Gestational diabetes insipidus. A systematic review of case reports

Mónica Bermúdez González; Esther Alvarez Silvares; Gonzalo Rubio Pérez

doi:10.1515/jpm-2024-0499

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Gestational diabetes insipidus. A systematic review of case reports

Mónica Bermúdez González , Esther Alvarez Silvares und Gonzalo Rubio Pérez

Veröffentlicht/Copyright: 28. Mai 2025

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Aus der Zeitschrift Journal of Perinatal Medicine

Abstract

Objectives

To evaluate the clinical characteristics and etiopathogenic factors associated with gestational diabetes insipidus (GDI), analyzing maternal and perinatal outcomes.

Methods

A systematic review was performed in PubMed, Embase and Scopus of articles on GDI published from January 1, 1980 to April 3, 2024. The review included 55 case reports on GDI, with a total of 64 women. Data on age, parity, diagnosis, management, and maternal and perinatal morbidity and mortality were collected. Descriptive statistical analysis was performed with SPSS version 17.0, considering a p value <0.05 as significant. Study quality was assessed with the Joanna Briggs Institute critical appraisal checklist.

Results

Of the 64 women studied, 65.6 % were primiparous and the mean gestational age at diagnosis was 32.7 weeks. There was a high prevalence of twin gestations (21.9 %) and a significant percentage of cesarean deliveries (54 %). Preeclampsia, Acute fatty liver of pregnancy and HELLP syndrome were significantly more prevalent. The incidence of prematurity was 54.7 % and the perinatal mortality rate was 78.1 ‰. These complications showed statistical significance (p<0.05), indicating the severity of GDI and its impact on obstetric outcomes.

Conclusions

GDI represents a complex clinical challenge with important implications for maternal-fetal health. The understanding of its aetiology, linked to vasopressinase activity and its relationship with various obstetric pathologies, is crucial for the diagnosis and proper management of this condition.

Keywords: diabetes insipidus; gestational; pregnancy; hypotonic polyuria; vasopressin

Introduction

Diabetes insipidus (DI) is an endocrine disorder characterized by a deficiency in the production or action of vasopressin (AVP), also known as antidiuretic hormone (ADH). Its symptoms include polyuria, polydipsia, dehydration and hypernatremia. It typically manifests with urinary output exceeding 3–3.5 L in 24 h and urinary osmolality less than 300 mOsmol/kg [1]. DI can be either of central origin, if there is dysfunction in the hypothalamus or neurohypophysis, or of nephrogenic origin, if there is no correct renal response to circulating AVP. It can be idiopathic or secondary to tumours, trauma, infections or genetic disorders [2], 3]. During pregnancy, gestational DI (GDI) – also known as transient DI – may arise, linked to excessive placental vasopressinase activity [4]. GDI is a rare disorder, affecting 2–4 of every 100,000 pregnancies, although the actual number may be higher due to undiagnosed cases [5], 6]. It usually shows up at the end of the second or third trimester and resolves spontaneously 4–6 weeks after delivery, without recurrence in future pregnancies [5], 7].

Pregnancy causes changes in blood volume physiology and osmoregulation, increasing AVP production, leading to water reabsorption, higher maternal plasma volume and lower plasma osmolality. However, placental vasopressinase increases endogenous AVP clearance [4]. As placental mass increases, plasma vasopressinase also rises, which increases AVP clearance 4-fold. Placental vasopressinase is detected as early as week 7 and its activity increases 20- to 50-fold towards the end of the second and beginning of the third trimester [8]. Despite these changes, the AVP concentration generally remains constant [8], 9].

At present, vasopressinase has been officially designated as leucyl/cystinyl aminopeptidase (LNPEP) by Human Genome Organization Gene Nomenclature Committee. LNPEP is known by several names, such as oxytocinase and placental leucine aminopeptidase (P-LAP), which indicate its broad substrate spectrum [10]. Increased levels of vasopressinase can lead to the development of GDI. This excess during pregnancy may be caused by excessive production of the enzyme by the placenta [11], or by a reduction in the liver’s ability to degrade vasopressinase [6], 12].

GDI has been associated in the scientific literature with various obstetric pathologies such as early birth [13], preeclampsia [14], Hellp syndrome [15], acute fatty liver disease of pregnancy (AFLP) [16] and oligohydramnios [5], 17]. The diagnosis of GDI is based on clinical evaluation and laboratory tests, such as sodium measurement and osmolality in blood and urine, and determination of copeptin [4]. Treatment aims to control symptoms and maintain water balance, using desmopressin (DDAVP), a vasopressin analog not degraded by vasopressinase, considered safe during pregnancy and lactation [6], 7], 18].

