EMPTY SELLA SYNDROME AND PITUITARY APOPLEXY

EMPTY SELLA SYNDROME AND PITUITARY APOPLEXY

774 those familiar with current scientific knowledge-and, sadly, attempts by vested interests to misrepresent it-the bias was evident. This showed in ...

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774 those familiar with current scientific knowledge-and, sadly, attempts by vested interests to misrepresent it-the bias was evident. This showed in the choice of speakers and chairmen. It showed, too, in the treatment of people who had been invited by Dr Thorne to be in the audience but not as speakers because she considered our views to be already well known to the public; when Professor Yudkin and I tried to put questions from the floor, the chairman (an employee of the industry-funded British Nutrition Foundation) dealt with us in a peremptory and even insulting manner, and prevented us from completing our questions, on the grounds that our views were familiar and outdated. It is a major strategy of the Sugar Bureau to influence doctors, dentists, nutritionists, and home economists. They do this by providing information, sponsoring conferences, and supporting nutrition research. Perhaps all of this has no influence whatsoever on the scientific consensus. If so, then I am glad. But in that case, why do they bother? Department of Community Dental Health and Dental Practice,

University College London,

A. SHEIHAM

London WC1E 6EA

EMPTY SELLA SYNDROME AND PITUITARY

APOPLEXY a syndrome that includes the sudden of headache with visual alterations and ophthalmoplegia, is caused by the ischaemic or haemorrhagic infarction of a hypophyseal adenoma. It happens in up to 10% of patients with a pituitary adenoma and is usually not diagnosed during the acute episode. Few large series of patients have been published. The neurological features have been well reviewed but the endocrine manifestations and the evolution are less well known.3 One suggestion is that the empty sella syndrome (ESS) is the result of pituitary apoplexy,4.5 a proposal based upon the history of an episode compatible with pituitary apoplexy in patients with the syndrome.3.6-8 We describe here three patients with acute-onset pituitary apoplexy in whom hormonal dysfunction with panhypopituitarism developed subsequently, with an empty sella on computerised

SIR,-Pituitary apoplexy,

aneurysm. Lindhohn et all-5 suggested that the ESS was due to necrosis of a hypophyseal adenoma. Reports on pituitary apoplexy evolving into ESS are rare.3,6-8 Not every patient with ischaemia or haemorrhage of a hypophyseal adenoma may progress to apoplexy; the degree of necrosis, and consequently the clinical manifestations, varies. Also pituitary apoplexy PA may sometimes be mistaken for other disorders such as brainstem ischaemic infarction or carotoid aneurysm, and the CT scan may sometimes appear negative if all the

right slices are not scanned. Pituitary apoplexy usually evolves into transient hypophyseal hypofunction. On the other hand, endocrinologically active tumours rarely resolve after an episode of apoplexy. 10 In two cases, the lack of neurological or endocrinological manifestations argues against previous adenohypophyseal insufficiency, but the third had panhypopituitarism and the hormonal dysfunction detected cannot be ascribed to pituitary apoplexy alone. Serum prolactin levels were low, perhaps indicative of prolactinoma.5 In all three cases global adenohypophyseal insufficiency rapidly ensued and the sella turcica appeared empty 6-18 months later. Some patients with pituitary apoplexy recover spontaneously and are not candidates for surgery. Surgical decompression is indicated if there is severe loss of vision or consciousness or in patients on a downhill course. Two of our with medical measures.

patients were in coma but recovered J. MONTALBÁN J. SUMALLA J. L. FERNANDEZ

onset

tomographic (CT) scan. The three patients, diagnosed between January and December, 1985, met the following criteria: sudden onset of headache, usually accompanied by nausea and vomiting and with or without decreased level of consciousness; CT evidence of

