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The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 3 1048-1053
Copyright © 2001 by The Endocrine Society

Original Studies

The Spectrum and Significance of Primary Hypophysitis

Carol C. Cheung, Shereen Ezzat, Harley S. Smyth and Sylvia L. Asa

The Freeman Center for Endocrine Oncology, Mount Sinai Hospital, Departments of Pathology and Laboratory Medicine (C.C.C., S.L.A.), Medicine (Endocrinology) (S.E.), and Surgery (H.S.S.), University of Toronto, Toronto, Ontario M5G 1X5, Canada

Address correspondence and requests for reprints to: Dr. Sylvia L. Asa, Department of Pathology, University Health Network, 610 University Avenue, Suite 4-302, Toronto, Ontario M5G 2M9, Canada. E-mail: sylvia.asa{at}uhn.on.ca


   Abstract
Top
 Abstract
Introduction
 Clinical Presentations
 Discussion
 References
 
Hypophysitis can present clinically as a mass lesion of the sella turcica. Secondary hypophysitis occurs in cases where a definite etiologic agent or process inciting the inflammatory reaction can be identified. In contrast, primary hypophysitis refers to inflammation confined to the pituitary gland with no identifiable etiologic associations. We report three cases of primary hypophysitis to illustrate the spectrum of three clinicopathological entities that encompass this disease: lymphocytic hypophysitis, granulomatous hypophysitis, and xanthomatous hypophysitis. Our three patients underwent surgery, with variable response. However, conservative, supportive treatment with or without surgical decompression is generally favored over aggressive and extensive surgical resection that results in hypopituitarism. We conclude that the optimal management of patients with hyophysitis requires a high index of suspicion before extensive surgical resection. Histological confirmation of the diagnosis of hypophysitis can be obtained by performing a biopsy or by requesting an intraoperative frozen section consultation.


   Introduction
Top
 Abstract
 Introduction
Clinical Presentations
 Discussion
 References
 
INFLAMMATORY LESIONS OF the pituitary gland, known as hypophysitis, are important for several reasons. They clinically and radiologically mimic tumors of the sellar region, causing mass effects such as headache and visual impairment (1). In addition, they may result in hypophysial and/or hypothalamic dysfunction from inflammatory destruction of the hypophysis or compression of the residual normal gland by edema (1, 2, 3). Hypophysitis secondary to infection or systemic disease, although common in the past, is relatively rare today. Idiopathic or primary hypophysitis is currently the most common form of pituitary inflammation. Three histopathological conditions are now recognized to fall within this category: lymphocytic hypophysitis, granulomatous hypophysitis, and xanthomatous hypophysitis. We describe three patients to illustrate the spectrum of primary hypophysitis.


   Clinical Presentations
Top
 Abstract
 Introduction
 Clinical Presentations
Discussion
 References
 
Case 1

A 24-yr-old G2, P2 woman presented with headaches and persistent galactorrhea. She had no significant past medical history apart from oligomenorrhea of 6 yr duration. Her first pregnancy was unremarkable; she breast fed with no difficulty for 8 months, then remained amenorrheic for another 8 months until she became pregnant again. Toward the end of her second pregnancy, she developed a bitemporal visual field defect and galactorrhea. Postpartum, her visual field defect worsened and she developed new headaches. Her family history was unremarkable for endocrine neoplasms or autoimmune conditions. Ophthalmologic evaluation revealed a symmetrical superior bitemporal quadrantic visual field defect. The remainder of the physical examination was unremarkable.

Relevant laboratory investigations included an elevated serum PRL of 77 µg/L (normal, <27 µg/L). TRH (200 µg) administration resulted in a further increase of PRL to 423 µg/L after 30 min. Insulin-induced hypoglycemia resulted in an appropriate rise in GH (peak, 7.5 µg/L) and cortisol (peak, 568 nmol/L), whereas GnRH administration resulted in peak LH and FSH values of 23 and 49 mIU/L, respectively.

