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Clinical Characteristics and Outcomes of Pediatric Craniopharyngioma Patients: A Descriptive Study
*Corresponding author: Ntombizodwa Mahlaba-Madi, Department of Paediatrics, University of the Witwatersrand, Faculty of Health, Chris Hani Baragwanath Hospital, Gauteng, South Africa. ntombizodwa.mahlaba2@wits.ac.za
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Received: ,
Accepted: ,
How to cite this article: Mahlaba-Madi N, Moosa FY, Thandrayen K. Clinical Characteristics and Outcomes of Pediatric Craniopharyngioma Patients: A Descriptive Study. Ann Child Health. 2025:2:71-8. doi: 10.25259/ACH_13_2025
Abstract
Objectives:
Craniopharyngiomas (CPs) are rare, benign but locally aggressive brain tumors that commonly impair the hypothalamic-pituitary axis, resulting in multiple endocrinopathies, including growth hormone (GH) deficiency. While recombinant human growth hormone (rhGH) therapy is available, data on its long-term benefits, especially in resource-limited settings, are limited. The objective of this study was to describe the clinical characteristics, growth outcomes, and quality of life (QOL) among pediatric CP patients, comparing those treated with rhGH to untreated peers.
Material and Methods:
A retrospective observational study was conducted at a tertiary hospital in South Africa between 2011 and 2024. Clinical records of 35 patients were reviewed for anthropometric data, endocrine profiles, treatment history, and QOL using the Pediatric Quality of Life Inventory v4.0. short form.
Results:
GH deficiency was diagnosed in 77% of patients, but only 10 (28.6%) received rhGH therapy. Among treated patients, 30% showed improved growth, while others had suboptimal outcomes due to delayed initiation and non-compliance. Overall QOL scores were poor, with no statistically significant difference between GH-treated and untreated groups. Radical surgical resection was associated with higher QOL scores compared to other interventions.
Conclusion:
In this cohort, endocrine dysfunction and neurodevelopmental morbidity were prevalent. Although rhGH therapy showed potential growth benefits, its impact was limited by late initiation and poor adherence. Surgical outcomes appeared to have a stronger influence on QOL than GH therapy. Comprehensive, multidisciplinary management remains essential in improving outcomes for pediatric CP patients in low-resource settings.
Keywords
Craniopharyngioma
Growth hormone
Pediatric endocrinology
Quality of life
Resource-limited settings
INTRODUCTION
Craniopharyngiomas (CPs) are rare, histologically benign, locally aggressive epithelial tumors that comprise approximately 3.5–10.5% of all pediatric intracranial neoplasms.[1,2] Despite their benign histology, their location in the sellar and suprasellar regions often results in significant morbidity due to involvement of the hypothalamic-pituitary axis and surrounding neurovascular structures. Affected children present with visual disturbances, endocrine dysfunctions, particularly growth hormone deficiency (GHD), and neurocognitive impairments.[2-4]
The management of CP is complex, requiring a balance between achieving tumor control and minimizing long-term complications. Treatment involves surgical resection, with or without radiotherapy. While gross total resection can achieve better tumor control, it carries a higher risk of hypothalamic injury, whereas subtotal resection followed by radiotherapy may preserve neurological function but increase the risk of recurrence.[3,5,6]
Growth hormone (GH) replacement therapy using recombinant human GH (rhGH) is well established in children with GHD, including those with CP. Evidence from high-income settings supports the safety and efficacy of rhGH in improving growth outcomes and certain aspects of quality of life (QOL), with no demonstrated increase in tumor recurrence.[7,8] However, in low- and middle-income countries (LMICs), challenges such as delayed diagnosis, limited access to diagnostics, and poor long-term follow-up may limit the effectiveness of endocrine therapies.[7,9]
This study aims to describe the clinical characteristics, endocrine complications, and QOL outcomes of pediatric CP patients managed at a tertiary hospital in South Africa. We also compare anthropometric and QOL outcomes in those who received rhGH therapy versus those who did not. These findings aim to inform context-specific strategies for comprehensive care in resource-constrained settings.
