Research on the relation between intrauterine infection and intrauterine growth retardation]

To investigate the relationship between intrauterine infection and IUGR, the following studies have been carried out: (1) measurement of specific antibodies of Toxoplasma (Toxo) and Cytomegalovirus (CMV) in the umbilical serum samples from 30 cases of IUGR with 26 normal newborn infants as controls; (2) follow-up exam on 14 positive cases in 17-25 months. The results showed that in 30 IUGR cases 14 were found to have Toxo and CMV infection, with an incidence significantly higher than that in the control group. One third of the infected patients were found to have retarded growth afterbirth and 63.63% of them appeared to have an increase in BAEP. This suggested that regular follow-up is indicated in these cases.     

Placenta in intrauterine growth retardation

Undernutrition and toxemia of pregnancy are considered to be important maternal causes for the fact that 15-30% of infants born at term in India are "small for date." The various changes of senescence in placenta were quantitatively studied in cases of toxemia, anemia, and unexplained growth retardation and compared with healthy controls. Placenta was studied in 100 term parturients admitted to the labor ward of the Lady Hardinge Medical College and Hospital in New Delhi, India. The parturients included the following: 1) group 1 -- 25 normal term parturients; 2) group 2 -- 25 intrauterine growth retardation, birth weight less than 2500 grams; 3) group 3 -- toxemia of pregnancy with blood pressure of 130 + 90 mm of Hg. and above with or without edema and/or proetinurea (25); and 4) group 4 -- anemia of pregnancy, Hb. less than 8.0 gm% (25). Despite extensive work no specific lesion in placental histology is found in toxemia of pregnancy and the same is true in cases of unexplained intrauterine growth retardation. The reason for this may be probable underlying multiple etiology in both conditions. The only significant finding which has been observed by many workers is decrease in size and weight of placentae in the IUGR group. Mean diameter was 15.3 cm compared to 17.54 in control cases, and mean weight was 288.0 gms compared to 466.8 in control cases.     

Genetic heterogeneity of prematurity and intrauterine growth retardation: clues from the Old Order Amish

We studied differences in the role of genetic factors in prematurity and intrauterine growth retardation with the use of data on 312 Amish singleton live children ascertained from Amish records in Lancaster county, Pennsylvania, between 1969 and 1980. Birth and death certificates were obtained on all children, and inbreeding coefficients of child, mother, and father were computed by use of the path method of tracing common ancestors in a unique genealogic registry of Amish ancestors dating back to the 1700s. Multivariate analysis with linear and log linear models showed that a lower mean gestational age and a higher risk of prematurity (less than 37 weeks) and borderline maturity (37 to 38 weeks) were significantly associated with increased maternal inbreeding but not child or paternal inbreeding. On the other hand, a higher risk of intrauterine growth retardation (less than the tenth percentile in birth weight for gestational age) and mild intrauterine growth delay (tenth to twenty-fifth percentile) were associated with increased child inbreeding but not maternal or paternal inbreeding. The analysis suggests the presence of genetic heterogeneity in the etiology of prematurity and intrauterine growth retardation; while prematurity is mostly related to the maternal genotype, intrauterine growth retardation is related to the fetal genotype. The study reemphasizes the need for separating low birth weight into prematurity and intrauterine growth retardation in genetic and epidemiologic studies.     

Inflammatory cytokines in intrauterine growth retardation

BACKGROUND: To evaluate maternal serum levels of two inflammatory cytokines in women with intrauterine growth retardation (IUGR), while studying separately women with or without placental insufficiency. METHODS: The study comprised 14 women with IUGR and Doppler-defined placental insufficiency, 14 women with IUGR without placental insufficiency, and 28 healthy pregnant women as a control group. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were measured using a commercially available kit. The Kruskal-Wallis test and the corrected Mann-Whitney U-test were used. RESULTS: There was a statistically significant difference in TNF-alpha levels among the three studied groups (p = 0.03). Women with IUGR and placental insufficiency showed statistically significant higher serum levels of TNF-alpha[2.2 pg/mL (1.3-4.1)] and a higher rate of detectable TNF-alpha[85.7% (12/14)] than those in the control group [0 pg/mL (0-2.7) and 32.1% (9/28)] (p = 0.01 and p = 0.001, respectively). On the contrary, there was no difference in either the TNF-alpha level [1.4 pg/mL (0-4.9)] or the rate of detectable TNF-alpha[57.1% (8/14)] between women with IUGR without placental insufficiency and women in the control group. The levels of IL-6 were similar in the three studied groups. CONCLUSION: TNF-alpha is increased in women with IUGR and placental insufficiency but normal in those with IUGR and normal placental perfusion. We suggest that elevations of TNF-alpha could be a specific phenomenon of certain subsets of IUGR, identifying cases with placental dysfunction.     

Fetal movements and intrauterine growth retardation

Fetal Movement (FM) rate was evaluated in cases of symmetrical and asymmetrical intrauterine growth retardation (IUGR) and was compared to the FM rate in normal pregnancy. In the 25–36th week of gestation there was a significant decrease of FM rate in both groups of IUGR which was more pronounced in the symmetrical group. Also shown, was a gradual trend of increase of the FM rate with advancing gestational age in both groups of IUGR. Cases of asymmetrical IUGR were noted, who had markedly decreased FM until cessation. In this group of IUGR decreased FM demands prompt hospitalization and fetal heart rate monitoring so that possible respiratory failure and impending fetal death can be detected.     

