ORIGINAL ARTICLE

PRENATAL
**DIAGNOSIS** WILEY

# Postnatal outcome of children with antenatal colonic hyperechogenicity

Florent Fuchs<fnref n="1" />,<fnref n="2" /> ID | Alexis Rodriguez<fnref n="1" /> | Eve Mousty<fnref n="3" /> | Denis Morin<fnref n="4" /> |
Agathe Roubertie<fnref n="5" />,<fnref n="6" /> | Constance F. Wells<fnref n="7" /> | Olivier Prodhomme<fnref n="8" /> |
Jean-François Benoist<fnref n="9" /> | Sophie Dreux<fnref n="10" /> ID | Jean-Michel Faure<fnref n="1" /> |
Marjolaine Willems<fnref n="6" />,<fnref n="7" /> ID

Correspondence

Marjolaine Willems, Service de Génétique Médicale, Hôpital Arnaud de Villeneuve, 371 avenue du Doyen Gaston Giraud, Montpellier 34295, France.

Email: m-willems@chu-montpellier.fr

Abstract

**Objective:** To evaluate the postnatal outcome of children with antenatal colonic hyperechogenicity, currently considered as a sign of lysinuria-cystinuria, but which may also be a sign of other disorders with a more severe prognosis.

**Method:** We carried out a French multi-centric retrospective study via 15 Multi-disciplinary Center for Prenatal Diagnosis from January 2011 to January 2021. We included pregnancies for which fetal colonic hyperechogenicity had been demonstrated. We collected the investigations performed during pregnancy and at birth as well as the main clinical features of the mother and the child. We then established the prevalence of pathologies such as lysinuria-cystinuria (LC), hypotonia-cystinuria syndrome (HC), or lysinuric protein intolerance (LPI).

**Results:** Among the 33 cases of colonic hyperechogenicity collected, and after exclusion of those lost to follow-up, we identified 63% of children with lysinuria-cystinuria, 8% with lysinuric rotein intolerance, and 4% with hypotonia-cystinuria syndrome.

**Conclusion:** Management of prenatal hyperechoic colon should include a specialized consultation with a clinical geneticist to discuss further investigations, which could include invasive amniotic fluid sampling for molecular diagnosis. A better understanding of diagnoses and prognosis should improve medical counseling and guide parental decision making.

Key points

What's already known about this topic ?

* Currently, colonic hyperechogenicity is a sign of lysinuria-cystinuria, but it can also be a sign of other disorders with a more severe prognosis.

<footnote n="1">¹CHU de Montpellier, Gynecology and Obstetrics, Montpellier, France</footnote>

<footnote n="2">²Desbrest Institute of Epidemiology and Public Health (IDESP), University Montpellier, INSERM, Montpellier, France</footnote>

<footnote n="3">³Centre Hospitalier Universitaire de Nimes, Gynecology and Obstetrics Nimes, Nimes, France</footnote>

<footnote n="4">⁴CHU de Montpellier, Pediatric Nephrology, Montpellier, France</footnote>

<footnote n="5">⁵CHU de Montpellier, Pediatric Neurology, Montpellier, France</footnote>

<footnote n="6">⁶Institute for Neurosciences of Montpellier, University Montpellier, INSERM, Montpellier, France</footnote>

<footnote n="7">⁷Medical Genetics Department, CHU de Montpellier, Montpellier, France</footnote>

<footnote n="8">⁸CHU de Montpellier, Radiologie Pédiatrique, Montpellier, France</footnote>

<footnote n="9">⁹Hôpital Necker-Enfants Malades, Biochimie Métabolomique et Protéomique, Paris, France</footnote>

<footnote n="10">¹⁰Hôpital Universitaire Robert Debré, Laboratoire de Biochimie-Hormonologie, Paris, France</footnote>
What does this study add?