MATERIAL AND METHODS
Study design and setting
This was a retrospective, observational study conducted at the pediatric endocrinology clinic of Chris Hani Baragwanath Academic Hospital, a tertiary public hospital in Johannesburg, South Africa. Medical records from January 01, 2011, to January 31, 2024, were reviewed.
Participants
All children with a confirmed diagnosis of CP during the study period were included in the analysis. Of the 40 eligible patients, 35 had complete records available for review. Diagnostic confirmation was based on neuroimaging (Magnetic Resonance Imaging [MRI]/computed tomography [CT]) and/or histopathology.
GH treatment details
Patients who received GH replacement were all treated with rhGH in the form of Norditropin® NordiFlex® (somatropin), selected based on availability.
Data collection
Clinical and demographic data were extracted from patient records and entered into REDCap. Variables collected included age at diagnosis, sex, race, presenting symptoms, anthropometry, bone age, imaging findings, surgical history, histopathology, and endocrine function. Endocrine evaluation included thyroid function, insulin-like growth factor 1 (IGF-1) levels, GH stimulation testing when performed, pubertal status, adrenal function, and the presence of diabetes insipidus (DI) or the syndrome of inappropriate antidiuretic hormone secretion (SIADH).
GH deficiency was diagnosed using standard clinical and biochemical criteria. Tumor status was documented through follow-up imaging. GH therapy adherence was assessed using clinical records and clinician or parent-reported compliance. QOL was evaluated using the Pediatric Quality of Life Inventory (PedsQL) version 4.0 (Short Form [SF]-15).
Follow-up and visit schedule
Patients were reviewed at intervals of 3–6 months, with regular assessments of anthropometry, laboratory tests, and imaging. QOL assessments were conducted during routine visits and telephonically.
Statistical analysis
All data were analyzed using Stata version 18. Categorical variables were summarized using frequencies and percentages. Continuous variables were first assessed for normality with the Shapiro–Wilk test. Variables that were normally distributed were reported as means with standard deviations (SDs), while non-normally distributed data were presented as medians with interquartile ranges. Anthropometric measurements were recorded at baseline and at each follow-up visit. Baseline anthropometric data were obtained at the child’s first endocrinology clinic visit after neurosurgical intervention. However, because referral times varied and documentation was inconsistent in retrospective records, the exact interval between surgery and baseline measurement could not be reliably determined across all patients. Z-scores for weight-forage, height-for-age, and weight-for-height were calculated using WHO reference standards, allowing longitudinal assessment of growth patterns. Repeated assessments allowed for longitudinal evaluation of growth trajectories and responses to GH therapy over time. Differences in growth and anthropometric outcomes between GH-treated and untreated groups were assessed using independent t-tests for normally distributed data and Mann–Whitney U-tests for skewed distributions. QOL was assessed using the PedsQL 4.0 SF-15, which includes four domains: Physical, emotional, social, and school functioning. Both patient-reported and parent-proxy scores were transformed to a 0–100 scale, with higher scores indicating better QOL. Comparisons between patient and parent scores were performed using paired t-tests or Wilcoxon signed-rank tests as appropriate. Differences in QOL between intervention groups, including GH therapy, radical surgery, and Ommaya reservoir placement, were evaluated using non-parametric tests due to small group sizes. All statistical analyses were two-tailed, and P < 0.05 was considered statistically significant.
RESULTS
Demographics and baseline characteristics
The cohort comprised 35 Black African children, with a mean age at presentation of 8.03 ± 4.5 years and a male predominance (54.3%). Visual disturbance was the most common presenting symptom (71.4%), followed by seizures (34.3%), neurodevelopmental delay (22.9%), and growth failure (8.6%). Other symptoms included headaches, vomiting, neuro-developmental regression, weakness, and syncope [Table 1].
