Symmetrical Intrauterine Growth Retardation Research Articles

Pattern of intrauterine growth retardation among low birth weight neonates

Background: There is an association between intrauterine growth retardation (IUGR) and subsequent development of diabetes mellitus, coronary artery disease and hypertension during adult life. With this context, it is vital to give attention about the patterns of body proportion of IUGR babies. The aim of this study was to determine the proportion of asymmetric distribution IUGR in contrast to symmetric distribution among babies with low birth weight (LBW).
 Methods: This cross-sectional study was conducted in the Department of Pediatrics, Sher-e-Bangla Medical College, Barisal,from January 2012 to June 2012, with a total 114 babies with LBW. All singleton newborns, within 24 hours of birth, having birth weight < 2.5 kg was were included. Weight was plotted in weight for gestation age centile chart. Then Ponderal index (PI) was calculated to determine asymmetric and symmetric IUGR by using the formula. Convenient sampling was used. Data were analyzed with SPSS. P value <0.05 was considered as significant.
 Results: Out of 114 LBW babies, 79 were IUGR babies. Among 79 IUGR babies, 45.6% were male and 54.4% were female. The mean age of the mothers of the IUGR babies was 24.2 ± 5.6 years. Most of the mothers were in the age group of 16 to 25 years. In this study, most of the IUGR was asymmetric (68.4%) and a majority of the asymmetric IUGR babies were from rural areas. The PI of the asymmetric IUGR was significantly (p =<0.001) lower than the symmetric IUGR.
 Conclusion: This study highlights that, among the LBW babies most of them were IUGR, the large population of IUGR babies were of asymmetric patterns. This group of patients carries immense importance to keep an eye on the risk of fetal origin of adult diseases.
 BIRDEM Med J 2022; 12(3): 177-181

Comparison of Head Circumference and Abdominal Circumference Ratio in Normotensive and patients with Pregnancy Induced Hypertensive Disorders after 28 weeks of gestation

Background: Hypertensive disorders are an important medical problem of gestation. Hypertensive disorders of pregnancy (HDP) are a significant cause for maternal and fetal morbidity as well as mortality. Intrauterine growth retardation (IUGR) commonly describes the condition of fetus whose size or growth is subnormal. IUGR fetus is frequently described as symmetrical and asymmetrical IUGR in term of their body proportions. Asymmetric growth retardation is typically linked to uteroplacental inadequacy. Hypertension is one of the maternal causes of placental insufficiency. Aim: To compare head circumference and abdominal circumference ratio in normotensive and patients with pregnancy induced hypertensive disorders after 28 weeks of gestation. Methodology: A cross sectional analytical study was carried on 113 pregnant females in which 57 women were normotensive and 56 women were hypertensive. All individuals were scanned by two- dimensional ultrasound following 28 weeks of pregnancy to evaluate sonographic parameters HC and AC. The HC/AC ratio was estimated by dividing head circumference with abdominal circumference. Results: Out of 57 normotensive patients 27 (36.48%) fetuses were diagnosed with IUGR having HC/AC ratio more than 1, while 30 had normal HC/AC ratio. In 56 hypertensive patients 47(63.51%) fetuses were diagnosed with IUGR having HC/AC ratio greater than 1, however 9(23.07%) fetuses had HC/AC ratio within normal range. So out of total 113 patients, 74 fetuses were found with IUGR while 39 fetuses had HC/AC ratio within normal ranges. Our study found that a cut off value of ≥ 1.0974 for HC/AC ratio could be used as diagnostic parameter in predicting IUGR. Conclusion: HC/AC ratio is a useful parameter for the detection of IUGR. Keywords: Head Circumference, Abdominal Circumference, Intra Uterine Growth Retardation

Dexamethasone-induced intrauterine growth restriction modulates expression of placental vascular growth factors and fetal and placental growth.

