Case Reports in Obstetrics and Gynecology
Volume 2018 (2018), Article ID 3869695, 8 pages
https://doi.org/10.1155/2018/3869695

Case Report

Abruptio Placentae Caused by Hypertriglyceridemia-Induced Acute Pancreatitis during Pregnancy: Case Report and Literature Review

Pınar Yalcin Bahat, Gokce Turan, and Berna Aslan Cetin

Department of Obstetrics and Gynecology, Kanuni Sultan Suleyman Training and Research Hospital, Istanbul Health Sciences University, Istanbul, Turkey

Correspondence should be addressed to Pınar Yalcin Bahat; dr_pinaryalcin@hotmail.com

Received 1 February 2018; Revised 16 August 2018; Accepted 27 August 2018; Published 5 September 2018

Academic Editor: Erich Cosmi

Copyright © 2018 Pınar Yalcin Bahat et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract.

Background. Hormonal effects during pregnancy can compromise otherwise controlled lipid levels in women with hypertriglyceridemia and predispose to pancreatitis leading to increased morbidity for mother and fetus. Elevation of triglyceride levels is a risk factor for development of pancreatitis if it exceeds 1000 mg/dL. Pancreatitis should be considered in emergency cases of abdominal pain and uterine contractions in Emergency Department at any stage of pregnancy. We report a case of abruptio placentae caused by hypertriglyceridemia-induced acute pancreatitis. Also, literature review of cases of acute pancreatitis induced by hypertriglycaemia in pregnancy has been made. Case. A 22-year-old woman presented to our Emergency Department, at 35 weeks of gestation, for acute onset of abdominal pain and uterine contractions. Blood tests showed a high rate of triglyceride. The patient was diagnosed with abruptio placentae caused by hypertriglyceridemia-induced acute pancreatitis. Immediate cesarean section was performed and it was observed that blood sample revealed a milky turbid serum. Insulin, heparin, and supportive treatment were started. She was discharged on the 10th day. Conclusion. Consequently, patients with known hypertriglyceridemia or family history should be followed up more closely because any delay can cause disastrous conclusions for mother and fetus. Acute pancreatitis should be considered in pregnant women who have sudden onset, severe, persistent epigastric pain and who have a risk factor for acute pancreatitis.

1. Introduction

Acute pancreatitis (AP) is a rare complication in pregnancy, occurring in approximately three in 10000 pregnancies [1, 2]. Hypertriglyceridemia is recognized as the third most common cause of gestational acute pancreatitis after gallstones and alcohol and occurs in about 4% of all cases [2]. An increase in plasma lipid level during pregnancy has been well documented. It is thought to represent a physiologic response to the hormonal changes; however, it is not sufficient to cause acute pancreatitis. Gestational pancreatitis due to hypertriglyceridemia usually occurs in pregnant women with preexisting abnormalities of the lipid metabolism. There are effective treatment choices during pregnancy such as dietary restriction of fat, intravenous heparin, and insulin and plasmapheresis. We report a case of abruptio placentae caused by hypertriglyceridemia-induced acute pancreatitis.

