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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 5 1362-1367
Copyright © 1997 by The Endocrine Society

Pediatric Endocrinology

Idiopathic Hypothalamic Diabetes Insipidus, Pituitary Stalk Thickening, and the Occult Intracranial Germinoma in Children and Adolescents1

Sudha L. Mootha2, Anthony J. Barkovich, Melvin M. Grumbach, Michael S. Edwards, Stephen E. Gitelman, Selna L. Kaplan and Felix A. Conte

Department of Pediatrics, Divisions of Neuroradiology (A.J.B.) and Pediatric Neurosurgery (M.S.E.), University of California, San Francisco, California 94143


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
We report nine consecutive children and adolescents [five females and four males; aged 2 yr 8 months (m) to 18 yr 1 m] studied over the last 5 yr with idiopathic central diabetes insipidus. In addition to vasopressin deficiency, anterior pituitary hormone deficiencies were detected, either on evaluation at presentation or during follow-up studies over the following 3 yr. Four patients had an increased concentration of plasma PRL. One patient had multiple pituitary hormone deficiencies at diagnosis, and two others developed the same by 21 m of follow-up. Brain magnestic resonance imaging scans, performed at presentation, were originally interpreted as normal in four of nine patients, except for absence of the bright posterior pituitary signal; after retrospective review, two of nine were considered normal. All of the brain magnetic resonance imaging (MRI) scans showed positive findings by 14 m of follow-up. The first abnormal finding in all patients was isolated pituitary stalk thickening. Evaluation of cerebrospinal fluid (CSF) for hCG was positive in three of eight evaluated patients; the three positive CSF values were found at presentation and 3 and 9 m after presentation. All eight patients assessed were negative for CSF {alpha}-fetoprotein and cytology, and no patient had serum tumor markers. Transsphenoidal biopsy of the lesion in seven of nine patients showed a germinoma in six patients and inflammatory cells in one. The six patients with documented germinoma comprise 31% of the intracranial germinomas diagnosed in this age group at the University of California-San Francisco during the last 5 yr. The patient with mononuclear inflammatory cells on biopsy along with one other patient have had spontaneous resolution of their stalk thickening. So-called "idiopathic" central diabetes insipidus warrants close follow-up to determine the etiology, especially if anterior pituitary hormone deficiencies are detected. Normal brain MRI scans or scans that show isolated pituitary stalk thickening merit follow-up with serial contrast enhanced brain MRI for the early detection of an evolving occult hypothalamic-stalk lesion. CSF evaluation is recommended at presentation because elevated CSF hCG may precede MRI abnormalities.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
CENTRAL diabetes insipidus (DI) is a rare disorder that can result as a consequence of diverse etiologies, including malformations, autoimmune, infiltrative (e.g. neoplastic or histiocytsis) or traumatic processes, as well as mutations in the gene encoding arginine vasopressin. Idiopathic central DI is a diagnosis of exclusion, and one that has been made less frequently through the decades. Of 188 patients in three series between 1955 and 1992, 15–30% with nonsurgical central DI were classified as idiopathic (1, 2, 3). With the increasing sensitivity of diagnostic imaging techniques, a specific etiology for at least some patients with idiopathic central DI can now be established. We report a study of nine consecutive patients referred with idiopathic central DI in whom an isolated thickened pituitary stalk and anterior pituitary hormone deficiencies were detected either at presentation or during follow-up studies.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Nine successive patients (five females and four males) were referred to the pediatric endocrine unit at the University of California-San Francisco (UCSF) between September 1991 and September 1996 with polyuria and polydipsia of undetermined etiology (Table 1Go). Seven patients presented without prior evaluation, and two were referred after initial workup proved inconclusive. None had neurological deficits or a family history of DI. Ages at presentation ranged from 2 yr 8 m months (m) to 18 yr 1 m (median age, 10.5 yr), and duration of symptoms at presentation was between 3 m to 4 yr (median, 17 m). All had polyuria and polydipsia; patient 9 also had secondary amenorrhea of 17 m duration, and patient 8 had arrested pubertal development. Although four of nine patients complained of poor growth, only two of these four had a demonstrable decrease in their growth rate. Patient 4 gave a family history of goiter. No other history for autoimmune disease was elicited. Past medical history was significant for patient 5 being small for gestational age and for in utero drug exposure in patient 3.