A computed tomographic scan of the head revealed a diffuse isodense sellar enlargement with upward displacement into the suprasellar space (Fig. 1Go).



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  		Figure 1. Radiological appearance of lymphocytic hypophysitis on computed tomographic scan. The sella is enlarged and filled with a diffuse isodense homogeneous mass with a bulging suprasellar component.

 
At the time of trans-sphenoidal surgery, the lesion appeared sticky, yellowish, and uniform. Histological examination revealed diffuse infiltration of the adenohypophysis by numerous lymphocytes with occasional plasma cells and macrophages (Fig. 2Go). No giant cells or granulomas were identified. No adenoma was identified.



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  		Figure 2. Histological appearance of lymphocytic hypophysitis. A, The pituitary contains a lymphoplasmacytic infiltrate with lymphoid aggregates (left); there is destruction of the underlying parenchyma. B, Higher magnification demonstrates the lymphocytes and plasma cells surrounding atrophic acini of adenohypophysial cells.

 
Postoperatively, her complaints of headaches, galactorrhea, and oligomenorrhea resolved. Serum PRL levels normalized to 27 µg/L, 17 µg/L, and 10 µg/L on the first, second, and third postoperative days, respectively. There was no evidence of associated autoimmune serology including antibodies to the thyroid, antinuclear antibodies, anticardiolipin antibodies, and antiadrenal antibodies were all negative. A 3-month postoperative magnetic resonance imaging (MRI) scan was normal. She continues to have normal pituitary and menstrual function with no requirement for hormone replacement after 6 yr of follow-up.

Case 2

A 39-yr-old nulliparous woman presented with rapidly progressive frontal headaches, nausea, vomiting, anorexia, weight loss, and cold and hot flashes. As a teenager, she had primary hyperthyroidism for which she received radioactive iodine treatment; she had been on thyroid hormone replacement since that time. Other significant past medical history included psoriasis. The patient had five sisters; three were hypothyroid, and one had undergone thymectomy for myasthenia gravis. There was no family history of endocrine neoplasms. She had no visual field deficits.

Endocrine laboratory investigations revealed modest hyperprolactinemia of 84 µg/L but marked reduction in random plasma cortisol (35 nmol/L), LH, FSH (<1 mIU/L), and GH (0.1 µg/L) levels. A MRI of the head revealed a 1.9-cm sellar mass with suprasellar extension (Fig. 3AGo).



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  		Figure 3. Radiological appearance of granulomatous hypophysitis on MRI. A, At presentation, the sella is distorted by a diffuse enhancing homogeneous mass with suprasellar extension. B, A postoperative scan shows complete resolution of the abnormality. C, Several months later, there is recurrence of sellar enlargement with an inhomogeneous lesion. (T1-weighted images; A, after gadolinium administration.)

 
The patient underwent trans-sphenoidal resection of the lesion. A postoperative MRI showed significant resolution of the lesion (Fig. 3BGo). In addition to her persistent anterior pituitary failure, which required replacement with glucocorticoids, T4, and estrogen/progestin, she also developed postoperative central diabetes insipidus requiring desmopressin supplements. Histological examination of the resected lesion showed necrotizing granulomatous inflammation (Fig. 4Go). There were variable numbers of plasma cells and foamy histiocytes with vacuolated cytoplasm. Areas of old hemorrhage with hemosiderin deposition were present. The lesion was well demarcated, and areas of interspersed normal adenohypophysis were identified. Investigations for infectious diseases including body fluid cultures and chest radiography were entirely negative. Six months later, her headaches returned and a MRI scan showed recurrence of the lesion (Fig. 3CGo). She was placed on high doses of dexamethasone (16 mg/day) with plans for a second trans-sphenoidal resection. She developed severe Cushing’s syndrome and type 2 diabetes mellitus. A MRI scan 3 months after treatment with corticosteroids showed complete resolution of her pituitary lesion, and surgery was, therefore, cancelled. Further investigations were unable to identify a cause for the pituitary inflammation. She was switched from dexamethasone to maintenance doses of cortisone acetate with resolution of her Cushingoid features and diabetes mellitus. Three years later, she remains disease free clinically and radiographically but continues to require full pituitary hormone replacement.



