Infantile cholestasis caused by pituitary stalk interruption syndrome: a case report and review of the literature
Case Report

Infantile cholestasis caused by pituitary stalk interruption syndrome: a case report and review of the literature

Xiaoqing Liao1,2, Shengxuan Liu1, Biao Zou1, Sainan Shu1, Chen Dong1 ORCID logo

1Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; 2Department of Pediatric Gastroenterology, Ganzhou Maternal and Child Health Care Hospital, Ganzhou, China

Contributions: (I) Conception and design: All authors; (II) Administrative support: None; (III) Provision of study materials or patients: All authors; (IV) Collection and assembly of data: All authors; (V) Data analysis and interpretation: C Dong; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Chen Dong, MD, PhD; Sainan Shu, MD, PhD. Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China. Email: dongchen98@tjh.tjmu.edu.cn; snshu@tjh.tjmu.edu.cn.

Background: Pituitary stalk interruption syndrome (PSIS) is a clinical syndrome caused by the absence or thinning of the pituitary stalk. This syndrome mainly impairs the transport of hormones from the hypothalamus to the posterior pituitary gland and affects the action of relevant hormones on the anterior pituitary gland, thereby leading to common clinical manifestations such as diabetes insipidus, growth retardation, gonadal dysplasia, hypothyroidism, and adrenocortical hypofunction. In PSIS, cases presenting with infantile cholestasis as the initial and prominent manifestation are relatively rare and prone to misdiagnosis.

Case Description: A boy aged 2 months was admitted for cholestatic liver disease, presenting with poor response to routine choleretic therapy, non-elevated gamma-glutamyl transferase (GGT) level, hypothyroidism and recurrent hypoglycemia. Difficulties were encountered in identifying the etiology of common infantile cholestatic liver disease with non-elevated GGT. Subsequently, cranial magnetic resonance imaging (MRI) and genetic testing were completed focusing on the symptoms related to the endocrine axis, leading to a definitive diagnosis of PSIS. The infant achieved stable and favorable therapeutic outcomes after receiving combined treatment by endocrinologists and gastroenterologists during follow-up.

Conclusions: The prominent feature of this case was infantile cholestatic liver disease accompanied by hypoglycemia and hypothyroidism. For infants, hypoglycemia and hypothyroidism should not be overlooked, and close monitoring is required. As pediatric gastroenterologists, when routine treatment fails for infantile cholestatic liver disease, we need to consider the possibility of cholestasis caused by hypothalamic-pituitary axis abnormality, and conduct relevant imaging examinations, hormone level tests and genetic tests when necessary. At this point, the joint diagnosis and treatment by gastroenterologists and endocrinologists is particularly important.

Keywords: Pituitary stalk interruption syndrome (PSIS); cholestatic liver disease; non-elevated gamma-glutamyl transferase (non-elevated GGT); hypothyroidism; case report

Submitted Dec 23, 2025. Accepted for publication Mar 18, 2026. Published online Apr 26, 2026.

doi: 10.21037/tp-2025-1-921

Highlight box

Key findings

• This study proposes a supplementary diagnostic strategy for infantile cholestasis characterized with low gamma-glutamyl transferase (GGT) levels.

What is known and what is new?

• For infants with cholestasis complicated with hypoglycemia and hypothyroidism, clinicians should be alert to the possibility of underlying central endocrine disorders.

• For infants with low-GGT cholestasis, pituitary stalk interruption syndrome should be taken into consideration.

What is the implication, and what should change now?

• Traditionally, bile acid synthesis defects and progressive familial intrahepatic cholestasis are prioritized in the differential diagnosis of infants with low-GGT cholestasis. Clinicians should additionally consider pituitary stalk interruption syndrome in future clinical practice.

Introduction

Pituitary stalk interruption syndrome (PSIS) is a clinical syndrome caused by the absence or thinning of the pituitary stalk. The change interrupts the transport of hormones secreted by the hypothalamus to the posterior pituitary. It also affects the action of related hormones on the anterior pituitary via the hypophyseal portal system (1).

The common clinical manifestations of PSIS include diabetes insipidus, growth retardation, gonadal dysgenesis, hypothyroidism, adrenocortical hypofunction, and so on. Cases presenting with infantile cholestasis as the initial and prominent manifestation are relatively rare and prone to misdiagnosis. Herein, we report an infantile PSIS case with non-elevated gamma-glutamyl transferase (GGT) cholestasis as the initial symptom. We present this article in accordance with the CARE reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-1-921/rc).