Prenatal exposure to glucocorticoids (GC) is a central topic of interest in medicine since GCs are essential for the maturation of fetal organs and intrauterine growth. Synthetic glucocorticoids, which are used in obstetric practice, exert beneficial effects on the fetus, but have also been reported to lead to intrauterine growth retardation (IUGR). In this study, a model of growth restriction in mice was established through maternal administration of dexamethasone during late gestation. We hypothesised that GC overexposure may adversely affect placental angiogenesis and fetal and placental growth. Female BALB/c mice were randomly assigned to control or dexamethasone treatment, either left to give birth or euthanised on days 15, 16, 17 and 18 of gestation followed by collection of maternal and fetal tissue. The IUGR rate increased to 100% in the dexamethasone group (8 mg/kg body weight on gestational days 14 and 15) and pups had clinical features of symmetrical IUGR at birth. Dexamethasone administration significantly decreased maternal body weight gain and serum corticosterone levels. Moreover, prenatal dexamethasone treatment not only induced fetal growth retardation but also decreased placental weight. In IUGR placentas, VEGFA protein levels and mRNA expression of VEGF receptors were reduced and NOS activity was lower. Maternal dexamethasone administration also reduced placental expression of the GC receptor, αGR. We demonstrated that maternal dexamethasone administration causes fetal and placental growth restriction. Furthermore, we propose that the growth retardation induced by prenatal GC overexposure may be caused, at least partially, by an altered placental angiogenic profile.

Assessment of Thyroid Function by Term and Gestational Age: A Retrospective Analysis Using the Ponderal Index

Background: Intrauterine growth retardation (IUGR) may prematurely impact the hormonal system by affecting its programming during growth and neurocognitive development. The aim of this study to evaluate thyroid function in preterm and term small for gestational age (SGA), and appropriate for gestational age (AGA) babies, and also in symmetrical and asymmetrical IUGR pattern. Methods: The study was conducted at a rural tertiary care center from 1st October 2016 to 30th September 2018. All babies born in the center …

Assessment of body length in infants born with different types of mild prenatal development delay

Objective. To assess the length of the body in infants from mothers with a burdened somatic and obstetric-gynecological history, including with a delay in the growth of the fetus of various types of mild severity, in comparison with each other, with healthy children from practically healthy mothers and with children from mothers with an aggravated somatic and obstetric-gynecological history, but without delayed fetal growth.
 Material and methods. 166 new-borns were monitored since birth, including 72 infants born after abnormal pregnancies with mild foetus growth and development retardation (gr. 1), and 69 infants born after abnormal pregnancies, but without any retardation (gr. 2), born by mothers with previous somatic and gynaecological disorders. The symmetrical intrauterine growth and development retardation was diagnosed in 15 infants (20.83%) (subgr. 1b), whereas the dissymmetric retardation was diagnosed in 57 children (79.17%) (subgr. 1a) from gr. 1. Practically healthy infants born by practically healthy mothers after normal pregnancies made up gr. 3 (25 subjects). Children are full-term, looked round in 1 (154), 3 (138), 6 (131), 12 (119 children) months. Comprehensive analysis of history, inspection, body height. Distribution-free statistical analysis methods.
 Results. The differences (p 0.01) in body length (Me, cm) in children at birth between the subgr. 1b (48) and gr. 2 (52); in 1 month between subgr. 1a (53) and 1b (52.5); in 3 months between subgr. 1a (60) and gr. 2 (62); in 6 months between subgr. 1a (66.5) and 1b (65.5); in 12 months between subgr. 1a (74.25) and 1b (73), subgr. 1a and gr. 2 (76), subgr. 1b and gr. 2. Increase of body length to 1 month in children subgr. 1a (4) and 1b (4.5) in comparison with children gr. 2 and 3 by 1 and 1.5 cm respectively more; to 3 months in children subgr. 1a (7) and gr. 2 (7) are comparable and more than children subgr. 1b. by 0.5 cm, gr. 3 by 1 and 0.5 cm respectively; to 6 months in children subgr. 1a (6.5) and 1b (6.5) more than the gr. 2 by 0.5 cm, less than the children gr. 3 by 0.5 cm; to 12 months in children subgr. 1a and 1b; gr. 1, 2 and 3 are comparable. To 12 months in children subgr. 1b in relation to children gr. 2 and 3 less by 0.5 cm.
 Conclusion. The established difference in body-length should be taken into account during the dispensary observation in order to decide whether to carry out corrective measures.

Somatic growth from birth to 6 months in low birth weight, in Bukavu, South Kivu, Democratic Republic of the Congo.

