Acute recurrent polyhydramnios and amniotic prolactin
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SHORT COMMUNICATION Acute recurrent polyhydramnios and amniotic prolactin Marco De Santis 1 *, Anna Franca Cavaliere 1 , Giuseppe Noia 1 , Lucia Masini 1 , Edoardo Menini 2 and Alessandro Caruso 1 1 Department of Obstetrics and Gynaecology, Catholic University of Sacred Heart, Rome, Italy 2 Department of Biochemistry, Hormone Laboratory, Catholic University of Sacred Heart, Rome, Italy A 25 year-old patient in her third pregnancy presented with acute polyhydramnios at 24 weeks’ gestation, which was the same time as in the two previous pregnancies. In both she had preterm premature rupture of membranes, preterm delivery and neonatal deaths. In the third pregnancy, amnioreductions combined with medical treatment resulted in the birth by Caesarean section of a normally formed live male at 31 weeks of pregnancy. Acute recurrent polyhydramnios is an extremely rare condition of unknown aetiology. We hypothesized that amniotic prolactin plays a role in this pathology. It was measured serially in amniotic fluid and high levels were found. Copyright # 2000 John Wiley & Sons, Ltd. KEY WORDS: prolactin; recurrent polyhydramnios; lactogen receptor; chorion laeve; amnioreduction INTRODUCTION Acute recurrent polyhydramnios (ARP) is an extre- mely rare condition which occurs in 1 in 12000 pregnancies (Pitkin, 1976). It is manifested at 20–24 weeks’ gestation and may cause premature delivery with a high fetal and neonatal mortality rate. Few cases of acute recurrent polyhydramnios treated with amnioreduction, combined with maternal administra- tion of indomethacin or isoxsuprine, have been reported in the literature and our experience confirms the efficacy of amnioreduction, particularly when combined with additional medical treatment (Malas and Hamlett, 1991; Pitkin, 1976; Queenan, 1970; Shimizu et al., 1988; Weissman and Zimmer, 1987). Only five cases of acute recurrent polyhydramnios have been reported in the literature: one was attributed to human leucocyte antigen compatibility (Shimizu et al., 1988); two refer to the role of amniotic prolactin (A-PRL) and its receptors without, however, any specific study having been carried out (Shimizu et al., 1988; Weissman and Zimmer, 1987); two reports do not propose any aetiologic hypothesis (Pitkin, 1976; Queenan, 1970). We report the first case of acute recurrent polyhydramnios in which prolactin (PRL) has been measured in amniotic fluid at different times and in which high levels were found. CASE REPORT A 25-year-old woman, gravida 3, para 2, with two early neonatal deaths, came under our care during the 24th gestational week following the appearance of severe polyhydramnios. Polyhydramnios had occurred at the same time in the previous two pregnancies, and resulted in premature rupture of the membranes with extremely premature vaginal delivery at the 27th week. During the course of the second pregnancy, amnio- reduction had been carried out at another centre. The woman had no family history of diabetes, thy- roid disease or hypertension. Maternal pathologies, TORCH group infections and maternal-fetal incom- patibility were excluded. All maternal blood chemical, urinary and microbiological examinations, as well as the oral glucose tolerance test (100 g), carried out at the 25th week and repeated at the 31st, were normal. Ultrasound examinations showed no morphologic changes or abnormal movements and the karyogram, previously performed on amniotic fluid at the 16th week, was normal (46,XY). Due to an increase in polyhydramnios and the presence of maternal symp- toms such as dyspnoea and abdominal pain the patient underwent a series of invasive and non- invasive therapeutic