Original Article
Lymphocytic Infundibuloneurohypophysitis as a Cause of Central Diabetes Insipidus
N Engl J Med 1993; 329:683-689September 2, 1993
- Abstract
Background
Central diabetes insipidus may be familial, secondary to hypothalamic or pituitary disorders, or idiopathic. Idiopathic central diabetes insipidus is characterized by selective hypofunction of the hypothalamic-neurohypophysial system, but its cause is unknown.
Methods
We studied 17 patients with idiopathic diabetes insipidus, in whom the duration of the disorder ranged from 2 months to 20 years. Only four patients had been treated with vasopressin before the study began. All the patients underwent endocrinologic studies and magnetic resonance imaging (MRI) with a 1.5-T superconducting unit, and two patients had biopsies of the neurohypophysis or the pituitary stalk.
Results
Nine of the 17 patients had thickening of the pituitary stalk, enlargement of the neurohypophysis, or both and lacked the hyperintense signal of the normal neurohypophysis. In the remaining eight patients, the pituitary stalk and the neurohypophysis were normal, although the hyperintense signal was absent. The abnormalities of thickening and enlargement were seen on MRI only in the patients who had had diabetes insipidus for less than two years, and the abnormalities disappeared during follow-up, suggesting a self-limited process. In addition to vasopressin deficiency, two patients had mild hyperprolactinemia and nine had impaired secretory responses of growth hormone to insulin-induced hypoglycemia. The two biopsies revealed chronic inflammation, with infiltration of lymphocytes (mainly T lymphocytes) and plasma cells.
Conclusions
Diabetes insipidus can be caused by lymphocytic infundibuloneurohypophysitis, which can be detected by MRI. The natural course of the disorder is self-limited.
Media in This Article
Figure 1
Sagittal T1-Weighted MRI Scans in Patient 1.Figure 2
Biopsy Specimens of the Pituitary Stalk in Patient 1 (Panel A and Panel C) and the Neurohypophysis in Patient 2 (Panel B).Article Activity
- Article
Central diabetes insipidus is a chronic disorder characterized by polyuria and polydipsia due to vasopressin deficiency. The disorder may be familial, idiopathic, or secondary. Familial diabetes insipidus is characterized by autosomal dominant inheritance and, at least in some families, mutations of the vasopressin-neurophysin II genes1,2. Secondary diabetes insipidus, the most common form of the disorder, is caused by tumors, infections, trauma, or other processes (such as histiocytosis and vascular lesions) that damage the hypothalamic-neurohypophysial system. Idiopathic diabetes insipidus, which accounts for 10 to 30 percent of cases of central diabetes insipidus,3,4 is characterized by selective hypofunction of the hypothalamic-neurohypophysial system. Antibodies against magnicellular neurons of the hypothalamus have been detected in some patients, leading to speculation that it is an autoimmune disorder5,6. Its pathogenesis, however, is unknown.
Magnetic resonance imaging (MRI) has shown that the normal neurohypophysis generates a hyperintense signal on T-weighted images7-9. Although the origin of this hyperintense signal is not known,10,11 it is seen on MRI scans from almost all normal subjects,8,9 and its intensity disappears after the injection of hypertonic saline10. The hyperintense signal is generally not seen in patients with idiopathic or secondary diabetes insipidus8,12,13.
We undertook this study in an attempt to determine the pathogenesis and pathophysiologic processes of idiopathic diabetes insipidus by MRI and endocrinologic testing. We found abnormalities on MRI scans of the pituitary stalk and neurohypophysis in nine patients and performed biopsies in two of them, which demonstrated lymphocytic inflammation. These investigations provide new insight into the pathogenesis of idiopathic diabetes insipidus.
Case Reports
We studied all 17 patients (4 men and 13 women, 28 to 73 years old) admitted to our hospital with idiopathic diabetes insipidus from 1986 to 1992 (Table 1Table 1
Clinical Characteristics of 17 Patients with Idiopathic Diabetes Insipidus, According to Results of MRI of the Pituitary Stalk or Neurohypophysis.). The diagnosis of idiopathic diabetes insipidus was based on normal computed tomographic (CT) scans of the head, the lack of symptoms and signs of hypothalamic damage other than diabetes insipidus, and the results of endocrine tests. The duration of the disorder ranged from 2 months to 20 years. Four of the 17 patients had been treated with vasopressin (an analogue of arginine vasopressin), which was discontinued at least one week before the study. None of the patients had a family history of diabetes insipidus. One patient (Patient 9) had had hyperthyroidism caused by Graves' disease 30 years before the onset of diabetes insipidus and had a small goiter on admission, but no other patient had any history of autoimmune disease. Patients 1, 2, 3, 4, 5, and 9 had had operations for appendicitis or ectopic pregnancy or had undergone cesarean section. Three patients had positive tests for antinuclear antibodies, and two had positive tests for rheumatoid factor. None of the nine patients tested had antithyroglobulin or antithyroid microsomal antibodies. Tests for antipituitary, antineuronal, and antivasopressin antibodies were not performed. The results of tuberculin skin tests were either positive or borderline in the 15 patients tested. Serum concentrations of angiotensin-converting enzyme were normal in the 12 patients tested. Chest and bone roentgenograms were normal in all 17 patients, except that Patient 2 had mild cardiomegaly due to mitral stenosis and aortic regurgitation and Patient 5 had pleural thickening. All the patients gave informed consent to the tests.The patients were divided into two groups. Group 1 consisted of the nine patients who had abnormalities in the pituitary stalk, neurohypophysis, or both on MRI. Group 2 consisted of the eight patients whose MRI scans were normal except for the absence of the normal hyperintense signal. The cases of the two patients in group 1 who had biopsies of the neurohypophysis or the pituitary stalk are described below.