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  		Table 1. Clinical findings

 
Methods

Polyuria and polydipsia were evaluated by either a modified water deprivation test or measurement of simultaneous urinary and serum osmolarity and antidiuretic hormone concentration, measured at SmithKline Laboratories (Dublin, CA) (4, 5). Insulin-like growth factor I (IGF-I) and IGF-binding protein-3 (IGFBP-3) were measured by RIA at Nichols Institute (San Juan Capistrano, CA). GH was measured by polyclonal RIA. An ACTH test was performed in two of nine, and a GnRH test was performed in four of seven pubertal aged patients. All stimulatory testing was conducted according to previously described standard protocols (6, 7).

All subjects had brain magnetic resonance imaging (MRI) performed at presentation. T1-weighted sagittal and coronal 3-mm sections were obtained without contrast enhancement in all patients. Eight MRIs were also performed after gadolinium contrast enhancement (0.1 mg/kg); four of the patients had postcontrast spinal MRI performed. Patients who had normal brain MRI scans (with the exception of a posterior pituitary bright spot) at presentation were followed with contrast-enhanced scans every 3–6 m. All MRI scans were evaluated for this study retrospectively by a pediatric neuroradiologist (A.J.B.).

Other diagnostic workup in all subjects included a skeletal survey to rule out Langerhans’ histiocytosis. The tumor marker hCG was measured in the cerebrospinal fluid (CSF) and serum. This assay was performed using a UCSF clinical laboratory assay preparation specific for the ß-subunit of hCG (normal value, <2 IU/L). Serum and CSF {alpha}-fetoprotein was determined by enzyme immunoassay; CSF cytology was assessed on a concentrated sample.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Endocrine profiles at presentation are summarized in Table 2Go. All nine patients had central DI. Six had inappropriately low arginine vasopressin concentrations (<1 ng/L) and low urinary osmolarity for the concentration of serum sodium and osmolarity measured in a random sample. The remaining three patients failed a water deprivation test. All patients concentrated their urine appropriately in response to exogenously administered 8-desamino-arginine vasopressin. Plasma PRL was elevated in four of eight patients. The peak GH concentrations after arginine and L-DOPA stimulations were less than 7 ng/mL in seven of eight patients tested; one of these seven patients had borderline GH deficiency and was growing at an appropriate rate. Plasma IGF-I was below the expected value for age in three of seven patients. Patient 8 had mild hypothalamic hypothyroidism at presentation. Patients 7, 8, and 9 required cortisol replacement 21 m after presentation, 3 m after presentation, and at presentation, respectively. Two pubertal aged patients had prepubertal LH response to GnRH; one of them presented with secondary amenorrhea of 17 m duration.


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  		Table 2. Hormonal studies at presentation

 
The initial brain MRIs were evaluated by various radiologists at UCSF and elsewhere (Table 3Go). These scans were interpreted as normal in four of nine patients (2, 3, 4, 8). Subsequently, all scans were reviewed by A.J.B., who found that the scans in two of nine subjects (patients 2 and 4) were normal and that seven of nine patients had diffuse thickening of the pituitary infundibulum (Fig. 1Go, a and b). Later, some exhibited lesion extension upward into the floor of the third ventricle or downward into the pituitary fossa (Fig. 2Go). The two patients with normal initial scans exhibited stalk enlargement at 3 m and 8 m follow-up, respectively. All patients had absence of the hyperintense signal normally seen in the neurohypophysis on the T1-weighted images. The four spinal MRI scans were interpreted as normal.


