AMERICAN JOURNAL OF PERINATOLOGY/VOLUME 7, NUMBER 3 July 1990
TRANSIENT DIABETES INSIPIDUS IN PREGNANCY COMPLICATED BY HYPERTENSION AND SEIZURES C. Andrew Combs, M.D., Ph.D., Cheryl Walker, M.D., Beth A. Matlock, M.D., and William Crombleholme, M.D.
ABSTRACT
Downloaded by: East Carolina University. Copyrighted material.
A case is presented of a primigravida with transient diabetes insipidus, gestational hypertension, and multiple seizures resistant to magnesium sulfate and diazepam. After addition of phenytoin, no further seizures occurred. Transient diabetes insipidus in pregnancy has been previously associated with hypertension, liver dysfunction, and fetal distress. Considered with previous cases, it is suggested that seizures may frequently be part of this syndrome.
Transient diabetes insipidus developing in late pregnancy is uncommon, despite the occurrence of several physiologic changes in water metabolism.1 Transient diabetes insipidus has been associated with such severe pregnancy complications as preeclampsia, liver dysfunction, and fetal distress,23 although the precise pathophysiology of these associations is unclear. Reported here is a case of seizures occurring in a patient with transient diabetes insipidus of pregnancy.
nephritis requiring hospitalization for intravenous antibiotics. Physical examination on admission showed a well-appearing young gravida in no apparent distress. Blood pressure was 150/100 mmHg sitting, but decreased to 140/80 mmHg after several minutes in the left lateral decubitus position. General physical examination, including fundoscopic examination, was normal. The deep tendon reflexes were brisk, but there was no clonus. No edema was noted. The cervix was long and closed, and rupture of membranes was confirmed by ferning and nitrazine tests. Her hematocrit was 32%, platelet count 305,000 per CASE REPORT ixl, AST 24 mg/dl, ALT 15 mg/dl, sodium 140 mEq/ liter, potassium 3.5 mEq/liter, chloride 108 mEq/liter, A 19-year-old black primigravida at 38 weeks' bicarbonate 23 mEq/liter, glucose 72 mg/dl, cregestation presented to the labor unit complaining of atinine 0.7 mg/dl, and blood urea nitrogen 2 mg/dl. fluid leaking from the vagina, severe frontal headThe fetal heart rate tracing was reactive and there ache, and blurred vision over the previous 2 hours. were no uterine contractions. One month before admission, she developed polyuria and polydipsia. She reported urinating sevThe admitting diagnosis was mild preeclampsia eral times nightly and her fluid intake was later estiwith premature rupture of membranes, and the plan mated at 18 liters/day. She had been told by the clinic was made to induce labor. Magnesium sulfate was staff that these were normal changes of pregnancy. given as a 4 gm intravenous bolus over 10 minutes, Six days before admission, she developed mild hythen an infusion of 2 gm/hour. Three minutes after pertension (150/90 mmHg), edema, and a weight the magnesium bolus was completed, the patient had gain of 2 kg over the previous week. There was no a generalized tonic-clonic seizure. The serum magproteinuria or other laboratory abnormality, and she nesium level was 4 mEq/liter. Diazepam was given as was advised to rest at home. a 5 mg intravenous bolus, but two more seizures Past medical history was significant for childoccurred, 20 and 30 minutes after the first. Phenyhood febrile seizures, but she had been seizure-free toin, 1 gm, was given intravenously at 50 mg/minute without medications for over 10 years. Two years and no further seizures occurred. before pregnancy, she had an Escherichia coli pyeloThe diagnosis of eclampsia was made. A central Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California San Francisco, San Francisco General Hospital, San Francisco, California Reprint requests: Dr. Combs, Department of Obstetrics and Gynecology (ML526), University of Cincinnati, Cincinnati, Ohio 45267-0526 Copyright © 1990 by Thieme Medical Publishers, Inc., 381 Park Avenue South, New York, NY 10016. All rights reserved.