an

intrasellar

mass, with or without suprasellar extension; ophthalmoplegia; and a

sudden decrease in visual acuity (this criterion being optional). CT scans (’Tomoscan 320’, with coronal cuts and/or CT1020) were done at diagnosis, 15 days later, and after 3,6,12, and in one case 18 months of follow-up. Hormone studies were done 3 days and 3, 6, 12, and in one case 18 months after diagnosis. The testing was done after the intravenous administration of 015 U/kg insulin, 400 ug thyrotropin releasing hormone, and 100 ug of luteinising-hormone releasing hormone. There were two men (aged 59 and 50) and a woman of 78. No patients had been previously diagnosed as having a hypophyseal tumour but case 3 had a history consistent with a global adenohypophyseal insufficiency. Two patients had altered consciousness and one a meningeal syndrome. Two patients had a contralateral lower limb motor deficit with a Babinski’s sign. CT scans revealed an intrasellar tumoural image with suprasellar extension. Aneurysm was ruled out by carotid arteriography. All three patients were given steroids. The two comatose patients recovered consciousness in 24 h, and the remaining neurological alterations cleared over 2-20 days. Surgery was not required. Hormonal profiles in the first week revealed global adenohypophyseal insufficiency;* this persisted and required replacement therapy. CT scans demonstrated ESS in all three cases 6 to 18 months later. ESS may be the result of lesions as diverse as pseudotumor cerebri9 and pituitary apoplexy. In one series of 44 patients with enlargement of the sella turcica4 20 patients had ESS and 50% of them had a history consistent with pituitary apoplexy 23 months earlier. In a series of 23 patients with acromegaly brain scans revealed an empty sella in 11, 6 of whom had a history of pituitary

Neurology, Neuroradiology, and Endocrinology Services, Hospital General Vall d’Hebron, Barcelona, Spam

A. MOLINS R. SIMÓ A. CODINA

*Detailed table available from J. M. 1. Cardoso

ER, Peterson EW. Pituitary apoplexy: a review. Neurosurgery 1984; 31: 363-73. 2. Reid R, Quigley E, Yen S. Pituitary apoplexy, a review. Arch Neurol 1985; 42: 712-19 3 Pelkonen R, Kuusisto A, Salmi J, et al. Pituitary function after pituitary apoplexy. Am J Med 1978; 65: 773-78. 4. Lindholm J, Bjerre P, Riishede J, Gyldensted C, Hagen C. Pituitary function in patients with evidence of spontaneous disappearance of a pituitary adenoma Clin Endocrinol 1983; 18: 599-603. 5. Bjerre P, Lindholm J, Videbaek H. The spontaneous course of pituitary adenomas and ocurrence of an empty sella in untreated acromegaly. J Clin Endocrinol Metab 1986, 63: 287-91. 6. Petersen P, Lindholm J. Pituitary apoplexy, the Houssay phenomenon, and accelerated proliferative retinopathy. Am J Med 1985; 79: 385-88. 7. Jones NS, Finer N. Pituitary infarction and development of the empty sella syndrome after gastrointestinal haemorrhage. Br Med J 1984; 289: 661-62. 8. Gutin PH, Cushard WG Jr, Wilson CB. Cushing’s disease with pituitary apoplexy leading to hypopituitarism, empty sella, and spontaneous fracture of the dorsum sellae. J Neurosurg 1979; 51: 866-69. 9. Foley KM, Posmer JB. Does pseudotumor cerebri cause the empty sella syndrome? Neurology 1975; 25: 565-69. 10. Dunn PJ, Donald RA, Espiner NA. Regression of acromegaly following pituitary apoplexy. Aust NZ J Med 1975; 5: 369-72.

ATYPICAL VIRUS PARTICLES IN HIV-1-ASSOCIATED PERSISTENT GENERALISED LYMPHADENOPATHY

SIR,-Ultrastructural studies of lymph nodes from patients with persistent generalised lymphadenopathy (PGL) have demonstrated that germinal centres harbour many retrovirus particles.1-5 Immunohistochemically, pl8and p24°6’ of HIV-1 can be visualised. Studies using in-situ hybridisation have shown that most cells expressing HIV-1 RNA are seen in germinal centres.5,8 Investigating repeated biopsy specimens we demonstrated HIV-1 in germinal centres for up to 2 years.5 Despite the persistence of virions in their lymph nodes, these patients have not progressed to AIDS. Generally, a subgroup of patients with PGL will proceed to AIDS but in most cases this process is slow and related to as yet undetermined factor(s). Recently, we investigated six lymph nodes removed 2-6 weeks after seroconversion and compared the ultrastructural changes with those seen in longstanding lymphadenopathy induced by HIV-1. A later group consisted of thirty-four lymph nodes obtained between 1983 and 1984. None of these patients with PGL have proceeded to