This study aims to conduct a comprehensive review of published cases of gestational diabetes insipidus (GDI) to characterize its clinical presentation, progression, and therapeutic management. By analyzing cases reported in the medical literature, we seek to describe the clinical and epidemiological characteristics of affected patients, as well as assess risk factors and associated comorbidities. Additionally, we examine the response to desmopressin treatment and maternal-fetal outcomes, including the incidence of preterm birth, mode of delivery, and perinatal mortality.

Since the low prevalence of this condition makes large-scale observational studies challenging, this work is based on the compilation and analysis of individual clinical cases. Our objective is to provide relevant information that contributes to the early identification of the disease and optimizes its clinical management, minimizing risks for both the mother and the fetus.

Methods

The present study systematically reviewed case reports and case series on GDI. A systematic search was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) [19].

This study does not require an Ethics Committee report as it is a compilation of published clinical cases.

Literature search strategy and inclusion criteria

Two authors (EAS and MBG) and an experienced librarian independently searched PubMed, Embase, and Scopus databases for articles on GDI published from January 1, 1980, to April 3, 2024. The combination of keywords and MeSH terms was used, according to the recommendations of each database. The key search in PubMed consisted of: (((diabetes insipidus[Title]) OR (“Diabetes Insipidus”[Mesh]))) AND ((pregnancy[Title]) OR (“Pregnancy”[Mesh]))))) OR ((gestational diabetes insipidus[Title]) OR (“Gestational Diabetes Insipidus” [Supplementary Concept]))) AND (1980:2024[pdat]). This strategy was subsequently adapted for use in the other selected databases (Supplementary Table 1).

Titles and abstracts obtained from the search were reviewed by the authors to determine eligibility and to exclude those that did not meet the inclusion criteria.

The full texts of all studies that were finally included were reviewed.

The search in electronic databases was complemented by a manual search of the reference lists of the included articles and Google Scholar to identify any grey literature on the subject. The full texts of potentially eligible case reports were retrieved and evaluated for final inclusion. Discrepancies were resolved through discussion and consensus. No language filters were applied.

Literature search strategy and inclusion criteria

Inclusion criteria were pregnant women with GDI diagnosis defined as pregnant women with hypotonic polyuria in the setting of elevated serum osmolality and polydipsia [4] that debuts during gestation and disappears a few weeks after the end of pregnancy.

The exclusion criteria consisted of cases diagnosed with (i) pre-gestational, central or nephrogenic diabetes insipidus, (ii) review articles, (iii) duplicate publications and (iv) studies lacking relevant results.

Data extraction and risk of bias assessment

Data extraction was performed using a standardized form designed for this review. Each author independently extracted and tabulated the following data from the included case reports: bibliographic information (author, country and year of publication. Supplementary Table 2) and clinical features of the pregnant women. Disagreements were resolved by discussion among all authors during data extraction.

Quality assessment

The Joanna Briggs Institute (JBI) Critical Appraisal Checklist was employed to assess the risk of bias in case reports and series included in our study [20]. For case reports, JBI domains included eight questions (Supplementary Table: Supplementary Table 4: Supplementary Table 2). For dat series publications, the methodology of the same institution was used [21] (Supplementary Table 3).

Pre-specified outcomes

The following outcomes were evaluated: (i) Maternal age at the onset of gestation; (ii) nulliparity: women who have never completed a pregnancy beyond 20 weeks; (iii) gestational age at disease onset; (iv) symptoms; (v) duration of symptoms prior to diagnosis; (vi) plasma osmolarity: quantitative; (vii) urinary osmolarity: quantitative; (viii) transaminases (alanine aminotransferase (ALT), aspartate aminotransferase (AST): quantitative; (ix) nuclear magnetic resonance; (x) treatment administered; (xi) maternal pathology associated with the course of GDI; (xii) time interval between GDI diagnosis and completion of pregnancy; (xiii) twin gestation; (xiv) oligohydramnios; (xv) amenorrhoea at the end of pregnancy; (xvi) type of delivery: vaginal vs. caesarean section; (xvii) perinatal morbidity and mortality; (xviii) maternal postpartum complications; (xix) resolution time.

Data synthesis

The descriptive statistical study was used with the Statistical Package for the Social Sciences (SPSS), version 17.0 (IBM, Chicago, IL, USA). Quantitative data obtained from the comparison of groups were analysed using unpaired Student’s t-tests and are presented as mean±standard deviation. For the analysis of qualitative data, Chi-square and Fisher’s exact tests were used and are expressed as number and percentage.

