- Email: [email protected]
Insulin resistance complicating pregnancy in a human immunodeficiency virus–infected patient treated with protease inhibitors and corticosteroids
REFERENCES 1. Sparkman RS. Rupture of the spleen in pregnancy: Report of two cases and review of the literature. Am J Obstet Gynecol 1958;76:587–98. 2. McCormick GM, Young DB. Spontaneous rupture of the spleen. A fatal complication of pregnancy. Am J Forensic Med Pathol 1995;16:132–4. 3. Denehy T, McGrath EW, Breen JL. Splenic torsion and rupture in pregnancy. Obstet Gynecol Surv 1988;43: 123–31. 4. Kaluarachchi A, Krishnamurthy S. Post-cesarean section splenic rupture. Am J Obstet Gynecol 1995;173:230–2. 5. Bhagrath R, Bearn P, Sanusi FA, Najjar S, Qureshi R, Simanovitz A. Postpartum rupture of the spleen. Br J Obstet Gynaecol 1993;100:954–5. 6. Orloff M, Peskin G. Spontaneous rupture of the normal spleen: A surgical enigma. Int Abst Surg 1958;106:1–5.
7. Barrilleaux PS, Adair D, Johnson G, Lewis DF. Splenic rupture associated with severe preeclampsia. J Reprod Med 1999;44:899–901. 8. Debnath D, Valerio D. A traumatic rupture of the spleen. J R Coll Surg Edinb 2002;47:437–45. 9. Klinkert P, Kluit AB, de Vries AC, Puylaert JBCM. Spontaneous rupture of the spleen: Role of ultrasound in diagnosis, treatment, and monitoring. Eur J Surg 1999;165: 712–3. 10. Ochsner MG. Factors of failure for nonoperative management of blunt liver and splenic injuries. World J Surg 2001;25:1393–6. 11. Firstenberg MS, Plaisier B, Newman JS, Malangoni MA. Successful treatment of delayed splenic rupture with splenic artery embolisation. Surgery 1998;123:584–6.
Insulin Resistance Complicating Pregnancy in a Human Immunodeficiency Virus–Infected Patient Treated With Protease Inhibitors and Corticosteroids
CONCLUSION: We found that HIV-positive pregnant women receiving highly active antiretroviral therapy may be at increased risk for development of glucose intolerance. The use of medications that impair glucose tolerance, for example, corticosteroids, may have a synergistic effect in aggravating insulin resistance. Additional screening for glucose intolerance later in the third trimester should be considered in these patients. (Obstet Gynecol 2003;102: 1210 –2. © 2003 by The American College of Obstetricians and Gynecologists.)
Sarit Aschkenazi, MD, Burton Rochelson, MD, James Bernasko, MD, and Jonathan Kaplan, MD Departments of Obstetrics and Gynecology and Internal Medicine, North Shore University Hospital, Manhasset, New York
BACKGROUND: Protease inhibitor therapy in human immunodeficiency virus (HIV)-infected adults has been associated with onset or aggravation of glucose intolerance. We report a case of a pregnant HIV-infected woman receiving highly active antiretroviral therapy who developed acute onset of severe insulin resistance during treatment for preterm labor. CASE: A 26-year-old multigravida with HIV infection treated with highly active antiretroviral therapy presented in preterm labor. During treatment, including corticosteroids for fetal lung maturity, severe hyperglycemia and ketonemia suggestive of diabetic ketoacidosis were detected. Aggressive intravenous fluid and insulin therapy was necessary to correct hyperglycemia. Address reprint requests to: Burton Rochelson, MD, North Shore University Hospital, Division of Maternal Fetal Medicine, 300 Community Drive, Manhasset, NY 11030; E-mail: [email protected].
1210
Received December 18, 2002. Received in revised form February 14, 2003. Accepted February 27, 2003.