287
venous line and Foley catheter were placed. Central venous pressure was 4 mmHg. The urine was clear and pale with a specific gravity of less than 1.005, trace protein, and no glucose. Over the next 4 hours, urine output totaled 3300 ml, despite a total fluid intake of less than 1200 ml. Labor was induced with oxytocin, and 10 hours after admission, she had a low forceps delivery of a vigorous 3440 gm male infant. Apgar scores were 4 and 9 at 1 and 5 minutes. Umbilical cord venous and arterial pH values were 7.33 and 7.24. Computed tomography obtained immediately postpartum showed no abnormality of the brain or pituitary. Urine output on the first postpartum day was 4525 ml, with a total intake, mostly oral, of 5990 ml. On the second postpartum day, urine output was 4670 ml and total intake was 3000 ml. On the third postpartum day, a formal water deprivation test was performed and the results are given in Table 1. Urine output continued greater than 200 ml/hr for most of the test, and only modest urine concentrating ability was demonstrated. The water deprivation test was discontinued after 10 hours because the patient developed a temperature of 38.5°C. No clear source of fever was identified, and she defervesced promptly. By the fourth postpartum day, her extreme thirst had completely resolved, her nocturia had decreased to once per night, and she was discharged. She failed to keep her appointment for repeat water deprivation testing and has been lost to follow-up. DISCUSSION
Although normal pregnancy is accompanied by increased urine output, the development of frank diabetes insipidus during pregnancy is uncommon. Blotner and Kunkel4 reviewed 18 cases of transient pregnancy-related diabetes insipidus reported before 1942. Since then, an additional 26 cases have been reported.2-22 Typically, polyuria and polydipsia develop in the third trimester and resolve spontaneously a few days or a few weeks after delivery. Diabetes insipidus may be produced by any of several pathophysiologic derangements in pregnancy. A functional classification was suggested by Diirr.1 First, patients who concentrate their urine in re-
Table 1. Water Deprivation Test
288
Time (hr)
Plasma Osmolality (mOsm/liter)
Urine Osmolality (mOsmlliter)
0 2 4 6 8 10
283 281 286 288 288 —
199 194 224 235 272 281
Urine Volume Weight (ml) (kg) 81.0 525 250 475 240 560
77.6
sponse to exogenous vasopressin are presumed to have a defect of central release of vasopressin. This may be due to subclinical pituitary insufficiency that is unmasked during pregnancy in some cases20,21 and may be idiopathic in others.19 Second, patients who do not respond to vasopressin but respond to the vasopressinase-resistant analogue deamino-8d-arginine vasopressin (desmopressin) are presumed to have increased activity of a circulating vasopressin-degrading enzyme.1318 Finally, diabetes insipidus that responds to neither vasopressin nor desmopressin is classified as nephrogenic, perhaps due to a prostaglandin-mediated resistance of the renal tubules to the action of vasopressin during pregnancy.11 In the present case, a precise classification was not possible, because the responses to vasopressin and desmopressin were not studied and the water deprivation test was performed at a time when the polyuria and polydipsia were clinically resolving. However, the clinical presentation and course were similar to the other reported cases of transient diabetes insipidus of pregnancy. Review of the 26 cases reported since 1942 reveals that transient diabetes insipidus of pregnancy is associated with a variety of other complications. Fourteen of the cases were associated with gestational hypertension with or without proteinuria.2-3'6-8'10-11'14-18'21-22 Dipstick tests for proteinuria may be insensitive in diabetes insipidus because the urine is diluted by large volumes of free water. Fourteen cases were associated with transaminase elevations2'5'7-9'13'15-17'22 and three with frank hepatic failure and encephalopathy.3,8,14 Xwo cases were complicated by stillbirth5'7 and six by intrapartum fetal distress.3-6-8'9'18'22 In patients with diabetes insipidus established before pregnancy, preeclampsia has been reported in fewer than 10% of cases.23"25 Interestingly, established diabetes insipidus seems to improve with the development of preeclampsia,2325 although the mechanisms are not clear. Seizures were observed in two previous cases. One patient with transient vasopressin-resistant diabetes insipidus, preeclampsia, and transaminase elevations had a seizure on the first postpartum day and was treated with magnesium sulfate and diazepam.8 In an earlier case, the patient developed polydipsia, polyuria, and hypertension 3 days postpartum and had a seizure 19 days later.26 The present case demonstrates that seizures may occur in patients with transient diabetes insipidus even in the absence of electrolyte disturbances and may be resistant to multiple anticonvulsants. It is not known whether the seizures have the same origin as typical eclamptic seizures. Although the cause-and-effect relationship between diabetes insipidus, preeclampsia, liver dysfunction, fetal distress, and seizures is not clear, the frequency and severity of the fetal and maternal complications have led to the recommendation that these pregnancies be followed with antepartum fetal surveillance and that consideration be given to delivery as soon as fetal pulmonary maturity is attained.3
Downloaded by: East Carolina University. Copyrighted material.