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  		Table 3. Imaging profile

 


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  		Figure 1. a and b, Saggital view brain MRI scans with contrast enhancement in patients 2 and 6. Pituitary stalk thickening is designated by the arrows.

 


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  		Figure 2. Serial coronal views of the contrast-enhanced brain MRI scans in patient 8, with arrows pointing to the pituitary stalk. The first scan was performed at presentation and is normal. The second scan was performed after the patient failed follow-up for 14 m. She had pituitary stalk thickening, with extension of the lesion to the floor of the third ventricle. The third scan is a normal scan performed after transsphenoidal biopsy and irradiation treatment.

 
hCG and {alpha}-fetoprotein were not detected in the serum of any of the subjects (Table 4Go). CSF was assessed in eight of nine patients (Table 4Go). Two were evaluated at presentation, and the others were examined between 3–46 m after presentation, either when the MRI became positive or when the mass lesion was biopsied. The CSF hCG was positive at low concentrations in three of eight subjects (patient 9 at presentation; patient 4, 3 m after presentation; patient 5, 9 m after presentation). The CSF was negative for hCG in the other five patients, and it was negative for {alpha}-fetoprotein and cytology in all eight patients.


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  		Table 4. Tumor markers

 
Biopsy of the stalk lesion was performed in seven of nine patients when their brain MRI scans showed extension of the lesion (to the hypothalamus, including the floor of the third ventricle) or if the CSF was positive for hCG. The biopsy was performed transsphenoidally in the six patients who had extension of the lesion to the pituitary fossa or to the hypothalamus. Patient 6 did not have extension of the lesion to the pituitary and had a craniotomy for biopsy. The transsphenoidal approach was preferred because of its lower morbidity and mortality compared to a craniotomy. All the patients were biopsied by the pediatric neurosurgeon (M.S.E.), and none had any operative complications. Six of the seven biopsied lesions were positive for germinoma (see Fig. 2Go). The biopsy of patient 6 showed mononuclear inflammatory infiltrates with no evidence of neoplastic cells. Patient 7 had a biopsy 2 yr after presentation; it was a small nondiagnostic sample, showing chronic inflammation and a granulomatous process. Over the ensuing 2 yr she had further progression of her lesion, and a second biopsy was consistent with germinoma.

Focal brain irradiation therapy (5000 cGy) was given to five of the patients with biopsy-proven germinoma, and they now have normal follow-up brain MRI scans. One patient (patient 5) with a germinoma is receiving chemotherapy with irradiation at another institution. Patient 6, whose biopsy showed an inflammatory lesion, had a decrease in stalk thickening at 3 m follow-up, but he continues to have evidence of multiple pituitary hormone deficiencies. He is Tanner stage I for genital development and pubic hair at the age of 12 yr. Patient 3 (not biopsied) has had resolution of his lesion on MRI, but continues to have central DI and GH deficiency without a decrease in the growth rate. Both of these patients are under observation with serial scans. Patient 1 is the youngest and most recent patient. He has isolated stalk thickening and no anterior pituitary hormone deficiencies, and is negative for serum and CSF tumor markers; he has not had a biopsy and is being followed with serial scans.


   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
All nine patients in this series presented with central DI and no clear etiology; however, each patient had a variable course with respect to duration of symptoms, presence of pituitary hormone deficiencies, and rate of progression. Anterior pituitary deficiencies were unmasked either after investigation at presentation or with follow-up studies. Four patients (no. 6–9) had multiple pituitary hormone deficiencies after having had symptoms of central DI for 18 m to 3 yr. In contrast, patient 4 presented with a 4-yr history of central DI and has only GH deficiency, with other anterior pituitary functions intact. The finding of anterior pituitary deficiencies in the presence of central DI greatly increased our suspicion of an occult hypothalamic lesion (8).

