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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 4 1891-1896
Copyright © 2004 by The Endocrine Society

COMMENT

Idiopathic Central Diabetes Insipidus Is Associated with Abnormal Blood Supply to the Posterior Pituitary Gland Caused by Vascular Impairment of the Inferior Hypophyseal Artery System

Mohamad Maghnie, Monica Altobelli, Natascia di Iorgi, Eugenio Genovese, Giulia Meloni, Maria Luisa Manca-Bitti, Amnon Cohen and Sergio Bernasconi

Departments of Pediatrics (M.M., M.A., N.d.I.) and Radiology (G.M.), Istituto di Ricovero e Cura a Carattere Scientifico Policlinico S. Matteo, University of Pavia, 27100 Pavia; Department of Radiology (E.G.), Università dell’Insubria, 21100 Varese; Department of Pediatrics (M.L.M.-B.), Rome "Tor Vergata", 00144 Rome; Ospedale S. Paolo (A.C.), 17100 Savona; and Department of Pediatrics (S.B.), University of Parma, 43100 Parma, Italy

Address all correspondence and requests for reprints to: Mohamad Maghnie, M.D., Ph.D., Department of Pediatrics, Istituto di Ricovero e Cura a Carattere Scientifico Policlinico S. Matteo, Viale Golgi 2, 27100 Pavia, Italy. E-mail: maghnie{at}smatteo.pv.it.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Central diabetes insipidus (CDI) has been linked to vascular central nervous system damage, although the pathophysiology of the mechanism has never been perfectly understood. Indeed, the vascular system of human pituitary gland has rarely been the subject of rigorous investigation except at postmortem. Recently, studies of pituitary gland blood supply have been carried out by means of a time evaluation of pituitary gland enhancement with noninvasive dynamic magnetic resonance (MR) imaging after contrast medium injection. In the present study, we decided to investigate the status of posterior pituitary blood supply by evaluating vascular pituitary patterns in a group of 19 patients with idiopathic CDI in whom previous standard MR imaging had failed to identify causal specific lesions. The control group was composed of 55 subjects with a median age of 12 yr (range, 4.2–17 yr) who had idiopathic isolated GH deficiency and normal pituitary morphology and 15 young adults (18–25 yr) who had normal pituitary gland and no endocrine dysfunction.

Nineteen patients (12 females and seven males), ranging in age at the time of diagnosis of CDI from 0.5–14.9 yr (median, 5 yr), were examined with dynamic MR imaging between 1990 and 1997 at a median age of 14.1 yr (range, 5.0–26.3 yr). CDI was diagnosed according to clinical findings of polyuria and polydipsia, water deprivation test, and desmopressin acetate therapeutic trial. All of the patients had permanent CDI and were being treated with satisfactory results with desmopressin, two to three times daily, either intranasally or orally. The previous MR imaging findings of the 19 CDI patients had shown the absence of posterior pituitary hyperintensity, normal pituitary stalk, and normal anterior pituitary size.

Enhancement of the straight sinus, representing a temporal reference point and occurring in normal subjects simultaneously to that of the posterior pituitary gland, was observed in all subjects after iv gadopentetate dimeglumine administration, with no substantial differences between patients and controls. However, the enhancement of the posterior pituitary lobe occurred simultaneously with the enhancement of the straight sinus in all of the controls but in only 14 of the 19 patients with CDI. In the remaining five patients, the enhancement of the straight sinus was not associated with the expected contrast enhancement of the posterior pituitary gland, suggesting abnormal blood supply to the posterior pituitary lobe. This is in keeping with vascular impairment of the inferior hypophyseal artery system and suggests that abnormal blood supply to the posterior pituitary gland is associated with what, until now, has been considered idiopathic CDI.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
CENTRAL DIABETES INSIPIDUS (CDI) is a heterogeneous condition characterized by the presence of polyuria and polydipsia due to a deficiency of arginine vasopressin. In many patients, CDI is caused by the destruction or degeneration of neurons that originate in the supraoptic and paraventricular nuclei of the hypothalamus. The demonstrated origins of these lesions include germinoma and craniopharyngioma; Langerhans-cell histiocytosis; inflammatory, autoimmune, and vascular diseases; trauma resulting from surgery or an accident; and, in rare cases, genetic defects in the synthesis of vasopressin, which are inherited as autosomal dominant or X-linked recessive traits (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13). However, 30–50% of CDI cases are considered idiopathic (1, 10, 12, 13).

