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The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 9 3047-3051
Copyright © 1999 by The Endocrine Society


Original Studies

A Longitudinal Study of Vasopressin Cell Antibodies, Posterior Pituitary Function, and Magnetic Resonance Imaging Evaluations in Subclinical Autoimmune Central Diabetes Insipidus

A. De Bellis, A. Colao, F. Di Salle, V. I. Muccitelli, S. Iorio, S. Perrino, R. Pivonello, C. Coronella, A. Bizzarro, G. Lombardi and A. Bellastella

Institute of Endocrinology (A.D.B., V.I.H., S.I., S.P., A.Be.) and Department of Clinical and Experimental Medicine (A.Bi.), Second University of Naples, and the Department of Molecular and Clinical Endocrinology and Oncology (A.C., R.P., G.L.) and the Institute of Radiological Sciences (F.D.S.), University Federico II, 80131 Naples, Italy

Address all correspondence and requests for reprints to: Annamaria De Bellis, M.D., Istituto di Endocrinologia Seconda Universitá di Napoli, Via S. Pansini 5, 80131 Naples, Italy. E-mail: bellaste{at}unina.it

Cytoplasmic autoantibodies to vasopressin-cells (AVPcAb) have been detected not only in patients with overt central diabetes insipidus (CDI), but also in patients with endocrine autoimmune diseases without CDI. This suggests that complete CDI can be preceded by a preclinical stage. Among 878 patients with endocrine autoimmune diseases without CDI, 9 patients found to be AVPcAb positive and 139 AVPcAb-negative controls were enrolled in this open prospective study. They were evaluated for AVPcAb and posterior pituitary function at least yearly for about 4 yr (range, 37–48 months); during this span, magnetic resonance imaging (MRI) of posterior pituitary and stalk was performed only in the AVPcAb-positive patients. Five of the 9 AVPcAb-positive patients had normal posterior pituitary function at study entry. They were AVPcAb positive throughout the follow-up period. At later stages of the study, 3 of them developed partial CDI, and 1 developed complete CDI. The remaining 4 patients showed impaired response to the water deprivation test at study entry and were diagnosed as having partial CDI. Two of them agreed to receive desmopressin replacement for 1 yr. After this treatment, the patients became negative for AVPcAb and displayed normal posterior pituitary function until the end of the follow-up. Conversely, the 2 untreated patients with partial CDI remained AVPcAb positive. One of them developed overt CDI. None of the controls became AVPcAb positive or developed CDI. The normal hyperintense MRI signal of the posterior pituitary, present at study entry, persisted subsequently in all 9 AVPcAb-positive patients, including those developing overt CDI, only disappearing in the late phase of complete CDI. In asymptomatic subjects, the monitoring of AVPcAb, but not MRI, seems to be useful to predict a progression toward partial/overt CDI. Early desmopressin therapy in patients with partial CDI could interrupt or delay the autoimmune damage and the progression toward clinically overt CDI.




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