The incidences of the associated pathologies were compared with the population incidence described for each entity in the medical literature.

Results

Study selection and characteristics

From the search in the different databases, potentially eligible articles were identified, as can be seen in the flow diagram [Figure 1]. After screening, 55 case reports were considered suitable and included in the study involving a total of 64 patients.

Figure 1:

PRISMA flowchart: summary of evidence search and selection.

The characteristics of the included studies are comprehensively elaborated in Table 1.

Table 1:

Detailed characteristics of the included studies.

Autor	Age	Parity	Amenorrhoea at diagnosis	Symptoms	Duration of symptoms before diagnosis, weeks	Amino-transferase	Associated maternal pathology	Interval between diagnosis and delivery, weeks	Twin gestation	Oligo-hydramnios	Amenorrhoea on delivery	Delivery	Perinatal mortality	Postpartum maternal complications	Resolution time, weeks
Marqués et al. [7]	38	Primipara	38	Polydipsia/polyuria	6	Normal	Gestational diabetes	2	No	No	39	–	No		8
Dashraath et al. [22]	31	Primipara	Postpartum	Headache abdominal pain	0	Increased	Pre-eclampsia Hellp syndrome	–	Yes	No	39	Caesarean	No		0.5
Giacobbe et al. [23]	40	Multiparae	33	Polydipsia/polyuria		Normal	Preterm labor	4	No	Yes	37	Caesarean	No		0.5
Mor A et al. [24]	41	Multiparae	Postpartum	Polydipsia/polyuria	0	Increased	Nothing	–	No	Yes	38	Caesarean	No		0.5
Chong et al. [5]	25	Multiparae	28	Polydipsia/poliuria Vomiting	0	Increased	Gestational diabetes	0.2	No	No	28	Vaginal	No		0.5
Krysiak et al. [25]	35	Multiparae	28	Polydipsia/poliuria Asthenia	0	Normal	Haemochromatosis	13	No	No	41	Vaginal	No		2
Krysiak et al. [25]	29	Primipara	24	Polydipsia/polyuria	0	Increased	Haemochromatosis	14	No	No	38	Vaginal	No		0.5
Hanson et al. [26]	14	Primipara	33	Polydipsia/polyuria	0	–	Nothing	5	No	Yes	38	Vaginal	No		0.5
Katz et al. [27]	31	Primipara	30	Polydipsia/polyuria	0	Increased	Preterm labor	0.1	Yes	No	30	Caesarean	No		3
Kennedy et al. [28]	24	Primipara	36	Polydipsia/poliuria Vomiting	–	Increased	Pre-eclampsia	0	No	No	36	Vaginal	No		3
Kennedy et al. [28]	24	Primipara	Postpartum	Polydipsia/polyuria	–	Increased	Pre-eclampsia	–	No	No	37	Vaginal	No		3
Kennedy et al. [28]	37	Multiparae	36	Polydipsia/polyuria	–	Increased	Gestational diabetes pre-eclampsia	0	No	No	36	Vaginal	No		3
Kennedy et al. [28]	23	Primipara	36	Polydipsia/poliuria Vomiting	–	Increased	Nothing	0	No	No	36	Vaginal	No		3
Kennedy et al. [28]	19	Primipara	39	Polydipsia/poliuria Vomiting	–	Increased	Gestational diabetes pre-eclampsia	0	No	No	39	Vaginal	No		3
Kennedy et al. [28]	29	Primipara	Postpartum	Polydipsia/poliuria Vomiting	–	Increased	Nothing	–	No	No	35	Vaginal	No	Disseminated vascular coagulation	3
Krege et al. [29]	27	Multiparae	34	Polydipsia/poliuria Vomiting	3	Increased	Pre-eclampsia	0.2	No	No	34	Caesarean	No		1