Arginine vasopressin is transported from the hypothalamus through the neural component of the pituitary stalk and stored in nerve terminals in the posterior pituitary. In the vast majority of normal subjects, the posterior pituitary is seen as a hyperintense signal on sagittal T1-weighted magnetic resonance (MR) imaging. The absence of this signal serves as a nonspecific indicator of CDI (1). A thickened infundibulum or pituitary stalk (or both), although not specific, suggests the presence of infiltration in the course of various diseases (1, 2, 3, 14). The percentage of these radiological abnormalities in patients with CDI has recently been reported in a large cohort of subjects; almost half of them did not have any detectable pituitary stalk lesions (1).

CDI may be caused by vascular brain damage, but the pathophysiology of such a mechanism has never been precisely understood. In 1950, the first case of CDI associated with embolic occlusions of the cerebral vessels was reported (15), and since then, several other cases of CDI with suspected vascular origin have been described (16, 17, 18, 19, 20, 21, 22, 23, 24). Due to a lack of noninvasive techniques, the human pituitary gland has not traditionally been a common subject of investigation, except at postmortem (25, 26). However, this has now changed due to dynamic MR imaging technology. Indeed, it is becoming increasingly more common to investigate diverse aspects of the pituitary gland; for example, hypothalamic-pituitary vascularization has been successfully studied in patients with hypopituitarism and Langerhans-cell histiocytosis-dependent CDI (27). Therefore, we chose to investigate vascular pituitary patterns in a group of 19 patients with idiopathic CDI in whom previous standard MR imaging had failed to identify associated local lesions (1).


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Nineteen patients (12 females and seven males), ranging in age at the time of diagnosis of CDI from 0.5–14.9 yr (median age, 5 yr), were investigated with dynamic MR imaging between 1990 and 1997 at a median age of 14.1 yr (range, 5.0–26.3 yr). This cohort represents a group of selected patients with CDI of unknown etiology, normal anterior pituitary gland and pituitary stalk findings at standard MR imaging study, and normal anterior pituitary function at the time of dynamic MR study. In particular, GH secretion was normal in 17 patients at the time of the first standard MR study, whereas two patients showed transitory GH deficiency (1), as demonstrated by a normalization of GH response at the time of GH reevaluation.

The patients were enrolled from a multicenter study of 79 patients with CDI; 60 of the patients had an identified cause of CDI, 18 had idiopathic pituitary stalk thickness suggestive of inflammatory/autoimmune disease, four had central nervous system malformations, 12 had Langerhans-cell histiocytosis, 18 had intracranial tumor, five had the autosomal dominant form of CDI, two had posttraumatic disease, and one had autoimmune polyendocrinopathy (1). CDI was diagnosed according to the clinical findings of polyuria and polydipsia, water deprivation test, and desmopressin acetate therapeutic trial. All patients had permanent CDI and were being successfully treated with desmopressin, two to three times daily, either intranasally or orally. Details on disease presentation, diagnostic modalities, and follow-up have been previously reported (1). The MR imaging findings in the 19 patients showed the absence of posterior pituitary hyperintensity and normal pituitary stalk and anterior pituitary size (1). The control group was composed of 55 patients with a median age of 12 yr (range, 4.2–17 yr) who had idiopathic isolated GH deficiency and normal pituitary morphology and 15 young adults (18–25 yr) who had normal pituitary gland and no endocrine dysfunction.

MR imaging

MR studies were performed with a spin-echo technique and use of a 1.5-T superconductive unit (Magnetom SP; Siemens, Erlangen, Germany). Sagittal and coronal T1-weighted images (time repetition/echo time, 310/15 msec; three acquisitions, 3-mm-thick sections, 256 x 256 matrix, and 20-cm field of view) were obtained (total acquisition time, ~8 min).