* In this retrospective study, among fetuses with hyperechoic colon, we identified 63% of children with lysinuria-cystinuria, 8% with lysinuric protein intolerance, and 4% with hypotonia-cystinuria syndrome. These data are likely to modify the management of patients in whom a hyperechogenic fetal colon is identified.

1 | INTRODUCTION

Intestinal (or digestive) hyperechogenicity is a common sign for which there are numerous publications in literature.¹⁻³ However, its exact definition, characteristics, and location are often poorly specified, resulting in significant differences in prevalence, imperfect etiologic guidance, and unclear codified care. Under the labeling of intestinal hyperechogenicity, two different features should be distinguished: small bowel hyperechogenicity and large bowel hyperechogenicity.

Small bowel hyperechogenicity has a prenatal prevalence of 0.1% to 1%–2%⁴ and is usually associated with chromosomal abnormalities, cystic fibrosis, viral infections or bleeding during pregnancy.² In contrast, the prevalence of colonic hyperechogenicity is unclear and is frequently described associated with lysinuria-cystinuria (Lysinuria Cystinuria (LC)).⁵

Hyperchogenic fetal colon is defined when the echogenicity of its contents is at least equal to that of the iliac bone prior to 36 weeks of gestation⁶ (Figure 1). According to current guidelines, such a finding should point to lysinuria-cystinuria.⁵,⁷⁻⁹ After 36 weeks, this sign has no pathological value, because it is hypothesized that dehydrated meconium could produce this ultrasonographic presentation late in pregnancy.¹⁰

Nevertheless, apart from LC or a physiologically hyperechoic colon after 36 weeks, other diagnoses are possible. In 2020, a Belgian team published the case of a primiparous woman with no previous history¹¹ whose fetus had isolated colonic hyperechogenicity at 26 weeks. The parents refused invasive prenatal sampling and an MRI was performed at 31 weeks and interpreted as normal. Prenatal counseling informed the parents of the possible diagnosis of LC and its postnatal care. After birth, the child developed hyperammonemia.

Exome sequencing revealed a homozygous pathogenic variant in the SLC7A7 gene leading to the diagnosis of lysinuric protein intolerance (LPI) with a more severe prognosis than LC.

Based on these findings, we decided to perform a retrospective, observational, multicenter, cohort study, aiming to evaluate the post-natal outcome of fetuses with colonic hyper echogenicity identified during prenatal ultrasound screening.

2 | MATERIAL AND METHODS

We retrospectively collected the cases of colonic hyperechogenicity discovered during prenatal screening between January 2011 and January 2021 whose case was referred in one of the 15 Multidisciplinary Centers for Prenatal Diagnosis (MCPD) in France: Marseille Timone, Marseille Nord, Grenoble, Lille, Port-Royal, Poitiers, Saint Brieuc, Créteil, Colombes-Pontoise, Strasbourg, Saint Denis de la Réunion, Bordeaux-Bagatelle, Lyon Est- Bron, Nîmes and Montpellier.

The cases were identified through three sources: (1) retrospective requests of cases followed by one of the 15 MCPDs through their own database analyses; (2) retrospective requests for amniotic fluid analysis (Amino Acids (AA) chromatography) at the National Biochemistry and Hormonology Laboratory of the Robert Debré Hospital (Paris); and (3) retrospective requests of infants referred to expert centers specialized in hereditary metabolic diseases.

All women between 15 and 45 years of age who were referred for the discovery of a fetal prenatal colonic hyperechogenicity at one of the MCPDS were included in the cohort study. Patients who refused the collection and use of their own data or of their child data were excluded. For each included patient, the following data were

