Correlation between magnetic resonance imaging of posterior pituitary and neurohypophyseal function in children with diabetes insipidus
M Maghnie, A Villa, M Arico, D Larizza, S Pezzotta, G Beluffi, E Genovese and F Severi
Department of Pediatrics, University of Pavia, Italy.
The posterior pituitary lobe and stalk were studied by magnetic resonance
imaging in 20 children with diabetes insipidus of different origins:
primary familial autosomal dominant (n = 2) or idiopathic (n = 2), and
secondary to craniopharyngioma (n = 6, resected in 5), to Langerhans cell
histiocytosis (n = 5), to excessive water intake (dipsogenic; n = 3), to
renal vasopressin insensitivity (n = 1), and to osmoreceptor dysfunction (n
= 1). Of the four children with primary diabetes insipidus, the posterior
bright signal was recognizable in two with the familial autosomal dominant
form and one with the idiopathic form; in the latter, the pituitary stalk
was thin, while it was normal in the first two patients; no posterior
hyperintense signal with enlarged and gadolinium-enhanced pituitary stalk
was observed in the fourth. The posterior hyperintense signal was absent
without evidence of ectopic posterior pituitary tissue regeneration in five
children with surgically removed craniopharyngioma and was doubtful in the
child with unresected craniopharyngioma; the stalk was unrecognizable in
all patients. In the five children with Langherans cell histiocytosis, the
posterior bright signal was absent, while the stalk was normal in two and
unexpectedly enlarged in three (uniformly in two and mainly at the level of
median eminence and hypothalamus in one). All five patients with dipsogenic
or nephrogenic diabetes insipidus or osmoreceptor dysfunction had normal
images of posterior pituitary lobe and stalk. Normal posterior pituitary
bright signal and stalk were found in all 25 healthy control children.
Plasma vasopressin was undetectable in all patients except in nephrogenic
one, in the child with osmoreceptor dysfunction, and in two of three
dipsogenic children, the third mimicking partial neurogenic diabetes
insipidus.(ABSTRACT TRUNCATED AT 400 WORDS)
This article has been cited by other articles:
A. Abu Libdeh, F. Levy-Khademi, M. Abdulhadi-Atwan, E. Bosin, M. Korner, P. C White, and D. H Zangen Autosomal recessive familial neurohypophyseal diabetes insipidus: onset in early infancy
Eur. J. Endocrinol.,
February 1, 2010;
162(2):
221 - 226.
[Abstract][Full Text][PDF]
C. P. Mahoney, E. Weinberger, C. Bryant, M. Ito, J. L. Jameson, and M. Ito Effects of Aging on Vasopressin Production in a Kindred with Autosomal Dominant Neurohypophyseal Diabetes Insipidus Due to the {Delta}E47 Neurophysin Mutation
J. Clin. Endocrinol. Metab.,
February 1, 2002;
87(2):
870 - 876.
[Abstract][Full Text][PDF]
M. Maghnie, G. Cosi, E. Genovese, M. L. Manca-Bitti, A. Cohen, S. Zecca, C. Tinelli, M. Gallucci, S. Bernasconi, B. Boscherini, et al. Central Diabetes Insipidus in Children and Young Adults
N. Engl. J. Med.,
October 5, 2000;
343(14):
998 - 1007.
[Abstract][Full Text][PDF]
E. Genovese, M. Maghnie, G. Maggiore, C. Tinelli, F. Lizzoli, C. D. Giacomo, S. Pozza, and R. Campani MR Imaging of CNS Involvement in Children Affected by Chronic Liver Disease
AJNR Am. J. Neuroradiol.,
May 1, 2000;
21(5):
845 - 851.
[Abstract][Full Text]
G. A. Kaltsas, T. B. Powles, J. Evanson, P. N. Plowman, J. E. Drinkwater, P. J. Jenkins, J. P. Monson, G. M. Besser, and A. B. Grossman Hypothalamo-Pituitary Abnormalities in Adult Patients with Langerhans Cell Histiocytosis: Clinical, Endocrinological, and Radiological Features and Response to Treatment
J. Clin. Endocrinol. Metab.,
April 1, 2000;
85(4):
1370 - 1376.
[Abstract][Full Text]
J. A. Brothers Morbid Obesity in a Young Child
Clinical Pediatrics,
March 1, 2000;
39(3):
169 - 171.
[PDF]
A. De Bellis, A. Colao, F. Di Salle, V. I. Muccitelli, S. Iorio, S. Perrino, R. Pivonello, C. Coronella, A. Bizzarro, G. Lombardi, et al. A Longitudinal Study of Vasopressin Cell Antibodies, Posterior Pituitary Function, and Magnetic Resonance Imaging Evaluations in Subclinical Autoimmune Central Diabetes Insipidus
J. Clin. Endocrinol. Metab.,
September 1, 1999;
84(9):
3047 - 3051.
[Abstract][Full Text]
J. Leger, A. Velasquez, C. Garel, M. Hassan, and P. Czernichow Thickened Pituitary Stalk on Magnetic Resonance Imaging in Children with Central Diabetes Insipidus
J. Clin. Endocrinol. Metab.,
June 1, 1999;
84(6):
1954 - 1960.
[Abstract][Full Text]
M. Maghnie, G. Bossi, C. Klersy, G. Cosi, E. Genovese, and M. Arico Dynamic Endocrine Testing and Magnetic Resonance Imaging in the Long Term Follow-Up of Childhood Langerhans Cell Histiocytosis
J. Clin. Endocrinol. Metab.,
September 1, 1998;
83(9):
3089 - 3094.
[Abstract][Full Text]
P. C. Gagliardi, S. Bernasconi, and D. R. Repaske Autosomal Dominant Neurohypophyseal Diabetes Insipidus Associated with a Missense Mutation Encoding Gly23->Val in Neurophysin II
J. Clin. Endocrinol. Metab.,
November 1, 1997;
82(11):
3643 - 3646.
[Abstract][Full Text][PDF]
M. Maghnie, E. Genovese, S. Lundin, F. Bonetti, and M. Arico Hyatrogenic Extrapontine Myelinolysis in Central Diabetes Insipidus: Are Cyclosporine and 1-Desamino-8-D-Arginine Vasopressin Harmful in Association?
J. Clin. Endocrinol. Metab.,
June 1, 1997;
82(6):
1749 - 1751.
[Full Text][PDF]
D. R. Repaske, R. Medlej, E. K. Gultekin, M. R. S. Krishnamani, G. Halaby, J. W. Findling, and J. A. Phillips III Heterogeneity in Clinical Manifestation of Autosomal Dominant Neurohypophyseal Diabetes Insipidus Caused by a Mutation Encoding Ala-1->Val in the Signal Peptide of the Arginine Vasopressin/Neurophysin II/Copeptin Precursor
J. Clin. Endocrinol. Metab.,
January 1, 1997;
82(1):
51 - 56.
[Abstract][Full Text][PDF]
H. Imura, K. Nakao, A. Shimatsu, Y. Ogawa, T. Sando, I. Fujisawa, and H. Yamabe Lymphocytic Infundibuloneurohypophysitis as a Cause of Central Diabetes Insipidus
N. Engl. J. Med.,
September 2, 1993;
329(10):
683 - 689.
[Abstract][Full Text]