Recurrent diabetes insipidus associated with pregnancy: Pathophysiology and therapy

Jm, Hughes; Barron, W. M.; Vance, M A

doi:10.1016/0020-7292(89)90243-9

Cited by 12 publications

(5 citation statements)

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“…Only two patients have been described as having recurrent, histologically proven acute fatty liver of pregnancy (Barton et al 1990; Schoeman et al 1991), both associated with underlying disorders of urea cycle enzyme or fatty acid oxidation deficiency. Recurrent cranial diabetes insipidus has been reported (Baylis et al 1986; Hughes et al 1989) and is not a surprising finding. Recurrent vasopressin‐resistant transient diabetes insipidus in association with hepatorenal dysfunction also has been reported (Goodman et al 1984), but the risk of recurrence of transient diabetes insipidus and acute fatty liver of pregnancy is probably extremely low.…”

Section: Discussionmentioning

confidence: 82%

Transient diabetes insipidus and acute fatty liver of pregnancy

Kennedy

Hall

Seymour

et al. 1994

BJOG

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Objective To review the association of transient diabetes insipidus and acute fatty liver of pregnancy. Design A retrospective study. Setting Six women presenting with polyuria and polydipsia in the third trimester or in the immediate postpartum period, referred over a two and a half year period; five out of six were primigravida. All had raised liver transaminases and biopsy‐proven acute fatty liver of pregnancy. Four out of six also had pre‐eclampsia. Subjects Tertiary referral centre. Main outcome measures There were no maternal deaths and only one fetal death. Desamino‐cys‐1‐D‐arg‐8‐vasopressin administration produced a reduction in urine output in all five women to whom it was administered. In all cases symptoms had resolved by the end of the fourth postpartum week. Three of the women have had subsequent pregnancies uncomplicated by either transient diabetes insipidus or acute fatty liver of pregnancy. Conclusions The association of transient diabetes insipidus and acute fatty liver of pregnancy appears more common than previously recognised. Both may be part of the spectrum of pre‐eclampsia.

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Section: Discussionmentioning

confidence: 82%

Transient diabetes insipidus and acute fatty liver of pregnancy

Kennedy

Hall

Seymour

et al. 1994

BJOG

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“…The disease presents during gestation, brought to the fore with the increase in the MCR of AVP that normally occurs in pregnancy. Cases described by Baylis (49), Hughs (50) and Iwasaki (51) and their respective colleagues, as well as the transient postpartum polyuria noted in women with Sheehan's syndrome, may fit this category (52,53). Finally, there are instances where female carriers of the X-linked disorder nephrogenic diabetes insipidus have developed hormone-resistant polyuria during pregnancy, the reasons for which appear obscure (Drs Bichet and Robertson, personal communications).…”

Section: Transient Of Pregnancymentioning

confidence: 82%

Osmoregulation, the secretion of arginine vasopressin and its metabolism during pregnancy

Lindheimer

Davison

1995

European Journal of Endocrinology

155

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This review stresses changes in osmoregulation as well as the secretion and metabolism of arginine vasopressin during pregnancy, focusing on human gestation. Pregnant women experience a decrease in body tonicity, plasma osmolality decreasing immediately after conception to a nadir approximately 10 mosmol/kg below non-pregnant levels early in pregnancy, after which a new steady state is maintained until term. Data from both human and rodent gestation have led to a formation of how these changes occur. The osmotic thresholds for thirst and antidiuretic hormone release decrease in parallel. Lowering the threshold to drink stimulates increased water intake and dilution of body fluids. Because arginine vasopressin (AVP) release is not suppressed at the usual level of body tonicity, the hormone continues to circulate and the ingested water is retained. Plasma osmolality declines until it is below the osmotic thirst threshold, and a new steady state with little change in water turnover is established. Pregnancy is characterized by increments in intravascular volume, but volume-sensing AVP release mechanisms appear to adjust as gestation progresses so that each new volume status is "sensed" as normal. The metabolic clearance of AVP increases fourfold, the rise paralleling that of circulating cystine aminopeptidase (vasopressinase), and enzyme produced by the placenta. Furthermore, the disposal rate of 1-deamino-8-D-AVP, and AVP analogue resistant to inactivation by vasopressinase, is unaltered in pregnancy. Thus, the increase in AVP's metabolism and the high circulating aminopeptidase levels have been implicated in certain forms of transient diabetes insipidus that occur in late pregnancy. Finally, mechanisms responsible for the altered osmoregulation in pregnancy are obscure, but chorionic gonadotropin and relaxin may be implicated in the changes.

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“…Whereas most reported cases within the second group seem to be associated with unmasking of subclinical cranial DI (Hime & Richardson, 1978;Hughes et a/., 1989), there has been only a handful of reports of pregnancy related exacerbations of nephrogenic DI (Ford & Lumpkin, 1986;Iwasaki et al, 1991), probably due to the male preponderance of inherited nephrogenic DI. Several cases in the past have been erroneously categorized as transient, recurrent nephrogenic DI (Goodman et al, 1984).…”

Section: Discussionmentioning

confidence: 99%

Pathophysiology of transient cranial diabetes insipidus during pregnancy

Williams

Metcalfe

Skingle

et al. 1993

Clinical Endocrinology

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These studies indicate that subclinical cranial diabetes insipidus may be unmasked in late pregnancy. This effect is not related to AVP resistance resulting from PGE2 production or excessive vasopressinase activity, but may be due to a combination of physiological vasopressinase secretion with reduced AVP secretory capacity and reduction in the thirst threshold that accompanies normal pregnancy. We relate these findings to a previously described group of women with transient diabetes insipidus during pregnancy who had impaired liver function.

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Recurrent diabetes insipidus associated with pregnancy: Pathophysiology and therapy

Cited by 12 publications

References 0 publications

Transient diabetes insipidus and acute fatty liver of pregnancy

Transient diabetes insipidus and acute fatty liver of pregnancy

Osmoregulation, the secretion of arginine vasopressin and its metabolism during pregnancy

Pathophysiology of transient cranial diabetes insipidus during pregnancy

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