AMERICAN JOURNAL OF PERINATOLOGY/VOLUME 7, NUMBER 3 July 1990
TRANSIENT DIABETES INSIPIDUS IN PREGNANCY/Combs, Walker, Matlock, et al.
14. 1. Diirr JA: Diabetes insipidus in pregnancy. Am J Kidney Dis 9:276-283, 1987 2. Krege J, Katz VL, Bowes WA Jr: Transient diabetes insipidus of pregnancy. Obstet Gynecol Surv 44:789-795, 1989 3. Harper M, Hatjis CG, Appel RG, Austin WE: Vasopressinresistant diabetes insipidus, liver dysfunction, hyperuricemia and decreased renal function. A case report. J Reprod Med 32:862-865, 1987 4. Blotner H, Kunkel P: Diabetes insipidus and pregnancy. Report of two cases. N Engl J Med 227:287-292, 1942 5. McLaren HC, McLeod M: A case of diabetes insipidus in pregnancy. J Obstet Gynaecol Br Emp 49:51-58, 1942 6. Millar DG, Robertson EG, Hall R: Transient diabetes insipidus in pregnancy: A case report. In Irvine WJ, Loraine
15. 16. 17.
18. 19.
JA (eds): Reproductive Endocrinology. Proceedings of sym-
7. 8. 9. 10. 11. 12.
13.
posium of the Royal Society of Medicine. Edinburgh: Livingstone, 1970, pp 152-156 Ferrara JM, Malatesta R, Kemmann E: Transient nephrogenic diabetes insipidus during toxemia in pregnancy. Diagn Gynecol Obstet 2:227-230, 1980 Barron WM, Cohen LH, Ulland LA, et al: Transient vasopressin-resistant diabetes insipidus of pregnancy. N Engl J Med 310:442-444, 1984 Goodman H, Sachs BP, Phillippe M, Moore T: Transient, recurrent nephrogenic diabetes insipidus. Am J Obstet Gynecol 149:910-912, 1984 Korbert SM, Corwin HL, Lewis EJ: Transient nephrogenic diabetes insipidus associated with pregnancy. Am J Nephrol 5:442-444, 1985 Ford SM, Lumpkin HL: Transient vasopressin-resistant diabetes insipidus of pregnancy. Obstet Gynecol 68:726— 728, 1986 Baylis PH, Thompson C, Burd J, Tunbridge WMG, Snodgrass CA: Recurrent pregnancy-induced polyuria and thirst due to hypothalamic diabetes insipidus: An investigation into possible mechanisms responsible for polyuria. Clin Endocrinol 24:459-466, 1986 Diirr JA, Hoggard JG, Hunt JM, Schrier RW: Diabetes insipidus in pregnancy associated with abnormally high
20. 21.
22.