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  		Figure 4. Histological appearance of granulomatous hypophysitis. This disorder is characterized by necrotizing granulomas that are formed by histiocytes and plasma cells surrounding areas of necrosis. Occasional giant cells can be seen.

 
Case 3

A 32-yr-old G1, P1 woman presented with oligomenorrhea and hyperprolactinemia 3 yr after an uneventful pregnancy. She had resumed normal menses 8 weeks postpartum and did not have persistent galactorrhea. Her PRL level was 96 µg/L (normal, <27 µg/L). Magnetic resonance imaging revealed a 1-cm inhomogeneous lesion that was bright on T1- and T2-weighted images, strongly suggestive of a cyst (Fig. 5Go). She was started on bromocriptine (up to 5 mg/day), which resulted in normalization of her PRL levels and menstrual function. Two years later, however, the size of the lesion did not regress on repeat magnetic resonance imaging. Preoperative evaluation of her pituitary function using insulin-induced hypoglycemia, TRH, and GnRH revealed no evidence of compromise including GH (peaking to 6.8 µg/L) concentrations. At the time of surgery, a cyst filled with syrupy orange/amber material with floating crystals was noted. The cavity appeared smooth with a fibrous wall. An apparently normal gland was visualized separately. Histological examination of the resected lesion showed chronic hypophysitis with fibrosis, lymphoplasmacytic infiltration, necrosis, hemorrhage, hemosiderin deposition, and foamy histiocytes (Fig. 6Go). There was no evidence of either an adenoma or of cyst wall remnants. Postoperatively, the patient’s PRL levels normalized (11 µg/L) without dopaminergic inhibition. Two years later, she continues to have normal pituitary function, including PRL levels (10 µg/L) and regular menstrual function.



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  		Figure 5. Radiological appearance of xanthomatous hypophysitis on MRI. The pituitary contains a discrete inhomogeneous cystic lesion that enhances with contrast (A, coronal; B, sagittal; T1-weighted images after gadolinium administration).

 


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  		Figure 6. Histological appearance of xanthomatous hypophysitis. A, The pituitary contains a localized process that consists primarily of foamy histiocytes (right); the adjacent gland (left) is focally infiltrated by lymphocytes. B, Higher magnification illustrates the lipid-laden macrophages with abundant clear cytoplasm and scattered lymphocytes.

 

   Discussion
Top
 Abstract
 Introduction
 Clinical Presentations
 Discussion
References
 
We describe three cases of primary hypophysitis to illustrate the histological and clinical spectrum of this entity. Although the most common pituitary mass is adenoma, other mass lesions include metastatic tumors, cysts, hyperplasia, infections, and inflammation (4). The potentially transient endocrine and compressive features of inflammation require a high index of suspicion because conservative management may eliminate the need for aggressive pituitary surgery. Primary hypophysitis should be considered in the differential diagnosis of pituitary lesions in women around the time of pregnancy, in those with rapidly progressive lesions, and in those in whom PRL levels are discordant with the size of the lesion or response to dopaminergic therapy.

Hypophysitis can be primary or secondary. In secondary hypophysitis, an etiologic agent or defined systemic disease is implicated (5). Bacterial, viral, and fungal pathogens have been reported; opportunistic infections are usually associated with HIV (6). Systemic inflammatory diseases that can involve the pituitary include sarcoidosis (7), Wegener’s granulomatosis (8), Takayasu’s disease (9), Crohn’s disease (10), and Langerhans cell histiocytosis (11, 12).

The causative agent(s) of primary hypophysitis is currently unknown. However, three distinct clinicopathological entities have been described (Table 1Go).