There are several reports of adverse metabolic disorders, including hypergycemia, associated with highly active antiretroviral therapy in general and protease inhibitor therapy in particular.1–5 Pregnancy per se is a predisposing factor to glucose intolerance, and several frequently used medical interventions during pregnancy may further increase this predisposition. If hyperglycemia is unrecognized or untreated for prolonged periods, significant maternal or fetal morbidity and/or mortality may occur. It is, therefore, important to identify clinical situations that may be associated with glucose intolerance, such as the administration of highly active antiretroviral therapy. CASE A 26-year-old multigravida was diagnosed with human immunodeficiency virus (HIV) infection 10 years before the current pregnancy. Before, and throughout the current pregnancy, the patient received highly active antiretroviral treatment consisting of two nucleoside reverse transcriptase inhibitors, lamivudine and stavudine, and one protease inhibitor, nelfinavir. Viral load remained undetectable throughout the second and third trimesters.
VOL. 102, NO. 5, PART 2, NOVEMBER 2003 © 2003 by The American College of Obstetricians and Gynecologists. Published by Elsevier.
0029-7844/03/$30.00 doi:10.1016/S0029-7844(03)00166-2
She was coinfected with hepatitis C virus. High-grade squamous intraepithelial cervical lesions had been detected by colposcopy and confirmed by biopsy, but conization had been deferred because of the pregnancy. She was receiving maintenance methadone therapy because of a history of intravenous drug dependence. She denied any personal or family history of diabetes. Her prenatal course before this hospitalization was uneventful, including a normal 1-hour diabetes screen (116 mg/ dL) at 24 weeks, performed in the standard fashion. Random blood glucose and urine dipstick measurements had been normal on several occasions. The patient appeared to be reliable and compliant. Obstetric and gynecologic history consisted of an uncomplicated pregnancy delivered at term by normal vaginal delivery of a 7-lb, 2-oz infant, who was not HIV infected. She had a history of salpingectomy for ruptured tubal pregnancy. The patient presented at 32 weeks complaining of uterine contractions every 10 minutes. She denied headache, nausea, vomiting, fever, chills, vaginal bleeding, rupture of membranes, or urinary symptoms. Vital signs were as follows: blood pressure, 130/80 mm Hg; pulse, 87; respiratory rate, 18 breaths per minute; and temperature, 36.9C. Physical examination was unremarkable. Vaginal examination revealed cervical dilatation of 3 cm, with 90% effacement and bulging membranes. The fetal heart rate was approximately 120 beats per minute and reactive with uterine contractions noted every 10 minutes. Sonography revealed a single fetus in vertex presentation. Amniotic fluid index was 21 cm, and estimated fetal weight indicated a large for gestational age fetus at the 98th percentile. The diagnosis of preterm labor was made. She was given intravenous magnesium sulfate for tocolysis, ampicillin for GBS prophylaxis, and intramuscular betamethasone for acceleration of fetal lung maturity. The following laboratory information was obtained: white blood cell count, 8500/L; hemoglobin, 12 g/dL; and hematocrit, 35.1%. Serum electrolytes were as follows: sodium, 130 mmol/L; potassium, 4.1, which fell to 3.3 mmol/L; chloride (CL), 101 mmol/dL; blood urea nitrogen, 12 mg/dL; and creatinine, 0.8 mg/dL. Carbon dioxide was 22 mmol/L on admission, falling to 14. Blood glucose was 319 mg/dL. Serum ketones were positive. Arterial blood gases were performed to evaluate the patient for diabetic ketoacidosis. Results were as follows: pH, 7.38; carbon dioxide pressure (tension), 30 mm Hg; oxygen pressure (tension), 101 mm Hg; bicarbonate, 17 mmol/L; saturated oxygen, 98%; and base excess, ⫺6.3 mmol/L. Hemoglobin A1c was 8.8%, and fructosamine was normal at 2.3. Aspartate transaminase and alanine transaminase were 137 U/L and 25 U/L, respectively.