Dynamic sagittal images with a flip angle of 8°, a section thickness of 6 mm, a matrix of 128 x 128 pixels, and a field of view of 25 cm were also obtained. Twenty rapid images (time repetition/echo time, 6.5/3 msec; one acquisition) were obtained every 4.6 sec over a 90-sec interval after gadopentetate dimeglumine [gadopentetate dimeglumine-diethylenetriamine pentaacetic acid (GD-DTPA), 0.1 mmol/kg body weight] injection at the beginning of the first acquisition at a rate of 2–3 ml/sec. A 20-gauge needle was used for rapid injection. Interscan delay time was 1–2 sec. Inversion time was 600 msec. Dynamic MR was performed by the same radiologist, all images were carefully evaluated by the same investigator (E.G.), and the times to enhancement of the straight sinus, posterior pituitary, and anterior pituitary lobe were recorded. The study protocol was carried out after the appropriate approval from the Department of Pediatrics Institutional Board, and signed informed consent for the study was obtained from all patients or their family members and from controls.

Normal hypothalamic-pituitary vascular supply: dynamic MR imaging patterns

The posterior pituitary lobe is supplied with blood predominantly by the inferior hypophyseal arteries arising from the meningohypophyseal trunk of the internal-carotid artery. The hypothalamus is supplied with blood by the superior-hypophyseal arteries, which arise from the supraclinoid portion of the internal-carotid artery and from branches of the anterior and posterior cerebral arteries. These arteries form a ring around the infundibulum and serve as the arterial blood supply to the median eminence and infundibulum. The main blood supply to the anterior lobe is through the portal venous system. This complex system originates from specialized vascular structures located in the region of the median eminence. The system is composed of short-terminal arterioles surrounded by a dense capillary network. This network drains into the long-portal veins that run along the surface of the pituitary stalk and terminate in the sinusoidal capillaries of the anterior pituitary. The sinusoidal capillaries are continuous with the deeper short-portal veins. Both anterior and posterior lobes have direct venous drainage (inferior hypophyseal vein to the dural venous sinus) (25, 26).

The times to pituitary gland enhancement were studied to evaluate pituitary gland blood supply. Because the inferior hypophyseal arteries arise from the proximal portion of the carotid artery, the contrast medium will first reach the posterior pituitary lobe, followed by the infundibular stem, and then finally the anterior pituitary lobe. In normal subjects, initial enhancement of the posterior pituitary lobe occurred simultaneously with the enhancement of the straight sinus, which could be considered a reliable temporal reference point for evaluation of time to enhancement of the hypophyseal structures; the same pattern has been demonstrated in isolated GH deficiency (27). The possible pitfall of this technique is that careful attention must be paid to the early arterial phase after bolus iv injection of GD-DTPA, during which contrast diffusion occurs simultaneously in the straight sinus and in the posterior pituitary lobe. This phase may be affected by cardiac rate and output, arterial blood pressure, the caliber of the injection vessel, and the amount of contrast medium, as well as its injection modality. Any of these factors could possibly explain an interindividual variability in initial enhancement time in our subjects, but once the straight sinus has been enhanced, any delay in posterior pituitary enhancement suggests local vascular impairment. Dynamic MR studies performed both at the time of the diagnosis of GH deficiency and repeated at the time of the reevaluation of GH status in 35 patients who normalized their GH response after pharmacological stimulation test (transitory GH defect) showed an identical pituitary enhancement pattern, suggesting that this method is highly reproducible (our unpublished data).