interventions, starting from the 24th gestational week up to delivery. Seven amnio- reductions were carried out between the 24th and 30th gestational weeks with a minimum withdrawal of 284 ml on the first occasion and a maximum of 1260 ml at the 30th week, reaching a total of 5290 ml. During the of amnioreduction, isoxsuprine i.v. and a 2 mg dose of mezlocillin were administered to the mother. The therapeutic strategy included 12-hourly administrations of 100 mg of indomethacin via the rectal route on the day of the procedure, and repeated on the following day to reduce uterine contractions and diminish the rapid reformation of polyhydramnios. The interval between one amnior- eduction and the next was established on the basis of maternal clinical condition and the amniotic fluid index (AFI) with a minimum of four days to a maximum of six. AFI values were always above the *Correspondence to: M. De Santis, Department of Obstetrics and Gynaecology, Catholic University of the Sacred Heart, L.go A. Gemelli, 8, 00168 Rome, Italy. E-mail: [email protected] PRENATAL DIAGNOSIS Prenat Diagn 2000; 20: 347–348. Copyright # 2000 John Wiley & Sons, Ltd. Received: 17 September 1999 Revised: 7 November 1999 Accepted: 21 December 1999
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Transcript of Acute recurrent polyhydramnios and amniotic prolactin
SHORT COMMUNICATION
Acute recurrent polyhydramnios and amniotic prolactin
Marco De Santis1*, Anna Franca Cavaliere1, Giuseppe Noia1, Lucia Masini1, Edoardo Menini2 andAlessandro Caruso1
1Department of Obstetrics and Gynaecology, Catholic University of Sacred Heart, Rome, Italy2Department of Biochemistry, Hormone Laboratory, Catholic University of Sacred Heart, Rome, Italy
A 25 year-old patient in her third pregnancy presented with acute polyhydramnios at 24 weeks' gestation,which was the same time as in the two previous pregnancies. In both she had preterm premature rupture ofmembranes, preterm delivery and neonatal deaths. In the third pregnancy, amnioreductions combined withmedical treatment resulted in the birth by Caesarean section of a normally formed live male at 31 weeks ofpregnancy. Acute recurrent polyhydramnios is an extremely rare condition of unknown aetiology. Wehypothesized that amniotic prolactin plays a role in this pathology. It was measured serially in amniotic¯uid and high levels were found. Copyright # 2000 John Wiley & Sons, Ltd.
KEY WORDS: prolactin; recurrent polyhydramnios; lactogen receptor; chorion laeve; amnioreduction
INTRODUCTION
Acute recurrent polyhydramnios (ARP) is an extre-mely rare condition which occurs in 1 in 12000pregnancies (Pitkin, 1976). It is manifested at 20±24weeks' gestation and may cause premature deliverywith a high fetal and neonatal mortality rate. Fewcases of acute recurrent polyhydramnios treated withamnioreduction, combined with maternal administra-tion of indomethacin or isoxsuprine, have beenreported in the literature and our experience con®rmsthe ef®cacy of amnioreduction, particularly whencombined with additional medical treatment (Malasand Hamlett, 1991; Pitkin, 1976; Queenan, 1970;Shimizu et al., 1988; Weissman and Zimmer, 1987).Only ®ve cases of acute recurrent polyhydramnioshave been reported in the literature: one was attributedto human leucocyte antigen compatibility (Shimizuet al., 1988); two refer to the role of amniotic prolactin(A-PRL) and its receptors without, however, anyspeci®c study having been carried out (Shimizu et al.,1988; Weissman and Zimmer, 1987); two reports donot propose any aetiologic hypothesis (Pitkin, 1976;Queenan, 1970). We report the ®rst case of acuterecurrent polyhydramnios in which prolactin (PRL)has been measured in amniotic ¯uid at different timesand in which high levels were found.