VOL. 102, NO. 5, PART 2, NOVEMBER 2003
No anti-islet cell antibodies were detected. Urinalysis showed a glucose concentration of 500 mg/dL, no protein, and more than 80 mg/dL of ketonuria. An impression of acute onset diabetes was made, and intravenous hydration and insulin drip were begun to avert frank ketoacidosis. The patient remained extremely insulin resistant, requiring infusion rates of up to 25 U per hour to correct glucose levels as high as 484 mg/dL. Antiretroviral medication was continued, and intravenous zidovudine was added to prevent vertical transmission. Fetal heart rate remained reassuring. Magnesium sulfate was continued, but labor progressed, and approximately 48 hours later, she had an uncomplicated vaginal delivery of a viable male infant weighing 5 lb, with Apgar scores of 6 and 8 at 1 and 5 minutes, respectively. The postpartum course was essentially unremarkable. Complete blood count and serum electrolytes remained normal. Aspartate transaminase and alanine transaminase decreased to 63 U/L and 13 U/L, respectively. Blood glucose remained elevated (161–226 mg/dL), but returned to normal with medical nutritional therapy and daily multiple insulin injections. Antiretroviral medication was continued, and the patient was discharged from the hospital on postpartum day 3. COMMENT Several reports have drawn attention to the tendency of protease inhibitors to induce chronic hyperglycemia in HIV-positive individuals.1–5 Fasset et al, however, have reported that the incidence of gestational diabetes or aberrant fetal growth was no higher in a cohort of 34 HIV-infected pregnant women treated with protease inhibitors than in 41 nontreated controls (Fasset M, Kramer F, Stek A. Treatment with protease inhibitors in pregnancy is not associated with an increase in incidence of gestational diabetes [abstract]. Am J Obstet Gynecol 1999;182:S7). There may be a  error because of the small numbers in their study. Additionally, their series studied patients at 24 –28 weeks according to current protocol. This patient presented at 32 weeks. It is possible that patients on highly active antiretroviral therapy need to be studied later or twice during the pregnancy. The action of corticosteroids in inducing hyperglycemia in pregnancy is well documented. The precise mechanism for these adverse metabolic effects of protease inhibitors remains unknown. It has been postulated that these agents induce an insulinresistant state similar to type 2 diabetes.6 Reports that HIV-infected nondiabetic patients with abnormal glucose homeostasis respond well to metformin6 would not only confirm the theory of drug-induced peripheral in-
Aschkenazi et al
Insulin Resistance in Pregnancy and HIV
1211
sulin resistance but may also provide a model for effective treatment. Furthermore, anti-HIV protease inhibitors are weakly active against human proteases and may hinder the cleavage of proinsulin into insulin, thus inducing insulin resistance.3 The concomitant use of agents that aggravate hyperglycemia may thus precipitate diabetic ketoacidosis. Factors that predispose pregnant women to ketonemia include “accelerated starvation,” dehydration, lowered blood acid buffering capacity, and increased production of insulin antagonists in the third trimester. These changes make overtly diabetic pregnant women particularly prone to diabetic ketoacidosis especially after receiving medications that cause hyperglycemia, for example, corticosteroids or -sympathomimetic drugs. Two recent reviews contend that all women currently receiving highly active antiretroviral therapy should continue such therapy during pregnancy and furthermore that treatment of pregnant HIV-positive women with monotherapy may be inadequate for suppression of viral replication.7 At this time, however, zidovudine remains the only agent recommended specifically for prevention of vertical transmission.7 Zidovudine was, therefore, added to the treatment regimen when labor was confirmed. This patient presented in preterm labor with hyperglycemia, ketonemia, and ketonuria suggestive of diabetic ketoacidosis. Although the third-trimester diabetes screen was negative, the presence on admission of elevated hemoglobin A1c, fetal macrosomia, and polyhydramnios suggests that glucose intolerance more likely antedated this admission. The effects of corticosteroids and protease inhibitors may have been synergistic in producing an insulin-resistant state. Not only would it be prudent, therefore, to exercise caution when using these medications together, but it may also be advisable to repeat the diabetes screen later in the third trimester, for example at about 32 weeks.
Given the significant maternal and fetal morbidity and mortality associated with diabetic ketoacidosis in pregnancy, this case emphasizes the importance of a high degree of suspicion and surveillance for impaired glucose intolerance in HIV-positive pregnant patients treated with protease inhibitors.