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
In five patients, the enhancement of the straight sinus was not associated with contrast enhancement of the posterior pituitary, although a normally progressive enhancement of the anterior pituitary occurred. In these patients, the diagnosis of CDI was based on a history of polyuria and polydipsia in the age range of 4–11 yr, laboratory evidence of arginine vasopressin deficiency including the water deprivation test, the 1-desamino-8-D-arginine vasopressin (DDAVP) trial, and a computed tomography scan of the brain and pituitary gland (1). Anterior pituitary function was also assessed by measuring serum GH after insulin-induced hypoglycemia or using the arginine test as previously reported (1). Endocrine evaluation showed normal thyroid-adrenal-gonadal function except in one female patient (patient 2) who developed vitiligo and underwent puberty but with persistent irregular menses. The GnRH test showed hypergonadotropic hypogonadism (high peak levels of FSH and LH), suggesting autoimmune ovarian failure, which was successfully treated with sex steroids. Patient 1 developed anorexia nervosa during adolescence. The clinical, laboratory, and hormonal characteristics are summarized in Table 1Go.


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  		TABLE 1. Clinical, biochemical, hormonal, and imaging characteristics of patients with CDI and posterior pituitary vascular impairment

 
Standard MR imaging revealed normal morphology and height of the anterior pituitary gland, as well as normal pituitary stalk size with an absence of posterior pituitary hyperintensity in all patients (Table 2Go). Enhancement of the straight sinus was observed in all subjects after injection of GD-DTPA, with no substantial difference between patients and controls. The enhancement of the posterior pituitary lobe, however, occurred simultaneously with that of the straight sinus in all of the controls but in only 14 of 19 patients with CDI (Fig. 1Go).


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  		TABLE 2. Standard pituitary MR and dynamic MR imaging findings in patients with CDI: time to enhancement of straight sinus, posterior pituitary, and anterior pituitary after GD-DTPA administration

 


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  		FIG. 1. A–H, Sagittal dynamic MR images in a normal subject showing (C) simultaneous enhancement of the straight sinus (double white arrows) and of the posterior pituitary (white arrowhead). Progressive enhancement of the anterior pituitary in the remaining images (D–H, white arrows) is compatible with a normal superior hypophyseal artery system.

 
In the remaining five patients, the enhancement of the straight sinus was not associated with contrast enhancement of the posterior pituitary, although a normally progressive enhancement of the anterior pituitary occurred (Table 2Go, Fig. 2Go). There were no clinical, biochemical, or other radiological differences between the five patients who showed vascular impairment and the 14 patients with normal posterior pituitary enhancement pattern.



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  		FIG. 2. A–H, Sagittal dynamic MR images in a patient with idiopathic CDI and an abnormal enhancement pattern. Enhancement of the straight sinus (D, double white arrows) was not associated with the enhancement of the posterior pituitary (white arrowhead); absence of posterior pituitary enhancement is shown in the remaining pictures (E–H). Enhancement of the anterior pituitary is clearly evident in E with progressive centripetal completion (F–H, white arrow).

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
Recent advances in pituitary gland imaging techniques have provided a new paradigm for the study of hypothalamic-pituitary vascularization and raise questions about the relationship between pituitary vascular impairment and pituitary dysfunction. The use of MR imaging in the work-up of suspected hypothalamic-pituitary disorders has amply proven to be an extraordinary tool for the diagnosis and prognosis of children with idiopathic GH deficiency (28, 29). Indeed, the pituitary MR phenotype may even represent an important criterion for the selection of the candidate gene involved in abnormal pituitary development (30).

Our improved understanding of vascular pituitary anatomy with dynamic MR clearly shows the temporal sequence of contrast enhancement in the various portions of the pituitary gland (31, 32). Data suggest that the early sequential images from postcontrast dynamic MR studies give the truest and most reliable representation of the posterior pituitary lobe (33). Moreover, the time-dependent enhancement patterns in pituitary adenomas confirm the findings of angiographic studies (34), reinforcing the essential role that dynamic MR technique plays in the evaluation of patients with hypothalamic-pituitary ischemic disorders. The importance of dynamic MR technique is further demonstrated both by studies that show that delayed enhancement of the anterior pituitary gland is associated with pituitary vasculopathy in patients with evolving pituitary hormone deficiency (27) and by studies that have reported abnormal pituitary vascularization in the course of lymphocytic hypophysitis (35, 36).