Case presentation

Patient information

A 2-month-old male infant was admitted to Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. He developed jaundice on the 7th day after birth, accompanied by refractory hypothyroidism and recurrent hypoglycemia. The conventional treatments with ursodeoxycholic acid and levothyroxine were ineffective. The infant was the second child (Gravida 2, Para 2) of the family, born at full term via spontaneous vaginal delivery with a birth weight of 4.2 kg. There was no similar family history.

Clinical findings

Physical examination on admission: weight 4.4 kg, length 52.5 cm. Jaundice was observed on the entire skin and sclera. The patient appeared emaciated with thin subcutaneous fat. Heart sounds were slightly dull, with no obvious murmurs heard. The liver was palpable 2 cm below the costal margin, with moderate texture; the spleen was not palpable below the costal margin.

Diagnostic assessment

The results of liver function and endocrine tests are shown in Table 1. Before cortisol replacement treatment, alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bile acid (TBA), total bilirubin (TBiL) and direct bilirubin (DBiL) were all abnormally elevated, while GGT was at a normal level. The child had recurrent hypoglycemia, with the lowest blood glucose level of 1.45 mmol/L. Thyroid stimulating hormone (TSH) was significantly decreased. Levels of adrenocorticotropic hormone (ACTH), fasting cortisol, insulin-like growth factor (IGF-1) and insulin-like growth factor binding protein 3 (IGFBP-3) were significantly decreased. Blood tandem mass spectrometry, urine organic acid assay, TORCH test, blood ammonia, lactic acid, and coagulation function showed no obvious abnormalities.

Table 1

Laboratory findings of the patient at the time of admission

Laboratory variables Pre-treatment‡ 5 days post-routine treatment† 5 days post-supplementary treatment‡ 1 month post-supplementary treatment‡ 1 year post-supplementary treatment‡ Normal range
ALT (U/L) 58 68 147 47 35 7–40
AST (U/L) 164 157 126 71 53 13–35
GGT (U/L) 20 18 131 118 10 6–42
TBA (μmol/L) >300 >300 207.15 33.1 10.0 ≤9.67
TBil (μmol/L) 178.9 179.0 145.1 47.1 5.1 ≤8
DBil (μmol/L) 162.9 158.2 137.3 41.9 <2.0 ≤12.9
TSH (μIU/mL) 0.260 – 0.099 0.016 <0.005 0.27–4.20
FT3 (pmol/L) 1.45 – 3.90 5.95 5.44 3.1–6.8
FT4 (pmol/L) 9.43 – 18.60 19.90 17.20 12–22
ACTH (pg/mL) 1.8 – 1.7 1.6 1.8 7.2–63.3
Fasting cortisol (μg/dL) – <0.4 0.6 13.6 21.2 6.7–22.6
IGF-1 (ng/mL) – <1.00 – – <1.00 35±8
IGFBP-3 (ng/mL) – 420.00 – – 362.00 2,058±1,107

†, routine treatment: herein refers to hepatoprotective and cholagogic treatment; ‡, supplementary treatment: herein refers to cortisol replacement treatment. ACTH, adrenocorticotropic hormone; ALT, alanine aminotransferase; AST, aspartate aminotransferase; DBiL, direct bilirubin; FT3, free triiodothyronine; FT4, free thyroxine; GGT, gamma glutamyl transpeptidase; IGF-1, insulin-like growth factor; IGFBP-3, insulin-like growth factor binding protein 3; TBA, total bile acid; TBiL, total bilirubin; TSH, thyroid stimulating hormone.

Pituitary and cranial magnetic resonance imaging (MRI) showed sella turcica dysplasia, almost invisible pituitary gland, absent pituitary stalk (considered aplasia or severe dysplasia), and ectopic posterior pituitary gland in the hypothalamus (Figure 1).

Figure 1 Plain MRI of the cranium (including the pituitary gland). (A) T1-weighted image. Long white arrow indicates the optic nerve, short white arrow indicates empty sella, and short red arrow indicates ectopic posterior pituitary lobe. (B) T1-weighted image. Short red arrow indicates ectopic posterior pituitary lobe. (C) T2-weighted image. Short white arrow indicates empty sella. MRI, magnetic resonance imaging.

