Hypopituitarism

Coronary artery bypass grafting is being performed with increasing frequency and to great benefit. The number of operations performed in the United Kingdom has risen steadily from 16 000 in 1990 to 22 000 in 1995; mortality fell from 3.7% to 2.7% at the same time (C Munsch, personal communication). A wide range of non-cardiac sequelae are recognised, which include varying degrees of cerebral dysfunction.[1]

The occurrence of pituitary infarction after such surgery can be remarkably silent but may have a seriously debilitating effect, as is clearly described by Davies and Scanlon. Appropriate endocrine replacement treatment is, however, effective. The symptoms which occurred in their two patients are similar to those found in Sheehan's syndrome, especially the long latency before the appearance of clinical features.[2]

The occurrence of pituitary apoplexy after cardiac bypass surgery is well documented and is unlikely to go unnoticed and undiagnosed. The importance of the two cases reported here is the subtle presentation of symptoms of malaise, sexual dysfunction, and persistent biochemical abnormalities without any clinical features of intracranial catastrophe. I have had similar experiences with a handful of patients--as, I suspect, have other clinicians. Thus what has been described here may be the tip of a sizeable iceberg, the existence of which clinicians should be more aware.

The authors emphasise that the persistent hyponatraemia was an important indicator of the occurrence of pituitary infarction, and they emphasise the likely role of hypoadrenalism as the cause. They dismiss the possibility that the syndrome of inappropriate antidiuretic hormone secretion caused the symptoms; all too often this seems to be the first, and sometimes only, condition thought to cause hyponatraemia. It is important to identify hypoadrenalism when it is the cause of low sodium concentration because treatment with corticosteroids can be life saving, whereas simply restricting fluid intake would be inappropriate. The attribution of hyponatraemia to failure of pituitary adrenocorticotrophic hormone may seem puzzling since this hormone primarily affects cortisol secretion rather than aldosterone; however, the reasons are found in the function of glucocorticoid influences on free water clearance in the kidney, rather than the primary influences on sodium metabolism. The osmolar cut off point for the secretion of antidiuretic hormone is reduced in hypocortisolism, so there may be an element of the syndrome of inappropriate antidiuretic hormone secretion in these cases.[3] A further clue to the possibility of hypoadrenalism is the persistent low grade fever seen in both patients; it is, of course, necessary to exclude any infective cause.

These patients were clearly deficient in all six hormones of the anterior pituitary. In cases of partial hypopituitarism in patients with pituitary adenomas there is early loss of secretion of growth hormone and gonadotrophin, although adrenocorticotrophic hormone secretion is preserved, as is thyroid stimulating hormone. Prolactin concentration is unaffected or increased. When hypopituitarism has a vascular aetiology, isolated losses of hormones stimulated by the pituitary-adrenal or pituitary-thyroid axes may occur together with preservation of secretion of gonadotrophin and growth hormone. Additionally, hypoprolactinaemia often occurs. On magnetic resonance imaging or computed tomography, loss of pituitary volume is seen. This is also common in idiopathic hypopituitarism of old age.[4 5]

The cause of pituitary infarction after coronary artery bypass grafting presumably relates to the cardioplegia, non-pulsatile blood flow, hypotension, and, possibly, embolism or haemorrhage, as discussed by the authors. Acute neuroendocrine changes during cardiopulmonary bypass have been documented.[6 7]

The susceptibility of patients to this complication may be caused by unsuspected pituitary tumours and their vulnerable blood supplies. Hypopituitarism affects mortality from cardiovascular problems. Most pituitary hormone deficiencies are adequately recognised and replaced, with the exception of growth hormone.[8] Growth hormone deficiency is associated with poor cardiac risks factors such as an adverse lipid profile and splanchnic obesity.[9]

[1] Smith PL, Taylor KM, eds. Cardiac surgery and the brain. London: Edward Arnold, 1993.

[2] Sheehan HL, Davis JC. Post-partum hypopituitarism. Springfield, IL: Charles C Thomas, 1982.

[3] Aubrey RH, Nankin HR, Moses AM, Streeten DHP. Measurement of osmotic threshold for vasopressin release in normal subjects, and its modification by cortisol. J Clin Endocrinol Metab 1965;25:1481-92.

[4] Belchetz PE. Idiopathic hypopituitarism in the elderly. BMJ 1985;291:247.

[5] Belchetz PE. Clinical recognition of idiopathic hypopituitarism in the geriatric patient. Geriatr Med Today 1987;6:27-42.

[6] Taylor KM, Wright G S, Reid JM, Bain WH, Caves PK, Walker MS, et al. Comparative studies of pulsatile and non-pulsatile flow during cardiopulmonary by-pass, II. The effects on adrenal secretion of cortisol. J Thorac Cardiovasc Surg 1978;75:574-8.

[7] Taylor KM, Wright GS, Bain WH, Caves PK, Walker MS. Comparative studies of pulsatile and non-pulsatile flow during cardiopulmonary by-pass. III. Anterior pituitary response to thyrotropin - releasing hormone. J Thorac Cardiovasc Surg 1978;75:579-84.

[8] Rosen T, Bengtsson B-A. Premature mortality due to cardiovascular disease in hypopituitarism. Lancet 1990;336:285-8.

[9] Cuneo RC, Salomon F, McGauley GA, Sonksen PH. The growth hormone deficiency syndrome in adults. Clin Endocrinol 1992;37:387-97.

Department of Endocrinology, General Infirmary at Leeds, Leeds LS1 3EX

P E Belchetz, consultant physician and endocrinologist

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