Patient 1
Patient 1 was a 47-year-old woman admitted in 1987. Five months earlier, she had experienced a sudden onset of polyuria and polydipsia, and one month earlier her vision had suddenly become blurred. Her menstrual cycles had been regular. Physical examination was normal except for mild papilledema. The results of routine laboratory tests, skull and other bone roentgenograms, and CT scans of the head were normal. A tuberculin skin test was positive. The cerebrospinal fluid obtained by lumbar puncture had a protein concentration of 32 mg per deciliter and 1 cell per cubic millimeter. The cerebrospinal fluid pressure was normal. MRI revealed thickening of the pituitary stalk and a slight enlargement of the neurohypophysis, but no ventricular dilatation (Figure 1Figure 1
Sagittal T1-Weighted MRI Scans in Patient 1.). Because the patient was thought to have a tumor or histiocytosis of this region, frontal craniotomy was performed. A small biopsy specimen obtained from the thickened pituitary stalk showed lymphocytic inflammation (Figure 2AFigure 2Biopsy Specimens of the Pituitary Stalk in Patient 1 (Panel A and Panel C) and the Neurohypophysis in Patient 2 (Panel B).); therefore, no further surgery was performed. Postoperatively, the patient was treated with betamethasone for seven days and then with hydrocortisone, which was gradually withdrawn over the following six months. The papilledema disappeared 40 days after surgery and did not reappear after the cessation of hydrocortisone therapy. The patient's diabetes insipidus was treated with vasopressin. She has remained well, but continues to require vasopressin therapy.Patient 2
Patient 2 was a 55-year-old man who had a sudden onset of polyuria and polydipsia two months before admission in 1988. Physical examination was normal, except for a heart murmur due to valvular disease. A test for antinuclear antibody was positive (with a speckled pattern), but other serologic tests were negative. A tuberculin skin test was positive. The cerebrospinal fluid protein concentration was 34 mg per deciliter, and the cell count was 13 lymphocytes per cubic millimeter. A CT scan of the head was normal, but MRI revealed enlargement of the neurohypophysis (Figure 3Figure 3
Sagittal T1-Weighted MRI Scans from Patient 2.). Because of the suspicion of an intrasellar tumor, transsphenoidal surgery was performed. The neurohypophysis was enlarged, but because a biopsy specimen showed chronic inflammation (Figure 2B), no further surgery was performed. The patient was treated with prednisolone for four months and continues to receive vasopressin; he has remained well since that time.Methods
MRI
A 1.5-T superconducting MRI unit (Sigma, General Electric) was used. MRI scans were obtained with the spin-echo technique. T1-weighted images were obtained with a repetition time of 400 or 500 msec and an echo time of 20 or 25 msec. T1-weighted images enhanced with gadolinium-diethylenetriamine pentaacetic acid were obtained immediately after the injection of 0.1 mmol of the contrast agent per kilogram of body weight.
Endocrinologic Studies
All endocrinologic tests were performed after an overnight fast, with the patient at rest. Plasma vasopressin was measured by radioimmunoassay14 before and after four to eight hours of water deprivation. We measured plasma concentrations of growth hormone, prolactin, luteinizing hormone, follicle-stimulating hormone, thyrotropin, cortisol (all Daiichi Radioisotope Laboratories kits), testosterone (Japan DPC kit), thyroxine (Dainabot Laboratories kit), and thyroxine corticotropin (Mitsubishi Petrochemical kit). Provocative tests were performed on separate days as follows: for thyrotropin and prolactin, a bolus injection of 500 μg of thyrotropin-releasing hormone; for luteinizing hormone and follicle-stimulating hormone, 100 μg of gonadotropin-releasing hormone; for growth hormone, 100 μg of growth hormone-releasing hormone and 0.1 unit of regular insulin per kilogram of body weight (also for corticotropin and cortisol). Multiple blood samples were collected to measure plasma hormone concentrations before and for up to 120 minutes after the injections.
Histologic Studies
Biopsy specimens were fixed routinely in 10 percent buffered formalin, embedded in paraffin, and stained with hematoxylin and eosin. Immunohistochemical staining with the avidin-biotin complex technique was also carried out in paraffin sections with monoclonal and polyclonal antibodies specific for B or T lymphocytes, Langerhans-cell histiocytosis cells, or endothelial cells. The monoclonal antibodies used were as follows: L26 (Dako) to detect CD20 B cells, antibody MT1 (Bio-Science Products) to detect CD43 T cells, antibody UCHL1 (Dako) to detect CD45-RO T cells,15 and antibody LN3 (Techniclone International) to detect HLA-DR. The polyclonal antibodies used were antibodies against immunoglobulin light chains (Dako), CD3 T cells (Dako),16 S-100 protein of Langerhans cells (Dako), and factor VIII-related antigen of endothelial cells (Dako).
Results
The clinical characteristics of the 17 patients are shown in Table 1. There were two men in each group. Of the 13 women, all 6 who were premenopausal had regular menstrual cycles. All the women in both groups had had children; all had resumed their menstrual cycles after their pregnancies, and none had had a complicated delivery.
All the patients in group 1 had had diabetes insipidus for less than two years, whereas four of the eight patients in group 2 had had the disease for more than two years. None of the patients had symptoms of anterior pituitary hormone deficiency at the time of admission, and none were taking any medication that might contribute to polyuria, such as a diuretic agent. After Patients 1 and 2, the patients in group 1 were followed without surgery, because the abnormalities on MRI were mild (except in Patient 4) and because, on the basis of our experience in Patients 1 and 2, we expected spontaneous regression of the abnormalities. All the patients received vasopressin therapy. We discontinued this therapy on more than one occasion in all the patients in group 1, but diabetes insipidus immediately reappeared, except in Patient 4. This patient had little polyuria for 10 months, but it then reappeared, and vasopressin therapy was resumed. Eight of the nine patients in group 1 and four of the eight patients in group 2 were followed for more than two years. In none of them did symptoms or signs of hypopituitarism or hypothalamic disturbances other than diabetes insipidus develop.
MRI Scans
The T1-weighted images in all the patients in both groups lacked the hyperintense signal of the neurohypophysis that is seen in almost all normal subjects. The anterior pituitary was normal. As Table 1 and Figure 1 and Figure 3 indicate, seven patients in group 1 had thickening of the pituitary stalk whose intensity was enhanced after the administration of gadolinium. Enlargement of the neurohypophysis was seen in four patients on sagittal images (Figure 3), and its intensity was also enhanced by gadolinium.
The thickening of the pituitary stalk in Patient 1 regressed after surgery and steroid treatment, was a little greater one year after steroid treatment ended, and had almost disappeared four years after surgery (Figure 1). In Patient 2, the enlargement of the neurohypophysis decreased rapidly after biopsy and steroid treatment (Figure 3). The remaining seven patients in group 1 received only vasopressin therapy. Six had repeated MRI studies more than two years later; in all six the abnormalities on MRI were markedly improved (Table 1), although the hyperintense signal of the neurohypophysis remained absent. The four patients in group 2 who had repeat imaging studies had no changes.