| Variable | N (%) |
|---|---|
| Age (mean ± SD) | 8.03 ± 4.5 |
| Gender | |
| Male | 19 (54.29) |
| Female | 16 (45.71) |
| Presenting complaints | |
| Seizures | 12 (34.29) |
| Visual symptoms | 25 (71.43) |
| Neurodevelopmental delay | 8 (22.86) |
| Growth failure | 3 (8.57) |
| Other (headaches, vomiting, regression of milestones, weakness, syncope) | 16 (45.71) |
| Anthropometry | |
| Weight Z-score (mean ± SD) | −1.80 ± 2.6 |
| Height Z-score (mean ± SD) | −2.75 ± 1.7 |
| Weight-height Z-score (mean ± SD) | −0.16 ± 2.25 |
| Head circumference (median, IQR) | 53 (50–54) |
| Visual acuity | |
| Normal | 6 (17.14) |
| Abnormal | 29 (82.86) |
| Neurological examination | |
| UMN signs | 12 (34.29) |
| Hemiplegia/hemiparesis/quadriplegia | 7 (20.00) |
| Cranial nerve palsy | 9 (25.71) |
| Normal examination | 10 (28.57) |
| Bone age | |
| Normal | 7 (20.00) |
| Delayed | 27 (77.14) |
| Advanced | 1 (2.86) |
| CT/MRI brain findings | |
| Suprasellar mass | 35 (100) |
| Hydrocephalus | 20 (57.14) |
| Surgical procedures | |
| Ommaya reservoir | 23 (65.71) |
| Radical surgery | 13 (37.14) |
| VP shunt | 19 (54.29) |
| Tumor not amendable to surgery | 1 (2.86) |
| Endocrine and post-operative complications | |
| None | 7 (20.00) |
| Growth hormone deficiency | 27 (77.14) |
| SIADH | 8 (22.86) |
| DI | 13 (37.14) |
| Hypocortisolemia | 9 (25.71) |
| Seizures | 2 (5.71) |
| Visual impairment | 6 (17.14) |
| Central hypothyroidism | 17 (48.57) |
| Intracranial hemorrhage | 2 (5.71) |
| Meningitis | 3 (8.57) |
| Other (Precocious puberty, pneumocephalus, and subdural hematomas) | 2 (5.71) |
| Histological results | |
| No malignant cells/craniopharyngioma | 28 (80.00) |
| None | 5 (14.29) |
| Other (Inconclusive: Diffuse fibrillary astrocytoma) | 2 (5.71) |
SIADH: Syndrome of inappropriate antidiuretic hormone secretion, DI: Diabetes insipidus, VP: Ventriculoperitoneal, CT/MRI: Computed tomography/Magnetic resonance imaging, UMN: Upper motor neuron, IQR: Interquartile range, SD: Standard deviation
Anthropometric assessment revealed a mean height-forage Z-score of −2.75 ± 1.7, and a mean weight-for-height Z-score of −0.16 ± 2.25. These findings indicate that most children in the cohort had short stature. On neurological and visual assessment, 29 patients (82.9%) exhibited impaired visual acuity, whereas 6 patients (17.1%) had normal vision. Neurological examination identified upper motor neuron signs in 12 patients (34.3%), hemiplegia or quadriplegia in 7 patients (20.0%), and cranial nerve palsies in 9 patients (25.7%), while 10 patients (28.6%) had a normal neurological examination [Table 1].
Radiological evaluation confirmed the presence of suprasellar masses consistent with CP in all patients. Hydrocephalus was present in 20 patients (57.1%). Surgical interventions included placement of an Ommaya reservoir in 23 patients (65.7%), radical tumor resection in 13 patients (37.1%), and ventriculoperitoneal shunting in 19 patients (54.3%). One tumor (2.9%) was deemed inoperable. Bone age assessment revealed a delay in 27 patients (77.1%), was normal in 7 patients (20.0%), and advanced in 1 patient (2.9%). Pubertal evaluation demonstrated predominantly prepubertal gonadotropin levels, consistent with the cohort’s mean age. One patient presented with precocious puberty, characterized by markedly elevated estrogen levels, advanced bone age, and ovarian cysts [Table 1].