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  		Table 1. Summary of distinguishing features between the different forms of primary hypophysitis

 
Since the first report of lymphocytic hypophysitis in 1962 (13), more than 100 cases have been described. Females are affected more frequently than males (8:1). The mean age of diagnosis is 34.5 yr for females and 44.7 yr for males. In females, lymphocytic hypophysitis classically presents during late pregnancy or early postpartum (14). In our earlier review of 16 cases (1), the most common manifestations were hypopituitarism (63%), mass effects (56%), hyperprolactinemia (38%), and diabetes insipidus (19%). Unrecognized and untreated hypopituitarism can result in death. In most cases, radiological studies suggest a pituitary tumor (15, 16, 17). Features indicative of lymphocytic hypophysitis, however, include loss of the hyperintense "bright spot" signal of the posterior pituitary, thickening of the pituitary stalk, or enlargement of the posterior gland (18, 19, 20). Histologically, lymphocytic hypophysitis is characterized by diffuse infiltration of the pituitary by inflammatory cells, predominantly lymphocytes that form lymphoid follicles; there is variable reactive fibrosis. Although the pathogenesis of lymphocytic hypophysitis is unknown, it is thought to be an autoimmune phenomenon. The histopathology resembles that of other autoimmune endocrine disorders (4), and up to one quarter of patients have other autoimmune disorders. Antipituitary antibodies have been detected in a few patients (21, 22). Most cases involve the anterior lobe and are assumed to be due to antibodies against adenohypophysial cells. In some patients, the clinical presentation and biochemical findings implicate a single hormone-secreting cell type as the target (23, 24, 25). Rarely, patients present with isolated diabetes insipidus and the inflammatory process is restricted to the posterior lobe and stalk, which can exhibit localized enlargement; this disorder has been named infundibular neurohypophysitis (18, 26, 27).

Granulomatous hypophysitis, first described in 1917, has an annual incidence of 1 in 10 million and accounts for less than 1% of all pituitary disorders (5). In contrast to lymphocytic hypophysitis, there is no gender predilection. The mean age of diagnosis is 21.5 yr for females and 50 yr for males. Most reported cases are diagnosed at autopsy. Patients present with nausea, vomiting, meningitis, hyperprolactinemia, and/or diabetes insipidus. Radiologically, there is an intrasellar mass that may show suprasellar extension. Histologically, granulomatous hypophysitis is characterized by collections of histiocytes, multinucleated giant cells, and variable numbers of lymphocytes and plasma cells (4). Although some cases are attributable to infection, most are idiopathic. An autoimmune pathogenesis has also been proposed for this disorder (28, 29), and some authors believe that granulomatous and lymphocytic hypophysitis are different manifestations of the same disease, but epidemiological data do not support this hypothesis.

Xanthomatous hypophysitis, the least common form of primary hypophysitis, was first described in three cases in 1998 (3). It is defined histologically by the presence of lipid-rich foamy histiocytes with variable numbers of lymphocytes and resembles xanthomatous inflammatory processes elsewhere, such as xanthomatous cholecystitis, endometritis, or pyelonephritis, in which the inflammation is attributed to cell debris of endogenous or infectious origin. Unlike the other hypophysitidies, these lesions are more likely to be cystic on radiological or surgical evaluation. It may be that the inflammation is a response to components of a ruptured cyst, however, no confirmation of a preexisting cyst has been identified. No infectious process has been implicated. Any attempt to characterize this entity based on the few cases reported would be speculative.

Currently, it is unclear whether these three conditions are truly distinct entities, or merely different manifestations of the same disease. They share clinical and radiological features, and there is no reliable way to distinguish the hypophysitidies from each other without histological examination. Nevertheless, they are important in the differential diagnosis of the sellar mass.

Conservative management may lead to resolution without the need for surgery (30). Transsphenoidal surgery is, however, both diagnostic and therapeutic and, therefore, should be performed in cases with progressive compression or those in whom radiographical and/or clinical progression occurs during conservative medical management (1, 31, 32). Hyperprolactinemia (33, 34, 35) and pituitary insufficiency (36, 37) resolve after pituitary surgery, in most cases (1). In rare instances, surgical intervention has resulted in further deterioration of visual field deficits (38) and/or hypopituitarism (33, 38, 39, 40). These complications highlight the importance of early suspicion of the diagnosis and conservative management in patients with nonprogressive disease. In the event of surgery, intraoperative pathology consultation will confirm the diagnosis and prevent aggressive resection of potentially viable pituitary tissue (1, 2, 41).