Low birth weight (LBW) is one of the leading causes of perinatal and infant morbidity and mortality, as well as of impaired growth and neurocognitive development. This study aimed to evaluate the evolution of anthropometric parameters and the nutritional status of LBW infants and to analyze factors influencing the growth failure during their first 6 months of life (or adjusted age). This was a prospective cohort study for 6 months, including 100 infants born with LBW and 100 infants born at full-term and with normal weight. The z-scores weight for age, height for age, head circumference for age and weight for height were computed with the software Epinut and WHO Anthro 2005. Descriptive statistics, bivariate analysis and multivariable logistic regression analyses were employed to identify factors associated with growth failure. Growth failure was defined as a decrease in weight z-score (standard deviation score) of over 0.67 during one of the study's periods. The statistical significance threshold was fixed at 0.05. At 6 months of life (or adjusted age), 15.3% of LBW were underweight, 51.4% were stunted, 4.2% had an emaciation and 25% had a head circumference for age<-2 z-scores. Risk factor for growth failure was male sex (OR=1.56 [95% CI: 1.03-2.23]). The symmetrical intra-uterine growth retardation was a protector factor for growth failure (OR=0.49 [95% CI: 0.25-0.98]). In the short term, LBW infants may have growth disorders. It is necessary to emphasize the importance of growth assessment of LBW children and proper education of their mothers about nutrition of their children for early and timely diagnosis and management of growth retardation and prevention of subsequent problems.

Expanding the FANCO/RAD51C associated phenotype: Cleft lip and palate and lobar holoprosencephaly, two rare findings in Fanconi anemia

Fanconi anemia is a rare chromosome instability disorder with a highly variable phenotype. In the antenatal and neonatal periods, the diagnosis is usually suggested by the presence of typical congenital abnormalities such as intrauterine growth retardation, microcephaly and radial ray defects. We report a newborn female with a prenatal diagnosis of Fanconi anemia, complementation group O (FANCO). Antenatal ultrasounds identified symmetrical intrauterine growth retardation, complex heart defect as well as brain anomalies, overlapping fingers and cleft lip and palate. Imperforate anus was detected after birth. Compound heterozygous RAD51C variants c. [571+5G > A]; [c.935G > A] were detected by prenatal whole exome sequencing and cellular hypersensitivity to DNA interstrand crosslinking agents (DEB, MMC) was confirmed after birth. With only one previously described homozygous RAD51C variant to date, our findings expand the phenotypic spectrum of FANCO and suggest it should be part of the antenatal differential diagnosis for trisomy 13 and 18, due to the presence of atypical findings such as cleft lip and palate, holoprosencephaly, growth restriction and overlapping fingers.

A novel heterozygous IGF-1 receptor mutation associated with hypoglycemia.

Mutation in the insulin-like growth factor-1 receptor (IGF1R) gene is a rare cause for intrauterine and postnatal growth disorders. Patients identified with IGF1R mutations present with either normal or impaired glucose tolerance. None of the cases described so far showed hypoglycemia. We aimed to identify the genetic basis for small for gestational age, short stature and hypoglycemia over three generations in one family. The proband, a 9-year-old male, presented in infancy with recurrent hypoglycemic episodes, symmetric intrauterine growth retardation and postnatal growth retardation. Blood DNA samples from the patient, his parents, a maternal sister and maternal grandmother underwent Sanger sequencing of the IGF1R gene. Primary skin fibroblast cultures of the patient, his mother and age- and sex-matched control donors were used for gene expression and receptor functional analyses. We found a novel heterozygous mutation (c.94 + 1g > a, D1105E) affecting the splicing site of the IGF1R mRNA in the patient, his mother and his grandmother. Primary fibroblast cultures derived from the patient and his mother showed reduced proliferation and impaired activation of the IGF1R, evident by reduced IGF1R and AKT phosphorylation upon ligand binding. In conclusion, the newly identified heterozygous missense mutation in exon 1 of IGF1R (D1105E) results in impaired IGF1R function and is associated with small for gestational age, microcephaly and abnormal glucose metabolism. Further studies are required to understand the mechanisms by which this mutation leads to hypoglycemia.

Features of the cardiovascular system in babies born with different types of intrauterine growth restriction

Based on the data of clinical and anamnestic examination, cardiointervalography, electrocardiography, and Doppler echocardiography, the investigators examined the features of the cardiovascular system in children born by women with compromised somatic and gynecological histories in the outcome of complicated pregnancy. Groups 1 and 2 included 72 and 69 infants with and without fetal growth restriction, respectively. Group 1 comprised Subgroup 1a of 57 infants with asymmetrical intrauterine growth restriction and Subgroup 1b of 15 children with symmetrical one; of them there were 13 and 2 infants with hypoplastic and dysplastic types. Apparently healthy infants born by apparently healthy mothers in the outcome of physiological pregnancies made up Group 3 (n = 25). There is proof that there are significantly important features of autonomic regulation of cardiac activity and morphofunctional characteristics of the heart. The infants with symmetrical intrauterine growth retardation, unlike those with asymmetrical one, were observed to have impaired autonomic regulation of cardiac activity, which was less obvious at birth, deteriorating over time. At birth, the babies had morphological features of the heart and a greater frequency of functioning of fetal communications. Impaired myocardial metabolic processes prevailed within the first month of life and there was a large frequency of changes similar to those in hypertrophic cardiomyopathy by the end of the first half of life. The featuresrevealed in the infants with different types of intrauterine growth restriction require electrocardiographic and ultrasound examinations, a pediatric cardiologist’s consultations at a maternity hospital, and a subsequent personalized follow-up with corrective measures at an outpatient setting.