Acute Postpartum Mental Status Change and Coma Caused by Previously Undiagnosed Ornithine Transcarbamylase Deficiency
BACKGROUND: Acute postpartum mental status change usually represents postpartum blues or depression. Psychosis and coma are rare. This is a case report of a patient with previously undiagnosed ornithine transcarbamylase deficiency presenting as postpartum acute mental status change and coma.
Dirk E. Peterson, MD, PhD
Address reprint requests to: Dirk E. Peterson, MD, PhD, Lee Physician Group, 16271 Bass Road, Fort Myers, FL 33908; E-mail: [email protected].
Lee Memorial Health System, Lee Physician Group, Fort Myers, Florida 1212
REFERENCES 1. Lee ECC, Walmsley S, Fantus IG. New-onset diabetes mellitus associated with protease inhibitor therapy in an HIV-positive patient: Case report and review. CMAJ 1999; 161:161–4. 2. Besson C, Jubault V, Viard JP, Pialoux G. Ketoacidosis associated with protease inhibitor therapy. AIDS 1998;12: 1399–400. 3. Kan VL, Nylen ES. Diabetic ketoacidosis in an HIV patient: A new mechanism of HIV protease inhibitor-induced glucose intolerance. AIDS 1999;13:1987–9. 4. Dube MP, Johnson DL, Currier JS, Leedom JM. Protease inhibitor-associated hyperglycemia. Lancet 1997;350: 713–4. 5. Tsiodras S, Mantzoros C, Hammer S, Samore M. Effects of protease inhibitors on hyperglycemia, hyperlipidemia, and lipodystrophy: A 5 year cohort study. Arch Intern Med 2000;160:2050–6. 6. Hughes CA, Taylor GD. Metformin in an HIV-infected patient with protease inhibitor-induced diabetic ketoacidosis. Ann Pharmacother 2001;35:877–80. 7. Center for Disease Control and Prevention. Public Health Service Task Force recommendations for the use of antiretroviral drugs in pregnant women infected with HIV-1 for maternal health and for reducing perinatal HIV-1 transmission in the United States. MMWR 1998;47(RR-2):1–30.
Received July 15, 2002. Received in revised form September 17, 2002. Accepted September 26, 2002.
CASE: A 28-year-old multipara developed acute mental status change and coma 3 days after cesarean delivery. A
VOL. 102, NO. 5, PART 2, NOVEMBER 2003 © 2003 by The American College of Obstetricians and Gynecologists. Published by Elsevier.
0029-7844/03/$30.00 doi:10.1016/S0029-7844(03)00165-0
7. Barrilleaux PS, Adair D, Johnson G, Lewis DF. Splenic rupture associated with severe preeclampsia. J Reprod Med 1999;44:899–901. 8. Debnath D, Valerio D. A traumatic rupture of the spleen. J R Coll Surg Edinb 2002;47:437–45. 9. Klinkert P, Kluit AB, de Vries AC, Puylaert JBCM. Spontaneous rupture of the spleen: Role of ultrasound in diagnosis, treatment, and monitoring. Eur J Surg 1999;165: 712–3. 10. Ochsner MG. Factors of failure for nonoperative management of blunt liver and splenic injuries. World J Surg 2001;25:1393–6. 11. Firstenberg MS, Plaisier B, Newman JS, Malangoni MA. Successful treatment of delayed splenic rupture with splenic artery embolisation. Surgery 1998;123:584–6.
Insulin Resistance Complicating Pregnancy in a Human Immunodeficiency Virus–Infected Patient Treated With Protease Inhibitors and Corticosteroids
CONCLUSION: We found that HIV-positive pregnant women receiving highly active antiretroviral therapy may be at increased risk for development of glucose intolerance. The use of medications that impair glucose tolerance, for example, corticosteroids, may have a synergistic effect in aggravating insulin resistance. Additional screening for glucose intolerance later in the third trimester should be considered in these patients. (Obstet Gynecol 2003;102: 1210 –2. © 2003 by The American College of Obstetricians and Gynecologists.)
