Imaging and pathological features of pediatric sclerosing angiomatoid nodular transformation of the spleen: a case series and hypothesis-generating perspective on non-operative management

Introduction

Solid tumors of the spleen are rare, accounting for approximately 0.007% of all surgical and autopsy specimens (1), Sclerosing angiomatoid nodular transformation (SANT) was originally considered a variant of splenic hamartoma, but is now recognized as a benign non‑neoplastic lesion characterized by red pulpderived angiomatoid nodules surrounded by stromal hyperplasia (2-4). Most SANT cases occur in middle‑aged adults with a female predominance (female:male ≈2:1). In contrast, SANT is extremely rare in children, where splenic masses are more commonly hemangiomas or lymphomas, and SANT is often not considered in the differential diagnosis (2,5,6).

The clinical presentation of SANT is non‑specific (e.g., occasional abdominal pain or asymptomatic), and no specific biomarkers exist. Imaging [ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI)] may show a solitary, well‑circumscribed mass with progressive centripetal or “spoke‑wheel” enhancement, but these findings are not uniformly present. SANT can mimic other splenic lesions (hemangioma, hamartoma, lymphoma), making preoperative diagnosis challenging. Pathological examination with immunohistochemistry (CD31+, CD34 variable, CD8−) remains the gold standard.

No large pediatric SANT series has been published; the natural history and optimal management in children remain unclear. Given the risks of splenectomy in children (e.g., overwhelming post‑splenectomy infection), non‑operative strategies such as observation or biopsy have gained interest, but their safety and feasibility are unproven in pediatrics. In this study, we report a consecutive case series of four pediatric patients with pathologically confirmed splenic SANT (one with a synchronous pancreatic calcifying fibrous tumor). We describe their clinical, imaging, and pathological features and present the imaging‑pathology correlation in a structured manner. Due to the small sample size, our conclusions are hypothesis‑generating regarding potential non‑operative management, aiming to provide a reference for clinicians and to highlight areas for future multicenter prospective studies. We present this article in accordance with the AME Case Series reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-1-0164/rc).

Case presentation

Patients and data collection

This was a retrospective descriptive case series. Consecutive pediatric patients who underwent partial splenectomy and were pathologically diagnosed with splenic SANT at the Children’s Hospital of Nanjing Medical University between June 2014 and December 2021 were enrolled. Inclusion criteria: (I) age <18 years; (II) splenic solid mass suspected on preoperative imaging; (III) underwent partial splenectomy; (IV) postoperative pathological diagnosis of SANT (including cases with coexisting benign lesions). Exclusion criteria: (I) incomplete clinical or imaging data; (II) lack of pathological confirmation. Four male patients were included, with a mean age of 90±53 months. Complete follow‑up was available for all cases.

Imaging examination methods

All imaging examinations adhered to the principle of radiation protection optimization for children. Ultrasonography, CT, and MRI images were independently reviewed by two senior radiologists. Disagreements were resolved by consensus discussion with a third senior radiologist when necessary. The radiologists were blinded to the final pathological diagnosis (SANT vs. others) at the time of image interpretation, although they were aware that all patients had undergone splenic mass resection.

Ultrasonography: a Toshiba Aplio 500 color Doppler ultrasound diagnostic instrument with a convex array probe (frequency 3.5–5.5 MHz) was used. The patient was positioned supine or on the right side, and the probe was placed between the left ribs for oblique scanning. When necessary, a gastric window was used. Spleen size was measured by two‑dimensional ultrasound, and the echo pattern of splenic parenchyma and adjacent tissues was recorded.

CT: all children underwent non‑contrast upper abdominal CT followed by dual‑phase contrast‑enhanced CT (late arterial and venous phases). Scanning was performed on a Philips CT scanner at 120 kVp with automated mA modulation and a slice thickness of 2–3 mm. A total of 20–80 mL of iodinated contrast agent (iodine concentration 300 mgI/mL, 1.5–2 mL/kg body weight) was injected via the antecubital vein at a rate of 3 mL/s. Late arterial phase imaging was acquired at 35 seconds and venous phase at 85 seconds after injection.