23. 24. 25. 26.
circulating vasopressinase activity. N Engl J Med 316: 1070-1074, 1987 Mizuno O: Transient nephrogenic diabetes associated with acute hepatic failure in pregnancy. Endocrinol Jpn 34:449_455( 1987 Grimaldi A, Champigneule A, Bosquet F, et al: Association d'un diabete sucre et d'un diabete insipide gestationnels. Presse Med 16:447, 1987 Katz VL, Bowes WA: Transient diabetes insipidus and preeclampsia. South Med J 80:524-525, 1987 van der Weiden RMF, Visser W, Peeters LLH, van Leeuwen AP, Wallenburg HCS: Transient diabetes insipidus of pregnancy. Eur J Obstet Gynecol Reprod Biol 25:331334, 1987 Shah SV, Thakur V: Vasopressinase and diabetes insipidus of pregnancy. Ann Intern Med 109:435-436, 1988 Hughes JM, Barron WM, Vance ML: Recurrent diabetes insipidus associated with pregnancy: Pathophysiology and therapy. Obstet Gynecol 73:462-464, 1989 Feldberg D, Samuel N, Dicker D, Goldman J: Diabetes insipidus in pregnancy. Isr J Med Sci 21:695-697, 1985 Barbieri RL, Randall RW, Saltzman DH: Diabetes insipidus occurring in a patient with Sheehan's syndrome during a gonadotropin-induced pregnancy. Fertil Steril 44:529— 531, 1985 Cammu H, Velkeniers B, Charels K, Vincken W, Amy JJ: Idiopathic acute fatty liver of pregnancy associated withtransient diabetes insipidus. Case report. Br J Obstet Gynaecol 94:173-174, 1987 Hime MC, Richardson JA: Diabetes insipidus and pregnancy. Case report, incidence and review of literature. Obstet Gynecol Surv 33:375-379, 1978 Campbell JW: Diabetes insipidus and complicated pregnancy. JAMA 243:1744-1745, 1980 Hadi HA, Mashini IS, Devoe LD: Diabetes insipidus during pregnancy complicated by preeclampsia. A case report. J Reprod Med 30:206-208, 1985 Laurentie A, Basiliou BJ: Crises eclamptiques sans albuminurie ayant apparu le 22e jour des suites de couches amaurose et diabete insipide: Contribution a l'etude pathogenique du diabete insipide dans ses rapports avec l'eclampsia. Gynecol Obstet 13:321-331, 1926
Downloaded by: East Carolina University. Copyrighted material.
REFERENCES
289
TRANSIENT DIABETES INSIPIDUS IN PREGNANCY COMPLICATED BY HYPERTENSION AND SEIZURES C. Andrew Combs, M.D., Ph.D., Cheryl Walker, M.D., Beth A. Matlock, M.D., and William Crombleholme, M.D.
ABSTRACT
Downloaded by: East Carolina University. Copyrighted material.
A case is presented of a primigravida with transient diabetes insipidus, gestational hypertension, and multiple seizures resistant to magnesium sulfate and diazepam. After addition of phenytoin, no further seizures occurred. Transient diabetes insipidus in pregnancy has been previously associated with hypertension, liver dysfunction, and fetal distress. Considered with previous cases, it is suggested that seizures may frequently be part of this syndrome.
Transient diabetes insipidus developing in late pregnancy is uncommon, despite the occurrence of several physiologic changes in water metabolism.1 Transient diabetes insipidus has been associated with such severe pregnancy complications as preeclampsia, liver dysfunction, and fetal distress,23 although the precise pathophysiology of these associations is unclear. Reported here is a case of seizures occurring in a patient with transient diabetes insipidus of pregnancy.
