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Decreasing the plasma triglyceride level in hypertriglyceridemia-induced pancreatitis in pregnancy: A case report
Decreasing the plasma triglyceride level in hypertriglyceridemia-induced pancreatitis in pregnancy: A case report Chee-Chuen Loo, FRCA, and Jackie Y. L. Tan, MRCP(Ireland) Republic of Singapore We report a case of hypertriglyceridemia-induced pancreatitis in pregnancy in which continuous intravenous heparin was used effectively and safely to lower the plasma triglyceride level within 24 hours. (Am J Obstet Gynecol 2002;187:241-2.)
Key words: Pancreatitis, hypertriglyceridemia, pregnancy, heparin
We used continuous intravenous heparin to lower the plasma triglyceride level in a case of hypertriglyceridemia-induced pancreatitis in pregnancy. Case report The patient was a 29-year-old woman, gravida 3, para 2. She had two uneventful normal vaginal deliveries complicated by mild pregnancy-induced hypertension (PIH) and gestational diabetes mellitus (GDM). She was admitted at 26 weeks of gestation for a 1-day history of severe epigastric pain and mild PIH. The serum amylase (64 U/L) and ultrasound scan of the hepatobiliary system were normal. The blood glucose level was 10.9 mmol/L. The impression was severe gastritis with PIH and GDM; the patient was treated with oral cimetidine, oral methyldopa, and soluble insulin injection. During blood drawing, the blood was noted to be lipemic and tests confirmed hypertriglyceridemia (53.53 mmol/L) and hypercholesterolemia (total 18.12 mmol/L). On the third day of admission, the patient became breathless and was transferred to the intensive care unit (ICU). Her blood glucose level was 16.3 mmol/L, urine ketones were 3+, and she had metabolic acidosis (pH 7.257, partial pressure of carbon dioxide [PCO2] 16.1 mm Hg, bicarbonate [HCO3–] 6.9 mmol/L). Her partial pressure of oxygen
From the Department of Anaesthesia, KK Women’s and Children’s Hospital,a and the Department of General Medicine, Tan Tock Seng Hospital.b Received for publication August 15, 2001; revised December 7, 2001; accepted December 20, 2001. Reprint requests: Chee-Chuen Loo, FRCA, Department of Anaesthesia, KK Women’s and Children’s Hospital, 100, Bukit Timah Road, S229899, Republic of Singapore. E-mail: [email protected] © 2002, Mosby, Inc. All rights reserved. 0002-9378/2002 $35.00 + 0 6/1/122422 doi:10.1067/mob.2002.122422
(PO2) was 121.9 mm Hg (fractional concentration of oxygen in inspired gas [FiO2] 0.4). The impression was diabetic ketoacidosis; she was treated with continuous intravenous insulin. However, she still had intractable epigastric pain, and a repeat serum amylase level was found to be markedly raised (956 U/L). A repeat ultrasound examination revealed fluid over the pancreas and enlargement of the pancreatic head. A diagnosis of acute pancreatitis secondary to hypertriglyceridemia was made. The worst laboratory results recorded during the patient’s ICU stay were total white blood cells 14.5 109/L, albumin 19 g/L, total bilirubin 72 µmol/L, HCO3– 6.8 mmol/L, ionized calcium 1.09 mmol/L, and PO2 83.2 mm Hg (FiO2 0.4). There was no hypotension, abnormal chest x-ray film, renal impairment, or coagulopathy. The liver enzymes and hematocrit were normal. She was treated conservatively with intermittent nasogastric suction and intravenous ranitidine 50 mg three times a day. The hypertriglyceridemia was treated with intravenous heparin infusion. We started at an empiric continuous intravenous dose of 20,000 U per day but had to decrease to 10,000 U per day because of a prolonged activated partial thromboplastin time (aPTT, 40 seconds, 104 seconds, 39.8 seconds). The triglyceride level decreased dramatically to 12.76 mmol/L after 18 hours and the serum amylase was 39 U/L after 24 hours. Ultrasound examination of the fetus showed normal growth and cardiotocography and umbilical artery pulsatile index were normal. The patient was discharged to the general ward after 6 days in the ICU and was discharged home 14 days from the time of hospital admission. Hypertriglyceridemia was treated with dietary control and at 31 weeks’ gestation the triglyceride level was 4.99 mmol/L and the total cholesterol was 7.26 mmol/L. Labor was induced at 37 weeks’ gestation because of PIH; the patient had an uneventful normal vaginal delivery. 241
