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Published on: June 11, 2012
Acquired central diabetes insipidus in children: a 12-year Brisbane experience
A E Al-Agha1, M J Thomsett, J F Ratcliffe
1Department of Endocrinology and Diabetes, Royal Children's Hospital Brisbane, Queensland, Australia. abdulmoa@nch.edu.au
Insights
Acquired diabetes insipidus (CDI) in children often presents with isolated anti-diuretic hormone deficiency. Careful follow-up is crucial for undiagnosed cases, with some showing improvement on MRI scans over time.
Area of Science:
- Pediatric Endocrinology
- Neuroendocrinology
- Clinical Research
Background:
- Acquired diabetes insipidus (CDI) is an uncommon condition in children.
- Understanding its clinical, endocrine, and radiological features is essential for diagnosis and management.
Purpose of the Study:
- To investigate the clinical, endocrine, and radiological characteristics and the progression of acquired diabetes insipidus in pediatric patients.
- To identify common etiologies and outcomes in children with CDI.
Main Methods:
- A retrospective chart review was conducted on children diagnosed with CDI.
- Data were collected from pediatric endocrine clinics between 1987 and 1999.
- Clinical, endocrine, and radiological (MRI) data were analyzed.
Main Results:
- Thirty-nine children with CDI were identified, with various etiologies including head trauma, CNS tumors, and malformations.
- Most cases presented with isolated anti-diuretic hormone deficiency, and many did not develop further endocrine deficits.
- Seven cases remained undiagnosed, with some showing spontaneous improvement in MRI findings over time.
Conclusions:
- Children with undiagnosed acquired diabetes insipidus require vigilant follow-up.
- More intensive initial investigations may reduce the number of undiagnosed cases.
- Pituitary stalk biopsies are reserved for progressive MRI changes; otherwise, yearly MRI follow-up may suffice.
Objective:
To study the clinical, endocrine and radiological features and progress of children presenting with acquired diabetes insipidus (CDI).
Methodology:
Chart review of children presenting because of CDI to Brisbane paediatric endocrine clinics between 1987 and 1999.
Results:
Thirty-nine children (female/male ratio 21/18) aged 0.1-15.4 years (mean age 6.7 years) were identified. Aetiologies were head trauma or familial in eight cases (20.5%) each, central nervous system (CNS) tumours in five cases (12.8%), CNS malformations in four cases (10.2%), histiocytosis in three cases (7%) and hypoxia and infection in two cases (5.1%) each. Seven cases (17.9%) remain undiagnosed. Of the 32 (82%) cases with isolated anti-diuretic hormone deficiency at presentation, 24 cases (61.5%) experienced no further endocrine deficit. Additional endocrine deficits occurred mainly in the tumour or undiagnosed groups. On follow-up brain magnetic resonance imaging (MRI) scans in the seven undiagnosed cases, six patients had mild or no change and one patient had marked improvement of MRI findings. These changes occurred 10-48 months (mean 18 months) after presentation.
Conclusions:
Children without an aetiological diagnosis for the uncommon condition of acquired CDI require careful follow-up. More intensive investigation at presentation (e.g. estimation of cerebrospinal fluid human chorionic gonadotrophin) promises to lessen the number of such cases. Pituitary stalk biopsies should be reserved for those patients with progressive MRI changes. If these changes do not occur early, our experience suggests that follow-up MRI scans may need to be performed only yearly.
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