CASE REPORT
Indonesia Journal of Biomedical Science (IJBS) 2026.
Volume 20.
Number 1: 1-7 P-ISSN.
E-ISSN.
Published by Indonesia Journal of Biomedical Science Neurocutaneous melanosis with giant congenital melanocytic nevus: a case report Made Cynthia Mahardika Putri1*.
I Gusti Ngurah Made Suwarba1.
Dewi Sutriani Mahalini1.
I Gusti Ngurah Agung Jayadhi Widyakusuma1
ABSTRACT
Background: Congenital melanocytic nevus syndrome is a rare neurocutaneous disorder characterized by congenital melanocytic nevus with extracutaneous involvement, most commonly neurocutaneous melanosis (NCM).
Symptomatic NCM usually presents early in life with seizures, hydrocephalus, or developmental delay, and carries a poor prognosis.
This study aimed to present a unique case of NCM in a child with giant congenital melanocytic nevus accompanied by a DandyAeWalker variant and unusual multisystem involvement.
Case presentation: We report a 5-year-old girl with a giant congenital melanocytic nevus who presented with status epilepticus.
Brain magnetic resonance imaging (MRI) revealed hyperintense lesions in both amygdalae and the left pons consistent with NCM, accompanied by a DandyAeWalker variant.
Skin biopsy confirmed congenital melanocytic nevi (CMN).
Systemic evaluation demonstrated pancytopenia, chronic kidney disease stage V, and hypoparathyroidism with vitamin D deficiency.
The patient was managed with intravenous and oral antiepileptic drugs, electrolyte correction, packed red cell transfusion, vitamin D supplementation, and multidisciplinary Conclusion: This case illustrates a rare presentation of neuricur with seizures at the age of five, multifocal NCM, and multisystem involvement.
Prognosis remains poor in multifocal disease where surgical intervention is not feasible, emphasizing the importance of optimal medical therapy, systemic correction, and long-term multidisciplinary management to improve quality of life.
Department of Pediatrics and Child Health.
Faculty of Medicine Udayana University/Prof.
Ngoerah Hospital.
Denpasar/Bali.
Indonesia *Corresponding author:
Made Cynthia Mahardika Putri.
Department of Pediatrics and Child Health.
Faculty of Medicine Udayana University/Prof.
Ngoerah Hospital.
Denpasar/Bali.
Indonesia.
cynthiamahardika22@gmail.
Received: 2025-11-26 Accepted: 2026-01-16 Published: 2026-02-23 Keywords: congenital melanocytic nevus.
DandyAeWalker variant, neurocutaneous melanosis, pediatric neurology, status epilepticus.
Cite this Article: Putri.
Suwarba.
Mahalini.
Widyakusuma.
Neurocutaneous melanosis with giant congenital melanocytic nevus: a case report.
IJBS 20.
: 1-7.
DOI: 10.
15562/ijbs.
INTRODUCTION
Neurocutaneous characterized by abnormal proliferation of melanocytes in the skin and central nervous system.
Its pathogenesis is thought to be related to disturbances in neural crest development during early Normally, melanocyte precursor cells migrate from the neural crest to the skin, leptomeninges, and other However, in NCM, dysregulated proliferation or differentiation of melanocytes occurs during this migration, leading to abnormal melanocytic accumulation in the skin as congenital melanocytic nevi and in the leptomeninges or brain parenchyma.
Melanocytic infiltration of the leptomeninges may disrupt cerebrospinal fluid circulation, causing hydrocephalus and, in some cases, malignant transformation into melanoma.
Genetic factors, such as somatic mutations in neuroblastoma RAS viral oncogene homolog (NRAS) or B-Raf proto-oncogen (BRAF), have also been reported to trigger abnormal melanocytic proliferation, explaining the link between cutaneous and neurological manifestations.
6 This mechanism indicates that NCM is not merely a cutaneous disorder, but rather a systemic condition originating from aberrant neural crest development.
Clinical manifestations of NCM typically appear in infancy or early childhood, usually before the age of two years, and include seizures, hydrocephalus, signs of raised intracranial pressure, and developmental delay.
7,8 The prognosis is generally poor once neurological Open access:
http://ijbs-udayana.
Published by Indonesia Journal of Biomedical Science | IJBS 2026.
: 1-7 | doi: 10.
15562/ijbs.