<figure><img src="image_1.png" /><figcaption>**FIG URE 1** Prenatal third trimester ultrasound examination of a fetus. Transverse view of the fetal abdomen showing (A) normal size and aspect of fetal colon (↑) and (B) hyperechoic content of fetal colon without dilatation (↓). [Colour figure can be viewed at wileyonlinelibrary.com]</figcaption></figure>
collected: medical history, intake of medical or recreational drugs, gravidity, parity, pregnancy evolution and occurrence of complications, gestational age at ultrasound finding, associated ultrasound signs, occurrence of prenatal invasive testing, maternal serologies, fetal karyotype, fetal or parental CFTR gene analysis, and abdominal fetal MRI conclusions. The results of amino acid chromatography on amniotic fluid were also collected from the national prenatal biochemistry center of the University Hospital of Robert Debré (APHP). For each included child, we collected gestational age at birth, mode of delivery, height, weight, head circumference, umbilical cord pH, Apgar, and type of feeding. The postnatal investigations, suspected or confirmed diagnosis, performed by either metabolic analysis or molecular analysis, and the existence of a pediatric follow-up were also collected.

The objective of this study was to evaluate the neonatal outcome of children with antenatal colonic hyperechogenicity. The primary outcome was the occurrence of post-natal pathology. The secondary outcome were the frequency of LC, hypotonia-cystinuria syndrome (HC), LPI, or other conditions in this population, as well as the clinical, ultrasound, or MRI criteria allowing to distinguish them.

Diagnosis of LC was based on urinary amino acid chromatography showing high levels of cystine. Diagnosis of HC was based on an evocative urinary amino acid chromatography with a genetic analysis (whichever its type: targeted analysis, NGS-panel, exome), confirming the homozygous deletion of the SLC3A1 gene and adjacent genes including PREPL, PPM1B and C2orf34. The diagnosis of LPI was an evocative urinary amino acid chromatography and a genetic analysis (whichever its type: targeted analysis, NGS-panel, exome), confirming the presence of biallelic pathogenic variations of the SLC7A7 gene.

Data are presented as mean (extremes) or percentage (n/N) (%) according to the variable studied and its distribution. The study was approved by the institutional review board of the Montpellier University Hospital IRB under the notification number n 202100816.

## 3 RESULTS

Between January 2011 and January 2021, 33 patients with a prenatal diagnosis of colonic hyperechogenicity were included in our study. The mean age of the patients was 29.7 years (19-43 years). The sample consisted of 44% nulligravida, 52% nulliparous, 33% primiparous, and 15% multiparous women. Two patients had an autoimmune disease (lupus, APS), none had inflammatory bowel disease, and one had an anti-JK1A allo-immunisation. No other relevant medical history was present.

Mean gestational age at diagnosis of fetal colonic hyperechogenicity was 30.1 weeks (17 weeks- 36.9 weeks), with 23% of diagnoses performed during 2nd trimester of pregnancy (14-28 weeks) and 77% during the 3rd trimester (>28 weeks). Most of the ultrasound did not precisely describe the colonic location of the hyperechogenicity; however, it generally appeared to involve the entire colon. In 12 cases (36%), other ultrasound abnormalities were observed: polyhydramnios (3%), urachal cyst (3%), bilateral

pyelectasis (3%), anorectal malformation (3%), short long bones (3%), single kidney (3%), megacystis (3%), posterior urethral valve (3%), polymalformative syndrome (3%), ascitis (3%) and intra-uterine growth restriction (6%).

Among the patients, 19/33 (58%) had an invasive sampling with systematic biochemical amniotic fluid analysis (AA chromatography) and 18 had fetal chromosomal study including CGH-array and karyotype that did not reveal any anomaly. Amino Acids chromatography had in 53% a result suggestive of LC or LPI without being able to distinguish the two pathologies on the chromatogram. Parental CFTR gene was studied in 16 cases (48%) and did not lead to any identification of pathogenic or likely pathogenic variation. Sixteen women (48%) had prenatal serology testing for CMV and toxoplasmosis with no sign of recent infection and 7 (21%) had an abdominal fetal MRI with normal results.

