[Case Study] A Case of Hyponatremia Caused by Central Hypocortisolism

Gabriele Parenti; Valdo Ricca; Alessia Zogheri; Mario Serio; Massimo Mannelli; Alessandro Peri*

Disclosures

Nat Clin Pract Endocrinol Metab. 2007;3(4):369-375. 

In This Article

Summary and The Case

Summary

Background: A 43-year-old woman was referred to the Psychiatric Unit of the University of Florence Hospital, 1 year after the development of a clinical picture characterized by nausea, hyporexia, muscle weakness, insomnia, weight loss, amenorrhea and severe depression. These clinical manifestations had started 2 months after delivery of her first child. Initial laboratory investigations revealed hypoglycemia and hyponatremia. The patient was, therefore, transferred to the Endocrine Unit of the same hospital for further evaluation of the case.
Investigations: Physical examination to evaluate extracellular volume status, standard laboratory investigations, and evaluation of plasma and urinary osmolality and urinary sodium excretion. Basal and dynamic evaluation of anterior pituitary function and a pituitary MRI were also performed.
Diagnosis: Hyponatremia caused by central hypocortisolism (isolated adrenocorticotropic hormone deficit).
Management: Glucocorticoid therapy (25 mg cortisone acetate tablets, 1.5 tablets per day).

The Case

In March 2005, a 43-year-old woman was referred to the Psychiatric Unit at the University of Florence Hospital. She reported that since June 2004, 2 months after her first delivery, she started to suffer from nausea, severe hyporexia, muscle weakness and insomnia. Her weight was then 62 kg (BMI 22.8 kg/m2). A few months later, she began to suffer from severe depression, a marked diminution of interest in most activities, diminished ability to concentrate, profound loss of energy, loss of sexual desire, feelings of worthlessness, and subjective chills without fever. She was still amenorrheic. She had no family or personal past history for Axis I clinical syndromes of mental dysfunction.

At admission, her weight was 47 kg (BMI 17.2 kg/m2). She was not taking any medication. Diagnostic and Statistical Manual of Mental Disorders IV criteria for major depressive episode were fulfilled. The main values for routine laboratory investigations revealed low fasting glucose levels (2.8 mmol/l; normal range 3.6-6.1 mmol/l) and sodium levels (125 mmol/l; normal range 135-146 mmol/l). The patient was transferred to the Endocrine Unit of the same hospital. Clinical examination revealed normal extracellular volume status (EVS) (i.e. normal skin moisture, no distended or flat veins, no sunken eyes), hypotonic and hypotrophic limb muscles, no melanodermia, moderately diminished axillary and pubic hair, blood pressure 100 over 65 mmHg without relevant postural changes, pulse rate 78 beats per minute. There were no abnormal neurologic findings.

Baseline evaluation confirmed the presence of hypoglycemia and hyponatremia ( Table 1 ). Dynamic testing for anterior pituitary hormone reserve revealed a normal TSH, follicle-stimulating hormone, luteinizing hormone and growth hormone response (Figure 1A-C). Conversely, no changes in adrenocorticotropic hormone (ACTH) and serum cortisol levels were observed after corticotropin-releasing hormone stimulation (Figure 1D). In agreement with the psychiatrist's suggestion, no insulin tolerance test was performed, because of the very severe psychiatric condition of the patient. MRI of the head showed a thickened (2.7 mm) pituitary stalk. Glucocorticoid therapy was started (one 25 mg cortisone acetate tablet at 0800 h, and half of a 25 mg tablet at 1600 h) and within 2 days, serum sodium levels gradually increased and ultimately returned to normal (136 mmol/l). After 1 year of follow-up, the patient had completely recovered from depression, her muscle tone and strength dramatically improved, a 10 kg weight gain was observed and regular menses returned. At that time, a repeat hormonal assessment (performed off therapy) confirmed the previous diagnosis ( Table 1 ) and, therefore, glucocorticoid replacement treatment was continued. All the patient's other anterior pituitary hormones were within the normal range.

Figure 1.

Results of dynamic tests for evaluation of pituitary hormones. (A) Response of TSH and prolactin after intravenous administration of 200 μg TRH. To convert prolactin values to pmol/l multiply by 2.043. (B) Response of FSH and LH after intravenous administration of 100 μg GnRH. (C) Response of GH after intravenous administration of 1 μg/kg GHRH plus 0.5 g/kg arginine. (D) Plasma levels of ACTH and cortisol after intravenous administration of 100 μg CRH. Abbreviations: ACTH, adrenocorticotropic hormone; CRH, corticotropin-releasing hormone; FSH, follicle-stimulating hormone; GH, growth hormone; GHRH, growth-hormone-releasing hormone; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone; TRH, TSH-releasing hormone.

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