Although CDI has been described as occurring after brain blood hypoperfusion, including respiratory failure, carbon monoxide poisoning, cardiorespiratory arrest, or hypoxic encephalopathy (22, 23, 24, 37, 38, 39), no systematic studies have so far been carried out in patients who might have vascular-dependent CDI. The present study attempts to examine the questions of whether vascular impairment of the inferior hypophyseal arteries could affect posterior pituitary function in idiopathic CDI and precisely how to define such impairment through the use of a noninvasive diagnostic technique.

In our study, we identified patients with idiopathic CDI who displayed similar standard MR imaging features such as normal anterior pituitary and pituitary stalk size with absent posterior pituitary hyperintensity. In addition to these findings, we determined that 14 of 19 CDI patients showed (with the straight sinus as a reliable temporal reference point at dynamic MR evaluation) an enhancement of the anterior and posterior pituitary lobes within the normal expected time, as well as a normal enhancement pattern. On the contrary, in the remaining five patients, no enhancement of the posterior pituitary lobe was observed, whereas a normal enhancement of the anterior pituitary gland occurred. The normal pattern of contrast diffusion within the posterior pituitary that was observed in the controls and in the majority of patients with idiopathic CDI, together with the lack of posterior pituitary enhancement in our five patients, cannot simply be considered a chance occurrence; rather, it strongly suggests a causal link. It seems clear that such an abnormal pattern of contrast enhancement, one never seen in more than 250 MR exams in controls or in other patients with CDI of various etiologies (our unpublished data), deserves close attention. Indeed, the association of abnormal arterial local blood flow with posterior pituitary dysfunction in some patients with idiopathic CDI emphasizes the importance of the inferior hypophyseal artery route in the pathophysiology of CDI. Our data are not comparable with the only reported study showing delayed enhancement of the posterior pituitary lobe in patients with idiopathic CDI because, unlike our study, its conclusions were affected by the use of a long framing time (40).

Our data suggest that vascular injury with consequent reduction of blood flow through the inferior hypophyseal artery is associated with CDI. The causal mechanism affecting posterior pituitary blood supply remains largely undefined, even if we cannot completely rule out arterial vasospasm or vasoconstriction phenomena or other mechanisms including cytokine modulation from adjacent osseous lesions or an autoimmune effect. CDI has been induced by selective embolization (with hypertonic and pure ethanol solutions) of the meningohypophyseal trunk (composed of three branches, namely the inferior hypophyseal, the dorsal meningeal, and the tentorial arteries) supplying an indirect carotid cavernous fistula (41). Moreover, CDI has been also described as a complication of systemic fat embolism or after transient ischemic attacks (16, 17, 18, 42). The high frequency of posterior pituitary lesions observed postmortem has been attributed to the large blood flow derived from the inferior hypophyseal artery. It is worth pointing out that anterior pituitary dysfunction may also occur in the absence of structural changes visible upon imaging and has been attributed to microinjury leading to vascular impairment and scarring (27). The possibility of a congenital lack or poor development of the posterior pituitary vascular system, without any evidence of macroscopic morphological abnormality of the pituitary gland at MR imaging or secondary changes of vascular supply due to a local inflammatory process (vasculitis?), cannot be ruled out.

In conclusion, the lack of posterior pituitary enhancement in patients with idiopathic CDI suggests abnormal vascularization of the posterior pituitary and provides additional valuable information for understanding this heterogeneous condition. Whereas in the past only severe conditions like hypoxic/ischemic encephalopathy were clearly associated with the onset of CDI, our data suggest that even selective vascular damage affecting the inferior hypophyseal arteries can be causally linked to CDI. We believe that by drawing attention to this disease entity, better understanding of its etiological variability will be possible as more cases of vascular-dependent CDI are identified.


   Acknowledgments
 
We thank Patti Grunther for her help in the revision of this paper.


   Footnotes
 
Abbreviations: CDI, Central diabetes insipidus; GD-DTPA, gadopentetate dimeglumine-diethylenetriamine pentaacetic acid; MR, magnetic resonance.

Received September 15, 2003.

Accepted January 8, 2004.


   References
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 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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