Combs et al. [30]	19	Primipara	34	Polydipsia/polyuria	0	Increased	Eclampsia	4	No	No	38	Caesarean	No		2
Kalelioglu et al. [31]	35	Multiparae	35	Polydipsia/poliuria Vomiting	3	Normal	Nothing	3	No	No	38	Caesarean	No		2
El-Hennawy	19	Multiparae	38	Vomiting	–	Normal	Nothing	0.1	No	No	38	Vaginal	No		0.5
El-Hennawy et al. [32]	32	Multiparae	37	Vomiting polydipsia/poliuria	0	Normal	Nothing	0.5	No	No	38	Caesarean	No		2
Hughes et al. [33]	19	Primipara	36	Polydipsia/poliuria	8	Normal	Nothing	0.2	No	No	36	Vaginal	No		8
Hughes et al. [33]	21	Multiparae	20	Polydipsia/poliuria	4	Normal	Nothing	12	No	No	36	Caesarean	No		10
Benchetrit et al. [34]	29	Primipara	24	Polydipsia/poliuria	–	Normal	Pre-eclampsia	1	No	No	25	Caesarean	No		2
Gambito et al. [35]	47	Primipara	Postpartum	Polydipsia/poliuria Lethargy	4	Increased	Hellp syndrome	–	Yes	No	34	Caesarean	Yes		0.5
Siristatidis et al. [36]	23	Primipara	33	Polydipsia/poliuria	4	Normal	Nothing	1.3	No	Yes	34.8	Caesarean	No		6
Ford et al. [37]	24	Primipara	29	Polydipsia/poliuria	–	Normal	Nothing	8	No	No	37	Vaginal	No		0.5
Frenzer et al. [38]	35	Primipara	31	Polydipsia/poliuria Abdominal pain	–	Normal	Hellp syndrome	1	No	No	32	Caesarean	No		1.1
Sainz Bueno et al. [39]	31	Primipara	33	Polydipsia/poliuria	–	Increased	Preterm labor Acute fatty liver	0.1	No	No	33.4	Vaginal	No		1
Kondo et al. [13]	16	Primipara	25	Polydipsia/poliuria	–	Normal	Preterm labor	7	No	No	32	Vaginal	No		0.1
Wallia et al. [40]	31	Multiparae	Postpartum	Polydipsia/poliuria	–	Increased	Preterm labor Placental abruption	–	Yes	No	33	Caesarean	No		6
Alvarez-Bernabeu et al. [41]	38	Primipara	30	Polydipsia/poliuria	–	Increased	Gestational diabetes	2	Yes	No	31	Caesarean	No		–
Vilouta et al. [42]	19	Primipara	38	Polydipsia/poliuria Anorexia	2	Normal	Acute fatty liver	0.3	No	No	38	Caesarean	No		0.1
Berteau et al. [43]	30	Primipara	32	Polydipsia/poliuria Paraplegia	2	Normal	Guillen-Barre syndrome	2	No	No	34	Caesarean	No	Pulmonary thromboembolism	–
De Mesmay et al. [44]	28	Primipara	28	Polydipsia/poliuria	6	Normal	Gestational diabetes preterm labor	7	Yes	No	35	Caesarean	No		1
Mizuno et al. [45]	29	Primipara	31	Polydipsia/poliuria Vomiting Anorexia	2	Increased	Pre-eclampsia	4	No	No	35	Vaginal	No	Liver failure Disseminated vascular coagulation	1
Passannante et al. [46]	30	Multiparae	32	Seizures	–	Increased	Eclampsia	0	Yes	No	32	Caesarean	No		0.6
Yamanaka et al. [47]	26	Primipara	Postpartum	Hypertension Proteinuria	0	Normal	Hellp syndrome	–	Yes	No	36	Caesarean	No		4
Raziel et al. [48]	23	Primipara	Postpartum	Polydipsia/poliuria	–	Increased	Nothing	–	No	No	42	Caesarean	No		0.5
Raziel et al. [48]	36	Multiparae	Postpartum	Polydipsia/poliuria	–	Increased	Gestational diabetes	–	No	No	40	Caesarean	No		1.3
Ellidokuz et al. [49]	23	Primipara	Postpartum	Polydipsia/poliuria	0	Increased	Hellp syndrome	–	No	No	35	Caesarean	Yes		2
English et al. [50]	33	Primipara	Postpartum	Vomiting Abdominal pain	–	Increased	Acute fatty liver pancreatitis	–	No	No	35	Caesarean	No	Liver failure	–