242 Loo and Tan
Comment Hypertriglyceridemia-induced pancreatitis in pregnancy has been well reported. However, most of the treatment of hypertriglyceridemia during the acute phase of the disease was with dietary control, lipoprotein apheresis, bezafibrate, or gemfibrozil. Heparin can be used effectively to decrease the triglyceride level by liberating into the plasma the endothelial-bound lipoprotein lipase (LPL). However, a MEDLINE search from 1960 to 2001 yielded only one such case report. Henzen et al1 described the use of intravenous heparin 10,000 U per day in five patients with hypertriglyceridemia-induced pancreatitis, of whom one was pregnant. The triglyceride level was decreased to <10 mmol/L within 2.8 days (range 1 to 6 days), and the amylase and lipase levels returned to normal after 3 and 4 days, respectively. We had similar results because the triglyceride level in our patient decreased to 12.76 mmol/L after 18 hours and the serum amylase was 39 U/L after 24 hours. A heparin dose of 10,000 U per day seems to be safe, as evidenced by a nor-
July 2002 Am J Obstet Gynecol
mal aPTT. However, the reduction of the triglyceride level by heparin is only temporary and long-term use may paradoxically result in an increase in the triglyceride level as a result of depletion of LPL.2 This should not be of concern with short-term use of heparin. Heparin can be stopped once the triglyceride level falls below 11 mmol/L. Methyldopa can cause pancreatitis, but it is unlikely to be the cause in our patient because her symptoms preceded ingestion of methyldopa. We conclude that intravenous heparin 10,000 U per day is an effective, simple, and safe method of lowering the triglyceride level in hypertriglyceridemia-induced pancreatitis in pregnancy. REFERENCES
1. Henzen C, Rock M, Schnieper C, Heer K. Heparin and insulin in the treatment of acute hypertriglyceridemia-induced pancreatitis. Schweiz Med Wochenschr 1999;129:1242-8. 2. Watts GF, Cameron J, Henderson A, Richmond W. Lipoprotein lipase deficiency due to long-term heparinization presenting as severe hypertriglyceridemia in pregnancy. Postgrad Med J 1991;67:1062-4.
Key words: Pancreatitis, hypertriglyceridemia, pregnancy, heparin
We used continuous intravenous heparin to lower the plasma triglyceride level in a case of hypertriglyceridemia-induced pancreatitis in pregnancy. Case report The patient was a 29-year-old woman, gravida 3, para 2. She had two uneventful normal vaginal deliveries complicated by mild pregnancy-induced hypertension (PIH) and gestational diabetes mellitus (GDM). She was admitted at 26 weeks of gestation for a 1-day history of severe epigastric pain and mild PIH. The serum amylase (64 U/L) and ultrasound scan of the hepatobiliary system were normal. The blood glucose level was 10.9 mmol/L. The impression was severe gastritis with PIH and GDM; the patient was treated with oral cimetidine, oral methyldopa, and soluble insulin injection. During blood drawing, the blood was noted to be lipemic and tests confirmed hypertriglyceridemia (53.53 mmol/L) and hypercholesterolemia (total 18.12 mmol/L). On the third day of admission, the patient became breathless and was transferred to the intensive care unit (ICU). Her blood glucose level was 16.3 mmol/L, urine ketones were 3+, and she had metabolic acidosis (pH 7.257, partial pressure of carbon dioxide [PCO2] 16.1 mm Hg, bicarbonate [HCO3–] 6.9 mmol/L). Her partial pressure of oxygen
From the Department of Anaesthesia, KK Women’s and Children’s Hospital,a and the Department of General Medicine, Tan Tock Seng Hospital.b Received for publication August 15, 2001; revised December 7, 2001; accepted December 20, 2001. Reprint requests: Chee-Chuen Loo, FRCA, Department of Anaesthesia, KK Women’s and Children’s Hospital, 100, Bukit Timah Road, S229899, Republic of Singapore. E-mail: [email protected] © 2002, Mosby, Inc. All rights reserved. 0002-9378/2002 $35.00 + 0 6/1/122422 doi:10.1067/mob.2002.122422