CASE REPORT
A 25-year-old woman, gravida 3, para 2, with twoearly neonatal deaths, came under our care during the24th gestational week following the appearance of
severe polyhydramnios. Polyhydramnios had occurredat the same time in the previous two pregnancies, andresulted in premature rupture of the membranes withextremely premature vaginal delivery at the 27th week.During the course of the second pregnancy, amnio-reduction had been carried out at another centre.The woman had no family history of diabetes, thy-roid disease or hypertension. Maternal pathologies,TORCH group infections and maternal-fetal incom-patibility were excluded. All maternal blood chemical,urinary and microbiological examinations, as well asthe oral glucose tolerance test (100 g), carried out atthe 25th week and repeated at the 31st, were normal.Ultrasound examinations showed no morphologicchanges or abnormal movements and the karyogram,previously performed on amniotic ¯uid at the 16thweek, was normal (46,XY). Due to an increase inpolyhydramnios and the presence of maternal symp-toms such as dyspnoea and abdominal pain thepatient underwent a series of invasive and non-invasive therapeutic interventions, starting from the24th gestational week up to delivery. Seven amnio-reductions were carried out between the 24th and30th gestational weeks with a minimum withdrawalof 284 ml on the ®rst occasion and a maximum of1260 ml at the 30th week, reaching a total of 5290 ml.During the of amnioreduction, isoxsuprine i.v. and a2 mg dose of mezlocillin were administered to themother. The therapeutic strategy included 12-hourlyadministrations of 100 mg of indomethacin via therectal route on the day of the procedure, andrepeated on the following day to reduce uterinecontractions and diminish the rapid reformation ofpolyhydramnios. The interval between one amnior-eduction and the next was established on the basis ofmaternal clinical condition and the amniotic ¯uidindex (AFI) with a minimum of four days to amaximum of six. AFI values were always above the
*Correspondence to: M. De Santis, Department of Obstetrics andGynaecology, Catholic University of the Sacred Heart, L.go A.Gemelli, 8, 00168 Rome, Italy. E-mail: [email protected]
PRENATAL DIAGNOSIS
Prenat Diagn 2000; 20: 347±348.
Copyright # 2000 John Wiley & Sons, Ltd. Received: 17 September 1999Revised: 7 November 1999
Accepted: 21 December 1999
97.5th percentile, with a minimum of 332 at the 24thweek and a maximum of 603 at the 31st. Duringthree of the amnioreductions amniotic infusions of L-thyroxine were administered at a dose of 250 mg atthe 25th week, and 500 mg at the 26th and 27thweeks, in order to induce fetal lung maturity andreduce the risk of bronchial dysplasia (Mashiachet al., 1978). The levels of amniotic prolactin (A-PRL), assessed by the radioimmunoassay (RIA)technique (BIODATA-SERONO), gave the followinghigh values: 1510 ng/ml at 24 weeks; 3387 ng/ml at 25weeks; 3248 at 26 weeks; and 1121 ng/ml at 27 weeks.(Andersen, 1982; Clements et al., 1977; Luciano andVarner, 1984). Maternal serum prolactin was175.5 ng/ml at 30 weeks, and this was within thenormal range (Clements et al., 1977; Tyson et al.,1972). The lecithin±sphyngomyelin ratio increasedfrom 0.6 at the 25th week, before L-thyroxineinfusion, to 1.7 at the 30th gestational week afterthree infusions of thyroid hormone. Dexamethasone12 mg i.m. was given twice. Labour started in the31st week of pregnancy and delivery by Caesareansection resulted in the birth of a normally formed livemale with a birth weight of 1500 g. Paediatricexamination carried out at one year of age showednormal development.
