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Table of Contents    
LETTER TO EDITOR
Year : 2016  |  Volume : 64  |  Issue : 5  |  Page : 1047-1048

Central precocious puberty in children with devastating brain damage: Two cases


1 Department of Pediatrics, Chonbuk National University Medical School, Jeonju 561-712, Korea
2 Department of Pediatrics, Chonbuk National University Medical School; Research Institute of Clinical Medicine of Chonbuk National University-Biomedical Research Institute of Chonbuk National University Hospital, Jeonju 561-712, Korea

Date of Web Publication12-Sep-2016

Correspondence Address:
Sun Jun Kim
Department of Pediatrics, Chonbuk National University Medical School; Research Institute of Clinical Medicine of Chonbuk National University.Biomedical Research Institute of Chonbuk National University Hospital, Jeonju 561-712
Korea
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.190266

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How to cite this article:
Kim H, Kim J, Kim MS, Lee DY, Kim SJ. Central precocious puberty in children with devastating brain damage: Two cases. Neurol India 2016;64:1047-8

How to cite this URL:
Kim H, Kim J, Kim MS, Lee DY, Kim SJ. Central precocious puberty in children with devastating brain damage: Two cases. Neurol India [serial online] 2016 [cited 2019 Nov 15];64:1047-8. Available from: http://www.neurologyindia.com/text.asp?2016/64/5/1047/190266




Sir,

Apart from idiopathic causes, central nervous system abnormalities or injuries in early childhood are the main causes of central precocious puberty (CPP).[1] CPP shows isosexual activation through an early stimulation of the hypothalamic-pituitary-gonadal axis. We briefly reviewed the clinical course of 2 male cases having CPP whom the disease occurred consequent to their suffering a devastating brain injury.

A 3-year-old male patient was admitted with facial acne and pubic hair. The patient had a history of hypoxic brain damage and symptomatic epilepsy at birth. He had been taking phenobarbital, valproic acid, and oxcarbazepine for 3 years. Luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels after stimulation with gonadotropin-releasing hormone (GnRH) were 44 mIU/ml and 3.3 mIU/ml, respectively (typical LH level after puberty, >6.9 mIU/ml). Magnetic resonance imaging (MRI) of the brain showed severe brain atrophy with encephalomalacic changes throughout both cerebral hemispheres [Figure 1]a. There was no evidence of a mass lesion in the pituitary gland or the hypothalamus [Figure 1]b. Electroencephalogram (EEG) showed disorganized and asynchronous background activity. The second case was of a 7-year-old male patient who visited our department because of penile growth. One year prior to his admission, after a motor vehicle accident, he was diagnosed with multiple traumatic brain injuries. After the accident, he experienced frequent intractable focal seizures, for which he was treated with phenytoin, valproic acid and oxcarbazepine for 2 years. No seizure recurrence was noted after the initiation of antiepileptic drugs. Prior to the presentation, the patient showed signs of pubertal development with pubic hair, testis volume of 5 ml, and bone age of 11 years. LH and FSH levels 1 hour after stimulation with GnRH were 31.4 mIU/ml and 15.9 mIU/ml, respectively. Brain magnetic resonance imaging (MRI) showed diffuse brain atrophy with extensive brain tissue loss with multiple cystic encephalomalatic changes [Figure 2]a. There was no mass lesion in the pituitary gland or the hypothalamus [Figure 2]b. Electroencephalogram showed the presence of frequent multifocal seizure activity.
Figure 1: (a) Magnetic resonance image (MRI) (FLAIR axial, TR = 8000 ms, TE = 95 ms) of the first patient shows severe brain atrophy with encephalomalacic changes in both cerebral hemispheres. (b) Sagittal MRI (T1 sagittal, TR = 345 ms, TE = 10 ms) of the first patient demonstrates no mass lesion in the pituitary gland

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Figure 2: (a) Magnetic resonance imaging (MRI) of the brain (T2 axial, TR = 3590 ms, TE = 96 ms) of the second patient shows diffuse brain atrophy with ventriculoperitoneal shunt in situ. Extensive brain damage with cystic encephalomalacic changes in the left cerebral hemisphere and the right frontotemporoparietal lobes are present. (b) Sagittal MRI (T1 sagittal, TR = 1510 ms, TE = 2.3 ms) of the second patient demonstrates no mass lesion in the pituitary gland

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The mechanism of hormonal disturbance in prepubescent children with severe brain damage is unclear. Van den Berghe [2] discussed the uncertainty regarding whether such an imbalance arises secondary to direct structural hypothalamic–pituitary injury or reflects temporary adaptive changes due to the underlying acute illness. These 2 patients experienced intractable seizures and were prescribed antiepileptic drugs including valproic acid for more than 1 year. It has been suggested that the reproductive endocrinal effects of valproic acid contribute to the development of hyperandrogenism and polycystic ovary syndrome in female patients.[3] The standard treatment of CPP consists of depot parenteral preparations of GnRH analogue, usually at 4-week intervals.[4] The clinical features of associated disorders are consistent with the hypothesis that extrahypothalamic areas inhibit pituitary gonadotropin secretion before puberty, and that damage to these areas can result in precocious puberty.

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Conflicts of interest

There are no conflicts of interest

 
  References Top

1.
Robben SG, Oostdijk W, Drop SL, Tanghe HL, Vielvoye GJ, Meradji M. Idiopathic isosexual central precocious puberty: Magnetic resonance findings in 30 patients. Br J Radiol 1995;68:34-8.  Back to cited text no. 1
[PUBMED]    
2.
Van den Berghe G. Novel insights into the neuroendocrinology of critical illness. Eur J Endocrinol Eur Fed Endocr Soc 2000;143:1-13.  Back to cited text no. 2
    
3.
Zaiem A, Aouinti I, Lakhoua G, Kastalli S, Daghfous R, Lakhal M, et al. Precocious puberty in an epileptic child treated with valproate. Thérapie 2012;67:537-8.  Back to cited text no. 3
    
4.
Partsch CJ, Sippell WG. Treatment of central precocious puberty. Best Pract Res Clin Endocrinol Metab 2002;16:165-89.  Back to cited text no. 4
    


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