The mean gestational age at birth was 39.4 weeks (36 weeks-41.4 weeks). Mean birth weight was 3045 g (2085-3840 g), whereas the mean height and head circumference were 48.5 cm (45-52.5 cm) and 34.3 cm (32.5-36 cm), respectively. The mean Apgar score was 8.4 (3-10) in 1 min, 9.5 (8-10) in 5 min, and 10 (10-10) in 10 min, and the mean arterial pH was 7.18 (6.94-7.29). The presence of colonic hyperechogenicity did not modify labor management or the mode of delivery. In our series, 89.5% of deliveries were vaginal and 10.5% were by caesarean section. Feeding was predominantly maternal, with 59% of babies being breast-fed versus 41% formula-fed (Table 1).

Among our 33 patients, nine new-borns (27%) were lost to follow-up after the immediate neonatal period, thus leading to a lack of data concerning the health status of the child.

<table><caption>TABLE 1 Maternal, fetal and neonatal data.</caption><thead><tr><td>Variable</td><td>Average (extreme) or n/N (%)</td></tr></thead><tbody><tr><td>Maternal age</td><td>29.7 years (19-43 years)</td></tr><tr><td>Genetic/nephrological history</td><td>0 (0%)</td></tr><tr><td>History of autoimmune disease</td><td>2/33 (6%)</td></tr><tr><td>Term at diagnosis</td><td>30 + 1 weeks (17 weeks-36 + 6 weeks)</td></tr><tr><td>Ultra-sonographic association</td><td>12/33 (36%)</td></tr><tr><td>Karyotype</td><td>18/33 (55%)</td></tr><tr><td>Chromatography</td><td>19/33 (58%)</td></tr><tr><td>Serology CMV/Toxoplasmosis</td><td>16/33 (48%)</td></tr><tr><td>Sequencing of frequent CFTR variants</td><td>16/33 (48%)</td></tr><tr><td>Fetal abdominal MRI</td><td>7/33 (21%)</td></tr><tr><td>Term of birth</td><td>39 + 3 weeks (36 weeks-41 + 3 weeks)</td></tr><tr><td>Birth weight</td><td>3045 g (2085-3840 g)</td></tr><tr><td>Birth height</td><td>48.5 cm (45 cm - 52.5 cm)</td></tr><tr><td>Head circumference</td><td>34.3 cm (32.5-36 cm)</td></tr><tr><td>Apgar (1 min 5 min 10 min)</td><td>8.4 (3-10)/9.5 (8-10)/10 (10-10)</td></tr></tbody></table>
Among the 24 patients for whom the outcome of the child was known, the final diagnosis was 15 cases (63%) of LC, 2 cases (8%) of LPI, 1 case (4%) of HC, and 6 cases with other prenatal malformations (25%). Except those 6 last cases, all 18 cases of hyperechogenic colon were prenatally isolated. No other ultrasound signs were associated with hyperechogenicity in the LC, LPI, or HC groups.

Regarding the cases of LC, 87% of the diagnoses were made at birth and 6.5% at 1 month; the remaining 6.5% were diagnosed before the age of 1 year. For the two cases of LPI, diagnosis was established later (at 5 and 7 years); whereas in the sole case of HC (2p21 microdeletion syndrome), the diagnosis was made at 12 months of age.

Regarding the six other cases (25%) with prenatal malformations, we found 1 urachal cyst, 1 adrenal calcification, 1 hypothyroidism with hypo-cortisolism, 1 unlabeled uropathy, 1 posterior urethral valve and one case with multiple congenital anomalies that ended with a late termination of pregnancy (Figure 2). Hyperechogenicity in those six cases had the same ultrasound appearance as hyper-echogenicity in the three diseases presented.

4 | DISCUSSION

In our retrospective study, performed between January 2011 and January 2021 in 15 French Prenatal Diagnostic Centers, 33 cases of hyperechoic colon were diagnosed antenatally. The final outcome, known for 24 cases (27% lost to follow-up), included 63% LC, 8% LPI, 4% HC and 25% other conditions.