Endocrine and laboratory findings
Endocrine complications were common in this cohort [Table 2]. GHD was diagnosed in 27 of 35 patients (77.1%) based on anthropometric and biochemical findings. Among the three patients who underwent formal clonidine stimulation testing, all demonstrated a peak GH concentration below 10 ng/mL. Central hypothyroidism was present in 17 patients (48.6%), hypocortisolemia and DI each occurred in 37.1%. SIADH was diagnosed in 22.9%, delayed puberty in 13 (37.1%), and obesity and panhypopituitarism in 14.3% of patients. Histopathological confirmation of CP was available in 28 cases (80%). Five patients did not undergo biopsy, and two were initially reported as inconclusive but were later confirmed as consistent with CP based on imaging and intraoperatively.
| Variables | n (%) |
|---|---|
| Endocrine and metabolic | |
| Panhypopituitarism | 5 (14.29) |
| Central hypothyroidism | 20 (57.14) |
| Delayed puberty | 13 (37.14) |
| Diabetes insipidus | 3 (8.57) |
| GHD | 27 (77.14) |
| Hypocortisolemia | 13 (37.14) |
| Obesity | 5 (14.29) |
| Neurodevelopmental outcome | |
| Normal | 10 (28.57) |
| Severe neurodevlopemental delay | 18 (51.43) |
| Growth outcome | |
| Normal growth | 1 (2.86) |
| Normal growth on GH treatment | 3 (8.57) |
| Poor growth on GH treatment | 7 (20.0) |
| Poor growth without GH treatment | 21 (60.0) |
| Missing data | 3 (8.57) |
| Morbidity outcome | |
| Lost to follow-up. | 14 (40.0) |
| Epilepsy | 7 (20.0) |
| Hearing impairment | 1 (2.86) |
| Vision impairment | 8 (22.86) |
| Paraplegia/hemiplegia | 5 (14.29) |
| Mortality | |
| Died | 2 (5.71) |
| Alive | 33 (94.2) |
GHD: Growth hormone deficiency, GH: Growth hormone
GH treatment patterns and compliance
Ten patients (28.6%) received rhGH therapy. The most common reason for non-initiation was loss to follow-up (40%), followed by normal growth parameters, residual tumor, severe impairment, or parental refusal. GH therapy was well tolerated, with no tumor recurrence temporally associated with treatment. Adherence data were inconsistently documented [Figure 1].
- (a) Growth Hormone treatment status: 10 out of the 35 patients were treated with rhGH, visit documentation revealed inconsistent reporting of drug administration or missed follow-ups, complicating analysis of adherence and growth response. (b) Reasons for not initiating rGH treatment. The majority of patients were lost to follow up.
Follow-up imaging, surgical outcomes, and complications
Among the 27 patients with available imaging follow-up data, a total of 192 MRI scans were reviewed, corresponding to an average of 10 clinic visits per patient. Imaging outcomes indicated that 80.7% of patients had no evidence of tumor recurrence, while 13.0% had residual tumor. Hydrocephalus was identified in 2.6% of scans, and 4.2% were reported as normal. Repeat surgery was required in 6 patients (22.2%), primarily due to cyst recurrence or persistent hydrocephalus.
Post-operative complications were evaluated in 24 patients over 169 clinic visits [Table 2]. Most patients (86.4%) experienced no complications. DI was observed in 10.7% of patients, central hypothyroidism in 11.8%, SIADH in 4.2%, and hypocortisolemia in 4.7%. Neurodevelopmental outcomes were documented in 28 patients. Of these, 10 children (28.6%) demonstrated normal development, whereas 18 patients (51.4%) exhibited severe neurodevelopmental delay. Delays were assessed clinically during routine follow-up visits by pediatricians using standard age-appropriate developmental milestones.
Growth outcomes and anthropometric trends
Anthropometric data were analyzed over ten clinical visits. Graph 2 illustrates longitudinal trends in z-scores for weight-for-age, height-for-age, and weight-for-height. Weight-for-height z-scores remained close to the normative reference (z ≈ 0), while both weight-for-age and height-for-age scores consistently tracked below average, indicating linear growth and weight gain failure in most patients [Figure 2].
- Anthropometric trends over 10 follow-up visits.
When we compared the anthropometric outcomes between the GH-treated group (n = 10) and untreated patients (n = 25). The patients who received rhGH therapy (n = 10) demonstrated higher mean height-for-age z-scores (−1.58) compared to untreated patients (−2.47), with this difference reaching statistical significance (P = 0.00064). Similarly, weight-for-age z-scores were significantly higher in the treatment group (mean: −1.12 vs. −1.85; P = 0.00027). However, weight-for-height z-scores were similar between groups (−0.03 vs. −0.22; P = 0.01575), suggesting proportionality of weight to height was preserved.