Endocrinologic Studies
The results of the endocrinologic studies are shown in Table 2Table 2
Results of Endocrinologic Tests in 17 Patients with Idiopathic Diabetes Insipidus, According to Results of MRI of the Pituitary Stalk and Neurohypophysis.. Urinary osmolality and plasma vasopressin concentrations during water deprivation were low in group 1 despite high plasma osmolality; in only one patient (Patient 8) did urinary osmolality exceed plasma osmolality. In group 2, two patients had slight increases in urinary osmolality and plasma vasopressin concentrations during water deprivation. All the patients had an increase in urinary osmolality in response to exogenous vasopressin (data not shown). Thus, one patient in group 1 and two patients in group 2 could be considered to have partial diabetes insipidus, whereas in the remaining patients it was complete.Plasma luteinizing hormone and follicle-stimulating hormone responses to gonadotropin-releasing hormone were normal for age in the men and menstrual status in the women. Plasma testosterone concentrations were within normal limits in all three men tested. All the patients had normal plasma thyroxine concentrations. The plasma thyroid-stimulating hormone responses to thyrotropin-releasing hormone were normal in all 14 patients tested, as were the plasma cortisol responses to insulin-induced hypoglycemia. The basal plasma prolactin concentrations were slightly elevated in 1 patient in each group, and the concentrations increased 160 to 1000 percent in response to thyrotropin-releasing hormone in the 13 patients tested. The plasma growth hormone responses to insulin-induced hypoglycemia were low in one patient, slightly low in five patients, and normal in three patients in group 1 and low in one patient and slightly low in two patients in group 2. The four patients tested with growth hormone-releasing hormone had peak plasma growth hormone concentrations of more than 5 ng per milliliter. These tests were not repeated, because no patient had symptoms or signs of anterior pituitary hormone deficiency during follow-up.
Histologic Studies
Microscopical examination of the biopsy specimens from Patients 1 and 2 revealed inflammatory infiltrates composed mainly of lymphocytes and plasma cells, with scattered eosinophils, neutrophils, and histiocytes (Figure 2). Most of the infiltrating lymphocytes stained with MT1, UCHL1 and the antibody against CD3, indicating that they were T cells (Figure 2C). The plasma cells were polyclonal in terms of immunoglobulin light-chain types. Although some histiocytes were seen, especially in the biopsy specimen from Patient 2, they did not contain S-100 protein. Endothelial cells that stained with antibodies against factor VIII-related antigen and scattered lymphocytes that stained with LN3 were seen in both biopsy specimens. There was no evidence of caseous necrosis or epithelioid granulomas, and no neuronal elements were seen. These findings excluded the possibility of tuberculosis, sarcoidosis, Langerhans-cell histiocytosis, malignant lymphoma, and meningioma.
Discussion
The 17 patients we studied all had clinical features and laboratory findings compatible with idiopathic diabetes insipidus. The diabetes insipidus was complete in 14 patients and partial in 3 patients. The only exceptional finding was transient papilledema in Patient 1, probably caused by inflammation in the pituitary stalk. Some patients, mostly in group 1, had subnormal responses of plasma growth hormone to insulin-induced hypoglycemia, as have been reported in other patients with idiopathic diabetes insipidus17,18. The reason for these subnormal responses is unknown. The plasma growth hormone responses to growth hormone-releasing hormone were normal in all four patients tested, three of whom had slightly low responses to insulin. It appears that there are derangements in the regulation of growth hormone secretion in some patients with idiopathic diabetes insipidus, in either the hypothalamus or the median eminence.
The MRI scans in all 17 patients were compatible with the diagnosis of idiopathic diabetes insipidus, in that the anterior pituitary gland and hypothalamus were normal and the hyperintense signal of the normal neurohypophysis on T1-weighted images was not seen12,13. Although the hyperintense signal may be present in some patients with idiopathic diabetes insipidus,19,20 it is generally absent. In addition, 9 of the 17 patients had thickening of the pituitary stalk, enlargement of the neurohypophysis, or both. The abnormalities were marked in Patients 1, 2, and 4, and we performed biopsies in the first two patients because we suspected a tumor. Histologic examination of the biopsy specimens showed inflammatory infiltrates composed of lymphocytes and plasma cells, with scattered granulocytes. Because the MRI abnormalities regressed in these patients, subsequent patients were simply followed. We cannot be certain that the patients who did not have biopsies had the same abnormalities, but we think it likely, given their MRI results and subsequent courses.
The pituitary stalk may be thickened in patients with Langerhans-cell histiocytosis,19,21,22 which should be carefully differentiated from lymphocytic infundibuloneurohypophysitis. Our patients had no signs of histiocytosis in other tissues and no hypopituitarism, which is often present in this disorder. The histologic findings in the two patients studied differed from those of Langerhans-cell histiocytosis, and staining for S-100 protein, the presence of which is characteristic of histiocytosis, was negative. Primary intracranial plasma-cell granuloma, a rare disorder with plasma-cell and lymphocytic infiltration,23,24 can occur anywhere in the brain. If it occurs in the hypothalamus, it can cause diabetes insipidus and hypopituitarism. The histologic findings in our patients were similar to those in patients with plasma-cell granuloma, but no tumor formation was seen, and the clinical course was different. Rare meningiomas contain plasma-cell and lymphocytic components25. Our patients had no meningoepithelial components and no tumor formation. Tuberculosis and sarcoidosis can be ruled out by the absence of granuloma, and the possibility of plasmacytoma can be excluded by the polyclonality of the plasma cells. Lymphoma is also unlikely, because of the lack of atypia and the T-cell phenotype; lymphoma in the central nervous system is almost exclusively of the B-cell type26. Germinoma can also be excluded, given the age and clinical course of the patients.
Only a few previous reports have described patients with lymphocytic inflammation confined to the hypothalamic-neurohypophysial system. In one patient who had acute onset of diabetes insipidus and subsequently died of bronchopneumonia27 and another patient who died of an acute attack of bronchial asthma,28 autopsy revealed lymphocytic inflammation limited to the hypothalamic-neurohypophysial system. An additional patient with diabetes insipidus had biopsies that showed chronic inflammation in the neurohypophysis29. The inflammatory cells in these patients consisted of lymphocytes and plasma cells. A few patients with lymphocytic (adeno)hypophysitis who also had diabetes insipidus have been reported30,31. In these patients, the anterior pituitary was the principal site of inflammation, and anterior pituitary cells were seen among the plasma cells and lymphocytes. In most patients with lymphocytic hypophysitis the lymphocytes are mostly CD4 cells,32,33 and there is unequivocal evidence of hypopituitarism. Amenorrhea is the most common initial symptom,34 but in some women the disorder first becomes evident during pregnancy33-35. MRI usually reveals a large intrasellar mass, which frequently extends toward the suprasellar region35. These findings in patients with lymphocytic hypophysitis are distinct from those in our patients. It is therefore likely that the lymphocytic infundibuloneurohypophysitis we describe here is not a variety of lymphocytic hypophysitis.
The natural course of this disorder is also unique. In the two patients who received glucocorticoid treatment after surgery, the width of the pituitary stalk or the size of the neurohypophysis diminished. The lesions regressed spontaneously in other patients. These results suggest that the inflammatory process was self-limited and regressed spontaneously, perhaps after the destruction of all neurons. This sequence is compatible with the autoimmune hypothesis of idiopathic diabetes insipidus. The preponderance of women among our patients and the presence of T-cell infiltration in the tissue also favor this hypothesis, although few of the patients had other autoimmune diseases. We think it likely that patients in group 2, half of whom had had diabetes insipidus for longer than any of the patients in group 1, had the same disorder but that it had regressed before we studied them. Although we have not confirmed the histologic features in many patients with abnormalities on MRI, we think that lymphocytic infundibuloneurohypophysitis is a common cause of what was previously considered to be idiopathic diabetes insipidus.