(PO2) was 121.9 mm Hg (fractional concentration of oxygen in inspired gas [FiO2] 0.4). The impression was diabetic ketoacidosis; she was treated with continuous intravenous insulin. However, she still had intractable epigastric pain, and a repeat serum amylase level was found to be markedly raised (956 U/L). A repeat ultrasound examination revealed fluid over the pancreas and enlargement of the pancreatic head. A diagnosis of acute pancreatitis secondary to hypertriglyceridemia was made. The worst laboratory results recorded during the patient’s ICU stay were total white blood cells 14.5 109/L, albumin 19 g/L, total bilirubin 72 µmol/L, HCO3– 6.8 mmol/L, ionized calcium 1.09 mmol/L, and PO2 83.2 mm Hg (FiO2 0.4). There was no hypotension, abnormal chest x-ray film, renal impairment, or coagulopathy. The liver enzymes and hematocrit were normal. She was treated conservatively with intermittent nasogastric suction and intravenous ranitidine 50 mg three times a day. The hypertriglyceridemia was treated with intravenous heparin infusion. We started at an empiric continuous intravenous dose of 20,000 U per day but had to decrease to 10,000 U per day because of a prolonged activated partial thromboplastin time (aPTT, 40 seconds, 104 seconds, 39.8 seconds). The triglyceride level decreased dramatically to 12.76 mmol/L after 18 hours and the serum amylase was 39 U/L after 24 hours. Ultrasound examination of the fetus showed normal growth and cardiotocography and umbilical artery pulsatile index were normal. The patient was discharged to the general ward after 6 days in the ICU and was discharged home 14 days from the time of hospital admission. Hypertriglyceridemia was treated with dietary control and at 31 weeks’ gestation the triglyceride level was 4.99 mmol/L and the total cholesterol was 7.26 mmol/L. Labor was induced at 37 weeks’ gestation because of PIH; the patient had an uneventful normal vaginal delivery. 241
242 Loo and Tan
Comment Hypertriglyceridemia-induced pancreatitis in pregnancy has been well reported. However, most of the treatment of hypertriglyceridemia during the acute phase of the disease was with dietary control, lipoprotein apheresis, bezafibrate, or gemfibrozil. Heparin can be used effectively to decrease the triglyceride level by liberating into the plasma the endothelial-bound lipoprotein lipase (LPL). However, a MEDLINE search from 1960 to 2001 yielded only one such case report. Henzen et al1 described the use of intravenous heparin 10,000 U per day in five patients with hypertriglyceridemia-induced pancreatitis, of whom one was pregnant. The triglyceride level was decreased to <10 mmol/L within 2.8 days (range 1 to 6 days), and the amylase and lipase levels returned to normal after 3 and 4 days, respectively. We had similar results because the triglyceride level in our patient decreased to 12.76 mmol/L after 18 hours and the serum amylase was 39 U/L after 24 hours. A heparin dose of 10,000 U per day seems to be safe, as evidenced by a nor-
July 2002 Am J Obstet Gynecol
mal aPTT. However, the reduction of the triglyceride level by heparin is only temporary and long-term use may paradoxically result in an increase in the triglyceride level as a result of depletion of LPL.2 This should not be of concern with short-term use of heparin. Heparin can be stopped once the triglyceride level falls below 11 mmol/L. Methyldopa can cause pancreatitis, but it is unlikely to be the cause in our patient because her symptoms preceded ingestion of methyldopa. We conclude that intravenous heparin 10,000 U per day is an effective, simple, and safe method of lowering the triglyceride level in hypertriglyceridemia-induced pancreatitis in pregnancy. REFERENCES
1. Henzen C, Rock M, Schnieper C, Heer K. Heparin and insulin in the treatment of acute hypertriglyceridemia-induced pancreatitis. Schweiz Med Wochenschr 1999;129:1242-8. 2. Watts GF, Cameron J, Henderson A, Richmond W. Lipoprotein lipase deficiency due to long-term heparinization presenting as severe hypertriglyceridemia in pregnancy. Postgrad Med J 1991;67:1062-4.