Since most cases of primary hypophysitis present clinically like neoplasms, they usually undergo surgical resection; histological examination reveals their true nature. This, and their variable natural history, makes it is difficult to accurately assess the efficacy of nonsurgical treatments. For example, all reported cases of xanthomatous hypophysitis have been diagnosed after surgical resection, and, therefore, there are no data reflecting the effects of medical treatment on this entity (3).

Spontaneous recovery of pituitary function with resolution of the pituitary mass has been described in cases with histologically proven hypophysitis (36, 37, 42, 43). Some patients, however, require active treatment. Although the administration of bromocriptine can improve visual field deficits and lower the hyperprolactinemia, the beneficial impact of this agent on the course of the disease is unproven. Moreover, lack of tumor shrinkage, as in our cases, should raise the suspicion of hypophysitis. Glucocorticoid therapy has been advocated to reduce inflammation and has been temporarily effective in some patients (35, 37, 39). The true efficacy of corticosteroid therapy in this condition, however, also remains uncertain.

In summary, the hypophysitidies are a heterogeneous group of inflammatory conditions involving the pituitary gland. Secondary hypophysitis is more easily diagnosed because patients will likely have other systemic manifestations of their underlying disorder. Primary hypophysitis encompasses three clinicopathological entities: lymphocytic hypophysitis, granulomatous hypophysitis, and more recently, xanthomatous hypophysitis. Unlike secondary hypophysitis, these conditions are usually confined to the pituitary gland and, therefore, require a higher level of clinical suspicion to ensure optimal management.


   Acknowledgments
 
We thank Dr. K. Kovacs for sharing material with us for this review.

Received March 14, 2000.

Revised October 9, 2000.

Revised November 2, 2000.

Accepted November 14, 2000.


   References
Top
 Abstract
 Introduction
 Clinical Presentations
 Discussion
 References
 