Only 3 patients on GH therapy (8.57% of the total cohort) were formally diagnosed with GHD using clonidine stimulation testing. The remaining seven patients were initiated on therapy based on clinical and biochemical indicators, such as subnormal IGF-1 levels and growth failure, without formal stimulation testing. Among the GH-treated group, 3 patients (30%) attained normal growth (height-for-age z-score > −2), while 7 (70%) continued to demonstrate growth faltering despite therapy. Of the untreated group, only 1 patient (2.86%) achieved normal growth. In total, 21 patients (60%) who did not receive GH therapy had persistently poor growth (z-scores < −2).
Compliance data were inconsistently documented. Adherence could only be evaluated in 24 patients (68.57%), of whom 50% demonstrated moderate to good adherence. However, compliance information was missing for 11 patients (31.43%), limiting definitive conclusions regarding the effectiveness of therapy.
QOL results
QOL was assessed using the PedsQL 4.0 short form tool. The assessment was conducted prospectively during routine clinic visits and telephonically. Data were available for 30 of the 35 patients [Table 3]. Mean total QOL scores were low across the cohort, with patient-reported scores averaging 32.8 (SD: 12.2) and parent-reported scores averaging 36.7 (SD: 12.8). These scores fall within the “Poor” category based on established cutoffs. Emotional (mean: 22.3) and social domains (mean: 21.7) had the lowest scores, reflecting substantial psychological and social challenges.
| Domain | Patient | Parent | t/z | P-value | QoL category |
|---|---|---|---|---|---|
| Physical | |||||
| Mean (SD) | 28.9 (12.0) | 29.1 (11.5) | −0.04 | 0.967 | Poor |
| Median (IQR) | 30 (22–38) | 32 (21–40) | −0.10 | 0.305 | |
| Emotional | |||||
| Mean (SD) | 22.3 (7.1) | 23.8 (6.6) | −1.48 | 0.160 | Very Poor |
| Median (IQR) | 20 (18–25) | 23 (20–25) | −1.56 | 0.119 | |
| Social | |||||
| Mean (SD) | 21.69 (15.5) | 22.9 (19.0) | −0.178 | 0.861 | Very poor |
| Median (IQR) | 20 (10–30) | 16.5 (10–28.5) | −0.454 | 0.650 | |
| School | |||||
| Mean (SD) | 27.19 (11.9) | 34.63 (13.2) | −2.19 | 0.045 | Poor |
| Median (IQR) | 30 (20–38) | 40 (30–40) | −3.075 | 0.002 | |
| Total | |||||
| Mean (SD) | 32.8 (12.2) | 36.7 (12.8) | −4.22 | 0.0006 | Poor |
| Median (IQR) | 35 (25–42) | 40 (31–43) | −3.09 | 0.002 | |
IQR: Interquartile range, SD: Standard deviation. The bold values showing P< 0.05 was considered statistically significant.
When comparing GH-treated (n = 10) and untreated patients (n = 25), there was no statistically significant difference in overall QOL (patient-reported P = 0.2519; parent-reported P = 0.1473). Mean scores were slightly lower in the GH-treated group across all domains, but this difference was not significant and may reflect underlying disease severity or treatment burden (e.g., injections, frequent follow-ups), rather than a direct effect of GH.
Table 4 summarizes QOL comparisons across other interventions. Notably, radical tumor resection was significantly associated with higher QOL (P = 0.0029), while patients with Ommaya reservoir placement had significantly lower scores (P = 0.0156). The comparison between patient and parent responses showed broad alignment in physical and emotional domains, though parents tended to rate school-related QOL more favorably than patients (P = 0.002), possibly reflecting differing perceptions of functioning.
| Intervention | Higher QOL score? | P-value | Interpretation |
|---|---|---|---|
| GH treatment | No | 0.2519 | No significant impact |
| Ommaya reservoir | No | 0.0156 | Lower QOL in those with a reservoir |
| Radical surgery | Yes | 0.0029 | Significantly improved QOL |
| VP shunt | No | 0.242 | No significant impact |
QOL: Quality of life, VP: Ventriculoperitoneal, GH: Growth hormone, VP: Ventriculoperitoneal. P < 0.05 was considered statistically significant.
