AEG-electrolux TG 100
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BRITISH MEDICAL JOURNAL
17 APRIL 1976
Spontaneous pituitary necrosis
Spontaneous pituitary necrosis follows a variable clinical course. Three different clinical presentations are reported.
A 44-year-old woman with acromegalic features and 27 years' amenorrhoea presented in coma which had been preceded by severe headache. She had pale nipples, fever (38C), signs of meningeal irritation, and no pubic or axillary hair. The fundi and visual fields were normal. The cerebrospinal fluid (CSF) was under increased pressure and contained g/l of protein and 0-02 x 109 lymphocytes/I (20/mm3). Her skull x-ray film showed an enlarged pituitary fossa, and spontaneous infarction of a pituitary tumour was diagnosed. Corticosteroid treatment rapidly improved her condition. Two years later endocrine assessment showed mild hypothyroidism (protein bound iodine (PBI) 240 nmol/l (3-1 Zg/l00 ml); normal 315-630 nmol/l (4-0-8-0 ,tg/ ml)) and low plasma 11 -hydrocorticosteroids (1 -OHCS: 70 nmol/l (2-5 tg/100 ml) at 9 am; normal 190-720 nmol/l (6-9-26 tg/100 ml)). A standard insulin tolerance test produced hypoglycaemia with a minimum blood sugar level of mmol/l (20 mg/ 100 ml) when the maximum values of plasma 1l-OHCS and growth hormone (GH) were below normal (88 nmol/l (3-2 tg/l100 ml) and Hg/l respectively). GH levels were not suppressed during a standard glucose tolerance test (minimum GH level 8-2 ,ug/l), confirming autonomous GH production by the pituitary tumour. Serum luteinising hormone was U/1 and serum follicle stimulating hormone was 5-4 U/1, compared with normal postmenopausal levels of 20 U/I and U/I respectively. The fundi and visual fields remained normal. L-thyroxine was combined with cortisol therapy and regular follow-up was maintained. Seven years later bitemporal hemianopia had developed with further enlargement of the pituitary fossa and irregular destruction of the floor and anterior wall. A huge intrasellar tumour containing fresh blood stretching the optic nerves was removed. Histology showed a pituitary adenoma containing predominantly chromophobe cells with 15-20 acidophilic cells. Postoperative irradiation was given to avoid recurrence. She is currently well on replacement therapy and her visual fields have improved since surgery.
The basic pathology of spontaneous haemorrhage into a pituitary tumour' 2 iS unclear; it may be due to rapid enlargement of the adenoma with infarction or rupture of the fine-walled vessels in the tumour.3 There is rarely enough tissue left to maintain normal function. We are unaware of reports of further growth of a pituitary tumour after apparent infarction sufficient to cause compression of the visual pathways as seen in case 1. The visual fields and skull x-ray picture should obviously be checked periodically after spontaneous infarction of a pituitary tumour. Pituitary infarction precipitated by AEG is rare but has been reported in a patient with acromegaly.5 Spontaneous pituitary necrosis is more common although it is of interest that the clinical features of hypopituitarism in the third patient were not apparent for two years.
Bleibtreu, L, Munchener medizinische Wochenschrift, 1905, 52, 2079. Brougham, M, Heusner, A P, and Adams, R D, Jfournal of Neurosurgery, 1950, 7,421. List, C F, Williams, J R, and Balyeat, G W,J3ournal of Neurosurgery, 1952, 9, 177. 4Muller, W, and Pia, H W, Deutsche Zeitschrift fur Nervenheilkunde, 1953 170, 326. Belchetz, P E, and Mason, A S, Proceedings of the Royal Society of Medicine, 1972, 65, 20.
Endocrine Unit, Department of Medicine, Royal Victoria Infirmary, University of Newcastle upon Tyne, Newcastle upon Tyne NE1 4LP Y SACHDEV, MD, MAMS, clinical fellow D C EVERED, MD, MRcP, consultant physician R HALL, MD, FRcP, professor of medicine
A 26-year-old woman presented with amenorrhoea and galactorrhoea after oral contraceptive therapy. Skull x-ray films showed an enlarged pituitary fossa, and air encephalography (AEG) was performed to delineate the extent of the tumour. Thirty minutes after AEG she developed a severe headache, neck rigidity, and hypotension. The CSF protein content was 0-9 g/l with 013 x 109 lymphocytes/l (130/mm3). She recovered well on parenteral corticosteroids. Results of endocrine assessment performed two months after AEG showed that the adrenocortical response to hypoglycaemia had disappeared and the GH response remained impaired (table). Cortisol therapy was prescribed and she is currently well though her periods have not restarted.
Rapid clonidine withdrawal with blood pressure overshoot exaggerated by beta-blockade
A disconcerting problem in treating hypertension with clonidine is the possibility of a severe rebound rise in blood pressure if the drug is stopped abruptly.The reaction may resemble the crisis seen in patients with a phaecochromocytoma. The combination of a betaadrenoreceptor blocker with one of the vasodilator group of antihypertensive drugs (hydrallazine, prazosin, clonidine) has become popular. Since beta-blocking drugs increase peripheral vascular resistance, theoretically a hypertensive crisis after a rapid withdrawal of clonidine could be aggravated in a patient who was also taking a beta-blocker. We report a case in which the patient started taking timolol and at the same time suddenly discontinued clonidine, and subsequently suffered a devastating blood pressure rebound.
Insulin tolerance test results in case 2 before and after air encephalogram (AEG). Clinical hypoglycaemia was achieved in both tests. Values in brackets obtained after AEG
Time (min): Blood sugar (mmol/l). Plasma ll-OHCS (nmol/l). Serum GH (,ug/l).
40 (3-9) 550 (60) 38 (15)
3-8 (5 0) 420 (50) 5-1 (1-4)
540 (30) 48 (4 3)
690 (30) 6-1 (1-9)
Conversion: SI to traditional units-Glucose: 1 mmol/lz 18 mg/ 100 ml. 1 1-OHCS: 1 nmol/lz 0-036 jig/ 100 ml.
A 69-year-old man reported persistent headache. Two days later he was admitted in coma with fever (39C), neck rigidity, right oculomotor nerve palsy, and right hemiplegia. Skull x-ray films showed an enlarged pituitary fossa. The CSF was xanthochromic with many red and white cells; the protein content was increased to 2-5 g/l. An intracerebral haemorrhage was diagnosed and treated. He was discharged after a few days. Two years later he presented with progressive lethargy, drowsiness, confusion, and hypotension. PBI was 250 nmol/l (3-2 tcg/lOO ml), Thyopac-(normal 92-117), and 9 am plasma ll-OHCS 80 nmol/I (2-9 Hug/l00 ml). Investigations confirmed that he had developed pituitary failure. He is currently well on L-thyroxine and cortisol replacement therapy.
A 60-year-old woman with a 10-month history of rapidly progressive glomerulonephritis and complicating hypertension was receiving prednisone 15 mg/day, warfarin 2 mg/day, and clonidine 0-15 mg eight-hourly. When seen for assessment she was well but her blood pressure was 180/140 mm Hg, her retinal arterioles were narrowed, and there were moderate arteriovenous crossing changes. The blood urea was mmol/l (90 mg/100 ml) and the serum creatinine 186 Hmol/l (2-1 mg/100 ml). The beta-adrenoreceptor blocking drug timolol 5 mg daily was added to the patient's antihypertensive regimen. In error, she immediately discontinued the clonidine. Forty-eight hours later she developed a throbbing frontal headache, mild confusion, and profound lethargy. Over the next 24 hours the headache became excruciating, the confusion more marked, she developed
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