DISCUSSION
This is the ®rst case report of acute recurrentpolyhydramnios in which PRL was measured inamniotic ¯uid. PRL covers an important roà le inwater homeostasis of amniotic ¯uid through a receptormechanism which modi®es the permeability of amnio-tic membranes. The prolactin produced by the deciduapasses into the amniotic compartment, does notin¯uence maternal and fetal blood prolactin levels, isindependent of dopaminergic control and is notin¯uenced by administration of bromocriptine (Ander-sen, 1982; Luciano and Varner, 1984). Wide variationsin amniotic prolactin (A-PRL) levels have beenreported by various authors regardless of the gesta-tional week. However, a typical trend emerges, i.e.increases start from the 10th gestational week andreach maximum values at approximately 20±25 weeks,diminishing toward the conclusion of pregnancy(Andersen, 1982; Clements et al., 1977; Luciano andVarner, 1984). Compared to results obtained byClements et al. (1977), and Pahnke et al. (1985) innormal pregnancy, the values obtained by us in thepresence of acute recurrent polyhydramnios are abovenormal limits. According to results obtained by Tysonet al. (1972) and Kletzky et al. (1985), also in normalpregnancy, our values are within normal limits, butcloser to the upper limits. In chronic polyhydramnios,
several authors have reported low levels of A-PRL dueto decreased PRL production by decidua (Lucianoand Varner, 1984; Pahnke et al., 1985; Phocas et al.,1987), and Healy et al. (1985) demonstrated PRLresistance subsequent to a defect in chorion laevereceptors that might produce chronic polyhydramnios.Thus, our elevated values in the presence of acuterecurrent polyhydramnios contrast with low levels ofA-PRL in chronic polyhydramnios. This leads to thehypothesis that acute recurrent polyhydramnios is notrelated to a reduced production of PRL but probablyto a numeric or functional de®cit in the chorionicreceptors for PRL. Despite the rarity of this condition,we suggest that further studies of the PRL receptors inacute recurrent polyhydramnios are indicated.
REFERENCES
Andersen JR. 1982. Prolactin in amniotic ¯uid and maternal serumduring uncomplicated human pregnancy. Dan Med Bull 29:266±274.
Clements JA, Reyes FI, Winter JSD, Faiman C. 1977. Studies onhuman sexual development IV. Fetal pituitary and serum, andamniotic ¯uid concentrations of prolactin. Clin Endocrinol Metab44: 408±413.
Healy DL, Herington AC, O'Herlihy C. 1985. Chronic polyhy-dramnios is a syndrome with a lactogen receptor defect in thechorion laeve. Br J Obstet Gynec 92: 461±467.
Kletzky OA, Rossman F, Bertolli SI, Platt LD, Mishell DR. 1985.Dynamics of human chorionic gonadotropin, prolactin, andgrowth hormone in serum and amniotic ¯uid throughoutnormal human pregnancy. Am J Obstet Gynec 151: 878±884.
Luciano AA, Varner MW. 1984. Decidual, amniotic ¯uid, maternaland fetal prolactin in normal and abnormal pregnancies. ObstetGynec 63: 384±388.
Malas HZ, Hamlett JD. 1991. Acute recurrent polyhydramnios-management with indomethacin. Br J Obstet Gynaecol 98:583±587.
Mashiach S, Barkai G, Sack J, Stern E, Goldman B, Brish M, SerrDM. 1978. Enhancement of fetal lung maturity by intramnioticadministration of thyroid hormone. Am J Obstet Gynecol 130:289±293.
Pahnke VG, Goepel E, Kitschke HJ. 1985. Fruchtwasser-prolaktin,ein osmoregulatorisches hormon mit klinischer bedeutung?Geburts Frauenheilk 45: 462±469.
Phocas I, Salamalekis E, Sarandakou A, Zourlas PA. 1987.Hormonal and biochemical parameters in polyhydramnios. EurJ Obstet Gynec Reprod Biol 25: 277±286.
Pitkin RM. 1976. Acute polyhydramnios recurrent in successivepregnancies. Obstet Gynecol 48: 42S±43S.
Queenan JT. 1970. Recurrent acute polyhydramnios. Am J ObstetGynec 106: 625±626.
Shimizu T, Ihara Y, Kawaguchi K, Fujiwara T, Ando N. 1988.Human leukocyte antigen compatibility in a couple withidiopathic recurrent hydramnios. Am J Obstet Gynec 159:463±464.
Tyson JE, Hwang P, Guyda H, Friesen HG. 1972. Studies ofprolactin secretion in human pregnancy. Am J Obstet Gynec 113:14±20.
Weissman A, Zimmer EZ. 1987. Acute polyhydramnios recurrent infour pregnancies. JRM 32: 65±66.
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Copyright # 2000 John Wiley & Sons, Ltd. Prenat Diagn 2000; 20: 347±348.