Woelk et al. [15]	18	Primipara	34	Polydipsia/poliuria Abdominal pain Headache	0	Increased	Hellp syndrome	0.7	Yes	No	35	Caesarean	No		0.6
Brewster et al. [51]	34	Multiparae	35	Polydipsia/polyuria Headache	0	Normal	Nothing	1	No	No	36	Vaginal	No		1.4
Brewster et al. [51]	32	Primipara	Postpartum	Polydipsia/polyuria Headache	0	Normal	Gestational diabetes	–	No	No	38	Vaginal	No		–
Weinberg et al. [52]	29	Primipara	29	Polydipsia/poliuria	9	Normal	Preterm labor	0.3	No	No	29	Vaginal	No		0.2
Jin-No et al. [53]	33	Primipara	33	Polydipsia/poliuria	–	Normal	Nothing	5	No	No	38	Vaginal	No		0.3
Aragon-Charris et al. [54]	16	Primipara	Postpartum	Polydipsia/poliuria	3	Increased	Pre-eclampsia	–	No	No	38	Caesarean	No		0.4
Barbey et al. [55]	32	Primipara	29	Polydipsia/poliuria Abdominal pain	1	Increased	Acute fatty liver pancreatitis	3	Yes	No	32	Vaginal	No		1
Price et al. [56]	25	Multiparae	23	Anorexia abdominal pain Vomiting	–	Increased	Pancreatitis Guillen Barre syndrome rhabdomyolysis	3	Yes	No	26	Caesarean	Yes		1
van der Weiden et al. [57]	28	Multiparae	38	Polydipsia/polyuria Headache Abdominal pain	1	Increased	Nothing	1	No	No	39	Vaginal	No		1.5
Sherer DM et al. [58]	–	Multiparae	Postpartum	Polydipsia/poliuria	7	Increased	Gestational diabetes	–	No	Yes	40	Vaginal	No	0	0.4
Wiser A et al. [59]	24	Primipara	35	Polydipsia/poliuria	7	Increased	Pre-eclampsia	3	Yes	No	35	Vaginal	Yes	0	1
Lacassie HJ et al. [60]	25	Multiparae	30	Polydipsia/poliuria Vomiting	3	Normal	Preterm labor	0.1	No	No	30	Vaginal	No	0	0.2
Carpio-Orantes et al. [61]	20	Primipara	Postpartum	Polydipsia/poliuria Seizures	–	Normal	Nothing	–	No	No	39	Caesarean	No	0	0.1
Sum M et al. [62]	28	–	33	Polydipsia/poliuria	8	Increased	Acute fatty liver	0	Yes	No	33	Caesarean	No	Acute fatty liver	3
Goldrich el al [14]	39	Multiparae	Postpartum	Polydipsia/polyuria Headache	–	Increased	Pre-eclampsia	–	No	No	39	Vaginal	No	Pre-eclampsia	0.3
Rodrigo et al. [63]	48	Multiparae	Postpartum	Polydipsia/polyuria Headache	–	Normal	Gestational diabetes	–	No	No	38	Caesarean	No	Pre-eclampsia	1
Abramova et al. [64]	32	Primipara	36	Polydipsia/poliuria	–	Normal	Nothing	5	No	No	41	Caesarean	No	0	4
Nakamura et al. [65]	16	Primipara	25	Polydipsia/poliuria	9	Normal	Preterm labor	7	No	No	32	Vaginal	No	Deep vein thrombosis	0
Wang et al. [16]	35	Primipara	33	Polydipsia/poliuria	–	Increased	Preterm labor Acute fatty liver	0	Yes	No	33	Caesarean	No	Disseminated vascular coagulation	0.2
Maharajh et al. [66]	33	–	23	Polydipsia/poliuria	0	Normal	Nothing	16	No	No	39	Vaginal	No	0	0.2
Elkhomri et al. [67]	34	–	28	Polydipsia/poliuria	–	Normal	Nothing	10	No	No	38	Vaginal	No	0	2
Razavi et al. [68]	38	Primipara	36	Polydipsia/poliuria Vomiting	2	Increased	Nothing	0	No	No	36	Caesarean	No		2
Alkaabi et al. [69]	25	Multiparae	29	Polydipsia/polyuria Headache Vomiting	8	Normal	Preterm labor	8	Yes	No	37	Caesarean	No	0	1

