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| Year : 1999 | Volume
: 47
| Issue : 2 | Page : 161-2 |
Regression of acromegaly following pituitary apoplexy.
Thomas N, Simon R, Chacko G, Chacko A, Chandy MJ, Seshadri MS
How to cite this article:
Thomas N, Simon R, Chacko G, Chacko A, Chandy M J, Seshadri M S. Regression of acromegaly following pituitary apoplexy. Neurol India 1999;47:161 |
Pituitary apoplexy is a known complication in patients with pituitary adenomas. It is often followed by hypopituitarism. Occasionally patients with functioning tumours may show remission of symptoms after an apoplectic episode. We report this in an acromegalic who not only developed remission but hypopituitarism following pituitary apoplexy.
A forty years old policeman noticed a progressive increase in his shoe size and coarsening of facial features over a period of 5 years. He developed diabetes mellitus one year prior to presentation and was prescribed glybenclemide 5mg twice a day at another hospital. Acromegaly was not diagnosed at that time. Two months prior to his visit to endocrinology clinic, he had severe holocranial headache, vomiting and lost consciousness for 6 hours. Subsequently, he noticed a reduction in the size of his extremities, had to discontinue his antidiabetic medication because of hypoglycaemic episodes and experienced erectile dysfunction. On examination he was moderately built and had acromegalic features [Figure 1]. His blood pressure was 110/80mm Hg. He had left temporal hemianopia and right upper temporal quadrantonopia. Examination of the cardiovascular, respiratory system and abdomen revealed no abnormality. The volume of his testes was 30 ml bilaterally and the pubic hair was Tanner's stage V. His deep tendon reflexes were sluggish.
Investigations revealed a normal haemogram, electrolytes and renal function. Plasma glucose values were normal. Total thyroxine 52.7nmol/1 (normal : 64.3-154.3nmol/1), plasma cortisol 8:00 AM : 3.03nmol/1 (nr: 19.53-58.6nmol/1), 4:OOPM: 4.74nmol/1 (nr :11.16-30.7nmol/1), FSH : <0.5IU/1 (nr: 4-201U/1), LH : <0.51U/1 (nr: 4-20 IU/1), total testosterone: 2.1nmol/l (nr:6.4-34.67nmol/1) and serum prolactin:2.3micg/l (nr:2.5 - 20micg/1), were all low, consistent with a diagnosis of panhypopituitarism. Serum Growth hormone, 1 hour after a 75G load of glucose was <0.1 micg/1 (nr: <10micg/1). As the basal hormonal profile revealed typical hypopituitarism, stimulation tests were not performed. Coronal cuts of CT scan revealed an isodense mass lesion with minimal contrast enhancement in the sellar and suprasellar regions. The patient underwent transsphenoidal surgery for relief of optic chiasmal compression. Histopathological examination of tissue removed at surgery, revealed a small cluster of cuboidal cells with round nuclei and eosinophilic cytoplasm with extensive areas of necrosis with foci of haemorrhage and calcification consistent with past pituitary apoplexy [Figure 2].
In most instances Pituitary apoplexy occurs spontaneously,[1-3] but some patient develop this after diabetic ketoacidosis, pregnancy, anticoagulant therapy, trauma, radiation therapy or bromocriptine administration. Of the functioning pituitary tumours with apoplexy, growth hormone and ACTH producing tumours predominate in several series, even though prolactin secreting tumours are the commonest functioning pituitary tumours.[2] A number of patients recover spontaneously[4] though most patients with visual field defects do require surgery.[1] In a large series of acromegalics, pituitary apoplexy occurred in 3.5% of all cases with spontaneous recovery in 75-88%. Empty sella syndrome may occur after pituitary apoplexy. Magnetic resonance imaging[5] is very useful in the diagnosis of asymptomatic or mildly symptomatic pituitary apoplexy.[2],[5] Occasionally normal pituitary function is retained after selective apoplexy of tumour alone.[6]
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