Supported in part by a grant from the Japanese Ministry of Health and Welfare.
Source Information
From the Departments of Medicine (H.I., K.N., A.S., Y.O., T.S.) and Radiology (I.F.), Kyoto University Faculty of Medicine, and the Laboratory of Anatomical Pathology, Kyoto University Hospital (H.Y.), both in Kyoto, Japan.
Address reprint requests to Dr. Imura at Kyoto University, Kyoto 606-01, Japan.
- References
References
1
Ito M ,Mori Y ,Oiso Y ,Saito H . A single base substitution in the coding region for neurophysin II associated with familial central diabetes insipidus. J Clin Invest 1991;87:725-728
CrossRef | Web of Science | Medline2
Bahnsen U ,Oosting P ,Swaab DF ,Nahke P ,Richter D ,Schmale H . A missense mutation in the vasopressin-neurophysin precursor gene cosegregates with human autosomal dominant neurohypophyseal diabetes insipidus. EMBO J 1992;11:19-23
Web of Science | Medline3
Moses AM ,Notman DD . Diabetes insipidus and syndrome of inappropriate antidiuretic hormone secretion (SIADH). Adv Intern Med 1982;27:73-100
Medline4
Greger NG ,Kirkland RT ,Clayton GW ,Kirkland JL . Central diabetes insipidus: 22 years' experience. Am J Dis Child 1986;140:551-554
Web of Science | Medline5
Scherbaum WA ,Czernichow P ,Bottazzo GF ,Doniach D . Diabetes insipidus in children. IV. A possible autoimmune type with vasopressin cell antibodies. J Pediatr 1985;107:922-925
CrossRef | Web of Science | Medline6
Scherbaum WA ,Wass JA ,Besser GM ,Bottazzo GF ,Doniach D . Autoimmune cranial diabetes insipidus: its association with other endocrine diseases and with histiocytosis X. Clin Endocrinol (Oxf) 1986;25:411-420
CrossRef | Web of Science | Medline7
Nishimura K ,Fujisawa I ,Togashi K , et al. Posterior lobe of the pituitary: identification by lack of chemical shift artifact in MR imaging. J Comput Assist Tomogr 1986;10:899-902
CrossRef | Web of Science | Medline8
Gudinchet F ,Brunelle F ,Barth MO , et al. MR imaging of the posterior hypophysis in children. AJR Am J Roentgenol 1989;153:351-354
Web of Science | Medline9
Fujisawa I ,Asato R ,Nishimura K , et al. Anterior and posterior lobes of the pituitary gland: assessment by 1.5 T MR imaging. J Comput Assist Tomogr 1987;11:214-220
CrossRef | Web of Science | Medline10
Fujisawa I ,Asato R ,Kawata M , et al. Hyperintense signal of the posterior pituitary on T1-weighted MR images: an experimental study. J Comput Assist Tomogr 1989;13:371-377
CrossRef | Web of Science | Medline11
Kucharczyk J ,Kucharczyk W ,Berry I , et al. Histochemical characterization and functional significance of the hyperintense signal on MR images of the posterior pituitary. AJR Am J Roentgenol 1989;152:153-157
Web of Science | Medline12
Fujisawa I ,Nishimura K ,Asato R , et al. Posterior lobe of the pituitary in diabetes insipidus: MR findings. J Comput Assist Tomogr 1987;11:221-225
CrossRef | Web of Science | Medline13
Colombo N ,Berry I ,Kucharczyk J , et al. Posterior pituitary gland: appearance on MR images in normal and pathologic states. Radiology 1987;165:481-485
Web of Science | Medline14
Yamada T ,Nakao K ,Morii N , et al. Central effect of atrial natriuretic polypeptide on angiotensin II-stimulated vasopressin secretion in conscious rats. Eur J Pharmacol 1986;125:453-456
CrossRef | Web of Science | Medline15
Shima N ,Kobashi Y ,Tsutsui K , et al. Extranodal non-Hodgkin's lymphoma of the head and neck: a clinicopathologic study in the Kyoto-Nara area of Japan. Cancer 1990;66:1190-1197
CrossRef | Web of Science | Medline16
Mason DY ,Cordell J ,Brown M , et al. Detection of T cells in paraffin wax embedded tissue using antibodies against a peptide sequence from the CD3 antigen. J Clin Pathol 1989;42:1194-1200
CrossRef | Web of Science | Medline17
Youlton R ,Kaplan SL ,Grumbach MM . Growth and growth hormone. IV. Limitations of the growth hormone response to insulin and arginine and of the immunoreactive insulin response to arginine in the assessment of growth hormone deficiency in children. Pediatrics 1969;43:989-1004
Web of Science | Medline18
Czernichow P ,Pomarede R ,Basmaciogullari A ,Brauner R ,Rappaport R . Diabetes insipidus in children. III. Anterior pituitary dysfunction in idiopathic types. J Pediatr 1985;106:41-44
CrossRef | Web of Science | Medline19
Maghnie M ,Ville A ,Arico M , et al. Correlation between magnetic resonance imaging of posterior pituitary and neurohypophyseal function in children with diabetes insipidus. J Clin Endocrinol Metab 1992;74:795-800
CrossRef | Web of Science | Medline20
Cacciari E ,Zucchini S ,Carla G , et al. Endocrine function and morphological findings in patients with disorders of the hypothalamo-pituitary area: a study with magnetic resonance. Arch Dis Child 1990;65:1199-1202
CrossRef | Web of Science | Medline21
Tien RD ,Newton TH ,McDermott MW ,Dillon WP ,Kucharczyk J . Thickened pituitary stalk on MR images in patients with diabetes insipidus and Langerhans cell histiocytosis. AJNR Am J Neuroradiol 1990;11:703-708
Web of Science | Medline22
Tien R ,Kucharczyk J ,Kucharczyk W . MR imaging of the brain in patients with diabetes insipidus. AJNR Am J Neuroradiol 1991;12:533-542