Colonic hyperechogenicity is often confused with intestinal hyper-echogenicity. However, it is very important to distinguish them as the causes and underlying conditions leading to these separate sonographic presentations are different. In the case of colonic

hyperechogenicity, notably in the case of LC, only the colon is affected. The sonographic sign originates from an accumulation of cystine in the lumen making the meconium hyperechoic.⁵,⁷⁻⁹ The pathophysiology behind hyperechoic small intestine is different and it can have many different causes: bleeding during pregnancy, infectious causes (CMV...), Down syndrome, cystic fibrosis, or spontaneous resolution without identified etiology. The hyperechogenicity only affects the small intestine and not the colon. To our knowledge, there are no cases of intestinal hyperechogenicity leading to the prenatal diagnosis of LC or LPI. In our series, after the identification of fetal hyperechoic colon, genetic counseling had led frequently to CFTR gene testing and chromosomal fetal analysis, without identifying any anomaly. However, cystic fibrosis can cause a hyperechoic small intestine rather than colon.

In the case of LC, prenatal amniotic fluid chromatography analysis shows an increase in the dibasic AA cystine and lysine. Postnatally, the pathology is confirmed either by an elevated cystine level in the urine or by analysis of one of the collected lithiases. The elevated urinary excretion of sediment is the cause of lithiasis.¹² The condition is autosomal recessive and genetic testing in the child and parents (using targeted sequencing, gene panel sequencing, or exome sequencing) may reveal a biallelic pathogenic variant of the SLC3A1 gene on chromosome 2 or SLC7A9 on chromosome 19 in the context of type A or B lysinuria. The management of this condition consists of a multidisciplinary approach with dietary measures, sometimes associated with drug prescription aimed at decreasing urinary free cystine concentration and regulating urinary pH.⁸,¹³ If LC disease/syndrome is suspected, counseling with a nephrologist who will explain the disease, prognosis, post-natal investigations, and treatment is advised. The prognosis is good with appropriate management.

In the context of LPI, amniotic fluid chromatography will theoretically also show an increase in dibasic AA. The two patients of our

<figure><img src="image_2.png" /><figcaption>FIGURE 2 Flow chart. [Colour figure can be viewed at wileyonlinelibrary.com]</figcaption></figure>
study did not have any amino acid chromatography on the amniotic fluid sample. The disease was confirmed after birth with abnormally low plasma or high urine levels of arginine, ornithine, and lysine. Low plasma amino acid levels will lead to hyperammonaemia by blocking ureagenesis and the urea cycle. Moreover, as this condition is autosomal recessive, genetic analysis in the child and parents (targeted sequencing, gene panel sequencing, or exome sequencing) may reveal a biallelic pathogenic variation of the SLC7A7 gene on chromosome 14. This condition is severe and can affect different systems.¹⁴⁻¹⁷ It leads to hepatic, renal, pulmonary, neurological, hematological, metabolic failure, growth retardation, autoimmune diseases and macrophagic activation, all of which can lead to premature death without effective curative treatment.

In the case of HC, antenatal chromatography on amniotic fluid will show an increase in dibasic AA, as in the case of classical LC. In our sole case, as in previously reported cases, the disease was confirmed after birth by an abnormally high cystine level in the urine and by identifying a homozygous 2p21 deletion encompassing the SLC3A1 and the PREPL gene. Aside from the kidney toxicity, the deletion leads to a defect in cytochrome C oxidase and mitochondrial disease.¹⁸ The condition causes neonatal and infantile hypotonia, growth retardation, and morphological features. Neurodevelopmental delay, sometimes associated with intellectual disability, can be part of the clinical presentation since the deletion involves other genes.¹⁹

The main challenge in prenatal care is to differentiate these three diseases, which widely differ regarding their prognoses. Lysinuric protein intolerance as well as HC are challenging to diagnose in the prenatal setting. If detected, they require multidisciplinary management starting with counseling with a clinical geneticist and a metabolic specialist to clearly explain the prognosis and post-natal management. The risk of post-natal hyperammonaemia requires a pediatric team ready to treat newborns and prevent neurotoxicity. Unlike LC, LPI and HC are associated with a poor prognosis. This can lead women in some countries to ask to terminate their pregnancy on medical grounds, which can be accepted in France since the law allows it until delivery.