nephritis requiring hospitalization for intravenous antibiotics. Physical examination on admission showed a well-appearing young gravida in no apparent distress. Blood pressure was 150/100 mmHg sitting, but decreased to 140/80 mmHg after several minutes in the left lateral decubitus position. General physical examination, including fundoscopic examination, was normal. The deep tendon reflexes were brisk, but there was no clonus. No edema was noted. The cervix was long and closed, and rupture of membranes was confirmed by ferning and nitrazine tests. Her hematocrit was 32%, platelet count 305,000 per CASE REPORT ixl, AST 24 mg/dl, ALT 15 mg/dl, sodium 140 mEq/ liter, potassium 3.5 mEq/liter, chloride 108 mEq/liter, A 19-year-old black primigravida at 38 weeks' bicarbonate 23 mEq/liter, glucose 72 mg/dl, cregestation presented to the labor unit complaining of atinine 0.7 mg/dl, and blood urea nitrogen 2 mg/dl. fluid leaking from the vagina, severe frontal headThe fetal heart rate tracing was reactive and there ache, and blurred vision over the previous 2 hours. were no uterine contractions. One month before admission, she developed polyuria and polydipsia. She reported urinating sevThe admitting diagnosis was mild preeclampsia eral times nightly and her fluid intake was later estiwith premature rupture of membranes, and the plan mated at 18 liters/day. She had been told by the clinic was made to induce labor. Magnesium sulfate was staff that these were normal changes of pregnancy. given as a 4 gm intravenous bolus over 10 minutes, Six days before admission, she developed mild hythen an infusion of 2 gm/hour. Three minutes after pertension (150/90 mmHg), edema, and a weight the magnesium bolus was completed, the patient had gain of 2 kg over the previous week. There was no a generalized tonic-clonic seizure. The serum magproteinuria or other laboratory abnormality, and she nesium level was 4 mEq/liter. Diazepam was given as was advised to rest at home. a 5 mg intravenous bolus, but two more seizures Past medical history was significant for childoccurred, 20 and 30 minutes after the first. Phenyhood febrile seizures, but she had been seizure-free toin, 1 gm, was given intravenously at 50 mg/minute without medications for over 10 years. Two years and no further seizures occurred. before pregnancy, she had an Escherichia coli pyeloThe diagnosis of eclampsia was made. A central Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California San Francisco, San Francisco General Hospital, San Francisco, California Reprint requests: Dr. Combs, Department of Obstetrics and Gynecology (ML526), University of Cincinnati, Cincinnati, Ohio 45267-0526 Copyright © 1990 by Thieme Medical Publishers, Inc., 381 Park Avenue South, New York, NY 10016. All rights reserved.
287
venous line and Foley catheter were placed. Central venous pressure was 4 mmHg. The urine was clear and pale with a specific gravity of less than 1.005, trace protein, and no glucose. Over the next 4 hours, urine output totaled 3300 ml, despite a total fluid intake of less than 1200 ml. Labor was induced with oxytocin, and 10 hours after admission, she had a low forceps delivery of a vigorous 3440 gm male infant. Apgar scores were 4 and 9 at 1 and 5 minutes. Umbilical cord venous and arterial pH values were 7.33 and 7.24. Computed tomography obtained immediately postpartum showed no abnormality of the brain or pituitary. Urine output on the first postpartum day was 4525 ml, with a total intake, mostly oral, of 5990 ml. On the second postpartum day, urine output was 4670 ml and total intake was 3000 ml. On the third postpartum day, a formal water deprivation test was performed and the results are given in Table 1. Urine output continued greater than 200 ml/hr for most of the test, and only modest urine concentrating ability was demonstrated. The water deprivation test was discontinued after 10 hours because the patient developed a temperature of 38.5°C. No clear source of fever was identified, and she defervesced promptly. By the fourth postpartum day, her extreme thirst had completely resolved, her nocturia had decreased to once per night, and she was discharged. She failed to keep her appointment for repeat water deprivation testing and has been lost to follow-up. DISCUSSION