Web of Science | Medline23
Cannella DM ,Prezyna AP ,Kapp JP . Primary intracranial plasma-cell granuloma: case report. J Neurosurg 1988;69:785-788
CrossRef | Web of Science | Medline24
Gochman GA ,Duffy K ,Crandall PH ,Vinters HV . Plasma cell granuloma of the brain. Surg Neurol 1990;33:347-352
CrossRef | Web of Science | Medline25
Horten BC ,Urich H ,Stefoski D . Meningiomas with conspicuous plasma cell-lymphocytic components: a report of five cases. Cancer 1979;43:258-264
CrossRef | Web of Science | Medline26
Aozasa K ,Ohsawa M ,Yamabe H , et al. Malignant lymphoma of the central nervous system in Japan: histologic and immunohistologic studies. Int J Cancer 1990;45:632-636
CrossRef | Web of Science | Medline27
Kojima H ,Nojima T ,Nagashima K ,Ono Y ,Kudo M ,Ishikura M . Diabetes insipidus caused by lymphocytic infundibuloneurohypophysitis. Arch Pathol Lab Med 1989;113:1399-1401
Web of Science | Medline28
Saito T ,Yoshida S ,Nakao K ,Takanashi R . Chronic hypernatremia associated with inflammation of the neurohypophysis. J Clin Endocrinol Metab 1970;31:391-396
CrossRef | Web of Science | Medline29
Higuchi M ,Arita N ,Mori S , et al. Four cases of granulomatous lesion in the pituitary. Clin Endocrinol Tokyo 1992;40:Suppl:128-13330
Vanneste JA ,Kamphorst W . Lymphocytic hypophysitis. Surg Neurol 1987;28:145-149
CrossRef | Web of Science | Medline31
Nussbaum CE ,Okawara SH ,Jacobs LS . Lymphocytic hypophysitis with involvement of the cavernous sinus and hypothalamus. Neurosurgery 1991;28:440-444
CrossRef | Web of Science | Medline32
Jensen MD ,Handwerger BS ,Scheithauer BW ,Carpenter PC ,Mirakian R ,Banks PM . Lymphocytic hypophysitis with isolated corticotropin deficiency. Ann Intern Med 1986;105:200-203
Web of Science | Medline33
McCutcheon IE ,Oldfield EH . Lymphocytic adenohypophysitis presenting as infertility: case report. J Neurosurg 1991;74:821-826
CrossRef | Web of Science | Medline34
Asa SL ,Bilbao JM ,Kovacs K ,Josse RG ,Kreines K . Lymphocytic hypophysitis of pregnancy resulting in hypopituitarism: a distinct clinicopathologic entity. Ann Intern Med 1981;95:166-171
Web of Science | Medline35
Cosman F ,Post KD ,Holub DA ,Wardlaw SL . Lymphocytic hypophysitis: report of 3 new cases and review of the literature. Medicine 1989;68:240-256
CrossRef | Web of Science | Medline
- Citing Articles (85)
Citing Articles
1
Keisuke Suzuki, Naoki Izawa, Toshiki Nakamura, Kenichi Hashimoto, Keita Ouchi, Hideki Sakuta, Yohei Asakawa, Ayaka Numao, Koichi Hirata. (2011) Lymphocytic Hypophysitis Accompanied by Aseptic Meningitis Mimics Subacute Meningoencephalitis. Internal Medicine 50:18, 2025-2030
CrossRef2
Satoshi Saito, Chiaki Mori, Keiichiro Toma, Tamotsu Kubori, Kazuto Nishinaka, Fukashi Udaka. (2011) A case of optic neuritis associated with lymphocytic hypophysitis revealed by pattern-reversal VEP. Rinsho Shinkeigaku 51:1, 27-31
CrossRef3
Prasad Katulanda, Godwin R Constantine, Muditha I Weerakkody, Yashasvi S Perera, Mahesh G Jayawardena, Preethi Wijegoonewardena, David R Matthews, Mohamed H.R. Sheriff. (2011) Can we bridge the gap? Knowledge and practices related to Diabetes Mellitus among general practitioners in a developing country: A cross sectional study. Asia Pacific Family Medicine 10:1, 15
CrossRef4
Daniel G. Bichet. 2011. The Posterior Pituitary. , 261-299.
CrossRef5
Y. Nakata, N. Sato, T. Masumoto, H. Mori, H. Akai, H. Nobusawa, Y. Adachi, H. Oba, K. Ohtomo. (2010) Parasellar T2 Dark Sign on MR Imaging in Patients with Lymphocytic Hypophysitis. American Journal of Neuroradiology 31:10, 1944-1950
CrossRef6
Fabio Rotondo, Andres Quintanar-Stephano, Sylvia L. Asa, Matilde Lombardero, Istvan Berczi, Bernd W. Scheithauer, Eva Horvath, Kalman Kovacs. (2010) Adenohypophysitis in rat pituitary allografts. International Journal of Experimental Pathology 91:5, 445-450
CrossRef7
Ernesto García Vicente, Valentín Del Villar Sordo, Ernesto Luis García y García. (2010) Trastornos del sodio. Medicina Clínica 134:12, 554-563
CrossRef8
Takamasa Nishiuchi, Hitomi Imachi, Koji Murao, Mako Fujiwara, Makoto Sato, Yukiko Nishiuchi, Yoshio Kushida, Reiji Haba, Atsushi Shindo, Takashi Tamiya, Toshihiko Ishida. (2010) Suprasellar Germinoma Masquerading As Lymphocytic Hypophysitis Associated With Central Diabetes Insipidus, Delayed Sexual Development, and Subsequent Hypopituitarism. The American Journal of the Medical Sciences 339:2, 195-199
CrossRef9
Hiroshi Akahori, Tatsuho Sugimoto. (2010) Lymphocytic Hypophysitis with a Long Latent Period from Onset of Central Diabetes Insipidus to Development of Pituitary Enlargement. Internal Medicine 49:15, 1565-1571
CrossRef10
Masanori Yamazaki, Ai Sato, Shin-ichi Nishio, Takeshi Uehara, Mitsuhisa Komatsu. (2010) Transient Polyuria Related to Central Diabetes Insipidus Caused by Lymphocytic Infundibulo-neurohypophysitis in a Patient Treated for Graves' Disease. Internal Medicine 49:17, 1885-1890
CrossRef11
Bernd W. Scheithauer, Kalman Kovacs, Eva Horvath, Ana I. Silva, Ricardo V. Lloyd. 2010. Pathology of the Pituitary and Sellar Region. , 371-416.
