetal serum and amniotic fluid prolactin concentrations, increased amniotic fluid osmolality, sodium, chlorides and calcium. Amniotic fluid potassium level was significantly decreased, compared with controls. Maternal serum and fetal serum PTH‐M, 1,25‐dehydroxyvitamin D3 were significantly higher in patients with PPROM than in controls. Conclusions: Increased amniotic fluid prolactin leads to impairment of structural integrity of fetal membranes through electrolytes disturbances. Moreover, increased amniotic fluid calcium induced by increased fetal calcitropic hormones evokes myometrial contraction through prostaglandin E2 release. Both mechanisms may combine to trigger the onset of PPROM associated with intrauterine infection.