Pathophysiology of transient cranial diabetes insipidus during pregnancy

Abstract

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.

Pregnancy complicated by multiple pituitary hormone deficiencies

“…It has been reported previously that subclinical cranial DI can be unmasked by pregnancy. 8 Transection of the pituitary stalk was suspected to be a cause of central DI; this was confirmed on cranial MRI in the present case. 9 The patient had a birth history of breech delivery, suggesting the possibility that pituitary stalk transection had occurred during delivery.…”

“…In the present case report we described a rare case of pregnancy complicated by multiple pituitary hormone deficiencies. It has been reported previously that subclinical cranial DI can be unmasked by pregnancy 8 …”

Diabetes insipidus in pregnancy

“…This usually represents an unveiling of subclinical cranial DI, with the posterior pituitary unable to respond to the physiological demands of pregnancy. 20 In such cases, MRI shows loss of normal high signal intensity in the posterior pituitary in the TI-weighted images, consistent with loss of AVP secretion (Figure 1). …”

Osmoregulatory adaptation in pregnancy and its disorders

“…Durr, Hoggard, Hunt & Schrier (1987) have reported a unique case of transient DI due to abnormally high circulating vasopressinase levels but serial measure¬ ments of vasopressinase in a recently reported case of transient central DI were within a control range established in patients of similar gestation (Williams, Skingle, Metcalfe et al 1991). The latter workers also demonstrated that inhibition of renal prostaglandin production by aspirin failed to improve urine con¬ centrating capacity and concluded that increased renal PGE2 production was unlikely to be a major aetiological factor.…”

“…The latter workers also demonstrated that inhibition of renal prostaglandin production by aspirin failed to improve urine con¬ centrating capacity and concluded that increased renal PGE2 production was unlikely to be a major aetiological factor. Post-partum resolution of symp¬ toms is usually observed although urine concentrating capacity may remain subnormal confirming under¬ lying subclinical DI and in this situation relapse occurs at a predictable stage in subsequent pregnancies (Baylis et al 1986;Williams et al 1991).…”