  1. Thodou E, Asa SL, Kontogeorgos G, Kovacs K, Horvath E, Ezzat S. 1995 Lymphocytic hypophysitis: clinicopathological findings. J Clin Endocrinol Metab. 80:2302–2311.[Abstract]
  2. Scanarini M, d’Ercole AJ, Rotilio A, Kitromilis N, Mingrino S. 1989 Giant-cell granulomatous hypophysitis: a distinct clinicopathological entity. J Neurosurg. 71:681–686.[Medline]
  3. Folkerth RD, Price DL, Schwartz M, Black PM, De Girolami U. 1998 Xanthomatous hypophysitis. Am J Surg Pathol. 22:736–741.[CrossRef][Medline]
  4. Asa SL. 1998 Tumors of the pituitary gland, third series, fascicle 22. Washington, DC: Armed Forces Institute of Pathology.
  5. Sautner D, Saeger W, Lüdecke DK, Jansen V, Puchner MJA. 1995 Hypophysitis in surgical and autoptical specimens. Acta Neuropathol (Berl). 90:637–644.[Medline]
  6. Sano T, Kovacs K, Scheithauer BW, Rosenblum MK, Petito CK, Greco CM. 1989 Pituitary pathology in acquired immunodeficiency syndrome. Arch Pathol Lab Med. 113:1066–1070.[Medline]
  7. Sato N, Szem G, Kim JH. 1997 Cystic pituitary mass in neurosarcoidoisis. Am J Neuroradiol. 18:1182–1185.[Abstract]
  8. Lohr KM, Ryan LM, Toohill RJ, Anderson T. 1988 Anterior pituitary involvement in Wegener’s granulomatosis. J Rheumatol. 15:855–861.[Medline]
  9. Toth M, Szabo P, Racz K, et al. 1996 Granulomatous hypophysitis associated with Takayasu’s disease. Clin Endocrinol. 45:499–503.[CrossRef][Medline]
  10. De Bruin WI, van’t Verlaat JW, Graamans K, De Bruin TWA. 1991 Sellar granulomatous mass in a pregnant woman with active Crohn’s disease. Neth J Med. 39:136–141.[Medline]
  11. Schmitt S, Wichmann W, Martin E, Zachmann M, Schoenle EJ. 1993 Primary stalk thickening with dibetes insipidus preceding typical manifestations of Langerhans cell histiocytosis in children. Eur J Pediatr. 152:399–401.[CrossRef][Medline]
  12. Vadakekalem J, Stamos T, Shenker Y. 1995 Sometimes the hooves do belong to zebras! An unusual case of hypopituitarism. J Clin Endocrinol Metab. 80:17–20.[CrossRef][Medline]
  13. Goudie RB, Pinkerton PH. 1962 Anterior hypophysitis and Hashimoto’s disease in a young woman. J Pathol Bacteriol. 83:584–585.[CrossRef][Medline]
  14. Asa SL, Bilbao JM, Kovacs K, Josse RG, Kreines K. 1981 Lymphocytic hypophysitis of pregnancy resulting in hypopituitarism: a distinct clinicopathologic entity. Ann Intern Med. 95:166–171.
  15. Quencer RM. 1980 Lymphocytic adenohypophysitis: autoimmune disorder of the pituitary gland. Am J Neuroradiol. 1:343–345.[Medline]
  16. Mayfield RK, Levine JH, Gordon L, Powers J, Galbraith RM, Rawe SE. 1980 Lymphoid adenohypophysitis presenting as a pituitary tumor. Am J Med. 69:619–623.[Medline]
  17. Hungerford GD, Biggs PJ, Levine JH, Shelley Jr BE, Perot PL, Chambers JK. 1982 Lymphoid adenohypophysitis with radiologic and clinical findings resembling a pituitary tumor. Am J Neuroradiol. 3:444–446.[Medline]
  18. Imura H, Nakao K, Shimatsu A, et al. 1993 Lymphocytic infundibuloneurohypophysitis as a cause of central diabetes insipidus. N Engl J Med. 329:683–689.[Abstract/Free Full Text]
  19. Abe T, Matsumoto K, Sanno N, Osamura Y. 1995 Lymphocytic hypophysitis: case report. Neurosurgery. 36:1016–1019.[Medline]
  20. Ahmadi J, Meyers GS, Segall HD, Sharma OP, Hinton DR. 1995 Lymphocytic adenohypophysisits: contrast enhanced MRI imaging in five cases. Radiology. 195:30–34.[Abstract/Free Full Text]
  21. Crock P, Salvi M, Miller A, Wall J, Guyda H. 1993 Detection of anti-pituitary autoantibodies by immunoblotting. J Immunol Methods. 162:31–40.[CrossRef][Medline]
  22. Crock PA. 1998 Cytosolic autoantigens in lymphocytic hypophysitis. J Clin Endocrinol Metab. 83:609–618.[Abstract/Free Full Text]
  23. Bottazzo GF, Pouplard A, Florin-Christensen A, Doniach D. 1975 Autoantibodies to prolactin-secreting cells of human pituitary. Lancet. ii:97–101.