Sarit Aschkenazi, MD, Burton Rochelson, MD, James Bernasko, MD, and Jonathan Kaplan, MD Departments of Obstetrics and Gynecology and Internal Medicine, North Shore University Hospital, Manhasset, New York
BACKGROUND: Protease inhibitor therapy in human immunodeficiency virus (HIV)-infected adults has been associated with onset or aggravation of glucose intolerance. We report a case of a pregnant HIV-infected woman receiving highly active antiretroviral therapy who developed acute onset of severe insulin resistance during treatment for preterm labor. CASE: A 26-year-old multigravida with HIV infection treated with highly active antiretroviral therapy presented in preterm labor. During treatment, including corticosteroids for fetal lung maturity, severe hyperglycemia and ketonemia suggestive of diabetic ketoacidosis were detected. Aggressive intravenous fluid and insulin therapy was necessary to correct hyperglycemia. Address reprint requests to: Burton Rochelson, MD, North Shore University Hospital, Division of Maternal Fetal Medicine, 300 Community Drive, Manhasset, NY 11030; E-mail: [email protected].
1210
Received December 18, 2002. Received in revised form February 14, 2003. Accepted February 27, 2003.
There are several reports of adverse metabolic disorders, including hypergycemia, associated with highly active antiretroviral therapy in general and protease inhibitor therapy in particular.1–5 Pregnancy per se is a predisposing factor to glucose intolerance, and several frequently used medical interventions during pregnancy may further increase this predisposition. If hyperglycemia is unrecognized or untreated for prolonged periods, significant maternal or fetal morbidity and/or mortality may occur. It is, therefore, important to identify clinical situations that may be associated with glucose intolerance, such as the administration of highly active antiretroviral therapy. CASE A 26-year-old multigravida was diagnosed with human immunodeficiency virus (HIV) infection 10 years before the current pregnancy. Before, and throughout the current pregnancy, the patient received highly active antiretroviral treatment consisting of two nucleoside reverse transcriptase inhibitors, lamivudine and stavudine, and one protease inhibitor, nelfinavir. Viral load remained undetectable throughout the second and third trimesters.
VOL. 102, NO. 5, PART 2, NOVEMBER 2003 © 2003 by The American College of Obstetricians and Gynecologists. Published by Elsevier.
0029-7844/03/$30.00 doi:10.1016/S0029-7844(03)00166-2
She was coinfected with hepatitis C virus. High-grade squamous intraepithelial cervical lesions had been detected by colposcopy and confirmed by biopsy, but conization had been deferred because of the pregnancy. She was receiving maintenance methadone therapy because of a history of intravenous drug dependence. She denied any personal or family history of diabetes. Her prenatal course before this hospitalization was uneventful, including a normal 1-hour diabetes screen (116 mg/ dL) at 24 weeks, performed in the standard fashion. Random blood glucose and urine dipstick measurements had been normal on several occasions. The patient appeared to be reliable and compliant. Obstetric and gynecologic history consisted of an uncomplicated pregnancy delivered at term by normal vaginal delivery of a 7-lb, 2-oz infant, who was not HIV infected. She had a history of salpingectomy for ruptured tubal pregnancy. The patient presented at 32 weeks complaining of uterine contractions every 10 minutes. She denied headache, nausea, vomiting, fever, chills, vaginal bleeding, rupture of membranes, or urinary symptoms. Vital signs were as follows: blood pressure, 130/80 mm Hg; pulse, 87; respiratory rate, 18 breaths per minute; and temperature, 36.9C. Physical examination was unremarkable. Vaginal examination revealed cervical dilatation of 3 cm, with 90% effacement and bulging membranes. The fetal heart rate was approximately 120 beats per minute and reactive with uterine contractions noted every 10 minutes. Sonography revealed a single fetus in vertex presentation. Amniotic fluid index was 21 cm, and estimated fetal weight indicated a large for gestational age fetus at the 98th percentile. The diagnosis of preterm labor was made. She was given intravenous magnesium sulfate for tocolysis, ampicillin for GBS prophylaxis, and intramuscular betamethasone for acceleration of fetal lung maturity. The following laboratory information was obtained: white blood cell count, 8500/L; hemoglobin, 12 g/dL; and hematocrit, 35.1%. Serum electrolytes were as follows: sodium, 130 mmol/L; potassium, 4.1, which fell to 3.3 mmol/L; chloride (CL), 101 mmol/dL; blood urea nitrogen, 12 mg/dL; and creatinine, 0.8 mg/dL. Carbon dioxide was 22 mmol/L on admission, falling to 14. Blood glucose was 319 mg/dL. Serum ketones were positive. Arterial blood gases were performed to evaluate the patient for diabetic ketoacidosis. Results were as follows: pH, 7.38; carbon dioxide pressure (tension), 30 mm Hg; oxygen pressure (tension), 101 mm Hg; bicarbonate, 17 mmol/L; saturated oxygen, 98%; and base excess, ⫺6.3 mmol/L. Hemoglobin A1c was 8.8%, and fructosamine was normal at 2.3. Aspartate transaminase and alanine transaminase were 137 U/L and 25 U/L, respectively.