Our experience indicates that close clinical follow-up accompanied by serial brain MRIs are essential to determine a diagnosis in patients with so-called idiopathic DI. Germinoma was diagnosed in six of the nine patients because brain MRIs were performed on a frequent (every 3–6 m) basis, and a biopsy was performed when the lesion progressed or if the CSF markers were positive. Contrast enhancement was useful in the identification of subtle extension of the lesion. A time lag of up to 14 m between clinical presentation and development of brain MRI abnormalities was seen in our series. Reports of patients followed by computerized tomography of the head indicate that imaging follow-up for many years may be needed to establish a diagnosis (9, 10, 11). In our series it took between 1–46 m from presentation to establish a biopsy-proven diagnosis. Scans at presentation were interpreted as normal in four patients (no. 2, 3, 4, and 8), and even when reviewed retrospectively, scans of patients 2 and 4 were read as normal without evidence of a mass lesion. With follow-up brain MRIs initially performed every 3–6 m, we found that the rate of tumor progression was variable; it took only 3 m for patient 4 to progress from a normal scan to stalk thickening, whereas others in our series have taken up to 15 m for MRI changes to evolve. Discrepancies in MRI interpretation exist because stalk thickening is a nonspecific finding, and there are no useful published standards for pituitary stalk size in children and adolescents.

The importance of isolated pituitary stalk thickening became apparent in the evaluation of this consecutive group of patients. In all nine of our patients, stalk thickening was the first abnormal finding on brain MRI. Six of these patients had biopsy-proven germinoma, and two patients had spontaneous resolution of the stalk thickening, one is being followed at this time. The underlying etiology for the two patients with spontaneous resolution of the stalk thickening is unclear. Patient 6, one of these two patients, has multiple pituitary hormone deficiencies and a pituitary stalk biopsy that showed mononuclear inflammatory cells. Patient 3 was followed without biopsy and had spontaneous resolution of his stalk lesion 9 m after presentation.

The differential diagnosis of pituitary stalk thickening includes germinoma; however, germinomas commonly present with a hypothalamic/pineal mass and in the past only infrequently have been noted to have isolated stalk thickening (8, 12). Other considerations in the evaluation of pituitary stalk thickening in children or adolescents include Langerhans’ histiocytosis and putative antivasopressin cell antibody-induced central DI (10, 12, 13, 14, 15). A thickened pituitary stalk was also common in a series of 17 adult patients with lymphocytic infundibuloneurohypophysitis that resolved by the 2-yr follow-up visit in all patients, which suggested a self-limited process (16). Only isolated cases of this disorder have been described in children; those suspected of having such a lesion, which was aggressive in one child (17), need continued monitoring to confirm the diagnosis and to follow its progress (17, 18).

Intracranial germ cell tumors comprise 7.8% of primary pediatric brain tumors (19). Our series of 6 patients with a documented intracranial germinoma make up 6 of 19 (31%) of all the children and adolescents with intracranial germinomas who were studied at UCSF during the same 5-yr period. Although serum hCG and {alpha}-fetoprotein were undetectable in all of our patients, evaluation of the CSF hCG was useful. Three of 7 patients (no. 4, 5, and 9) had positive, but low, hCG concentrations (normal, <2 IU/L) in their CSF, a finding consistent with some pure germ cell tumors. Patient 4 presented with a normal scan, but progressed to stalk nodularity and thickening on MRI at the 4 m follow-up, at which time the CSF hCG level was 3 IU/L. Patient 5 presented with a large stalk and on the 9 m follow-up scan had extension of the lesion to the pineal gland and floor of the third ventricle; the CSF hCG level was 9 IU/L at that time. Patient 9 had a CSF hCG value of 6 IU/L when she presented with mild stalk enlargement. Others have reported positive CSF cytology 1 yr before radiological evidence of germinoma (20). We recommend CSF evaluation at presentation, and biopsy when the lesion extends beyond the stalk or if tumor markers are positive. Irradiation treatment should be given only after a biopsy-proven diagnosis is established.