In our series, the contribution of imaging by ultrasound or MRI did not allow us to differentiate between the three metabolic

conditions but may be performed to try to eliminate other diagnoses (25% of patients had diagnosis outside of LC, LPI and HC). The reason why those 6 cases had hyperechogenicity of the colon associated with another (or multiple) malformation remains unknown. However, most of those 6 cases presented with a urinary trouble (adrenal calcification, uropathy, urethral valve...) that raises questions about the link between the digestive and urinary system.

Chromatography of AA on amniotic fluid samples was seen as a possible candidate for early diagnosis differentiate between these three conditions, but there was no sample issued from LPI or HC patients. Moreover, the results obtained in cases of LC could not exclude the two other pathologies. Similarly, urine chromatography in the immediate postnatal period may be falsely reassuring. Indeed, breast milk, naturally low in protein, can induce a normal urine balance. Once food diversification is achieved, the pathology will be revealed by acute or chronic signs. This is why close pediatric follow up (1 month, 3 months, and after food diversification) is mandatory in this situation.

Genetic testing could be another candidate for early diagnosis. There is no genetic panel in France designed to diagnose LPI, LC, or HC syndrome during the prenatal period. However, the genetic diagnosis of any of these three diseases could be made on an exome analysis by asking the laboratory for a careful reading of the involved genes and verifying adequate coverage. We therefore advocate the possibility of exome sequencing for the prenatal diagnosis of LC, LPI, or HC in the context of colonic hyper-echogenicity.

The prevalence of LPI (less than 1 case in 70,000 births) and HC syndrome (1 case in 1,000,000) is much lower than that of LC (1 case in 7000).¹³,¹⁴,¹⁸ It is essential to provide parents this information, implying different a priori probabilities of each pathology, the most frequent being considered as benign, and the two severe ones very rare. As colonic hyperechogenicity is mostly discovered during the 3rd trimester of pregnancy, gestational age at diagnosis is an issue which should be considered and discussed with the parents, explaining them the possibility that birth might occur before obtaining the results of amniocentesis. Specialized genetic counseling should be mandatory (Table 2), explaining to parents all these elements, including severity, proposed treatment and follow-up, and

<table><caption>TABLE 2 Results of ante- and post-natal investigations for each of the 3 pathologies.</caption><thead><tr><th>Pathology</th><th>Prenatal ultrasound</th><th>Fetal MRI</th><th>Amniotic fluid AA chromatography</th><th>Post-natal urinary AA chromatography</th><th>Genetic analysis</th></tr></thead><tbody><tr><td>Lysinuria cystinuria (LC)</td><td>HE colic</td><td>Normal</td><td>Dibasic AA ↑<br>Cystine ↑↑</td><td>Dibasic AA ↑<br>Cystine ↑↑</td><td>Bi-allelic pathogenic variation<br>SLC3A1/SLC7A9</td></tr><tr><td>Hypotonia cystinuria syndrome (HC)</td><td>HE colic</td><td>Normal</td><td>Expected: Dibasic AA ↑<br>Cystine ↑↑</td><td>Dibasic AA ↑<br>Cystine ↑↑</td><td>Homozygous deletion 2p21,<br>including SLC3A1, PREP</td></tr><tr><td>Lysinuric protein intolerance (LPI)</td><td>HE colic</td><td>Normal</td><td>Expected: Dibasic AA ↑<br>Cystine ↑↑</td><td>Dibasic AA ↑<br>Orotic acid ↑</td><td>SLC7A7 bi-allelic pathogenic variation</td></tr></tbody></table>

