Posterior Lobe of the Pituitary in Diabetes Insipidus: Dynamic MR Imaging
| Title: | Posterior Lobe of the Pituitary in Diabetes Insipidus: Dynamic MR Imaging |
|---|---|
| Authors: | Sato, Noriko; Ishizaka, Hiroshi; Yagi, Hideki; Matsumoto, Mitsuomi; Endo, Keigo |
| Publisher: | Radiology |
| Date Published: | February 01, 1993 |
| Reference Number: | 141 |
Magnetic resonance (MR) imaging was performed in 10 subjects: four with central idiopathic diabetes insipidus (DI), two with nephrogenic DI, and four with normal pituitary glands. Characteristics high intensity of the posterior pituitary lobe was seen in all four control subjects and one case of nephrogenic DI. However, it was undetectable in all four cases of central idiopathic DI and one case of nephrogenic DI. Peak contrast enhancement of the posterior lobe occurred within 30 seconds after injection of gadopentetate dimeglumine in control subjects and in both cases of nephrogenic DI and at 30-60 seconds in one case of mild partial idiopathic DI. In contrast, no or faint early enhancement of the posterior pituitary lobe was observed in two cases of complete and one case of partial central DI. In patients with central DI, MR imaging reveals delayed enhancement of the posterior pituitary lobe compared with the early enhancement seen in subjects without central DI.
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This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
Sato, et al, performed MR on ten people: four with central diabetes insipidus (CDI), two with nephrogenic diabetes insipidus (NDI), and four with healthy pituitary glands. CDI is caused by a lack of the antidiuretic hormone, arginine vasopressin (AVP), which is normally synthesized in the hypothalamus. NDI patients have sufficient levels of AVP circulating in their blood, but their kidneys can not respond to it. Because the NDI patient's body does not respond to AVP, his or her posterior pituitary keeps secreting it to try and compensate. Because of this, the posterior pituitary is hyperstimulated and the NDI patient will have normal to elevated levels of AVP in their blood.
The authors injected the subjects with gadopentate dimeglumine, an agent used to heighten the lighting contrast in the pituitary for purposes of MR imagery. They saw the characteristic high intensity of the posterior pituitary in all four control subjects and in one of the people with NDI. However, the bright spot was undetectable in all four cases of CDI and in one case of NDI.
These results confirmed earlier research by other investigators who found the high intensity of the posterior pituitary lobe was absent in patients with CDI. The authors, however, were the first to perform an MR study on the pituitary glands of NDI patients.
There were two different MR findings in the NDI patients: one subject's posterior pituitary had the characteristic high intensity; the other's did not. In NDI, the functioning of the posterior pituitary is considered normal; it secretes AVP as it should. In fact, the high intensity seems to represent granules of AVP. The researchers speculate that the reason one NDI patient did not show high intensity was because enough AVP granules may not have been stored in his posterior pituitary because of his body's increased demand for AVP.
The low intensity of the CDI patients signifies their posterior pituitary's reduced or absent ability, and perhaps it indicates poor blood flow through the posterior lobe. It appears then that MR imagery is useful for evaluating the function of the posterior pituitary and differenciating between CDI and NDI.