Placental insufficiency and intrauterine growth retardation

AIM: Placental insufficiency is a pathological condition consisting of a placental functional deficit with multifactorial etiology; it can cause maternal complications such as edema, proteinuria, hypertension, etc. Our study aims to establish if placenta analysis after birth can lead to the identification of basic morphological alterations which can be easily documented and useful for the diagnosis of feto-neonatal pathologies. METHODS: We examined 60 pregnant women (45 primipara, 15 multipara). They were hospitalized in the period from March 1998 to March 2004 in different pregnancy periods because of fetus growth delay. After birth, a careful examination of the placenta has been carried out soon after spontaneous birth (weight, thickness, possible morphological alterations which could be macroscopically observed) and it was followed by an anatomo-pathological examination carried out at the Anatomopathology Unit of Ospedali Riuniti in Foggia. RESULTS: Macroscopic examination, in the group of women at the first pregnancy, showed that there were no morphological alterations in the placenta in all the cases, but the weight was normal (400- 500 g) in 8 cases and it was less than 400 g in the other 37 cases. In the group of multipara, placenta did not shown morphological alterations in all the cases, but the weight was normal in only 3 cases and it was lower in the remaining 12 cases. The placental microscopic examination pointed out: infarct focus in 34 cases (60%), 12 (35%) of which were recent and 22 (65%) were old infarct focuses; immaturity of chorionic villus in 15 (30%) of the examined placentas; increase in the cytotrophoblast mitotic index in 49 cases (90%) and placenta with normal histological appearance in 11 cases (10%). CONCLUSION: Placental examination, both with macroscopic and microscopic techniques, can lead to the identification of basic morphological alterations which can be easily documented and useful for the diagnosis of feto-neonatal pathologies. A good placental functionality influences both fetal life and postnatal life. Thus, a greater attention to the placental examination in obstetric practice is suggested, especially for maternal and fetal pathologies.     

Platelets and intrauterine growth retardation in pre-eclampsia.

In pre-eclampsia, but not essential hypertension of pregnancy, reduced maternal levels of circulating platelets were found to correlate with intrauterine growth retardation. This suggests that disseminated intravascular coagulation and fibrin deposition contribute to the placental damage of pre-eclampsia.     

Chorionic chromosome abnormalities and intrauterine growth retardation

Chorion, placental membranes, and embryo all arise from the same fertilized oocyte; therefore, chorionic cells are presumed to reflect fetal chromosome status. Progenitor cells of the embryo are selected from the blastocyst, however, at a very early stage of development. If mitotic nondisjunction were to occur in one of the blastocyst cells destined to become trophoblast, the resultant abnormal cell line would be restricted to extraembryonic tissues. Indeed, chromosome mosaicism confined to the placenta has been found repeatedly in diagnostic chorionic villus sampling, and occasionally in third trimester placentas. Cytogenetically abnormal placental cells are morphologically and perhaps functionally abnormal. Such aberrations might result in deficient oxygen or nutrient supply to the fetus, causing intrauterine growth retardation (IUGR). To investigate this hypothesis we studied chorion and cord blood samples after delivery from 11 confirmed IUGR pregnancies. A minimum of 10 cells were analyzed from each cord blood and chorion specimen (mean number of cells from cord blood = 27; from chorion = 17). None of the cases showed true mosaicism for a hyperdiploid line. We conclude from this preliminary study that few, if any, cases of IUGR are likely to be due to chorionic mosaicism.     

Experimental intrauterine growth retardation with indomethacin

The present study was undertaken to determine the influence of indomethacin, a potent inhibitor of prostaglandin synthetase, on the intrauterine fetal growth of rats. All experimental rats administered indomethacin on various days of gestation were sacrificed on day 22 of gestation. The following results were obtained. The intrauterine fetal growth retardation (IUGR) and maternal weight loss were found following intramuscular administration of indomethacin 2mg on day 19 of gestation. IUGR and maternal weight loss were also found after fasting from day 19 of gestation to day 22. IUGR was induced by the administration of indomethacin on days 15 to 21 of gestation, while not by that on day 10. The mean fetal weight of rats which received indomethacin on day 19 of gestation was 3.57 +/- 0.44g, which was as low as 67.9% of normal fetal weight. There seemed to be a critical period for the occurrence of IUGR in rat due to indomethacin. The possible jeopardy of fetal development due to the administration of indomethacin to pregnant women in the late pregnancy should be warned against.     

Patterns of intrauterine growth retardation.

A prospective study of 70 singleton pregnancies at high risk for intrauterine growth retardation (IUGR) was undertaken to determine 1) the differences in intrauterine growth patterns; 2) the diagnostic accuracy of obstetric techniques; and 3) the frequencies of perinatal complications. Thirty infants displayed signs of IUGR. Although only 14 infants had low birth weights, these 14, as well as the remaining 16 infants under study, displayed many other features of growth abnormalities, including a low ponderal index, short stature, and small head circumference. These data demonstrate various patterns of IUGR. Although the perinatal complications occurred primarily in the low-birth-weight group, the major growth abnormalities observed in the non-low-birth-weight group demonstrate the need for additional short- and long-term follow-up studies in both groups.