VOL. 102, NO. 5, PART 2, NOVEMBER 2003
No anti-islet cell antibodies were detected. Urinalysis showed a glucose concentration of 500 mg/dL, no protein, and more than 80 mg/dL of ketonuria. An impression of acute onset diabetes was made, and intravenous hydration and insulin drip were begun to avert frank ketoacidosis. The patient remained extremely insulin resistant, requiring infusion rates of up to 25 U per hour to correct glucose levels as high as 484 mg/dL. Antiretroviral medication was continued, and intravenous zidovudine was added to prevent vertical transmission. Fetal heart rate remained reassuring. Magnesium sulfate was continued, but labor progressed, and approximately 48 hours later, she had an uncomplicated vaginal delivery of a viable male infant weighing 5 lb, with Apgar scores of 6 and 8 at 1 and 5 minutes, respectively. The postpartum course was essentially unremarkable. Complete blood count and serum electrolytes remained normal. Aspartate transaminase and alanine transaminase decreased to 63 U/L and 13 U/L, respectively. Blood glucose remained elevated (161–226 mg/dL), but returned to normal with medical nutritional therapy and daily multiple insulin injections. Antiretroviral medication was continued, and the patient was discharged from the hospital on postpartum day 3. COMMENT Several reports have drawn attention to the tendency of protease inhibitors to induce chronic hyperglycemia in HIV-positive individuals.1–5 Fasset et al, however, have reported that the incidence of gestational diabetes or aberrant fetal growth was no higher in a cohort of 34 HIV-infected pregnant women treated with protease inhibitors than in 41 nontreated controls (Fasset M, Kramer F, Stek A. Treatment with protease inhibitors in pregnancy is not associated with an increase in incidence of gestational diabetes [abstract]. Am J Obstet Gynecol 1999;182:S7). There may be a  error because of the small numbers in their study. Additionally, their series studied patients at 24 –28 weeks according to current protocol. This patient presented at 32 weeks. It is possible that patients on highly active antiretroviral therapy need to be studied later or twice during the pregnancy. The action of corticosteroids in inducing hyperglycemia in pregnancy is well documented. The precise mechanism for these adverse metabolic effects of protease inhibitors remains unknown. It has been postulated that these agents induce an insulinresistant state similar to type 2 diabetes.6 Reports that HIV-infected nondiabetic patients with abnormal glucose homeostasis respond well to metformin6 would not only confirm the theory of drug-induced peripheral in-
Aschkenazi et al
Insulin Resistance in Pregnancy and HIV
1211
sulin resistance but may also provide a model for effective treatment. Furthermore, anti-HIV protease inhibitors are weakly active against human proteases and may hinder the cleavage of proinsulin into insulin, thus inducing insulin resistance.3 The concomitant use of agents that aggravate hyperglycemia may thus precipitate diabetic ketoacidosis. Factors that predispose pregnant women to ketonemia include “accelerated starvation,” dehydration, lowered blood acid buffering capacity, and increased production of insulin antagonists in the third trimester. These changes make overtly diabetic pregnant women particularly prone to diabetic ketoacidosis especially after receiving medications that cause hyperglycemia, for example, corticosteroids or -sympathomimetic drugs. Two recent reviews contend that all women currently receiving highly active antiretroviral therapy should continue