Risk of bias of included studies

The overall risk of bias of the case reports analyzed using the JBI Critical Appraisal Checklist was low. The question with the worst evaluation was Q4 when describing the diagnostic tests and their results (Figure 2A and B).

Figure 2:

Risk of bias. Description of the part labels: green box with symbol (+): answers the question adequately. Red box with symbol (−): does not answer the question. Orange box with symbol (¿): unclear or not applicable. A) Risk of bias: summary assessed through JBI critical appraisal checklist for case reports. (For the meaning of Q1–Q8 you should refer to Table suppl 3). Green box with symbol (+): answers the question adequately. Red box with symbol (−): does not answer the question. Orange box with symbol (¿): unclear or not applicable.) B) Risk of bias: summary and graph assessed through JBI critical appraisal checklist for case series (For the meaning of Q1–Q10 you should refer to Table suppl 4). Green box with symbol (+): answers the question adequately. Red box with symbol (−): does not answer the question. Orange box with symbol (¿): unclear or not applicable.

Statistical analyses

Data for 64 women diagnosed with GDI were analyzed in this study. The mean maternal age was 28.7 ± 7.5 years (14–48 years). Forty patients (65.6 %; 40/61) were primiparous (p=0.0008) compared to 34.4 %, which were multiparous.

There were 14 twin pregnancies. The twin gestation rate was 21.9 %, significantly higher when compared to the one described in the medical literature [70] (p=0.001).

The mean gestational age at onset of clinical symptoms was 32.7 ± 4.8 weeks (20–42 weeks). In 23.4 % (n=15/64) the GDI diagnosis was made in the puerperium. The distribution by gestational period can be seen in [Figure 3].

Figure 3:

Distribution by gestational period at diagnosis of GDI.

In 84.4 % (n=54) among the debut symptoms, polyuria with polydipsia associated with other symptoms was present. In 53.1 % (n=34) of the cases the only debut clinical manifestation was the presence of polyuria with polydipsia. Only in 9.4 % of the cases, polyuria was not a symptom at the onset of the clinical picture, but it was present in all cases during the course of the disease. The clinical features are shown in Table 2.

Table 2:

The clinical features.

Clinical features/symptoms	n	%
Polyuria/polydipsia	54	84.4
Hypertension	17	26.6
Nausea and vomiting	14	21.9
Headache	8	12.5
Abdominal pain	7	10.9
Epigastralgia	3	4.7
Anorexia	3	4.7
Seizures	2	3.1
Asthenia	1	1.6
Confusion	1	1.6

A total of 51.6 % (n=33) of the pregnant women reported isolated polyuria/polydipsia of long duration up to 9 weeks (4.6 ± 2.6 weeks), for which they had not consulted. In this group, it should be noted that the evolution of GDI was associated with other serious maternal pathologies in 36.4 % (preeclampsia, eclampsia, AFLP, Hellp syndrome, consumption coagulopathy, deep vein thrombosis and early placental abruption). It was also associated with three perinatal deaths. The maternal pathologies associated with the course of GDI are shown in Table 3.

Table 3:

Maternal pathologies associated with the course of GDI.

Associated maternal pathologies	n	%	Estimated frequency in the medical literatura, %	p-Value
Pre-eclampsia	19	29.7	4.6 [71]	0.000
Threatening premature labor	13	20.3	10 [72]	0.10
Gestational diabetes	9	14.1	17 [73]	0.77
Acute fatty liver of pregnancy	6	9.4	0.005 [74]	0.000
HELLP syndrome	5	7.8	0.5 [75]	0.005
Eclampsia	2	3.1	0.018 [76]	0.000
Haemochromatosis	2	3.1	*
Guillen Barre syndrome	1	1.6	*
Pancreatitis	1	1.6	*
Rhabdomyolysis	1	1.6	*

(*): There are no data in the literature on the incidence of these pathologies in pregnant women.

In the entire series, the association with oligohydramnios only occurred in 6 cases (9.4 %), without being associated with an increase in the reported perinatal mortality. Neither serum osmolarity nor urinary osmolarity were prognostic factors for maternal-fetal morbidity and mortality. A higher maternal morbidity and fetal mortality was observed when the liver profile was altered at diagnosis of GDI Table 4.

Table 4:

Maternal and fetal morbimortality in relation to liver profile.

	Normal transaminases (n=30)	Altered transaminases (n=34)	p-Value
Amenorrhoea at delivery	34.9 ± 3.9	34.4 ± 3.6	0.61
Preterm birth	22/33 (66.7 %)	13/29 (44.8 %)	0.14
Twin pregnancy	3 (10 %)	11 (32.3 %)	0.06
Caesarean section	8 (26.6 %)	18 (52.9 %)	0.06
Maternal morbidity	2 (6.7 %)	8 (23.5 %)	0.13
Perinatal mortality	0 (0 ‰)	5 (147 ‰)	0.000

The gestational age at delivery was 35.6 ± 3.5 weeks (25–42 weeks). The distribution by gestational age at birth can be seen in Table 5. The prematurity rate was 54.7 %.

Table 5:

Gestational age distribution at birth.

Amenorrhoea at delivery	n (64)	%
≥37	29	45.3
≥32<37 (moderate to late preterm)	28	43.7
≥28<32 (very preterm)	5	7.8
<28 (extremely preterm)	2	3.1
Rate of preterm	35	54.69 (WHO: 4–16 %)

WHO, World Health Organization.

Of the 35 cases of preterm birth (amenorrhoea<37 weeks), 51.4 % (n=18) were iatrogenic, severe maternal pathology being the most frequent cause (77.8 %). In one case the indication was abruptio placentae. In 7 % of the cases the authors do not specify the medical indication for premature termination.