Learning defects in Drosophila growth restricted chico mutants are caused by attenuated adenylyl cyclase activity.

BackgroundReduced insulin/insulin-like growth factor signaling (IIS) is a major cause of symmetrical intrauterine growth retardation (IUGR), an impairment in cell proliferation during prenatal development that results in global growth defects and mental retardation. In Drosophila, chico encodes the only insulin receptor substrate. Similar to other animal models of IUGR, chico mutants have defects in global growth and associative learning. However, the physiological and molecular bases of learning defects caused by chico mutations, and by symmetrical IUGR, are not clear.ResultsIn this study, we found that chico mutations impair memory-associated synaptic plasticity in the mushroom bodies (MBs), neural centers for olfactory learning. Mutations in chico reduce expression of the rutabaga-type adenylyl cyclase (rut), leading to decreased cAMP synthesis in the MBs. Expressing a rut+ transgene in the MBs restores memory-associated plasticity and olfactory associative learning in chico mutants, without affecting growth. Thus chico mutations disrupt olfactory learning, at least in part, by reducing cAMP signaling in the MBs.ConclusionsOur results suggest that some cognitive defects associated with reduced IIS may occur, independently of developmental defects, from acute reductions in cAMP signaling.

PC.121 The Different Presentations and Management of Congenital Cytomegalovirus Infection – A Case Series

IntroductionCongenital Cytomegalovirus (CCMV) infection is the most common intrauterine infection. We present three cases of babies and compare their symptoms and subsequent management. Treatment of CMV is with antivirals. The...

Aorto–Right Ventricular Tunnel Causing Functional Tricuspid Atresia

A girl with symmetrical intrauterine growth retardation and a birth weight of 2240 g was delivered at term by primary cesarean section to a 27-year-old primiparous woman. Fetal echocardiography had shown a nearly atretic tricuspid valve. Postnatally, the child stabilized rapidly but showed signs of heart failure with tachypnea and general weakness, as well as cyanosis (transcutaneous oxygen saturation, 85%). The presence of an aorto–right ventricular (RV) tunnel (ARVT) was confirmed by transthoracic echocardiography, which showed a 5 to 6×15–mm structure extending from the proximal ascending aorta to the outflow tract of the RV, with the left coronary artery originating from the aortic end of the tunnel. The ARVT caused a strong left-to-right shunt during diastole (Figure 1 and Movies I and II in the online-only Data Supplement). Figure 1. Echocardiographic views. A , Apical 4-chamber view. Arrow indicates the minimal tricuspid valve opening during diastole. B , Aorto–right ventricular tunnel (ARVT). C , Diastolic left-to-right shunt through the ARVT (arrow). RA …

Aplasia cutis congenita, terminal limb defects and periventricular leukomalacia in one sibling with minor findings in the other-probable autosomal recessive Adams-Oliver Syndrome

We report on siblings with probable Adams-Oliver syndrome. The older brother had symmetric intra-uterine growth retardation, plagiocephaly, a cardiac defect and periventricular calcification. The younger sister was born with abdominal and scalp skin defects and small fingers and toes. Prenatal cranial imaging in the younger sibling suggested possible bilateral closed lip schizencephaly and neuronal migrational defect. These siblings are thought to have Adams-Oliver syndrome with the older sibling's features at the milder end of the spectrum while the younger sibling is more severely affected. Several case reports have been published discussing the clinical variability and the possibility of autosomal recessive inheritance. Recently reports suggest an increased frequency of seizures and central nervous system involvement in autosomal recessive Adams-Oliver syndrome. We report affected siblings born to healthy non-consanguineous parents and review previously published similar sibships and case reports in relation to the clinical features.