A secondary analysis examined whether BMI was associated with patient- or parent-reported QOL. Among the 17 patients with complete anthropometric and QOL data, there was no evidence of a meaningful association between BMI and patient-reported QOL (Spearman ρ = 0.08, P = 0.76; 95% CI −0.42–0.54). Parent-reported QOL showed a weak, non-significant positive trend (Spearman ρ = 0.36, P = 0.15; 95% CI −0.14–0.72).
DISCUSSION
This study aimed to describe the clinical and endocrine characteristics, treatment patterns, and QOL outcomes in pediatric patients with CP at a tertiary hospital in South Africa. Although GH therapy was a focus, only a small subset of patients received treatment. Consequently, definitive conclusions regarding the efficacy of GH therapy in improving growth or QOL are limited by sample size and heterogeneity in diagnostic and treatment practices.
Endocrine dysfunction was common, with 77% of patients meeting clinical criteria for GH deficiency, and nearly half requiring thyroid hormone replacement. The high prevalence of endocrine dysfunction, particularly GHD (77%) and hypothyroidism (57.14%), aligns with extensive literature emphasizing the frequent hypothalamic-pituitary axis involvement in PCP.[3,10] GH therapy was underutilized, often initiated late (mean age 12.8 years), and hindered by loss to follow-up, incomplete documentation, and low adherence. The mean age of GH therapy initiation (12.8 ± 4.2 years) highlights a significant treatment delay, often due to prolonged neurosurgical recovery, delayed endocrine referral, or challenges in accessing rhGH supply. This delay likely contributed to the limited catch-up growth observed and underscores the need for earlier endocrine re-evaluation post-surgery. Among treated patients, only 30% achieved normal growth. This highlights the multifactorial barriers to effective GH therapy in resource-constrained environments. In contrast to international data, where post-operative obesity affects approximately 40–75% of children with CP and 12–19% are obese at diagnosis, only 14% of patients in our cohort were classified as obese.[11] This lower prevalence may reflect under-detection or incomplete documentation of weight gain over time. Another possibility is that most of our patients had hypothalamus-sparing surgery, and similar to a cohort described by Elowe-Gruau et al., they had lower rates of obesity.[12]
Importantly, GH therapy did not significantly influence QOL outcomes, as assessed by the PedsQL tool. Children receiving GH reported slightly lower scores across most domains compared to untreated peers, though these differences were not statistically significant. Instead, surgical outcomes had a clearer relationship with QOL: patients who underwent radical tumor resection reported significantly better QOL than those with more invasive disease requiring procedures such as Ommaya reservoir placement. This suggests that overall disease burden and tumor control may be more influential determinants of QOL than endocrine replacement alone. Among the 17 patients with complete anthropometric and QOL data, there was no evidence of a meaningful association between BMI and patient-reported QOL. The wide confidence intervals for both correlations reflect the small sample size and substantial uncertainty around the true effect.
This study contributes novel epidemiological data on CP in a LMIC context, where resource limitations impact diagnostic evaluation, treatment adherence, and long-term follow-up. While the endocrine sequelae of CP are well documented in international literature, this study adds insight into the implementation challenges of GH therapy in a public sector African setting and emphasizes the need for structured protocols, early intervention, and improved tracking systems.
Several limitations must be acknowledged. The retrospective design introduces potential for missing or incomplete data. Only a minority of patients underwent formal GH stimulation testing, limiting diagnostic accuracy. The timing of baseline anthropometry relative to surgery could not be consistently determined from retrospective records, which may have introduced variability in growth status at the initial assessment. QOL assessments were not available for all participants and were not controlled for socioeconomic or educational status. The study was also not powered to assess the effect of GH therapy due to the small number of treated patients and the variability in their underlying clinical characteristics. In addition, associations between QOL and treatment modality were exploratory and not adjusted for confounding variables such as residual tumor, neurodevelopmental status, or socioeconomic factors.