MRI: performed using a Siemens Aera 3.0T scanner. The protocol included: T1-weighted imaging (in-phase and opposed‑phase), T2-weighted imaging with fat suppression, diffusion-weighted imaging (DWI; b =0 and 800 s/mm²), and multi-phase dynamic contrast-enhanced T1-weighted imaging (arterial, portal venous, equilibrium, and delayed phases). Contrast-enhanced imaging was performed using a 3D volumetric ultra-fast multi-phase dynamic sequence after intravenous injection of 0.1 mmol/kg gadolinium-based contrast agent.non-contrast scan.

Image analysis parameters: number of lesions, size (maximum diameter in three planes), shape, margin, attenuation/signal intensity (qualitatively compared to normal spleen: hypodense, isodense, or hyperdense), enhancement pattern (arterial, venous, delayed phases), and degree of enhancement (visually graded as weak, moderate, or significant). No formal statistical testing was performed due to the small sample size.

Pathological examination

Each specimen was fixed with 10% neutral formaldehyde for 24 h, embedded in conventional paraffin, and the tissue was sectionalized with 4–5 µm thickness and stained with HE. The histopathological features were observed under light microscope. At the same time, the typical histological areas of each case were selected and immunohistochemical staining of CD34, CD31, CD8, IgG, IgG4 and other related indexes were performed by En Vision two-step method. The blank control group used phosphate-buffered saline (PBS) instead of primary antibody, and the positive control group used known positive tissue sections.

Case description

Case 1

A 36‑month‑old boy presented with occasional abdominal pain. Ultrasound showed a single, well‑defined, round, hypoechoic mass (8.5 cm × 5 cm × 4 cm) in the upper spleen with sparse blood flow signal. CT: non‑contrast scan showed a large, round mass with heterogeneous internal density and indistinct boundary; late arterial phase revealed marked enhancement of solid components with well‑defined boundary; venous phase showed uniform enhancement resembling splenic parenchyma. No spoke‑wheel pattern. MRI: T1 and T2 showed no clear abnormality; DWI not distinctive. Preoperative diagnosis: splenic hemangioma. The patient underwent open partial splenectomy. Postoperative pathology: isolated SANT (mass size 6.0 cm × 5.3 cm × 5.5 cm) with CD31+, CD34−, CD8−; hemosiderin deposition (+); central scar (+); no calcification; lymphoplasmacytic infiltrate (+). Follow‑up 96 months: no recurrence or metastasis.

Case 2

A 60‑month‑old asymptomatic boy. Ultrasound: regular spleen shape, clear boundary, uneven isoechoic interior, single mass (14 cm × 9 cm × 7 cm). CT: hypodense without central calcification; spoke‑wheel, centripetal, asymptotic enhancement from arterial to venous phase. MRI: T1 low signal, T2 slightly low signal, DWI low signal with interspersed strip‑like high signal. Preoperative diagnosis: splenic hamartoma. Laparoscopic partial splenectomy. Pathology: isolated SANT (4.5 cm × 4.5 cm × 4.2 cm), CD31+/CD34+/CD8−; hemosiderin deposition (+); central scar (+); no calcification; no lymphoplasmacytic infiltrate. Follow‑up 132 months: no recurrence.

Case 3

A 156‑month‑old asymptomatic boy. Ultrasound: regular shape, clear boundary, uneven internal hypoechoic mass (7 cm × 7 cm × 6 cm). CT: hypodense without central calcification; spoke‑wheel enhancement. MRI: no clear signal abnormality. Preoperative diagnosis: splenic hemangioma. Laparoscopic partial splenectomy. Pathology: isolated SANT (5.5 cm × 5.1 cm × 5.0 cm), CD31+/CD34+/CD8−; hemosiderin deposition (+); no central scar; no calcification; no lymphoplasmacytic infiltrate. Follow‑up 108 months: no recurrence.