such therapy during pregnancy and furthermore that treatment of pregnant HIV-positive women with monotherapy may be inadequate for suppression of viral replication.7 At this time, however, zidovudine remains the only agent recommended specifically for prevention of vertical transmission.7 Zidovudine was, therefore, added to the treatment regimen when labor was confirmed. This patient presented in preterm labor with hyperglycemia, ketonemia, and ketonuria suggestive of diabetic ketoacidosis. Although the third-trimester diabetes screen was negative, the presence on admission of elevated hemoglobin A1c, fetal macrosomia, and polyhydramnios suggests that glucose intolerance more likely antedated this admission. The effects of corticosteroids and protease inhibitors may have been synergistic in producing an insulin-resistant state. Not only would it be prudent, therefore, to exercise caution when using these medications together, but it may also be advisable to repeat the diabetes screen later in the third trimester, for example at about 32 weeks.
Given the significant maternal and fetal morbidity and mortality associated with diabetic ketoacidosis in pregnancy, this case emphasizes the importance of a high degree of suspicion and surveillance for impaired glucose intolerance in HIV-positive pregnant patients treated with protease inhibitors.
Acute Postpartum Mental Status Change and Coma Caused by Previously Undiagnosed Ornithine Transcarbamylase Deficiency
BACKGROUND: Acute postpartum mental status change usually represents postpartum blues or depression. Psychosis and coma are rare. This is a case report of a patient with previously undiagnosed ornithine transcarbamylase deficiency presenting as postpartum acute mental status change and coma.
Dirk E. Peterson, MD, PhD
Address reprint requests to: Dirk E. Peterson, MD, PhD, Lee Physician Group, 16271 Bass Road, Fort Myers, FL 33908; E-mail: [email protected].
Lee Memorial Health System, Lee Physician Group, Fort Myers, Florida 1212
REFERENCES 1. Lee ECC, Walmsley S, Fantus IG. New-onset diabetes mellitus associated with protease inhibitor therapy in an HIV-positive patient: Case report and review. CMAJ 1999; 161:161–4. 2. Besson C, Jubault V, Viard JP, Pialoux G. Ketoacidosis associated with protease inhibitor therapy. AIDS 1998;12: 1399–400. 3. Kan VL, Nylen ES. Diabetic ketoacidosis in an HIV patient: A new mechanism of HIV protease inhibitor-induced glucose intolerance. AIDS 1999;13:1987–9. 4. Dube MP, Johnson DL, Currier JS, Leedom JM. Protease inhibitor-associated hyperglycemia. Lancet 1997;350: 713–4. 5. Tsiodras S, Mantzoros C, Hammer S, Samore M. Effects of protease inhibitors on hyperglycemia, hyperlipidemia, and lipodystrophy: A 5 year cohort study. Arch Intern Med 2000;160:2050–6. 6. Hughes CA, Taylor GD. Metformin in an HIV-infected patient with protease inhibitor-induced diabetic ketoacidosis. Ann Pharmacother 2001;35:877–80. 7. Center for Disease Control and Prevention. Public Health Service Task Force recommendations for the use of antiretroviral drugs in pregnant women infected with HIV-1 for maternal health and for reducing perinatal HIV-1 transmission in the United States. MMWR 1998;47(RR-2):1–30.
Received July 15, 2002. Received in revised form September 17, 2002. Accepted September 26, 2002.
CASE: A 28-year-old multipara developed acute mental status change and coma 3 days after cesarean delivery. A
VOL. 102, NO. 5, PART 2, NOVEMBER 2003 © 2003 by The American College of Obstetricians and Gynecologists. Published by Elsevier.
0029-7844/03/$30.00 doi:10.1016/S0029-7844(03)00165-0