In 40 % (n=14) of the cases were spontaneous preterm deliveries, in all of them tocolysis was attempted and fetal lung maturation was performed. We did not observe that both therapies modified the course of the disease.

In 3 cases, the authors do not specify whether the delivery was spontaneous or medically indicated.

A total of 74.6 % (47/63) received treatment with desmopressin, with remission of polyuria/polydipsia symptoms.

54 % (34/63) terminated their pregnancy by cesarean section.

The main causes of cesarean section were:

Severe maternal pathology: 16 (47 %)
Risk of loss of fetal wellbeing: 7 (20.6 %)
Previous cesarean section: 3 (8.8 %)
Prematurity ± twin pregnancy: 2 (5.9 %)
Not cited: 6 (17.6 %)

In the group of patients with puerperal debut (n=15), the diagnosis was made between the 1st and 15th day. The 66.7 % (10/15) corresponded to term gestations. 80 % (12/15) occurred after cesarean section. In 73.3 % (11/15) of the cases it was associated with alteration of the hepatic profile.

The perinatal mortality rate was estimated at 78.1 ‰ (n=5). All of them occurred in mothers with extremely severe concomitant diagnoses: 2 Hellp syndromes, 1 rhabdomyolysis and 1 severe preeclampsia.

The estimated perinatal mortality rate in the literature [77] is 13.9 ‰ (p=0.000).

No maternal deaths were described in the entire series.

The mean time to resolution of GDI was 1.8 ± 2 weeks (2 days- 10 weeks). In 50.7 % of the cases total resolution occurred in less than 1 week. In 37.3 % clinical resolution was delayed for more than 2 weeks. Practical algorithm regarding evaluation and management of GDI Figure 4.

Figure 4:

Algorithm for the diagnosis and management of diabetes.

Discussion

GDI is a rare and transient disorder during pregnancy with potential maternal-fetal consequences. It is due to increased activity of the enzyme vasopressinase, officially known as LNPEP, produced by placental trophoblasts to degrade AVP. This enzyme activity increases with the growth of the placental mass, especially in the third trimester, and with an increased risk in multiple pregnancies. Generally speaking, GDI is resolved spontaneously within 4–6 weeks after delivery and rarely recurs in future pregnancies [7], 78].

In our analysis, most of the pregnant women were primigravid (65.6 %, p=0.000), with a mean gestational age at diagnosis of 32.7 ± 4.8 weeks. Furthermore, 21.9 % of the cases were found to correspond to twin pregnancies, a significantly higher frequency than that reported in the population, which stands at 3.1 % (p=0.001) [70]. As an initial clinical manifestation, we observed the presence of polyuria and polydipsia of long duration in more than half of the pregnant women (51.2 %). It is also noteworthy that more than half of the deliveries were by cesarean section (54 %), with a mean amenorrhea at delivery of 35.6 ± 3.5 weeks. The average time to resolution of the clinical picture was 1.8 weeks (2 days–10 weeks), being less than 1 week in 50.7 % of the sample. These findings are consistent with those described in the medical literature, highlighting the significant role of primigravid pregnant women, the high incidence of cesarean sections and prematurity.

It has been suggested that the placenta may synthesize vasopressinase as a preventive measure against preterm delivery [13]. Vasopressinase plays a crucial role in the degradation of oxytocin and AVP, increasing the metabolic clearance rate of oxytocin during gestation [79]. It has been observed that reduced vasopressinase levels are associated with spontaneous abortions and preterm deliveries [80], 81]. In our review, 20.3 % of pregnant women presented a threat of preterm delivery before or during the course of the disease, compared to 10 % reported in the medical literature [72] (p=0.1). Most of the deliveries were preterm (less than 37 weeks), reaching 54.7 %. In addition, the perinatal mortality rate was estimated at 78.1 ‰, significantly higher than the 13.9 ‰ referred to in the literature [77] (p=0.000). This highlights the potential perinatal mortality associated with this pathology, an aspect that has not been widely highlighted in the scientific literature.

Case reports have also associated DGI with oligohydramnios and fetal death, highlighting the importance of careful management and close surveillance in patients with this condition [5], 17]. However, in our study, only 6 cases of oligohydramnios (9.4 %) were observed, with no increase in fetal morbidity and mortality.