Case 4

A 108‑month‑old boy with limb weakness. Ultrasound: irregular spleen shape, unclear boundary, non‑uniform hypoechoic internal echo; multiple irregular hypoechoic masses in pancreatic body/tail with calcification. CT: mixed density with scattered calcifications in spleen; pancreatic tail mass with marked calcification. No spoke‑wheel enhancement. MRI: T1 low signal in phase, equal signal in reverse phase, low signal in lipid phase, slightly high signal in water phase; T2 heterogeneous slightly low signal; DWI low signal with interspersed strip‑like high signal; after contrast, splenic lesions showed significant heterogeneous multinodular enhancement, with a low‑signal radiating wheel pattern in the larger central nodule. The patient underwent partial splenectomy plus resection of the pancreatic tail tumor. Pathology: splenic SANT (11.4 cm × 10.5 cm × 6.2 cm) with CD31+/CD34+/CD8−; hemosiderin deposition (+); calcification (+); central scar (−); lymphoplasmacytic infiltrate (+); and a separate pancreatic calcifying fibrous tumor (dense collagenous fibrous tissue with psammomatous calcifications and chronic inflammation). No continuity between the two lesions. Follow‑up 52 months: no recurrence or metastasis.

Summary of clinical and pathological features

Table 1: clinical characteristics of four children (gender, age, clinical picture, nodule number, tumor size, preoperative diagnosis, surgical method, postoperative diagnosis, follow‑up months).

Table 2: comparison of pathological features (mass size, immunohistochemistry, hemosiderin deposition, calcification, central scar, lymphoplasmacytic infiltrate).

Table 3: comparative analysis of imaging manifestations (ultrasonography, CT scan, CT enhancement features including spoke‑wheel pattern).

Table 4: imaging‑pathology correlation (imaging finding, pathological correlate, example cases).

Table 5: differential diagnosis of SANT [CT, MRI, fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) features of SANT, splenic hemangioma, splenic lymphoma, splenic hamartoma, splenic lymphatic malformation].

Figure 1: light microscopic images.

Figure 1 Light microscopic image of SANT pathology. (A) Multiple scattered hemangiomatoid nodules were observed by H&E staining of splenectomy specimen ×100 image. (B) H&E staining ×400 image showed that hemangiomatous nodules were composed of fissure, honeycomb or irregular blood vessels lined with hypertrophy endothelial cells. The nodules are surrounded by a large number of fibrous sclerosis stroma. (C) Immunohistochemical CD31 (+). (D) Immunohistochemical CD34 (+). (E) IgG staining was sporadic positive. (F) IgG4 staining was sporadic positive. (G,H) Pancreatic calcified fibrous tumor with H&E staining ×100 image, collagen fibrous tissue hyperplasia with scattered calcium salt deposition and a large number of chronic inflammatory cell infiltration can be seen in pancreatic tissue. H&E, hematoxylin and eosin; SANT, sclerosing angiomatoid nodular transformation.

Figure 2: specimen of spleen.

Figure 2 The spleen measured 14.2 cm × 14 cm × 8 cm and weighed 620 g. The splenic capsule was intact. On cut section, an 11 cm × 11 cm × 6 cm mass was identified, which was grayish-red to grayish-white in color, solid, firm in consistency, and multinodular in appearance with the largest nodule measuring up to 4 cm in diameter. In some areas, the tumor protruded through the capsule, forming several nodular elevations on the splenic surface with a maximum diameter of 2.2 cm. The mass was in close proximity to the splenic capsule and hilum.

Figure 3: CT findings for Cases 1‑4.

Figure 3 CT findings. 1, 2, 3, 4: case number. (A) Non‑contrast scan. (B) Late arterial enhancement. (C) Venous enhancement. CT, computed tomography.

Figure 4: transverse and coronal CT images of multiple lesions (Case 4).

Figure 4 Comparison of transverse and coronal CT images of multiple lesions. (A) Non‑contrast scan. (B) Late arterial enhancement. (C) Venous enhancement. CT, computed tomography.

Figure 5: plain MRI of multiple lesions (Case 4).

Figure 5 Plain MRI scan of multiple lesions. (A) T1 lipid pressure phase. (B) DWI phase, b =800. (C,D) Transverse and coronal T2WI phase. DWI, diffusion-weighted imaging; MRI, magnetic resonance imaging; T2WI, T2-weighted imaging.

Figure 6: MRI enhancement in multiple lesions (Case 4).

Figure 6 MRI enhancement in multiple lesions. (A) Transverse. (B) Coronal. (C) Sagittal. MRI, magnetic resonance imaging.

