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QJM: An International Journal of Medicine, 2019, 123–124

doi: 10.1093/qjmed/hcy252
Advance Access Publication Date: 29 October 2018
Case report

CASE REPORT

Gestational diabetes insipidus

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P.L. Chong1, J. Pisharam2, A. Abdullah3 and V.H. Chong 4

From the 1Division of Diabetes and Endocrinology, Department of Internal Medicine, 2Department of Renal
Services, 3Department of Obstetrics and Gynaecology and 4Division of Gastroenterology and Hepatology,
Department of Internal Medicine, RIPAS Hospital, Bandar Seri Begawan BA1710, Brunei Darussalam
Address correspondence to Dr P. L. Chong, Division of Diabetes and Endocrinology, Department of Medicine, RIPAS Hospital, Bandar Seri Begawan BA1710,
Brunei Darussalam. email: lina.chong@moh.gov.bn

creatinine ratio 282; NR 0–45 mg/mmol), raised uric acid


Learning points for clinicians (588; NR: 150-350lmol/l), leucocytosis (white cell count 20.9; NR:
• Liver disease during pregnancy may precipitate gesta-
3.8–11.8  109g/l), microcytic anaemia (Haemoglobin 9.8;
NR: 10.9–14.3g/dl and mean corpuscular volume 69.3; NR:
tional diabetes insipidus (GDI) and evaluation of liver
75.5–95.3fl), normal platelet count (430; NR: 150–450  109).
function is necessary in patients who develop GDI.
• Desmopressin is the treatment of choice and is safe in
Haemolysis was considered unlikely with mild lactate dehydro-
genase (578; NR: 125–220 U/l) and haptoglobulin (0.09; NR: 0.35–
pregnancy.
• Clinician awareness, prompt diagnosis and treatment
2.50g/l) abnormalities.
On Day 8 of admission, foetal heartbeat became undetectable.
should minimize the risk of maternal morbidity and
Intranasal desmopressin (DDAVP) 10 mcg was administered for
mortality.
suspected gestational diabetes insipidus. A water deprivation
test was not performed in view of the risk of further dehydration.
After one dose of desmopressin, her urine output slowed down
to 20–50 ml/h and hypernatraemia improved (Figure 1).
Case
She developed spontaneous contractions the next day and
A 25-year-old housewife presented with reduced foetal move- delivered a dismorphic female foetus without signs of life.
ments at 28 weeks of her fourth pregnancy (G4P2). She had diet- Blood sampling was undertaken unsuccessfully for karyotype
controlled gestational diabetes mellitus and was not on any analysis. A pituitary magnetic resonance imaging was unre-
medications. Although foetal heartbeat was detected, a foetal markable with normal posterior pituitary and stalk. Her electro-
ultrasound revealed an anomalous baby with a three-chamber lytes and liver function test normalized and no further polyuria
heart and features of hydrops fetalis. She was counselled was reported. She had an uneventful recovery postnatally and
regarding the likelihood of intrauterine foetal death. has remained well on follow-up 2 years later without any symp-
Her initial admission was complicated by vomiting, gastritis, toms of liver dysfunction or features of diabetes insipidus.
hypokalaemia and hyperglycaemia. On day 6 of admission, she
developed osmotic symptoms and significant hypernatraemia
(serum Naþ 164 mmol/l). The following day, despite intravenous
Discussion
fluids, she remained clinically dehydrated with a sinus tachy- Diabetes insipidus (DI) is defined as an inability to concentrate
cardia (107 beats/min), BP 104/74 mmHg, and 24-h urine output urine with polyuria (urine output > 3 l/day) and polydipsia.1
of 5400 ml. Serum Naþ was 170 mmol/l, serum osmolality Gestational diabetes insipidus (GDI) is a rare complication of
342 mmol/kg (normal range [NR]: 275–305 mosmol/kg), urine pregnancy affecting 2–4 per 100 000 pregnancies. It tends to
osmolality 55 mmol/kg (50–1200 mosmol/kg) and urine specific occur at the end of the second trimester or during the third
gravity 1.010. Renal function was normal. trimester. GDI is usually transient with spontaneous resolution
Liver function test was deranged (Table 1) with negative viral 4–6 weeks after delivery. Excessive vasopressinase activity has
screen. Liver ultrasonography was unremarkable. Other results been implicated in the pathophysiology of GDI. Vasopressinase
include negative autoimmune screen, proteinuria (protein: is produced by placental trophoblasts from the seventh week of

Received: 22 October 2018; Revised (in revised form): 24 October 2018


C The Author(s) 2018. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved.
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123
124 | QJM: An International Journal of Medicine, 2019, Vol. 112, No. 2

Table 1. Trend of liver function test during admission

Day 7 Day 8 Day 9a Day 10 Day 12 Day 17 Day 18 Ref range

ALT 170 167 106 57 35 25 15 1–54 U/l


ALP 174 185 205 209 214 109 102 40–150 U/l
GGT 365 410 372 332 324 94 57 9–36 U/l
Bilirubin 47.2 56.3 70.7 47.2 14.9 10.4 9.5 3.4–20.5 umol/l
Albumin 19 18 16 16 17 26 34 35–50 g/l

a
Spontaneous delivery.
ALT, alanine aminotransferase; ALP, alkaline phosphatase; GGT, gamma-glutamyl transferase.

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Figure 1. Trend of serum Naþ (mmol/L).

gestation and degrades vasopressin. As trophoblast mass Conflict of interest: None declared.
increases during pregnancy, vasopressinase levels reach
1000-fold peaking in the third trimester. Its activity remains high
during labour and delivery, then decreases by 25% per day to
References
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