Three clinical entities occurred significantly more in women with GDI compared to the general obstetric population: preeclampsia, AFLP and HELLP syndrome, accounting for 46.9 % of the sample. Preeclampsia was diagnosed in 29.7 % of pregnant women with GDI, compared to 4.6 % reported in the medical literature [71] (p=0.000). Pregnant women diagnosed with AFLP accounted for 9.4 %, compared to 0.00005 % reported [74] (p=0.000). Those that developed HELLP syndrome constituted 7.8 %, compared to 0.5 % described in the literature [75] (p=0.005). This condition has been linked in the literature to liver dysfunction during pregnancy. Vasopressinase is metabolized in the liver, implying that patients with hepatic insufficiency are at risk for decreased enzymatic degradation, resulting in increased clearance of AVP and leading to GDI [14]. However, the pathophysiological mechanism previously described does not explain the cases of GDI without transaminase alteration found in our analysis. Although it has been suggested that preeclampsia may trigger GDI, it is also possible that the relationship is inverse, with GDI inducing preeclampsia. One explanation is put forward by Yoshihara et al. [82], who demonstrate that in severe preeclampsia the protective functions of P-LAP at the placental level are broken, leading to massive leakage of fetal vasopressin into the maternal circulation and subsequent contraction of both maternal vessels and the uterus.

In the series analyzed, 80 % of women with GDI with puerperal debut underwent cesarean section. Postpartum GDI has been associated with placental extraction that would result in the release of a large volume of placental vasopressinase into the bloodstream [40]. Another plausible explanation would be that some of these pregnant women had not previously reported symptoms of polyuria/polydipsia and balanced their GDI by increased water intake. After the cesarean section with water control and fluid restriction, the entity finally manifested itself.

An algorithm is presented that provides a practical tool to facilitate the evaluation and management of GDI.

We have identified several novel findings related to GDI. First, we observed a higher incidence of twin pregnancies, which was significantly higher in our sample than in the general population. We also highlighted the association of GDI with an increased frequency of preeclampsia, AFLP, and HELLP syndrome, which occurred more frequently compared to what has been reported in the literature. Another relevant finding was the higher percentage of cesarean sections and preterm deliveries in the affected pregnancies. Additionally, the perinatal mortality associated with GDI was considerably higher than expected, underscoring the severity of this condition. These results suggest that GDI has a significant impact on the course of pregnancy and emphasize the importance of early diagnosis and proper management.

Strength and limitations

To our knowledge, and as a strength of our work, this is the first systematic review on GDI. Until our study, the medical literature only included isolated clinical cases and small case series. From the analysis carried out, data can be extracted to help us in the early and adequate diagnosis of this entity, which is considered a pathology with a high potential to generate maternal morbidity and perinatal mortality. One of the limitations of our analysis is that it is based on case studies and case series. Therefore, it is necessary to carry out clinical studies with greater scientific robustness to obtain more conclusive results.

Conclusions

Corresponding author: Esther Alvarez Silvares, Department of Obstetrics and Gynecology, Ourense Hospital Complex, Ourense, Spain, E-mail: lacuentadealvarez@gmail.com

Research ethics: Not applicable.
Informed consent: Not applicable.
Author contributions: All authors have accepted responsibility for the entire content of this manuscript and approved its submission. EAS: protocol/project development, data collection or management, data analysis, manuscript writing/editing. MBG: protocol/project development, data collection or management, data analysis, manuscript writing/editing. GRP: protocol/project development, manuscript writing/editing.
Use of Large Language Models, AI and Machine Learning Tools: No AI, LLM or machine learning tools were used at any point during the study and writing of the manuscript.
Conflict of interest: The authors state no conflict of interest.
Research funding: None declared.
Data availability: The raw data can be obtained on request from the corresponding author.

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Supplementary Material

This article contains supplementary material (https://doi.org/10.1515/jpm-2024-0499).

Received: 2024-10-21

Accepted: 2025-04-19

Published Online: 2025-05-28

This work is licensed under the Creative Commons Attribution 4.0 International License.

Supplementary Material

https://doi.org/10.1515/jpm-2024-0499

Schlagwörter für diesen Artikel

diabetes insipidus; gestational; pregnancy; hypotonic polyuria; vasopressin

Creative Commons

BY 4.0

Gestational diabetes insipidus. A systematic review of case reports

Artikel

Abstract

Objectives

Methods

Results

Conclusions

Introduction

Methods

Literature search strategy and inclusion criteria

Literature search strategy and inclusion criteria

Data extraction and risk of bias assessment

Quality assessment

Pre-specified outcomes

Data synthesis

Results

Study selection and characteristics

Risk of bias of included studies

Statistical analyses

Discussion

Strength and limitations

Conclusions

References

Supplementary Material

Zusatzmaterial