Congenital melanocytic nevus syndrome is a rare neurocutaneous disorder defined by the presence of congenital melanocytic nevi (CMN) associated with extracutaneous involvement, most commonly neurocutaneous melanosis (NCM).
1,2 Congenital melanocytic nevi are pigmented lesions present at birth, arising from nevomelanocytes of neural crest origin.
Based on projected adult size, they are classified into small (<1.
5 c.
, medium .
5Ae20 c.
, and large/giant (>20 c.
3 The incidence of congenital melanocytic nevi is approximately 1% of newborns, while giant CMN occurs in only 1:20,000 to 1:500,000 live births.
NCM is even rarer, reported in 2Ae3% of patients with large or giant CMN.
CASE REPORT
symptoms develop, with many patients deteriorating within two to three years due to intractable epilepsy, hydrocephalus, or malignant transformation.
Diagnostic criteria for NCM were first proposed by Fox in 1972, requiring the presence of a large or multiple CMN with meningeal melanosis or melanoma, in the absence of cutaneous melanoma or other primary CNS melanoma.
Advances in MRI have improved early detection, particularly when T1-weighted hyperintensities are identified in the amygdala, hippocampus, or brainstem, which are known epileptogenic regions.
Additional structural malformations, such as the DandyAeWalker complex, may coexist and further worsen neurological Although congenital melanocytic nevus syndrome is primarily considered a cutaneous and neurological disorder, rare reports describe associations with hematologic, renal, endocrine, and musculoskeletal abnormalities, suggesting a broader systemic spectrum linked to neural crest-derived tissues.
13 This case
is unique because status epilepticus was the initial neurological presentation of NCM in a child with giant congenital melanocytic nevus, accompanied by a DandyAeWalker variant and unusual multisystem involvement, expanding the known clinical spectrum of this rare
CASE REPORT
Figure 1.
The skin lesions in patient with (NCM) melanocytic nevus (CMN) Figure 3.
The Dermoscopic Findings Figure 2.
Nevus was scattered discretely or in groups, and some with fine hair on them.
A 5-year-old girl was referred to the Emergency Department of Prof.
Dr.
G Ngoerah Hospital due to a prolonged The event was characterized by focal tonicAeclonic movements involving the left upper and lower extremities with associated upward eye deviation.
The seizure lasted for approximately 30 minutes and was accompanied by loss of consciousness, consistent with status Upon arrival, the patient was unresponsive to verbal and painful stimuli.
She had received diazepam suppository and intravenous phenobarbital prior to referral, with partial improvement.
Stabilization was continued in the ED, after which she was admitted to the pediatric high care unit for further monitoring and The child is the third of four siblings, all born to healthy, non-consanguineous Both older and younger siblings are healthy with no similar medical conditions reported.
She was delivered by cesarean section at term with a birth weight of 3200 gram and a length of 49 cm.
No history of birth asphyxia or perinatal complications was reported.
She had achieved normal developmental milestones until the onset of illness.
Immunizations were up to date according to the national schedule.
There was no family history of similar skin lesions, seizures, or neurological disorders.
Since birth, the patient had extensive blackish-brown pigmented skin lesions involving the trunk, extremities, and scalp.
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which progressively increased in number and extent with age.
Atrophy of the left foot has also been noted since infancy.
There was no history of trauma, bleeding, or infection associated with the lesions.
On examination, the patient appeared pale but was conscious and interactive after stabilization of the seizure.
Anthropometric measurements showed a weight of 13 kg and height of 99 cm, corresponding to mild malnutrition.
Head circumference was 49 cm, within normal limits for age.
Vital signs were Neurological examination revealed normal muscle tone and no focal deficits after seizure resolution.
Fundoscopic examination showed no papilledema.
CASE REPORT
Dermatological well-demarcated hyperpigmented macules and patches ranging in size from 0.
3 y 0.
8 cm to 22 y 10 cm, some associated with fine hair growth, diffusely distributed across the A large hyperpigmented plaque measuring approximately 22 y 10 cm extended from the left knee to the ankle, with overlying hypertrichosis, consistent with a giant CMN.
Smaller satellite lesions were scattered over both dorsal feet and the No ulceration or signs of secondary infection were observed (Figure 1 and Dermoscopic findings are shown in Figure 3.
Laboratory investigations revealed pancytopenia with hemoglobin 6.