Fasting ultrasound showed unfilled gallbladder. The results of ultrasound-guided fine needle aspiration showed mostly preserved hepatic lobule structure, swelling hepatocellular with bile pigment deposition, and multinucleated hepatic giant cells. Additionally, it showed scattered punctate necrosis in lobules, mild proliferation of fibrous connective tissue in portal areas, with local formation of fibrous septa (suspected). Immunohistochemistry results: cytokeratin 7 (CK7) (small bile ducts +), cluster of differentiation 8 (CD8) (scattered, slight +) (Figure 2).

Figure 2 Liver biopsy examination (hematoxylin-eosin staining, 200 times magnified image) (A,B). The lobular architecture of the liver is roughly preserved. Hepatocellular swelling with bile pigment deposition is noted, accompanied by multinucleated hepatic giant cells. Scattered spotty necrosis is present within the lobules. Mild proliferation of fibrous connective tissue is observed in the portal tracts, with focal potential formation of fibrous septa. Mild proliferation of small bile ducts and a small amount of acute and chronic inflammatory cell infiltration are also seen.

Therapeutic intervention

Based on the infant’s postnatal clinical manifestations, blood tests, and imaging findings, the possibility of PSIS was suggested. Whole-exome sequencing was performed for further evaluation. The results showed a point variation—a variant of unknown clinical significance (VUS) was detected in the ROBO1 gene. Diseases associated with this gene include combined or isolated pituitary hormone deficiency type 8 (CPHD8/IPHD8).

Then the patient was treated in collaboration with endocrinologists. On the basis of the original therapy for choleresis and jaundice reduction, hydrocortisone was added at a dose of 2 mg/kg via intravenous infusion for 5 days as hormone replacement therapy. After re-examination showed improvement, oral hydrocortisone was continued for maintenance treatment.

Follow‑up and outcomes

After discharge, the child was followed up regularly in the outpatient clinic, with simultaneous monitoring of liver function and endocrine-related indicators. At present, the child has recovered well and the condition is stable (Table 1).

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s parent for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

The incidence of infantile cholestasis is approximately 1/2,500 (2). The most common cause is biliary atresia, followed by genetic metabolic diseases, infectious diseases, etc. (3).

Cholestasis in this case was detected during the postnatal jaundice monitoring, while the relevant hormone levels were overlooked. Therefore, the child was initially monitored mainly at the primary care pediatric clinic. Later, due to poor control of cholestasis, the child was admitted to the Department of Pediatric Gastroenterology in our hospital for inpatient treatment.

After the child was admitted to our hospital, what impressed us most and also provided the main clue for diagnosis was the child’s non-elevated level of GGT. GGT is mainly distributed in the kidneys in the body, and in the liver, it is mainly located in cholangiocytes (4). It can catalyze the reaction between glutathione and amino acids to form glutamyl amino acids and cysteinylglycine, with its main function being involved in the transport activities of cell membranes. GGT has been used as an indicator to reflect liver function since the 1960s and 1970s. In recent years, multiple studies on infantile cholestatic liver disease have also taken the increased or non-elevated GGT level as an important indicator for preliminary grouping. Studies have found that most patients with non-elevated GGT levels are diagnosed with progressive familial intrahepatic cholestasis type 1 (PFIC1), PFIC2, or bile acid synthesis defects (5,6).

The child’s non-elevated level of GGT and elevated bile acid level led us to initially lean toward a diagnosis of familial intrahepatic cholestasis. However, the child experienced recurrent hypoglycemia during hospitalization, and normal blood glucose levels could only be maintained through 24-hour continuous infusion of glucose-containing fluids. The above findings reminded us that we also need to consider other diseases that may cause cholestasis. Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) is one of the common etiologies of cholestasis in infants, characterized by cholestasis accompanied by metabolic abnormalities such as hypoglycemia, galactosemia, citrullinemia, and hyperammonemia (7). However, inconsistent with this case, the GGT level is usually elevated in infants with neonatal intrahepatic cholestasis caused by NICCD (8). In addition, other diseases associated with both hypoglycemia and cholestasis include: mitochondrial inner membrane protein MPV17-related mitochondrial DNA maintenance defect, preterm neonates, mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes; deafness, hypertrophic cardiomyopathy, encephalopathy, lactic acidosis, and Leigh-like syndrome (MEGDHEL syndrome), etc. (9,10). However, the results of routine examinations such as liver function, coagulation function, and screening for metabolic diseases, as well as liver pathological examination, did not point us to a clear diagnostic direction. After routine cholagogic and hepatoprotective treatment, the results of the first re-examination did not indicate any improvement. And our clinical work was once stuck in a difficult situation.

