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Hypopituitarism after Tuberculous Meningitis in Childhood

Karen S. L. Lam, MD; Michael M. K. Sham, MD; Sidney C. F. Tam, MD; Matthew M. T. Ng, MD; and Hector T. G. Ma, MD
[+] Article and Author Information

From the University of Hong Kong, Queen Mary Hospital, and Ruttonje Hospital, Hong Kong. Requests for Reprints: Dr. Karen Lam, MD, University Department of Medicine, Queen Mary Hospital, Pokfulam Road, Hong Kong. Acknowledgments: The authors thank Gloria Chan, RN; research technician Lau Kam Shing; and secretary Venus Yuen for their contributions to this study. Grant Support: By grants from the Universities and Polytechnics Grant Committee (No. 337/041/0014) and the Medical Faculty Research Fund (No. 362/031/3405) of the University of Hong Kong. The WHO Matched Assay Reagents Program supplied the reagents for the radioimmunoassay of serum testosterone and estradiol.


Copyright 2004 by the American College of Physicians


Ann Intern Med. 1993;118(9):701-706. doi:10.7326/0003-4819-118-9-199305010-00007
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Objective: To study the prevalence and pathogenesis of hypopituitarism following tuberculous meningitis in childhood.

Design: A retrospective cross-sectional study.

Setting: A university teaching hospital and a tuberculosis referral center.

Patients: Forty-nine patients, aged 23.4 6.0 years (mean SD), who had tuberculous meningitis in childhood (age at diagnosis, 5.9 5.0 years) were studied.

Measurements: A detailed assessment of hypothalamicpituitary function, including conventional stimulation tests and responses to four hypothalamic releasing hormones, was done. Magnetic resonance imaging of the hypothalamicpituitary region was performed in patients with abnormal endocrine function.

Results: Ten patients were found to have abnormal pituitary function: Seven had growth hormone deficiency, four of whom also had gonadotropin deficiency; the other three had gonadotropin deficiency, corticotropin deficiency, and mild hyperprolactinemia, respectively; none had diabetes insipidus. Among those with growth hormone deficiency, a significant correlation (r = 0.749, P < 0.05) was found between the height standard deviation score and the age at diagnosis of tuberculous meningitis. Growth hormone, corticotropin, and gonadotropin responses to growth hormone releasing hormone, corticotropin releasing hormone, and gonadotropin releasing hormone, respectively, suggested a hypothalamic defect in five patients. Magnetic resonance imaging scans of the hypothalamicpituitary region were abnormal in five patients.

Conclusions: Hypopituitarism was documented in 20% of a small subset of patients years after recovery from tuberculous meningitis in childhood. The cause appears to be tuberculous lesions affecting the hypothalamus, pituitary stalk and, directly or indirectly, the pituitary itself. Early recognition and treatment can be beneficial.

Figures

Grahic Jump Location
Figure 1.
Magnetic resonance imaging scan after gadolinium injection.left panelright panel

Enhanceable tissue is present in the hypothalamus extending down to the upper half of the pituitary stalk () in patient 3 ( ) and near the right inferior cerebellar peduncle (A), in the pons (B), and within the suprasellar cistern (C and D) in patient 2 ( ).

Grahic Jump Location
Grahic Jump Location
Figure 2.
Magnetic resonance imaging scan.ABleft panelright panel

Hydrocephalus ( ) and atrophic pituitary ( ) are seen in scan of Patient 3 ( ) and gross pituitary atrophy () is seen in scan of Patient 4 ( ).

Grahic Jump Location

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