CrossRef12
Takumi Abe. (2008) Lymphocytic infundibulo-neurohypophysitis and infundibulo-panhypophysitis regarded as lymphocytic hypophysitis variant. Brain Tumor Pathology 25:2, 59-66
CrossRef13
Verena Gellner, Senta Kurschel, Michael Scarpatetti, Michael Mokry. (2008) Lymphocytic hypophysitis in the pediatric population. Child's Nervous System 24:7, 785-792
CrossRef14
Ji-Myoung Lee, Sang-Mi Park, Byung-Hee Hwang, Hyun-Sook Choi, Seong-Su Lee, Jee-Young Kim, Sung-Rae Kim, Kwang-Woo Lee, Ho-Young Son, Sung-Koo Kang, Soon-Jib Yoo. (2008) A Case of Lymphocytic Infundibuloneurohypophysitis Along with Central Diabetes Insipidus, and this Improved with Conservative Care. Journal of Korean Endocrine Society 23:2, 142
CrossRef15
Kazunori Kageyama, Maki Naraoka, Satoru Sakihara, Hidetoshi Ikeda, Toshiaki Sano, Toshihiro Suda. (2008) A Progressive Case of Lymphocytic Hypophysitis Accompanied by Paresis of the Left Abducens Nerve. Internal Medicine 47:13, 1245-1249
CrossRef16
LOUIS J. MUGLIA, JOSEPH A. MAJZOUB. 2008. Disorders of the Posterior Pituitary. , 335-373.
CrossRef17
Manjusha S. Rathi, Paul E. Jennings. (2008) Lymphocytic Hypophysitis Causing Hypopituitarism and Diabetes Insipidus, and Subsequent Association With Primary Autoimmune Hypothyroidism and Type 1 Diabetes Mellitus, in a Nonpregnant Female With Complete Recovery of Pituitary Function and Pregnancy. The Endocrinologist 18:1, 7-10
CrossRef18
Yasuyuki Arai, Koichiro Nabe, Hiroki Ikeda, Sachiko Honjo, Yoshiharu Wada, Yoshiyuki Hamamoto, Kazuhiro Nomura, Tomokazu Aoki, Toshiaki Sano, Hiroyuki Koshiyama. (2007) A case of lymphocytic panhypophysitis (LPH) during pregnancy. Endocrine 32:1, 117-121
CrossRef19
Ibrahim Kalelioglu, Ayse Kubat Uzum, Alkan Yildirim, Tulay Ozkan, Funda Gungor, Recep Has. (2007) Transient gestational diabetes insipidus diagnosed in successive pregnancies: review of pathophysiology, diagnosis, treatment, and management of delivery. Pituitary 10:1, 87-93
CrossRef20
Daisuke KITA, Osamu TACHIBANA, Yukihiro NAGAI, Hiroki SANO, Junkoh YAMASHITA. (2007) Granulomatous Pachymeningitis Around the Sella Turcica (Tolosa-Hunt Syndrome) Involving the Hypophysis. Neurologia medico-chirurgica 47:2, 85-88
CrossRef21
Seung Joon Chung, Seong Yong Lee, Choong Ho Shin, Sei Won Yang. (2007) Clinical, endocrinological and radiological courses in patients who was initially diagnosed as idiopathic central diabetes insipidus. Korean Journal of Pediatrics 50:11, 1110
CrossRef22
Mark E. Molitch, Mary P. Gillam. (2007) Lymphocytic Hypophysitis. Hormone Research 68:5, 145-150
CrossRef23
Suzanne Myers Adler, Joseph G. Verbalis. (2006) Disorders of Body Water Homeostasis in Critical Illness. Endocrinology & Metabolism Clinics of North America 35:4, 873-894
CrossRef24
Julie Buyst, Guy Massa, Catherine Christophe, Sylvie Tenoutasse, Claudine Heinrichs. (2006) Clinical, hormonal and imaging findings in 27 children with central diabetes insipidus. European Journal of Pediatrics 166:1, 43-49
CrossRef25
Mohamad Maghnie, Stefano Ghirardello, Annamaria De Bellis, Natascia di Iorgi, Linda Ambrosini, Andrea Secco, Mara De Amici, Carmine Tinelli, Antonio Bellastella, Renata Lorini. (2006) Idiopathic central diabetes insipidus in children and young adults is commonly associated with vasopressin-cell antibodies and markers of autoimmunity. Clinical Endocrinology 65:4, 470-478
CrossRef26
Yoko Mikami-Terao, Masaharu Akiyama, Takaaki Yanagisawa, Junko Takahashi-Fujigasaki, Kentaro Yokoi, Kohei Fukuoka, Mio Sakuma, Ichiro Miyata, Kohji Fujisawa, Shizuo Oi, Yoshikatsu Eto. (2006) Lymphocytic hypophysitis with central diabetes insipidus and subsequent hypopituitarism masking a suprasellar germinoma in a 13-year-old girl. Child's Nervous System 22:10, 1338-1343
CrossRef27
Ahmet Mesrur Halefoglu, Hakan Yildirim, Muzaffer Basak, Yuksel Altuntas. (2006) Pituitary stalk thickening on magnetic resonance imaging as a first sign of Langerhans cell histiocytosis in an adult. European Journal of Radiology Extra 59:2, 49-53
CrossRef28
Christopher Sonnier, Juraj Osterman, David Dubuisson, Jacob Vandersteenhoven. (2006) Lymphocytic Hypophysitis With Subsequent Development of Graves Disease. The Endocrinologist 16:4, 223-226
CrossRef29
Juan-Andres Rivera. (2006) Lymphocytic hypophysitis: Disease spectrum and approach to diagnosis and therapy. Pituitary 9:1, 35-45
CrossRef30
Helmut Prosch, Nicole Grois, Jos Bökkerink, Daniela Prayer, Ivo Leuschner, Milen Minkov, Helmut Gadner. (2006) Central diabetes insipidus: Is it Langerhans cell histiocytosis of the pituitary stalk? A diagnostic pitfall. Pediatric Blood & Cancer 46:3, 363-366
CrossRef31
Hee Joung Kim, Mi Yeon Kang, Kyung Won Kim, Hyun Seung Jeong, Hae Sung Kim, Sang Wan Kim, Seong Yeon Kim. (2006) Retrospective Observation of Long-Term Clinical Courses of Idiopathic Central Diabetes Insipidus in Adults. Journal of Korean Endocrine Society 21:6, 482
CrossRef32
Francisco Menor. (2005) El eje hipotálamo-hipófisis en el niño: consideraciones de imagen. Radiología 47:6, 305-321
CrossRef33
Rucha Jani, Andree de Bustros, Robert N. Stein. (2005) Heparin-Induced Thrombocytopenia Presenting as Central Diabetes Insipidus. The Endocrinologist 15:6, 374-376
CrossRef34
I. Hansenne. (2005) Thymic Transcription of Neurohypophysial and Insulin-Related Genes: Impact Upon T-Cell Differentiation and Self-Tolerance. Journal of Neuroendocrinology 17:5, 321-327