We note a decrease in the frequency of the diagnosis of idiopathic central DI. An underlying etiology must be pursued especially in the presence of anterior pituitary hormone deficiencies that increase the suspicion of an occult hypothalamic lesion (8). A normal brain MRI or an MRI with only pituitary stalk enlargement calls for serial scanning. An approach to a diagnosis in patients with idiopathic CDI is given in the algorithm in Fig. 3Go. Even though a brain MRI without contrast better detects the absence of the bright posterior pituitary signal, this observation only confirms the known clinical diagnosis of (nongenetic) central DI (12). More important in our view is the usefulness of a contrast-enhanced brain MRI in the detection of subtle abnormalities in the hypothalamic-pituitary region. For example, an MRI without contrast can miss subtle changes in the floor of the third ventricle that are crucial to establishing an early diagnosis. CSF evaluation for cytology and markers is recommended at presentation, given the possibility of a time lag before evidence of a lesion appears on the brain MRI (20). In cases with a normal brain MRI, our experience has shown that it may take up to 1 yr for the scans to become positive and up to 4 yr for a diagnosis to be established by biopsy. Accordingly, we recommend that a contrast-enhanced MRI brain scan be performed every 3–6 m for the first 1–2 yr after presentation, followed by a brain MRI every 6 m for at least 5 yr if a lesion is not detected. This approach will assure early detection of an expanding lesion that may be readily treatable.



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  		Figure 3. Algorithm for the evaluation of central DI with no clear etiology.

 


   Footnotes
 
Address requests for reprints to: Dr. Felix Conte, Department of Pediatrics, Box 0136, University of California, San Francisco, California 94143-0136.

1 This work was supported by a NIH grant from the NIDDK (5T32-DK-07161) and the NIH Pediatric Clinical Research Center (M01-RR-01271). Back

2 Trainee in Pediatric Endocrinology under a program sponsored by the NIDDK, NIH (Grant 5T32-DK-07161). Back

Received December 9, 1996.

Revised February 4, 1997.

Accepted February 12, 1997.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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  4. Frasier SD, Kutnik LA, Schmidt RT, Smith FG. 1967 A water deprivation test for the diagnosis of diabetes insipidus in children. Am J Dis Child. 114:157–160.[Abstract/Free Full Text]
  5. Richman RA, Post EM, Notman DD, Hochberg Z, Moses AM. 1981 Simplifying the diagnosis of diabetes insipidus in children. Am J Dis Child. 135:839–841.[Abstract/Free Full Text]
  6. Goodman HG, Grumbach MM, Kaplan SL. 1968 Growth and growth hormone. II. A comparison of isolated growth hormone deficiency and multiple hormone deficiencies in 35 patients with hypopituitary dwarfism. N Engl J Med. 278:57.
  7. Grumbach MM, Roth JC, Kaplan SL, Kelch RP. 1974 Hypothalamic-pituitary regulation of puberty in man: evidence and concepts derived from clinical research. In: Grumbach MM, Grave GD, Mayer FE, eds. The control of the onset of puberty. New York: Wiley and Sons; 115–166.
  8. Sklar CA, Grumbach MM, Kaplan SL, Conte FA. 1981 Hormonal and metabolic abnormalities associated with central nervous system germinoma in children and adolescents and the effect of therapy: report of 10 patients. J Clin Endocrinol Metab. 52:9–16.[Abstract/Free Full Text]
  9. Cianfarani S,, Nicholl RM, Medbach S, Charlesworth MC, Savage MO. 1993 Idiopathic hypothalamus-pituitary dysfunction: review of five cases. Horm Res. 39:47–50.[Medline]
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  16. Imura H, Nakao K, Shimatsu A, et al. 1993 Lymphocytic infundibuloneurohypophysitis as a cause of central diabetes insipidus. N Engl J Med. 329:683–689.[Abstract/Free Full Text]
  17. Bettendorf M, Frank S, Grulich-Henn J, Engenhart R, Heinrich U. Lymphocytic hypophysitis: malignant clinical course in prepubertal girl (Abstract no. P1-434; P243). Proc of the 10th Annual Meet of the Int Congr of Endocrinol. 1996.
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