Abbreviations: AA, Amino acid; HC, Hypotonia Cystinuria Syndrome; HE, Hyperechoic; LC, Lysinuria Cystinuria; LPI, Lysinuric protein intolerance.
probability of each diagnosis. Amniocentesis, which remains an invasive procedure with risks, should be discussed, as well as turn around time explained.²⁰ If prenatal confirmation is requested by the parents, obstetrical management of this delay should be taken into account. Multidisciplinary Centers for Prenatal Diagnosis plays a crucial role in this process, and it is essential that a sonographer refers to any suspected case of colonic hyperechogenicity for confirmation by a referent sonographer.

In our series, all children with colonic hyperechogenicity for whom a follow-up was known had a post-natal diagnosis of LC, HC, or LPI along with other pathologies, such as urological, digestive, or syndromes with multiple congenital anomalies. Given our results in this subpopulation, the medical outcome of the children who were lost to follow-up is essential and should be addressed (Figure 3).

The strength of this study lies in its multicentric character since it collects cases of colonic hyperechogenicity from many antenatal diagnostic centers in France. In addition, few studies have focused on the underlying pathologies of colonic hyperechogenicity apart from LC.

To date, it allows to highlight the occurrence of severe conditions associated with this ultrasound sign.

This study has several limitations. The retrospective nature of the study made exhaustive data retrieval difficult. We have, 27% of infants lost to follow up. The number of patients included

remains limited because the sonographic sign is rare and challenging to identify. Our study collected the short-term outcome in children; the evolution and follow-up in childhood could modify the results. Finally, we observed heterogeneity and a lack of inter-center consensus in these children's antenatal management and post-natal follow-up.

According to our findings, the next step should be a collaborative prospective study in the 46 French MCPD. Fetuses would be followed from the ultrasound sign of hyperechoic colon to definitive diagnosis. The goal would be a better understanding of diagnoses and prognoses, which would lead to recommendations to improve diagnosis and medical management of affected families.

5 | CONCLUSION

Fetal colonic hyperechogenicity can be the point of call for several pathologies, in the majority of cases leading to a diagnosis of LC, and in a minority of cases, a diagnosis of HC or a LPI, or a malformative pathology with very different prognoses.

We suggest a prenatal evaluation including genetic counseling to discuss an invasive sampling with exome sequencing in order to refine the diagnosis and specify the prognosis according to the couples wishes.

<figure><img src="image_3.png" /><figcaption>**FIGURE 3** Proposition of medical care during pre and postnatal stages in case of prenatal colonic hyperechogenicity. [Colour figure can be viewed at wileyonlinelibrary.com]</figcaption></figure>
## ACKNOWLEDGMENTS

We warmly thank the MCPD: Marseille Timone, Marseille Nord, Grenoble, Lille, Port-Royal, Poitiers, Saint Brieuc, Créteil, Colombes-Pontoise, Strasbourg, Saint Denis de la Réunion, Bordeaux-Bagatelle, Lyon Est-Bron, Nîmes and Montpellier who participated.

## CONFLICT OF INTEREST STATEMENT

None.

## DATA AVAILABILITY STATEMENT

Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.

## ORCID

Florent Fuchs https://orcid.org/0000-0003-3530-6328

Sophie Dreux https://orcid.org/0000-0003-1941-5516

Marjolaine Willems https://orcid.org/0000-0002-2959-0935

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## SUPPORTING INFORMATION

Additional supporting information can be found online in the Supporting Information section at the end of this article.

**How to cite this article:** Fuchs F, Rodriguez A, Mousty E, et al. Postnatal outcome of children with antenatal colonic hyperechogenicity. *Prenat Diagn.* 2024;44(1):28-34. https://doi.org/10.1002/pd.6475