CrossRef35
Annamaria De Bellis, Antonio Bizzarro, Antonio Bellastella. (2005) Pituitary antibodies and lymphocytic hypophysitis. Best Practice & Research Clinical Endocrinology & Metabolism 19:1, 67-84
CrossRef36
Chun-Hao Huang, Kang-Ju Chou, Po-Tsang Lee, Chien-Liang Chen, Hsiao-Ming Chung, Hua-Chang Fang. (2005) A case of lymphocytic hypophysitis with masked diabetes insipidus unveiled by glucocorticoid replacement. American Journal of Kidney Diseases 45:1, 197-200
CrossRef37
Akira Matsuno, Michi Nakashima, Haruko Katayama, Mineko Murakami, Hideki Tanaka, Tadashi Nagashima, Kazuto Yamazaki, Isamu Sugano. (2005) A Patient Presenting Partial Diabetes Insipidus Diagnosed as Pituitary Abscess With Paranasal Sinusitis. The Endocrinologist 15:1, 10-13
CrossRef38
G Oswald, A Kinch, E Ruddy. (2004) Transfer to a patient centred, carbohydrate counting and insulin matching programme in a shortened time frame. Practical Diabetes International 21:9, 334-338
CrossRef39
Helmut Prosch, Nicole Grois, Daniela Prayer, Franz Waldhauser, Manuel Steiner, Milen Minkov, Helmut Gadner. (2004) Central diabetes insipidus as presenting symptom of Langerhans cell histiocytosis. Pediatric Blood & Cancer 43:5, 594-599
CrossRef40
I. Runkle de la Vega, R. Boente Varela, N. García de la Torre Lobo, A. Charro Salgado. (2004) Enfermedades de la neurohipófisis. Diabetes insípida. Síndrome de secreción inadecuada de ADH.. Medicine - Programa de Formación Médica Continuada Acreditado 9:13, 798-806
CrossRef41
A. Shearer, A. Bagust, D. Sanderson, S. Heller, S. Roberts. (2004) Cost-effectiveness of flexible intensive insulin management to enable dietary freedom in people with Type 1 diabetes in the UK. Diabetic Medicine 21:5, 460-467
CrossRef42
Mitsunori Kanagaki, Yukio Miki, Jun A. Takahashi, Yuta Shibamoto, Takahiro Takahashi, Tetsuya Ueba, Nobuo Hashimoto, Junji Konishi. (2004) MRI and CT findings of neurohypophyseal germinoma. European Journal of Radiology 49:3, 204-211
CrossRef43
Tracy L. Breen, Kalmon D. Post, Sharon L. Wardlaw. (2004) Lymphocytic Hypophysitis. The Endocrinologist 14:1, 13-18
CrossRef44
Seong Jin LEE, Hyung Joon YOO, Sung Woo PARK, Moon Gi CHOI. (2004) A Case of Cystic Lymphocytic Hypophysitis with Cacosmia and Hypopituitarism. Endocrine Journal 51:3, 375-380
CrossRef45
Lorraine Lipscombe, Sylvia L. Asa, Shereen Ezzat. (2003) Management of Lesions of the Pituitary Stalk and Hypothalamus. The Endocrinologist 13:1, 38-51
CrossRef46
M. Necmettin Pamir, Koray ??zduman. (2002) Primary Hypophysitis: Idiopathic Inflammatory Disorders of the Pituitary Gland. Neurosurgery Quarterly 12:3, 197-215
CrossRef47
Seiji Hama, Kazunori Arita, Takashi Nishisaka, Toshiyuki Fukuhara, Atsushi Tominaga, Kazuhiko Sugiyama, Hiroyuki Yoshioka, Kuniki Eguchi, Masayuki Sumida, Yuji Heike, Kaoru Kurisu. (2002) Changes in the epithelium of Rathke cleft cyst associated with inflammation. Journal of Neurosurgery 96:2, 209-216
CrossRef48
Hiroshi Imoto, Eikoh Imamiya, Yu Momose, Yasuo Sugiyama, Hiroyuki Kimura, Takashi Sohda. (2002) Studies on Non-Thiazolidinedione Antidiabetic Agents. 1. Discovery of Novel Oxyiminoacetic Acid Derivatives. CHEMICAL & PHARMACEUTICAL BULLETIN 50:10, 1349-1357
CrossRef49
ICHIRO FUJISAWA, KYOSUKE UOKAWA, NAOTOSHI HORII, NORIHIKO MURAKAMI, NOBUYUKI AZUMA, SUMIKO FURUTO-KATO, KOHSUKE YAMASHITA, SATOSHI NAKAO, NAOKI KAGEYAMA. (2002) Bright Pituitary Stalk on MR T1-Weighted Image: Damming Up Phenomenon of the Neurosecretory Granules.. Endocrine Journal 49:2, 165-173
CrossRef50
KOZO HASHIMOTO, KOICHI ASABA, KANAE TAMURA, TOSHIHIRO TAKAO, TOSHIHIRO NAKAMURA. (2002) A Case of Lymphocytic Infundibuloneurohypophysitis Associated with Systemic Lupus Erythematosus.. Endocrine Journal 49:6, 605-610
CrossRef51
Masateru Nishiki, Yoshio Murakami, Yasunori Ozawa, Yuzuru Kato. (2001) Serum antibodies to human pituitary membrane antigens in patients with autoimmune lymphocytic hypophysitis and infundibuloneurohypophysitis. Clinical Endocrinology 54:3, 327-333
CrossRef52
Frederic Baleydier, Claire Galambrun, Anne Marie Manel, Laurent Guibaud, Marc Nicolino, Yves Bertrand. (2001) Primary lymphoma of the pituitary stalk in an immunocompetent 9-year-old child. Medical and Pediatric Oncology 36:3, 392-395
CrossRef53
Ji Hoon Shin, Ho Kyu Lee, Choong Gon Choi, Dae Chul Suh, Chang Jin Kim, Sung Kwan Hong, Dong Gyu Na. (2001) MR Imaging of Central Diabetes Insipidus: A Pictorial Essay. Korean Journal of Radiology 2:4, 222
CrossRef54
Cabot, Richard C.Scully, Robert E., Mark, Eugene J., McNeely, William F., Ebeling, Sally H.Ellender, Stacey M.Peters, Christine C., Madsen, Joseph R.Karluk, Diane. (2000) Case 34-2000. New England Journal of Medicine 343:19, 1399-1406
Full Text55
Maghnie, Mohamad, Cosi, Gianluca, Genovese, Eugenio, Manca-Bitti, Maria Luisa, Cohen, Amnon, Zecca, Silvia, Tinelli, Carmine, Gallucci, Massimo, Bernasconi, Sergio, Boscherini, Brunetto, Severi, Francesca, Aricò, Maurizio, . (2000) Central Diabetes Insipidus in Children and Young Adults. New England Journal of Medicine 343:14, 998-1007
Full Text56
Bernadette L. Koch. (2000) Langerhans Histiocytosis of Temporal Bone: Role of Magnetic Resonance Imaging. Topics in Magnetic Resonance Imaging 11:1, 66-74
CrossRef57