Although normal pregnancy is accompanied by increased urine output, the development of frank diabetes insipidus during pregnancy is uncommon. Blotner and Kunkel4 reviewed 18 cases of transient pregnancy-related diabetes insipidus reported before 1942. Since then, an additional 26 cases have been reported.2-22 Typically, polyuria and polydipsia develop in the third trimester and resolve spontaneously a few days or a few weeks after delivery. Diabetes insipidus may be produced by any of several pathophysiologic derangements in pregnancy. A functional classification was suggested by Diirr.1 First, patients who concentrate their urine in re-
Table 1. Water Deprivation Test
288
Time (hr)
Plasma Osmolality (mOsm/liter)
Urine Osmolality (mOsmlliter)
0 2 4 6 8 10
283 281 286 288 288 —
199 194 224 235 272 281
Urine Volume Weight (ml) (kg) 81.0 525 250 475 240 560
77.6
sponse to exogenous vasopressin are presumed to have a defect of central release of vasopressin. This may be due to subclinical pituitary insufficiency that is unmasked during pregnancy in some cases20,21 and may be idiopathic in others.19 Second, patients who do not respond to vasopressin but respond to the vasopressinase-resistant analogue deamino-8d-arginine vasopressin (desmopressin) are presumed to have increased activity of a circulating vasopressin-degrading enzyme.1318 Finally, diabetes insipidus that responds to neither vasopressin nor desmopressin is classified as nephrogenic, perhaps due to a prostaglandin-mediated resistance of the renal tubules to the action of vasopressin during pregnancy.11 In the present case, a precise classification was not possible, because the responses to vasopressin and desmopressin were not studied and the water deprivation test was performed at a time when the polyuria and polydipsia were clinically resolving. However, the clinical presentation and course were similar to the other reported cases of transient diabetes insipidus of pregnancy. Review of the 26 cases reported since 1942 reveals that transient diabetes insipidus of pregnancy is associated with a variety of other complications. Fourteen of the cases were associated with gestational hypertension with or without proteinuria.2-3'6-8'10-11'14-18'21-22 Dipstick tests for proteinuria may be insensitive in diabetes insipidus because the urine is diluted by large volumes of free water. Fourteen cases were associated with transaminase elevations2'5'7-9'13'15-17'22 and three with frank hepatic failure and encephalopathy.3,8,14 Xwo cases were complicated by stillbirth5'7 and six by intrapartum fetal distress.3-6-8'9'18'22 In patients with diabetes insipidus established before pregnancy, preeclampsia has been reported in fewer than 10% of cases.23"25 Interestingly, established diabetes insipidus seems to improve with the development of preeclampsia,2325 although the mechanisms are not clear. Seizures were observed in two previous cases. One patient with transient vasopressin-resistant diabetes insipidus, preeclampsia, and transaminase elevations had a seizure on the first postpartum day and was treated with magnesium sulfate and diazepam.8 In an earlier case, the patient developed polydipsia, polyuria, and hypertension 3 days postpartum and had a seizure 19 days later.26 The present case demonstrates that seizures may occur in patients with transient diabetes insipidus even in the absence of electrolyte disturbances and may be resistant to multiple anticonvulsants. It is not known whether the seizures have the same origin as typical eclamptic seizures. Although the cause-and-effect relationship between diabetes insipidus, preeclampsia, liver dysfunction, fetal distress, and seizures is not clear, the frequency and severity of the fetal and maternal complications have led to the recommendation that these pregnancies be followed with antepartum fetal surveillance and that consideration be given to delivery as soon as fetal pulmonary maturity is attained.3
Downloaded by: East Carolina University. Copyrighted material.
AMERICAN JOURNAL OF PERINATOLOGY/VOLUME 7, NUMBER 3 July 1990
TRANSIENT DIABETES INSIPIDUS IN PREGNANCY/Combs, Walker, Matlock, et al.
14. 1. Diirr JA: Diabetes insipidus in pregnancy. Am J Kidney Dis 9:276-283, 1987 2. Krege J, Katz VL, Bowes WA Jr: Transient diabetes insipidus of pregnancy. Obstet Gynecol Surv 44:789-795, 1989 3. Harper M, Hatjis CG, Appel RG, Austin WE: Vasopressinresistant diabetes insipidus, liver dysfunction, hyperuricemia and decreased renal function. A case report. J Reprod Med 32:862-865, 1987 4. Blotner H, Kunkel P: Diabetes insipidus and pregnancy. Report of two cases. N Engl J Med 227:287-292, 1942 5. McLaren HC, McLeod M: A case of diabetes insipidus in pregnancy. J Obstet Gynaecol Br Emp 49:51-58, 1942 6. Millar DG, Robertson EG, Hall R: Transient diabetes insipidus in pregnancy: A case report. In Irvine WJ, Loraine
15. 16. 17.
18. 19.