  24. Bottazzo GF, McIntosh C, Stanford W, Preece M. 1980 Growth hormone cell antibodies and partial growth hormone deficiency in a girl with Turner’s syndrome Clin Endocrinol (Oxf). 12:1–9.
  25. Scherbaum WA, Schrell U, Glück M, Fahlbusch R, Pfeiffer EF. 1987 Autoantibodies to pituitary corticotropin-producing cells: possible marker for unfavourable outcome after pituitary microsurgery for Cushing’s disease. Lancet. i:1394–1398.
  26. Hasimoto K, Takao T, Makino S. 1997 Lymphocytic andenohypophysitis and lymphocytic infundibuloneurohypophysitis. Endocr J. 44:1–10.[Medline]
  27. Kamel N, Dagci Illgin S, Corapicioglu D, Deda H, Gullu S. 1998 Lymphocytic infundibuloneurohypophysitis preesnting as diabetes insipidus in a man. J Endocrinol Invest. 21:537–540.[Medline]
  28. Hassoun P, Anayssi E, Salti I. 1985 A case of granulomatous hypophysitis with hypopituitarism and minimal pituitary enlargement. J Neurol Neurosurg Psychiatry. 48:949–951.[Abstract/Free Full Text]
  29. Klaer W, Nørgaard JOR. 1969 Granulomatous hypophysitis and thyroiditis with lymphocytic adrenalitis. Acta Pathol Microbiol Scand. 76:229–238.[Medline]
  30. Ezzat S, Josse RG. 1997 Autoimmune hypophysitis. Trends Endocrinol Metab. 8:74–80.[CrossRef][Medline]
  31. Nishioka H, Ito H, Miki T, Akada K. 1994 A case of lymphocytic hypophysitis with massive fibrosis and the role of surgical intervention. Surg Neurol. 42:74–78.[CrossRef][Medline]
  32. Prasad A, Madan VS, Sethi PK, Prasad ML, Buxi TBS, Kanwar CK. 1991 Lymphocytic hypophysitis: can open exploration of the sella be avoided? Br J Neurosurg. 5:639–642.[Medline]
  33. Levine SN, Benzel EC, Fowler MR, Shroyer JVI, Mirfakhraee M. 1988 Lymphocytic hypophysitis: clinical, radiological and magnetic resonance imaging characterization. Neurosurgery. 22:937–941.[Medline]
  34. Mazzone T, Kelly W, Ensinck J. 1983 Lymphocytic hypophysitis associated with antiparietal cell antibodies and vitamin B12 deficiency. Arch Intern Med. 143:1794–1795.[Abstract/Free Full Text]
  35. Nussbaum CE, Okawara S-H, Jacobs LS. 1991 Lymphocytic hypophysitis with involvement of the cavernous sinus and hypothalamus. Neurosurgery. 28:440–444.[CrossRef][Medline]
  36. McGrail KM, Beyerl BD, Black PM, Klibanski A, Zervas NT. 1987 Lymphocytic adenohypophysitis of pregnancy with complete recovery. Neurosurgery. 20:791–793.[Medline]
  37. Bitton RN, Slavin M, Decker RE, Zito J, Schneider BS. 1991 The course of lymphocytic hypophysitis. Surg Neurol. 36:40–43.[CrossRef][Medline]
  38. Pestell RG, Best JD, Alford FP. 1990 Lymphocytic hypophysitis. The clinical spectrum of the disorder and evidence for an autoimmune pathogenesis. Clin Endocrinol (Oxf). 33:457–466.[Medline]
  39. Stelmach M, O’Day J. 1991 Rapid change in visual fields associated with suprasellar lymphocytic hypophysitis. J Clin Neurol Ophthalmol. 11:19–24.[Medline]
  40. Reusch JE-B, Kleinschmidt-De Masters BK, Lillehei KO, Rappe D, Gutierrez-Hartmann A. 1992 Preoperative diagnosis of lymphocytic hypophysitis (adenohypophysitis) unresponsive to short course dexamethasone: case report. Neurosurgery. 30:268–272.[Medline]
  41. Oeckler RCT, Bise K. 1991 Non-specific granulomas of the pituitary: report of six cases treated surgically. Neurosurg Rev. 14:185–190.[CrossRef][Medline]
  42. Ozawa Y, Shishiba Y. 1993 Recovery from lymphocytic hypophysitis associated with painless thyroiditis: clinical implications of circulating antipituitary antibodies. Acta Endocrinol (Copenh). 128:493–498.[Abstract/Free Full Text]
  43. Ober KP, Elster A. 1994 Spontaneously resolving lymphocytic hypophysitis as a cause of postpartum diabetes insipidus. Endocrinologist. 4:107–111.



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