5 g/dL, 37 y 10A/AAL, and platelets 108 y 10A/AAL.
Peripheral blood smear anemia with leukopenia .
and thrombocytopenia, consistent with Electrolyte profile showed hyponatremia .
mmol/L) and severe hypocalcemia .
4 mg/dL).
Renal function tests demonstrated markedly elevated BUN .
5 mg/dL) and serum creatinine .
02 mg/dL), consistent with chronic kidney disease (CKD) stage V.
Endocrine profile revealed a markedly suppressed intact parathyroid hormone (PTH) level .
578 pg/mL, reference 9Ae59 pg/mL), confirming hypoparathyroidism, and vitamin D deficiency .
ng/mL).
Neuroimaging with brain MRI revealed hyperintense T1 lesions in the bilateral amygdala and left pons, consistent with (NCM).
Additional findings included a DandyAe Walker variant and multiple soft-tissue nodules of the scalp involving connective Figure 5.
tissue, aponeurosis, and periosteum (Figure 4A, 4B, 5, and .
Histopathological examination of the skin biopsy demonstrated nests and cords of nevus cells extending into the deep dermis with infiltration around adnexal structures such as hair follicles, sebaceous glands, and arrector pili muscles.
The nevus cells appeared small, round to oval, with uniform nuclei and finely pigmented No nuclear atypia, mitotic Figure 4.
Sagittal T1-weighted MRI demonstrates a posterior fossa cyst with hypoplasia of the cerebellar vermis .
, consistent with a DandyAeWalker variant.
activity, or necrosis was observed.
These features were consistent with a congenital melanocytic nevus.
The patient was managed acutely with intravenous antiepileptic drugs .
henobarbital and phenytoi.
and supportive therapy.
Electrolyte correction was provided with intravenous calcium gluconate, and packed red cell transfusions were administered to address anemia.
She was subsequently maintained on oral Brain MRI findings of neurocutaneous melanosis.
(A) Axial T1-weighted MRI shows hyperintense lesions in the left pons and cerebellum .
, consistent with parenchymal involvement of neurocutaneous melanosis.
(B) Axial and coronal T1-weighted MRI demonstrates bilateral hyperintense lesions in the amygdala .
, a typical feature of neurocutaneous melanosis and a potential epileptogenic focus associated with recurrent seizures.
Figure 6.
Sagittal post-contrast MRI reveals multiple soft tissue nodules in the scalp involving the right frontal, parietal, and left occipital regions .
, consistent with extracranial involvement of congenital melanocytic nevus.
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CASE REPORT
phenytoin for seizure prophylaxis and vitamin D supplementation.
During were successfully controlled with intravenous antiepileptic drugs and metabolic correction.
The patient experienced one brief seizure during hemodialysis, which improved after acute therapy, and was subsequently discharged on oral phenytoin and vitamin D supplementation.
In the postdischarge period, the patient remained seizure-free of antiepileptic medication.
However, chronic kidney disease stage V persisted, accompanied by hypoparathyroidism and severe vitamin D deficiency, which were managed with supplementation.
On longterm follow-up, the patient continued regular hemodialysis twice weekly.
She remains under multidisciplinary followup, focusing on seizure prevention, metabolic stabilization, and quality-of-life This case highlights a rare presentation of neurocutaneous melanosis associated with a giant congenital melanocytic nevus and a DandyAeWalker variant, further complicated by multisystem involvement including chronic kidney disease, pancytopenia, and endocrine Such a constellation of findings underscores the broad clinical spectrum of congenital melanocytic nevus syndrome and the importance of multidisciplinary management for optimizing long-term outcomes.
DISCUSSION
Congenital melanocytic nevus syndrome is a rare condition characterized by the presence of multiple or large congenital melanocytic nevi with extracutaneous involvement, most notably (NCM).
Congenital melanocytic nevus occurs in approximately 1% of newborns, while giant congenital melanocytic nevus is much rarer, with an estimated incidence of only 1:20,000 to 1:500,000 live births.
In general, congenital melanocytic nevus is classified as small (<1.
5 c.
, medium .
5Ae20 c.
, and large/giant (>20 c.
Compared to small or medium, giant CMN carries a higher risk of serious transformation into melanoma and central nervous system involvement through NCM.
4,5 These lesions originate from neural crest melanoblasts, and abnormal migration of these cells into the central nervous system leads to NCM.