VINCENT GEENEN, HENRI MARTENS, FABIENNE BRILOT, CHANTAL RENARD, DENIS FRANCHIMONT, OUAFAE KECHA. (2000) Thymic Neuroendocrine Self-Antigens: Role in T-Cell Development and Central T-Cell Self-Tolerance. Annals of the New York Academy of Sciences 917:1, 710-723
CrossRef58
Isaac O Donkor, Yasar S Abdel-Ghany, Peter F Kador, Tadashi Mizoguchi, Anita Bartoszko-Malik, Duane D Miller. (1999) Synthesis and biological activity of aldose reductase inhibitors with Michael acceptor substituents. European Journal of Medicinal Chemistry 34:3, 235-243
CrossRef59
Geenen, Kecha, Martens. (1998) Review Article Thymic Expression of Neuroendocrine Self-Peptide Precursors: Role in T Cell Survival and Self-Tolerance. Journal of Neuroendocrinology 10:11, 811-822
CrossRef60
Nicole G. Grois, Blaise E. Favara, Gerhard H. Mostbeck, Daniela Prayer. (1998) CENTRAL NERVOUS SYSTEM DISEASE IN LANGERHANS CELL HISTIOCYTOSIS. Hematology/Oncology Clinics of North America 12:2, 287-305
CrossRef61
Richard Donnelly, Xianqin Qu. (1998) MECHANISMS OF INSULIN RESISTANCE AND NEW PHARMACOLOGICAL APPROACHES TO METABOLISM AND DIABETIC COMPLICATIONS. Clinical and Experimental Pharmacology and Physiology 25:2, 79-87
CrossRef62
Isaac O. Donkor, Yasser S. Abdel-Ghany, Peter F. Kador, Tadashi Mizoguchi, Anita Bartoszko-Malik, Duane D. Miller. (1998) Synthesis and biological activities of aldose reductase inhibitors bearing acyl benzenesulfonamides as carboxylic acid surrogates. European Journal of Medicinal Chemistry 33:1, 15-22
CrossRef63
Fumio Otsuka, Satoshi Mizobuchi, Kiyoshi Morita, Hideo Matsumoto, Toshio Ogura, Masahisa Hirakawa, Hirofumi Makino. (1997) Postanesthetic Polyuria Attributable to Central Diabetes Insipidus. Anesthesia & Analgesia 85:4, 940-943
CrossRef64
Yuwen Lee, Mary Robinson, Nathan Wong, Eve Chan, M.Arthur Charles. (1997) The effect of pentoxifylline on current perception thresholds in patients with diabetic sensory neuropathy. Journal of Diabetes and its Complications 11:5, 274-278
CrossRef65
Mary Specker Stone. (1997) In Search of Patient Agency in the Rhetoric of Diabetes Care. Technical Communication Quarterly 6:2, 201-217
CrossRef66
Shereen Ezzat, Robert G Josse. (1997) Autoimmune Hypophysitis. Trends in Endocrinology & Metabolism 8:2, 74-80
CrossRef67
Henri Martens, Béatrice Goxe, Vincent Geenen. (1996) The thymic repertoire of neuroendocrine self-antigens: physiological implications in T-cell life and death. Immunology Today 17:7, 312-317
CrossRef68
Peter W. Bushunow, Victor Casas, David B. Duggan. (1996) Lymphomatoid Granulomatosis Causing Central Diabetes Insipidus: Case Report and Review of the Literature. Cancer Investigation 14:2, 112-119
CrossRef69
Fumio Otsuka, Tetsuki Amano, Toshio Ogura, Zensuke Ota. (1995) Diabetes insipidus with Behçet's disease. The Lancet 346:8988, 1494-1495
CrossRef70
P. H. Baylis. (1995) Investigation of suspected hypothalamic diabetes insipidus. Clinical Endocrinology 43:4, 507-510
CrossRef71
Mary Mackinnon. (1995) Blood glucose meters in practice. Practical Diabetes International 12:5, 206-207
CrossRef72
Aldo Maldonato, Donatella Bloise, Massimo Ceci, Emanuele Fraticelli, Franco Fallucca. (1995) Diabetes mellitus: lessons from patient education. Patient Education and Counseling 26:1-3, 57-66
CrossRef73
Takumi Abe, Kiyoshi Matsumoto, Naoko Sanno, Yoshiyuki Osamura. (1995) Lymphocytic Hypophysitis. Neurosurgery 36:5, 1016-1019
CrossRef74
P. J. Jenkins, S. L. Chew, D. G. Lowe, F. Afshar, M. Charlesworth, G. M. Besser, J. A. H. Wass. (1995) Lymphocytic hypophysitis: unusual features of a rare disorder. Clinical Endocrinology 42:5, 529-534
CrossRef75
Takumi Abe, Kiyoshi Matsumoto, Naoko Sanno, Yoshiyuki Osamura. (1995) Lymphocytic Hypophysitis. Neurosurgery 36:5, 1016???1019
CrossRef76
J. K. Powrie, Y. Powell, A. B. Ayers, C. Lowy, P. H. Sönksen. (1995) Lymphocytic adenohypophysitis: magnetic resonance imaging features of two new cases and a review of the literature. Clinical Endocrinology 42:3, 315-322
CrossRef77
Philip J. Randle. (1995) Metabolic fuel selection: general integration at the whole-body level. Proceedings of the Nutrition Society 54:01, 317-327
CrossRef78
Douglas N. Ishii, S. B. Lupien. (1995) Insulin-like growth factors protect against diabetic neuropathy: Effects on sensory nerve regeneration in rats. Journal of Neuroscience Research 40:1, 138-144
CrossRef79
R.Maarten Egeler, Mark E. Nesbit. (1995) Langerhans cell histiocytosis and other disorders of monocyte-histiocyte lineage. Critical Reviews in Oncology/Hematology 18:1, 9-35
CrossRef80
Anthony Peter Weetman. (1995) Autoimmunity to steroid-producing cells and familial polyendocrine autoimmunity. Baillière's Clinical Endocrinology and Metabolism 9:1, 157-174
CrossRef81
Cabot, Richard C.Scully, Robert E., Mark, Eugene J., McNeely, William F., McNeely, Betty U., Samuels, Martin A.de la Monte, Suzanne. (1994) Case 36-1994. New England Journal of Medicine 331:13, 861-868
Full Text82
K. D. Hepp. (1994) Implantable insulin pumps and metabolic control. Diabetologia 37:S2, S108-S111
CrossRef83
Peter GF Swift. (1994) A constantly moving target. Practical Diabetes International 11:4, 137-137
CrossRef84
P. H. Baylis. (1994) Understanding the cause of idiopathic cranial diabetes insipidus: a step forward. Clinical Endocrinology 40:2, 171-172
CrossRef85
Ken Shaw. (1994) The pendulum swings. Practical Diabetes International 11:1, 6-6
CrossRef
