alexa Pseudotumor Cerebri Associated with Leuprolide Acetate for Central Precocious Puberty-Case Report | OMICS International | Abstract
ISSN: 2155-9570

Journal of Clinical & Experimental Ophthalmology
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Case Report

Pseudotumor Cerebri Associated with Leuprolide Acetate for Central Precocious Puberty-Case Report

Renato Antunes Schiave Germano1, Ruth Rocha Franco2, Sandro Matas3 and Frederico Castelo Moura1*
1Department of Ophthalmology, Medical School, University of Sao Paulo, Brazil
2Department of Pediatrics, Medical School, University of Sao Paulo, Brazil
3Department of Neurology, Paulista School of Medicine, Federal University of Sao Paulo, Brazil
Corresponding Author : Frederico C Moura
Rua Mato Grosso, 306 – conj
414 – Higienópolis São Paulo – SP - Brasil
CEP: 01239-040
Tel: 55 11 3892-9232
E-mail: [email protected]
Received March 23, 2015; Accepted June 27, 2015; Published June 30, 2015
Citation: Germano RAS, Franco RR, Matas S, Moura FC (2015) Pseudotumor Cerebri Associated with Leuprolide Acetate for Central Precocious Puberty-Case Report. J Clin Exp Ophthalmol 6:444. doi: 10.4172/2155-9570.1000444
Copyright: © 2014 Germano RAS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

This article represents the fourth case in literature of an association between pseudotumor cerebri (PTC) and leuprolide acetate, the first with precocious puberty and severe visual loss. A 9-year-old girl with precocious puberty was treated with a once-monthly dose of leuprolide acetate (3.75 mg) for three months. In the 4th month of treatment, it was decided to increase the dosage of leuprolide acetate to 11.25 mg in once-quarterly doses. After 1 month, she complained of holocranial headache, transient visual obscuration followed by progressive visual loss. After 6 months, she persisted with holocranial headache and progressive visual loss associated with ocular deviation. Neuro-opthalmological examination revealed severe visual loss and bilateral papilledema. Cerebrospinal fluid (CSF) analysis showed opening pressure of 45 cm H2O. The most likely diagnosis was PTC associated with leuprolide acetate. Treatment was started immediately with oral acetazolamide and leuprolide was discontinued. Acetazolamide was discontinued for having induced metabolic acidosis. A ventriculoperitoneal shunt was performed to control intracranial pressure as an alternative to acetazolamide treatment. The follow-up of 18 months showed CSF pressure of 14 cm H2O, stabilization of visual acuity and resolution of papilledema. There appears to be a causal relationship between the onset of leuprolide acetate with the development of PTC. Children should have a complete ophthalmic evaluation if they report headache or visual disturbances after administration of leuprolide acetate.

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