Magnetic resonance imaging (MRI) is the primary diagnostic tool, with melanin typically appearing hyperintense on T1weighted sequences, most often affecting the amygdala, temporal lobes, cerebellum, and brainstem.
6,7 Furthermore, congenital melanocytic nevus syndrome may be associated with other neurodevelopmental anomalies, such as DandyAeWalker malformation, characterized by cerebellar vermis hypoplasia, fourth ventricle dilatation, and enlargement of the posterior fossa.
8 The association between NCM and DandyAeWalker malformation (DWM) is extremely rare, occurring in only about 10% of NCM patients.
Most reported cases present during the neonatal or infantile period, with poor prognosis and high mortality.
For instance.
Lookzadeh et al.
described a neonatal case with NCM and DandyAeWalker complex that rapidly progressed to severe neurological complications.
14 In this case, a 5-year-old girl presented with a giant congenital melanocytic nevus measuring 22 y 10 cm on the lower extremity with numerous satellite lesions across the body, fulfilling the criteria for giant CMN.
MRI of the brain demonstrated T1 hyperintense lesions in both amygdalae and the left pons, consistent with NCM, accompanied by a DandyAeWalker variant.
The coexistence of CMN, multifocal NCM, and structural CNS malformation is exceedingly rare and underscores the complexity of neurological involvement in this patient.
Moreover, our case is unique because neurological symptoms manifested only at the age of five years in the form of status epilepticus, much later than the majority of reported cases.
The development of neurocutaneous melanosis (NCM) and DandyAeWalker variant (DWV) can be traced back to Melanocytes, which later contribute to the formation of congenital melanocytic nevi, originate from neural crest cells, whereas posterior fossa structures, including the cerebellar vermis and fourth ventricle, derive from the hindbrain during closely overlapping periods of organogenesis.
Under normal conditions, these processes occur in a synchronized and coordinated manner.
However, when disturbances such as somatic mutations in the NRAS or BRAF genes arise, melanocyte proliferation may become dysregulated while simultaneously disrupting signaling mechanisms essential for the development of posterior brain This combined defect may lead to the accumulation of abnormal melanocytes in the leptomeninges or brain parenchyma (NCM), as well as morphological anomalies of the posterior fossa characteristic of DWV.
Thus, the coexistence of NCM and DWV is not coincidental but rather reflects overlapping embryogenic abnormalities, explaining why these conditions may occur together in a small subset of patients.
2,7,8 In this case, sagittal T1-weighted MRI revealed a posterior fossa cyst with partial hypoplasia of the cerebellar vermis, consistent with a DandyAeWalker variant.
Pathophysiologically, malformation disrupts the normal development of the fourth ventricle and posterior fossa, resulting in cystic dilatation and impaired cerebrospinal fluid (CSF) circulation.
On the other hand, neurocutaneous melanosis contributes through melanocytic infiltration of the leptomeninges in the posterior fossa.
This infiltration thickens the leptomeninges.
CSF obstruction and interfering with local neural tissue development.
These dual mechanisms CSF circulation impairment due to DWV and meningeal burden from melanocytic infiltration in NCM act synergistically to increase the risk of hydrocephalus, elevated intracranial pressure, and cortical hyperexcitability.
Such a pathophysiological process may account for the late-onset seizures observed in our patient, particularly as the amygdala and brainstem, which are commonly involved in NCM, are highly susceptible to becoming secondary epileptogenic foci.
Histopathological essential to differentiate CMN from CMN is characterized by nests of nevus cells extending into the dermis and subcutaneous tissue, often involving Published by Indonesia Journal of Biomedical Science | IJBS 2026.
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CASE REPORT
adnexal structures, but lacking atypia or mitotic activity.
15,16 In this case, skin biopsy confirmed a diagnosis of benign congenital melanocytic nevus without evidence of malignancy, supporting the interpretation that neurological manifestations were due to benign melanocytic infiltration of the CNS rather than malignant transformation.
Seizures are the most common neurological manifestation of NCM, reported in 50Ae70% of symptomatic Amygdala is highly epileptogenic and strongly associated with recurrent or refractory 6 Structural abnormalities such as the DandyAeWalker variant may further exacerbate epileptogenesis by disrupting cerebrospinal fluid dynamics and cortical excitability.
8 Beyond structural substrates, metabolic disturbances such as hyponatremia and hypocalcemia can further lower the seizure threshold and trigger prolonged convulsions.