Therefore, we must adopt a different approach to address the child patient’s problem. The abnormal thyroid function identified by routine screening and recurrent hypoglycemia prompted us to pay attention to potential abnormalities in the hormone secretion. Therefore, with the consent of the child’s parents, we completed hypothalamus + pituitary MRI and relevant hormone level tests for the child. The relevant results suggest a diagnosis of PSIS.

PSIS is a rare congenital abnormality, with an incidence of 0.5/100,000 live births (11). Most reported cases are sporadic, with less than 5% being familial (12). The male-to-female incidence ratio is approximately 2.3:1 (12). The child in this case is also a sporadic case; no pathogenic mutations were found in the parents, and the elder sister has no relevant clinical symptoms.

PSIS has a variety of etiologies, such as genetics, specific mutations, and different degrees of traction during childbirth (13). The patient was born via spontaneous vaginal delivery. Upon detailed inquiry, there was no traction applied during the delivery process. In recent years, genetic defects of some transcription factors have been reported to have phenotypic-genotypic correlations to varying degrees. For example, genes such as B3GAT3, BLM, BRAF, FGFR1, and ROBO1 have been shown to be associated with combined or isolated pituitary hormone deficiency (14).

In this case, the child’s mutation site is located in the ROBO1 gene. ROBO1 is a member of the immunoglobulin gene superfamily and encodes a membrane-integrated protein. This protein is the receptor for Slit homolog (Slit) proteins and plays a crucial role in axon guidance and neuronal precursor cell migration in the forebrain (15). The Slit2-Robo1 signaling pathway is associated with the development of the central nervous system; it also regulates leukocyte chemotaxis, mesoderm migration, and vascular smooth muscle migration. Recent studies have suggested that it is also related to tumors and liver fibrosis. The specific mechanism by which ROBO1 mutation causes pituitary stalk interruption remains unclear, but it may affect the differentiation of pituitary cells by influencing the Notch signaling pathway and its downstream factor Hes1 (16).

The clinical manifestations of PSIS are heterogeneous, depending on whether there is isolated or multiple anterior pituitary hormone deficiency (11). It is mainly diagnosed in the neonatal period or early infancy with hypoglycemia or hypothyroidism as the initial symptoms. Reports of cholestasis as the initial manifestation are relatively rare (17). There are few relevant reports on the mechanism by which pituitary stalk interruption syndrome causes cholestasis. Scholars have proposed that thyroid hormones and cortisol can promote bile acid-independent bile flow and bile formation, while growth hormone can regulate the synthesis and secretion of bile acids (17). In addition, ROBO1 not only affects pituitary cell differentiation through the Notch signaling pathway but may also regulate the differentiation of milk-producing alveolar cells, alveolar progenitor cells, and other cell types (18,19). In our preliminary study, we found that the Notch signaling pathway can influence hepatoblast differentiation, thereby inducing cholestasis (20,21).

An important factor causing cholestasis is the impairment in the quantity and function of bile acid transporters (BSEP protein, encoded by the ABCB11 gene) on the canalicular membrane of hepatocytes. In the normal liver, glucocorticoids can increase bile excretion by enhancing bile salt-dependent bile flow (22). They can also regulate the gene transcription of BSEP and MDR3 proteins through different receptors, and cholestasis may occur when glucocorticoid is deficient (23). BSEP plays a dominant role in bile secretion and bile flow; its deficiency reduces bile salt secretion and decreases bile flow.

Conclusions

In summary, when cholestasis is accompanied by endocrine abnormalities such as hypoglycemia and hypothyroidism, attention should be paid to diseases related to abnormalities of the hormone-secreting center. For younger infants and toddlers, the possibility of pituitary stalk interruption syndrome should be considered. If necessary, further cranial imaging examinations, pituitary-related hormone tests, and genetic tests should be performed to confirm the diagnosis. Such patients respond well to hormone replacement therapy; therefore, timely diagnosis and targeted treatment are crucial.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-1-921/rc

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-1-921/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-1-921/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s parent for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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Cite this article as: Liao X, Liu S, Zou B, Shu S, Dong C. Infantile cholestasis caused by pituitary stalk interruption syndrome: a case report and review of the literature. Transl Pediatr 2026;15(5):202. doi: 10.21037/tp-2025-1-921

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