Service de Néphrologie B, Hôpital Calmette, 1 Service de Suites de Couches, Maternité Jeanne de Flandre and 2 Service d'Endocrinologie, Clinique Marc Linquette, CHRU Lille, Lille, France
Correspondence and offprint requests to: Dr Eric Boulanger, Service de Néphrologie B, Hôpital Calmette, Boulevard du Pr. J. Leclerc, 59037 Lille Cedex, France.
Keywords: antidiuretic hormone; hyponatraemia; hypopituitarism; pregnancy; Sheehan syndrome
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Introduction |
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Case |
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The patient had normal biochemical data for 6 days in the intensive care unit. Ten days after hysterectomy, she complained of asthenia and failure to lactate. Hydration was clinically normal. Blood pressure was 120/75 mmHg. Red and white blood cell and platelet counts were within normal values. The biochemical data indicating acute hyponatraemia are presented in Table 1. Low blood osmolality and elevated urine osmolality suggested inappropriate secretion of antidiuretic hormone.
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With hormonal substitution, 30 mg/day hydrocortisone and 100 µg/day L-thyroxine, no relapse of inappropriate secretion of antidiuretic hormone has occurred 18 months after delivery. Subsequent magnetic resonance imaging showed pituitary atrophy.
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Discussion |
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Hyponatraemia as the presenting manifestation of Sheehan syndrome in the early post-partum period has been reported twice [4,5]. Several hypotheses have been proposed to explain hyponatraemia in the presence of hypopituitarism, i.e. dysfunction of the anterior hypophysis.
Inappropriate secretion of antidiuretic hormone is known to occur in states of adrenocorticotropin deficiency [6,7]. Glucosteroids have been shown to reverse the impaired water diuresis of this disorder by increasing the renal excretion of solute-free water. One study [8] reported that the plasma arginine vasopressin level was abnormally elevated during mild dehydration, and remained above the normal range despite haemodilution in patients with untreated adrenocorticotropin deficiency demonstrating a delayed water diuresis. Glucosteroid therapy lowered plasma arginine vasopressin to normal in dehydrated patients. A normal diuretic response to hydration was accompanied by a fall in plasma arginine vasopressin level to zero in steroid-treated patients. In this study, the results suggested that hypersecretion of arginine vasopressin may have played an important role in the abnormal water metabolism of adrenocorticotropin deficiency, and that glucosteroids promoted normal water diuresis by inhibiting the secretion of arginine vasopressin from the neurohypophysis.
Hypothyroidism can cause hyponatraemia. Montenegro recently reported a study of serum electrolytes concentration and glomerular filtration rate before and after thyroid replacement therapy in 41 patients with hypothyroidism [9]. The authors observed that creatinine clearance was slighty decreased in all and that the decrease was more noticeable in the elderly. Hyponatraemia was found more often in patients with elevated serum creatinine levels than in those with normal serum creatinine levels. All these defects were corrected by treatment with thyroid hormone. Hypothyroid patients have a diminished ability to excrete free water, fail to achieve maximum urine dilution, and show delayed excretion of a water load [10]. The correlation between plasma arginine vasopressin levels and the capacity to excrete a water load is weak [11].
Our patient had an acute onset of hypothyroidism and severe adrenocorticotropin deficiency which can explain both hyponatraemia and inappropriate secretion of antidiuretic hormone. The sodium concentration initially was corrected by water deprivation. After 6 months of hormonal substitution, the sodium concentration remained normal without any water deprivation.
Whereas post-partum hyponatraemia is not a uncommon disorder secondary to surgical procedure or inadequate rehydration, hyponatraemia secondary to panhypopituitarisum should be suspected if severe blood loss occurred during delivery.
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References |
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