17-19 In most reports, neurological manifestations of NCM occur within the first two years of life, typically presenting as seizures or signs of increased intracranial pressure.
In contrast, this patient developed neurological symptoms at the age of five years, which is considerably later than commonly reported.
This underscores the importance of long-term neurological surveillance in children with giant CMN, even in the absence of early symptoms.
She presented with status epilepticus requiring benzodiazepines and barbiturates.
Lesions in the amygdala and pons provided clear epileptogenic substrates, the DandyAeWalker variant increased seizure susceptibility, and severe hyponatremia .
mmol/L) together with hypocalcemia .
4 mg/dL) acted as additional triggers, resulting in a multifactorial etiology of One of the most frequently reported associations of neurocutaneous melanosis (NCM) is with the DandyAeWalker complex, which was also present in our The coexistence of this additional malformation has been recognized as a poor prognostic factor, as it increases the risk of symptomatic NCM.
Interestingly, the literature also describes rare and unusual associations with NCM, such as type 1 diabetes mellitus that resolved following treatment of CNS melanoma.
HirschsprungAos disease in a neonate, and acute disseminated encephalomyelitis (ADEM) in a child.
These reports reinforce the understanding that NCM represents a wide clinical spectrum and may involve multiple organ systems, depending on the extent and direction of abnormal neural crest cell migration.
13,14
This is consistent with our case, in which the combination of multifocal NCM, a DandyAeWalker variant, and multisystem involvement highlighted the extreme clinical complexity.
Hematologically, the patient presented with pancytopenia (Hb 6.
5 g/dL, leukocytes 3.
37 y10A/ AAL, platelets 108 y10A/AAL), most likely related to chronic disease and end-stage CKD.
This condition reduced cerebral oxygenation due to anemia and increased bleeding risk from thrombocytopenia, both of which exacerbated seizures.
Renally, stage V CKD (BUN 168.
5 mg/ 02 mg/dL) resulted in severe uremia and electrolyte imbalance, conditions known to lower neuronal membrane stability and promote seizures.
Endocrinologically, the patient exhibited an unusual profileAihypoparathyroidism with low PTH levels, in contrast to the secondary hyperparathyroidism typically seen in advanced CKD.
Together with severe vitamin D deficiency .
ng/mL), this further aggravated hypocalcemia, enhancing neuronal excitability and lowering the seizure threshold.
Therefore, in this patient, seizures were not only driven by epileptogenic substrates from NCM and the DandyAeWalker variant but were also compounded by hematological, renal, and endocrine dysfunction.
The convergence of these multisystem abnormalities rendered status epilepticus multifactorial and significantly worsened the prognosis.
The management of neurocutaneous melanosis (NCM) is essentially supportive, as no definitive curative therapy currently Several therapeutic approaches have been reported in the literature, although outcomes remain variable.
Surgical resection of intracranial or parenchymal lesions may be considered when the lesions are localized, operable, and cause significant mass effect.
such indications are rare.
20 In patients with hydrocephalus, placement of a ventriculoperitoneal shunt can reduce intracranial pressure and improve neurological symptoms.
21 More recently, the potential role of targeted molecular therapy has been highlighted, particularly in patients with somatic NRAS or BRAF Mitogen-activated protein kinase (MEK) and B-Raf proto-oncogen (BRAF) inhibitors, such as trametinib and dabrafenib, have been anecdotally reported to provide clinical responses in cases of leptomeningeal melanocytosis harboring NRAS mutations.
22,23 In and chemotherapy have generally demonstrated little long-term benefit and are not recommended as standard 24 Therefore, the management of NCM remains focused on seizure control, correction of metabolic disturbances, and long-term multidisciplinary follow-up aimed at maintaining the patientAos quality of life.
In this patient, acute seizures were managed with intravenous antiepileptic drugs .
henobarbital and phenytoi.
, followed by oral phenytoin as prophylaxis.
Electrolyte disturbances particularly severe hypocalcemia and hyponatremia were corrected with intravenous calcium gluconate and vitamin D supplementation, in accordance with the presence of hypoparathyroidism and severe vitamin D Anemia and pancytopenia were managed with packed red cell transfusions under hematology supervision.
Chronic kidney disease stage V required regular hemodialysis twice weekly, accompanied by strict fluid and electrolyte management.