Ethics statement

All procedures performed in this study were in accordance with the ethical standards of the institutional research committee and with the Helsinki Declaration and its subsequent amendments. The study was reviewed and approved by the Ethics Committee of the Children’s Hospital of Nanjing Medical University (No. 202402005-1). Written informed consent was obtained from the parents or legal guardians of all participating children for publication of this case series and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

SANT is an infrequent benign lesion of the spleen, with an even lower prevalence observed in pediatric populations (3,4). The pathogenesis of SANT remains poorly understood; however, it is predominantly hypothesized to be associated with IgG4-related autoimmune diseases (3,19,20). Clinically, some individuals with SANT present with elevated IgG levels (21,22). Histologically, certain SANT lesions are characterized by a dense infiltration of IgG4-positive plasma cells within the newly formed stroma and at the periphery of red blood cells (23,24). In our pediatric cohort, immunohistochemistry revealed only sporadic, small numbers of IgG4+ plasma cells, without dense infiltration. Thus, our data do not support a strong IgG4 association in pediatric SANT. We therefore limit discussion of this topic to a brief mention, without clinical or therapeutic implications. If more pediatric SANT cases can be collected in the future, the underlying causes of the differences in IgG4 expression could be further elucidated.

The primary challenge in managing this disease is its diagnosis; nonetheless, the present study offers a thorough examination of its characteristic manifestations. A non-contrast CT scan identified an ill-defined splenic mass, while contrast enhancement delineated a distinct boundary, corroborating findings in the existing literature. On MRI, the non-contrast images displayed well-defined boundaries, and DWI revealed multiple high-intensity regions surrounded by strip-like low-intensity regions, in full agreement with previous imaging reports. In summary, CT imaging is effective in delineating the morphological characteristics of calcification. In contrast, MRI provides superior capability in illustrating specific imaging features, such as the pathological boundary of SANT, hemorrhage, necrosis, stellate fibrous scars, hemosiderin deposition, and enhancement patterns, which can be distinctly identified. Consequently, MRI imaging characteristics demonstrate a high degree of concordance with pathological findings. The progressive enhancement of the spokewheel pattern is recognized as a distinctive feature of SANT (5,25,26). Therefore, we suggest that the diagnostic accuracy for SANT can be improved through the combined application of CT and MRI. In the presence of these characteristic imaging features, SANT should be prioritized in the differential diagnosis. However, in our series, this pattern was present in only two of four cases (Cases 2 and 3). Its absence (Cases 1 and 4) did not exclude SANT. Therefore, while the spokewheel sign is valuable when present, it is not universally observed in pediatric SANT, and its absence should not discourage consideration of the diagnosis. Additionally, calcification has been reported in approximately 50% of cases, highlighting the necessity of considering pathological calcification as a feature of the disease (8,25). In the present study, a case was identified as a pancreatic calcifying fibrous tumor, potentially representing a calcified variant of SANT, in alignment with prior reports. Furthermore, it is essential to distinguish this condition from other splenic pathologies, including splenic hemangioma, splenic lymphatic malformation, and malignant splenic lymphoma, during the diagnostic evaluation. In clinical practice, when a solitary, well-circumscribed splenic mass is identified in children with a benign clinical course and centripetal or spoke-wheel enhancement, the possibility of SANT should be considered. However, pathological examination combined with immunohistochemistry remains the gold standard.

Recent studies suggest that percutaneous ultrasound‑guided core‑needle biopsy is a safe and effective diagnostic technique for SANT, with lower morbidity and cost compared to surgical resection. Histological examination [hematoxylin and eosin (H&E) stain] typically reveals angiomatoid nodules surrounded by stromal fibrosis, containing capillaries, small veins, sinusoids, erythrocytes, and inflammatory cells. In a case reported by Mariano Gómez Rubio et al., an asymptomatic female patient with SANT was diagnosed via this method and managed conservatively; follow‑up CT after 10 years showed no disease progression. Thus, core‑needle biopsy represents a promising diagnostic tool for SANT and warrants further investigation. In conclusion, combining imaging with percutaneous ultrasound‑guided core‑needle biopsy offers an effective non‑surgical strategy for confirming SANT. This study included only male pediatric patients. Despite the limited sample size, future studies should enroll larger and more balanced pediatric cohorts to better elucidate potential gender‑related differences between children and adults with SANT.