An incomplete trisomy 3 rescue resulting in a marker chromosome and UPD(3)—difficulties in interpretation

Trisomy 3 and marker chromosomes derived from chromosome 3 are rare cytogenetic findings. Confined placental mosaicism (CPM) of trisomy 3 was reported and in such cases, intrauterine growth retardation (IUGR) and intrauterine fetal death (IUFD) were occasionally seen. A case of trisomy 3 mosaicism in amniotic fluid was once detected in a newborn with a normal phenotype at birth and symmetric IUGR, probably resulting from the placental trisomic cell lines (Zaslav et al., 2004). There are only four cases of mosaic trisomy 3 in liveborn infants (confirmed in blood lymphocytes) with all showing an abnormal phenotype (Schinzel, 2001). There are several (19) published reports of chromosome-3-derived marker chromosomes (patients with complex karyotype, unpublished cases and tumor cell lines were excluded; http://www.med.uni-jena.de/fish/ sSMC/03.htm#unclear). Nine cases showed a normal phenotype; however, three of them were prenatal cases not evaluated after birth. An abnormal phenotype was reported in ten cases. We present the first documented case of an ‘incomplete’ trisomy 3 rescue, which resulted in an extra chromosome-3-derived marker chromosome in the fetus. Fluorescent in situ hybridization (FISH) and DNA studies were performed in order to characterize the marker chromosome and to elucidate the mechanism of formation, respectively. In order to assess a genotype–phenotype correlation, we compared our case with similar cases in the literature.

Chromosomal aberrations as etiological factors of intrauterine growth retardation

Intrauterine growth retardation (IUGR) is a pathological condition of pregnancy characterised by birth weight below the 10th centile. A number of fetal, placental and maternal causes can lead to IUGR; although, in most cases no specific causes can be identified. The aim of this study was to determine the part of chromosomal abnormalities in IUGR etiology. Fetal blood karyotype taken by cordocentesis from 168 fetuses with diagnosed IUGR was analyzed. Chromosomal rearrangements both numerical and structural were detected in 14 cases (12.2%). Two cases were triploid. Patau syndrome, Edwards syndrome and Down syndrome were found in two cases each. There was one case of trisomy 7 (47, XY, +7) and one case of trisomy 16 (47, XX, +16); one translocation, 46, XY, t (2; 14)(q23; q32) and a deletion 46, XYdel (12) (p12) as well as two cases of sex chromosomes abnormalities, 45, X (Turner syndrome) and 47, XYY. These findings suggest that a consistent number of symmetrical IUGR cases (about 12%) can be associated with chromosomal rearrangements. Chromosomal aberrations that cause IUGR are heterogeneous, aberration of autosomes, mostly autosomal trisomies, being the most common.

Symmetrical fetal growth retardation after gestational cocaine exposure in the rat

Cocaine use during pregnancy results in an increase in different maternal and perinatal complications. The fetal effects of cocaine could be mainly related to the disturbances in the brain development, microcephaly being the most common brain abnormality. The aim of this study was to analyze maternal outcome and fetal somatic effects of cocaine and to evaluate the hypothesis that maternal cocaine exposure would specifically impair fetal global brain development. Fifty-four timed-pregnant female Sprague–Dawley rats were daily injected with 15 or 40 mg/kg per day from gestational day (GD) 1 or 8 and sacrificed at gestational day 20. By analyzing different maternal and fetal outcomes, it could be suggested that the cocaine exposure in pregnant rats decreased maternal weight gain without significant maternal mortality, did not affect the mean number of fetuses by litter, although notably increased stillbirths, reduced fetal birth weight, and reduced the fetal central nervous system weight. Present results are globally in agreement with the literature and underline a possible selective effect of cocaine on the fetal CNS resulting in symmetrical intrauterine fetal growth retardation in contrast to the asymmetrical retardation of undernutrition.

Activity of the brain isoenzyme creatine kinase in newborns with intrauterine growth retardation

The CK-BB activity in neonates with intrauterine growth retardation (IUGR) was investi-gated and the results were compared to their clinical condition in early neonatal period. The re-sults of the study have shown that the CK-BB activity was increased in neonates with symmetric IUGR and in the presence of chronic placental insufficiency of infectious genesis.

Clinical use of antenatal corticosteroids: benefits and risks.