Given the multifocal distribution of NCM lesions .
ilateral amygdala and pon.
, epilepsy surgery was not feasible.
Seizure control was therefore focused on optimization of medical therapy and metabolic stabilization.
The prognosis of symptomatic (NCM) is generally poor, with most patients experiencing neurological deterioration within three years of symptom onset.
Recurrent and refractory seizures are the main determinants of morbidity and mortality, and to date, no curative therapy is available.
Management therefore focuses on supportive approaches, including seizure control, correction of Published by Indonesia Journal of Biomedical Science | IJBS 2026.
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CASE REPORT
FUNDING
metabolic disturbances, and long-term To describe prognostic factors and therapeutic options in epilepsy associated with neurocutaneous melanosis (NCM), the distribution pattern of parenchymal melanosis is the strongest predictor of epilepsy outcomes in NCM Patients with isolated amygdala involvement have a higher likelihood of achieving seizure control, even seizure freedom, making epilepsy surgery a potential option.
In contrast, multifocal lesions significantly increase the risk of drug-resistant epilepsy, and surgical intervention is usually not beneficial due to the absence of a single resectable 25 In relation to our patient a 5-yearold girl with bilateral amygdala and pontine involvement, presenting with status epilepticus, chronic kidney disease stage V, hypoparathyroidism, vitamin D deficiency, and pancytopenia these findings support that epilepsy surgery is not a realistic option given the multifocal lesion pattern.
The best strategy is to optimize medical therapy .
ntiepileptic drug.
, correct metabolic abnormalities, and provide multidisciplinary care.
This approach aligns with the evidence from Pellino et al.
25 which emphasizes that failure to control seizures is strongly associated with worse long-term neurological and cognitive outcomes.
Routine MRI screening in patients with CMN remains controversial.
The prevalence of neurological involvement is approximately 6Ae7%, with developmental delay and seizures being the most common clinical manifestations, while CNS melanocytosis and hydrocephalus were the most frequent MRI findings.
6 However, current evidence was deemed insufficient to support strong recommendations for routine MRI in all CMN patients, as its clinical benefits remain uncertain.
The authors therefore emphasized the need for standardized study protocols and largescale, multi-center prospective research to clarify the role of MRI in long-term For the time being, clinical centers are advised to determine their own policies by weighing the advantages and disadvantages of MRI screening, although MRI remains recommended whenever new neurological signs or symptoms appear.
Our present case where neurological manifestations only emerged at the age of five further underscores the importance of long-term monitoring and a flexible approach in determining the timing of MRI in patients with Giant CMN.
In summary, this case illustrates that the coexistence of Giant CMN, multifocal NCM.
DandyAeWalker variant, and multisystem involvement can result in a highly complex clinical presentation with poor prognosis.
The unusual feature of late-onset seizures underscores the importance of long-term follow-up and integrated multidisciplinary management.
This report not only broadens the understanding of the clinical spectrum of NCM in children but also highlights the necessity of individualized management focused on symptom control, metabolic quality-of-life Published by Indonesia Journal of Biomedical Science | IJBS 2026.
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CONCLUSION
This case describes a rare presentation syndrome with giant CMN, multifocal (NCM), and a DandyAeWalker variant, further complicated by multisystem involvement including hematologic, renal, and endocrine abnormalities.
Unlike most reports where neurological symptoms appear in the neonatal or infantile period, our patient developed late-onset seizures at the age of five, representing an uncommon clinical course.
Multifocal melanosis involving the bilateral amygdala and pons, together with metabolic disturbances, contributed to recurrent and refractory seizures, highlighting the multifactorial pathogenesis.
Prognosis in symptomatic NCM remains poor, particularly in multifocal disease where surgical intervention is not feasible, underscoring the importance of optimal medical therapy, systemic correction, and long-term multidisciplinary care to preserve quality of life.
CONFLICT OF INTEREST
All authors declare there is no conflict of None.
AUTHOR CONTRIBUTION
All authors had contributed in manuscript writing and agreed for the final version of manuscript for publication.
ETHICAL CONSIDERATION
The patientAos legal guardian had signed written informed consent regarding publication of medical data in scientific medical journal with confidentiality to personal information.
GENERATIVE AI USAGE
DISCLOSURE
The authors explicitly state that the writing of this scientific case report did not use any generative AI technology.
REFERENCES