Nonetheless, the findings underscore the importance of comprehensive, multidisciplinary care for children with CP. Improving early diagnosis, streamlining endocrine assessment, and ensuring continuity of care through enhanced follow-up mechanisms are critical steps. While GH therapy may offer benefits, its implementation must be supported by systems that enable timely diagnosis, monitoring, and adherence.
CONCLUSION
This study provides important context-specific insights into the clinical course, endocrine complications, and treatment challenges faced by pediatric patients with CP in a resource-limited setting. GH therapy was associated with modest improvements in linear growth among a small subset of patients, but its overall impact on QOL was not statistically significant. Delayed initiation limited diagnostic confirmation, poor adherence, and systemic barriers all contributed to these outcomes.
More consistently, surgical outcomes – particularly radical tumor resection – were linked to improved QOL scores, suggesting that overall disease burden and surgical morbidity play a more critical role in shaping long-term well-being than endocrine therapy alone. These findings highlight the complexity of managing CP and the need for holistic, multidisciplinary strategies that integrate endocrine, surgical, and psychosocial care.
Future research should focus on prospective studies with standardized GH initiation protocols, robust adherence tracking, and larger sample sizes to better define the role of GH therapy in this population.
Authors contributions:
NM: Conceptualization, data collection, formal analysis, and drafting of the manuscript. FM: Database and drafting the protocol. KT: Database, statistical assistance, and drafting the protocol.
Ethical approval:
The research/study approved by the Institutional Review Board at University of the Witwatersrand, number M240355M240618A0001, dated June 18, 2024.
Declaration of patient consent:
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Conflicts of interest:
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that they have used artificial intelligence (AI)-assisted technology for assisting in editing the grammar of the manuscript and generating Figure 2.
Financial support and sponsorship: This study received partial funding from the Society for Endocrinology, Metabolism, and Diabetes of South Africa (SEMDSA) and Novo Nordisk. The funders had no role in study design, data collection, analysis, interpretation of results, or manuscript preparation.
References
- The 2016 world health organization classification of tumors of the central nervous system: a summary. Acta Neuropathol. 2016;131:803-20.
- [CrossRef] [PubMed] [Google Scholar]
- CBTRUS statistical report: primary brain and other central nervous system tumors diagnosed in the United States in 2011-2015. Neuro Oncol. 2018;20(Suppl 4):iv1-86.
- [CrossRef] [PubMed] [Google Scholar]
- Childhood-onset craniopharyngioma. J Clin Endocrinol Metab. 2021;106:e3820-36.
- [CrossRef] [PubMed] [Google Scholar]
- Childhood craniopharyngioma-changes of treatment strategies in the trials KRANIOPHARYNGEOM 2000/2007. Klin Padiatr. 2014;226:161-8.
- [CrossRef] [PubMed] [Google Scholar]
- Predictive factors for pediatric craniopharyngioma recurrence: an extensive narrative review. Diagnostics (Basel). 2023;13:1588.
- [CrossRef] [PubMed] [Google Scholar]
- Minimally-invasive endoscopic-assisted sinus augmentation. J Craniofac Surg. 2019;30:e359-62.
- [CrossRef] [PubMed] [Google Scholar]
- Reply to: Understanding treatment options in craniopharyngioma better. Nat Rev Dis Primers. 2020;6:27.
- [CrossRef] [PubMed] [Google Scholar]
- Safety of growth hormone replacement in survivors of cancer and intracranial and pituitary tumours: a consensus statement. Eur J Endocrinol. 2022;186:P35-52.
- [Google Scholar]
- National UK guidelines for the management of paediatric craniopharyngioma. lancet diabetes endocrinol. 2023;11:694-706.
- [CrossRef] [PubMed] [Google Scholar]
- Differential diagnosis of suprasellar tumors in children. Klin Padiatr. 2004;216:323-30.
- [CrossRef] [PubMed] [Google Scholar]
- Long-term weight gain in children with craniopharyngioma. Eur J Endocrinol. 2024;190:363-73.
- [CrossRef] [PubMed] [Google Scholar]
- Childhood craniopharyngioma: hypothalamus-sparing surgery decreases the risk of obesity. J Clin Endocrinol Metab. 2013;98:2376-82.
- [CrossRef] [PubMed] [Google Scholar]