Adrenal failure and subsequent alactogenesis: partial pituitary failure in pregnancy. — ASN Events

Adrenal failure and subsequent alactogenesis: partial pituitary failure in pregnancy. (#341)

Shannon McCarthy 1 2 , Elke Hendrich 3
  1. Endocrinology, Ballarat Base Hospital, Ballarat, VIC, Australia
  2. Barwon Health, Geelong, VIC, Australia
  3. Endocrinology, Ballarat Base Hospital, Ballarat, VIC, Australia

A G2P1 37 year old woman presented to an emergency department following a hypoglycaemic seizure at 18/40 weeks’ gestation. Her husband woke to witness her experiencing a generalised tonic-clonic seizure. Fingerprick BSL by paramedics was 1.9. The seizure resolved rapidly with intravenous glucose.

At initial assessment she was clinically well and afebrile. She was normotensive with a postural drop of 20mmHg systolic. Cardiovascular and respiratory examinations were otherwise unremarkable. Serum insulin was 45mIU/L, serum C-peptide 2.40nmol/L, and serum glucose 10.7mmol/L, likely elevated due to the intravenous glucose load.
She had been well recently. She had coeliac disease confirmed by endoscopy. Her pregnancy was so far uncomplicated, as was her previous pregnancy. She denied use of alcohol, recreational drugs, oral hypoglycaemic agents, or insulin. Her only medication was a multivitamin.

No further episodes of hypoglycaemia occurred during admission. Serum cortisol at 1130 was 58nmol/L, prolactin was low at 38mIU/L, and HbA1c was 4.5%. Thyroid function revealed subclinical hypothyroidism with TSH 5.86mIO/L, T4 7.0pmol/L. The patient was discharged without initiation of any treatment.

Months later, the obstetric registrar requested urgent endocrinology review regarding worsening subclinical hypothyroidism and possible adrenal insufficiency. Prior to pregnancy she menstruated regularly. She reported a lack of lactation after delivering her first child two years earlier, but denied any other symptoms of pituitary insufficiency.

Cardiovascular, respiratory, and neurological examinations including visual fields and cranial nerves were unremarkable. There was no increased pigmentation and no postural drop in blood pressure.

Secondary adrenal insufficiency was confirmed by a 250mcg Synacthen test [see table]. Anti-TPO Abs were positive at 73 kIU/L. Anti-IA2, anti-GAD, and anti-adrenal antibodies were negative. Prolactin was still low.

She was treated with cortisone, 25mg and 12.5mg, and thyroxine 150mcg daily, and following delivery, pituitary MRI demonstrated a partially empty sella, and no evidence of lymphocytic hypophysitis. She again experienced puerperal alactogenesis. Menses returned spontaneously.

                     ACTH pmol/L Cortisol nmol/L
0 minutes       <1.1                           84
1>30 minutes                                     100
60 minutes    <1.1                          113