After completing this article, readers should be able to: 1. Describe the rationale for the use of antenatal corticosteroids for human fetal maturation. 2. Delineate recommendations of the 1994 National Institutes of Health Consensus Conference on Antenatal Corticosteroids. 3. Review areas of controversy in the clinical use of antenatal corticosteroids. 4. Describe the potential risks of multiple courses of antenatal corticosteroids. 5. Delineate current recommendations for clinical use of antenatal corticosteroids to promote fetal maturation. Glucocorticoid administration initially was appreciated as a method for accelerating development of the intestine more than 40 years ago. Since that time, developmental effects of these agents have been defined in at least 16 tissues of mammals. More than 30 years ago, while studying the mechanism of initiation of labor in sheep, Liggins made the observation that infusion of corticosteroids into fetal lambs was associated with improved survival and decreased lung disease in animals delivered preterm. Subsequently, numerous studies in cell culture, animal models, and human fetal tissue have delineated the multiple effects of glucocorticoids on the developing lung. These include increases in both the total tissue and alveolar surfactant pools; a decrease in vascular permeability, with less protein leak into the alveolar spaces; enhanced clearance of lung water; maturation of parenchymal structure; increase in lung compliance and maximal lung volume; enhanced response to surfactant treatment; and improvement in respiratory function, outcome, and survival. (See accompanying article on scientific rationale for use of antenatal glucocorticoids.) In 1972, the first randomized clinical trial of administration of antenatal corticosteroids (ANCS) in humans demonstrated decreased mortality and a decreased incidence of respiratory distress syndrome (RDS) in preterm infants born at less than 34 weeks’ gestation, who were treated with betamethasone for at least 24 hours before delivery. Over the ensuing 20 years, multiple clinical investigations continued to document the effectiveness of ANCS on …

Plasmodium coatneyi in the rhesus monkey (Macaca mulatta) as a model of malaria in pregnancy.

Pregnant women with Plasmodium falciparum infection are at increased risk for complications such as anemia and cerebral malaria. In addition, the infants of these women suffer intrauterine growth retardation (IUGR), low birth weight (LBW), congenital infection, and high infant mortality. Although much has been learned from studies of malaria during human pregnancy, progress has been limited by the lack of a suitable animal model. Nonhuman primates are of particular interest because, other than the armadillo, they are the only animals with a discoidal, villous, hemochorial placenta like that of humans. We have established a model of malaria during human pregnancy by inoculating pregnant rhesus monkeys (Macaca mulatta) with Plasmodium coatneyi (a sequestering parasite) during the first trimester. In our initial experiment, four monkeys were inoculated with a fresh inoculum containing 10(8) viable parasites from an infected donor monkey. All four monkeys became parasitemic seven days postinoculation (PI) and three monkeys aborted 7-10 days PI coincident with high peak parasitemias (41,088-374,325 parasites/mm3). Although abortion is one of the outcomes observed in Plasmodium-infected women, the intent of this study was to examine the effects of Plasmodium infection throughout gestation. Since the rapid onset of high parasitemia may have been responsible for the abortions, a decision was made to reduce the size of the effective inoculum. Six additional pregnant monkeys were inoculated with a frozen isolate taken from the same donor containing 10(6) parasites. These six animals became parasitemic by 14 days PI and, along with monkey E412, carried their infants to term. These seven infants weighed significantly less at term than the infants of uninfected mothers (P = 0.0355). Symmetrical IUGR was detected by ultrasound in one fetus with an LBW of 334 g. Another LBW infant (300 g) had asymmetrical growth retardation, which has been associated with uteroplacental insufficiency and was consistent with the lower placental weights found in infected dams compared with controls (P = 0.0455). The infant with symmetric IUGR died at five days of age, while the other is alive but congenitally infected. The IUGR, LBW, congenital infection, postnatal infant mortality, and early abortions observed in these animals suggest that P. coatneyi in pregnant rhesus monkeys is a valid model of malaria in human pregnancy. This model should provide the opportunity to study questions about malaria in pregnancy that have been difficult to study in humans.

Aetiology, morphology and body composition of infants born small for gestational age.

Infants born small for gestational age (SGA) are a heterogeneous group. Both the timing and duration of the intrauterine insult determine the physical condition and body composition of the infant at birth. Infants with symmetrical intrauterine growth retardation (IUGR) have a similar body composition at birth to weight-matched infants born appropriate for gestational age. However, these infants are more likely to remain shorter and lighter than normal infants. In contrast, infants with asymmetrical IUGR have reduced fat deposition but are more likely to exhibit catch-up growth during the first few months of life. The low mortality and morbidity rates in infants born SGA observed in recent studies are linked to their appropriate perinatal management, including adequate early nutritional support.