Splenectomy or partial splenectomy remains the mainstay of treatment. However, in children, early splenectomy may compromise immune function, adversely affecting growth and development and increasing the risk of infections. One of the most severe complications is overwhelming postsplenectomy infection (OPSI). Although OPSI can occur at any age, children—especially those under two years—are at increased risk. Initial symptoms (abdominal pain, nausea) may progress to fever, chills, vomiting, and even coma or shock. In conclusion, OPSI represents a critical infection that can rapidly progress to fulminant sepsis, posing a significant threat to patient survival (27,28). Although all patients in our cohort underwent surgery without complications, the risks of splenectomy in children—particularly OPSI—cannot be ignored. Given that SANT is a benign, non-neoplastic lesion, non-operative strategies have been proposed in the literature, including percutaneous ultrasound-guided biopsy for diagnosis and follow-up observation without resection. However, our study does not provide direct evidence for the safety or efficacy of such an approach, as all our patients were treated surgically. Therefore, we frame the following discussion as hypothesis-generating rather than as a conclusion supported by our data. In carefully selected pediatric cases with typical imaging features (e.g., well-defined solitary mass, spoke-wheel enhancement on MRI if present) and a benign clinical course, follow-up observation might be considered as a potential alternative to surgery, provided that a preoperative diagnosis can be confirmed by core-needle biopsy. This strategy, however, requires prospective validation. Until such evidence is available, surgical resection (partial splenectomy) remains the standard of care when diagnostic uncertainty persists.

It is undeniable that this study has several limitations. First, the sample size is very small (four patients), which limits the generalizability of our findings and forces us to present the results as descriptive and hypothesis‑generating rather than conclusive. Second, the retrospective design carries inherent risks of selection and information bias. Third, this is a single‑center study, and our case series may not reflect the broader pediatric population or institutional practices elsewhere. Fourth, all patients underwent partial splenectomy; therefore, our data provide no direct evidence for the safety or feasibility of non‑operative management (e.g., observation or biopsy alone). Fifth, potential selection bias exists because the cohort was derived from a surgical database, likely missing children with SANT who were managed conservatively or never diagnosed. Sixth, the cohort is heterogeneous: three patients had isolated splenic SANT, while one (Case 4) had splenic SANT with a synchronous pancreatic calcifying fibrous tumor, which may confound the analysis of pure splenic SANT. Additionally, all patients were male, which does not reflect the female predominance reported in adult literature. Collectively, these limitations highlight important areas that warrant further investigation in larger pediatric cohorts.

Conclusions

The identification of the distinctive “spoke‑wheel” imaging characteristics and contrast enhancement patterns on CT or MRI is crucial for accurate diagnosis. Furthermore, percutaneous ultrasound-guided splenic biopsy serves as a valuable diagnostic tool for pediatric patients. If these diagnostic approaches confirm a diagnosis of SANT, Close follow-up and observation may be considered as an alternative to surgery.; however, if confirmation is not possible, splenectomy or partial splenectomy may be considered as a treatment option. This study primarily explores the potential of follow-up observation as an alternative to surgical intervention in pediatric patients with SANT. The suggestion of non-operative management for pediatric SANT is currently speculative. Future multicenter prospective studies are needed to evaluate the safety of observation or biopsy-only approaches. Until then, clinicians should balance the benign nature of SANT against the surgical risks and the need for definitive diagnosis. This area constitutes the focus of our future research efforts. We intend to conduct further multi-center collaborative studies with a larger pediatric cohort to elucidate the pathogenesis of SANT and to establish a standardized treatment protocol.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the AME Case Series reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-1-0164/rc

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-1-0164/prf

Funding: The project was supported by Jiangsu Provincial Health Commission Medical Research Project (No. MQ2024023).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-1-0164/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 research committee and with the Helsinki Declaration and its subsequent amendments. The study was reviewed and approved by the Ethics Committee of the Children’s Hospital of Nanjing Medical University (No. 202402005-1). Written informed consent was obtained from the parents or legal guardians of all participating children for publication of this case series 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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