JA (eds): Reproductive Endocrinology. Proceedings of sym-
7. 8. 9. 10. 11. 12.
13.
posium of the Royal Society of Medicine. Edinburgh: Livingstone, 1970, pp 152-156 Ferrara JM, Malatesta R, Kemmann E: Transient nephrogenic diabetes insipidus during toxemia in pregnancy. Diagn Gynecol Obstet 2:227-230, 1980 Barron WM, Cohen LH, Ulland LA, et al: Transient vasopressin-resistant diabetes insipidus of pregnancy. N Engl J Med 310:442-444, 1984 Goodman H, Sachs BP, Phillippe M, Moore T: Transient, recurrent nephrogenic diabetes insipidus. Am J Obstet Gynecol 149:910-912, 1984 Korbert SM, Corwin HL, Lewis EJ: Transient nephrogenic diabetes insipidus associated with pregnancy. Am J Nephrol 5:442-444, 1985 Ford SM, Lumpkin HL: Transient vasopressin-resistant diabetes insipidus of pregnancy. Obstet Gynecol 68:726— 728, 1986 Baylis PH, Thompson C, Burd J, Tunbridge WMG, Snodgrass CA: Recurrent pregnancy-induced polyuria and thirst due to hypothalamic diabetes insipidus: An investigation into possible mechanisms responsible for polyuria. Clin Endocrinol 24:459-466, 1986 Diirr JA, Hoggard JG, Hunt JM, Schrier RW: Diabetes insipidus in pregnancy associated with abnormally high
20. 21.
22.
23. 24. 25. 26.
circulating vasopressinase activity. N Engl J Med 316: 1070-1074, 1987 Mizuno O: Transient nephrogenic diabetes associated with acute hepatic failure in pregnancy. Endocrinol Jpn 34:449_455( 1987 Grimaldi A, Champigneule A, Bosquet F, et al: Association d'un diabete sucre et d'un diabete insipide gestationnels. Presse Med 16:447, 1987 Katz VL, Bowes WA: Transient diabetes insipidus and preeclampsia. South Med J 80:524-525, 1987 van der Weiden RMF, Visser W, Peeters LLH, van Leeuwen AP, Wallenburg HCS: Transient diabetes insipidus of pregnancy. Eur J Obstet Gynecol Reprod Biol 25:331334, 1987 Shah SV, Thakur V: Vasopressinase and diabetes insipidus of pregnancy. Ann Intern Med 109:435-436, 1988 Hughes JM, Barron WM, Vance ML: Recurrent diabetes insipidus associated with pregnancy: Pathophysiology and therapy. Obstet Gynecol 73:462-464, 1989 Feldberg D, Samuel N, Dicker D, Goldman J: Diabetes insipidus in pregnancy. Isr J Med Sci 21:695-697, 1985 Barbieri RL, Randall RW, Saltzman DH: Diabetes insipidus occurring in a patient with Sheehan's syndrome during a gonadotropin-induced pregnancy. Fertil Steril 44:529— 531, 1985 Cammu H, Velkeniers B, Charels K, Vincken W, Amy JJ: Idiopathic acute fatty liver of pregnancy associated withtransient diabetes insipidus. Case report. Br J Obstet Gynaecol 94:173-174, 1987 Hime MC, Richardson JA: Diabetes insipidus and pregnancy. Case report, incidence and review of literature. Obstet Gynecol Surv 33:375-379, 1978 Campbell JW: Diabetes insipidus and complicated pregnancy. JAMA 243:1744-1745, 1980 Hadi HA, Mashini IS, Devoe LD: Diabetes insipidus during pregnancy complicated by preeclampsia. A case report. J Reprod Med 30:206-208, 1985 Laurentie A, Basiliou BJ: Crises eclamptiques sans albuminurie ayant apparu le 22e jour des suites de couches amaurose et diabete insipide: Contribution a l'etude pathogenique du diabete insipide dans ses rapports avec l'eclampsia. Gynecol Obstet 13:321-331, 1926
Downloaded by: East Carolina University. Copyrighted material.
REFERENCES
289