2. Case Report

A 22-year-old patient, Para 1, Gravida 2, presented to our Emergency Department of Gynecology and Obstetrics, at 35 weeks of gestation for acute onset of abdominal pain and uterine contraction. It was learned that the patient’s history had no follow-up hypertriglyceridemia. On physical exam, her heart rate was at 100 pulses per minute, and her blood pressure was at 110/70 mm-Hg, respiratory rate 18 /min. Her abdomen was defensive. Her cervical os was dilated to 1-2 cm and minimal bleeding. The patient had mild epigastric tenderness. Decelerations were seen in pregnant cardiotocography follow-ups with abnormal abdominal pain and uterine contractions continued and simultaneous wide bleeding area (like abruptio placenta) was seen on the posterior part of placenta in ultrasound. Immediate cesarean section was performed under general anesthesia because of contraction of the tetanic type in the manual contraception. She gave birth to a healthy infant of 2980 g. Amylase, lipase, triglyceride, HDL, and LDL were studied in the patient’s blood after emulsion of chylous fluid from abdomen during the cesarean section. Liver enzymes were high: ast: 241, sub. 147. It was observed that blood sample revealed a milky turbid serum. Laboratory finding included a triglyceride at 3297 mg/dl and amylase 827 U/L, lipase 1576 U/L. Abdominal ultrasound showed thickened pancreas without necrosis; acute pancreatitis compatible with diffuse edema was observed on pancreas. Biliary tract was naturally observed. Other causes of cholestasis of pregnancy, such as cholangitis, acute hepatitis, and hemophagocytic syndrome, were ruled out. Oral intake of the patient was stopped; intravenous fluid replacement therapy, antibiotherapy, proton pump inhibitor, insulin, and heparin therapy were started. She was discharged on the 10th day of treatment. Even though the patient did not have previous history of diabetes or gestational diabetes, the baby was born 4 to 3 weeks earlier. It was thought that this condition might be related to maternal hyperlipidemia for newborn’s doctors.

3. Discussion

Acute pancreatitis (AP) is a rare complication in pregnancy. Diagnosis becomes difficult because it can interfere with the physiological findings in pregnancy. Acute pancreatitis should be considered in pregnancies with nausea, vomiting, and epigastric pain. Gallstones, hypertriglyceridemia, and alcohol especially play a role in the etiology of acute pancreatitis.

Hypertriglyceridemia is the second most common cause of acute pancreatitis in pregnancy. Diagnosis is made when the serum triglyceride is > 1000 mg/dl. Hypertriglyceridemia in pregnant patients can occur with preexisting dyslipidemia, associated with others diseases (hypertension, diabetes mellitus, and alcoholism), or without any predisposing factor. Triglycerides concentration rises gradually, 2.5-fold over prepregnancy levels, reaching a peak during the third trimester to almost twice as high value of nonpregnant value. This is thought to be due to estrogen-induced increases in triglyceride synthesis and very low-density lipoprotein secretion [29]. Therefore, AP is more common in the third trimester of pregnancy. Lipids decrease gradually postpartum to reach prepregnancy level in 6 weeks [30, 31]. Epigastric pain, spreading pain, nausea, vomiting, and distension can be seen at the beginning of the symptoms in acute pancreatitis cases. Findings of peritoneal irritation are not seen in general, especially when there is epigastric pain in mild cases as indicated by physical examination findings. In severe cases, epigastric tenderness and peritoneal irritation findings may be accompanied by ileus, fever, and tachycardia. The increase in serum amylase reaches peak values 6-12 hours after the onset of the event. The exact diagnosis of pancreatitis is based on the amylase/creatinine clearance rate. Serum lipase values also increase. Imaging methods can be used in the diagnosis of acute pancreatitis from ultrasonography, computed tomography, and magnetic resonance imaging. Ultrasound is the most appropriate method for pregnancy.

Acute pancreatitis treatment in pregnancy is similar to nonpregnant treatment of hyperlipidemia. Pregnancy pancreatitis treatment is primarily medicinal and approximately 90% of patients respond to medical treatment. Medical treatment of AP is mostly supportive. These treatments include low fat diet [32, 33], antihyperlipidemic therapy [32, 33], insulin [32, 34] (to increase lipoprotein lipase activity), heparin [33, 35] (to increase lipoprotein lipase activity), and even plasmapheresis [32, 35].

Our patient was admitted with acute onset of abdominal pain and uterine contraction to our clinics in the 35th week of gestation. She had lipid abnormality in her history, but her history had no follow-up hypertriglyceridemia. Pregnancy had induced aggravation of hypertriglyceridemia and associated pancreatitis. In addition, acute pancreatitis induced by the pregnancy was accompanied by abruptio placenta and delivery was performed with an emergency cesarean section. It was observed that blood sample revealed a milky turbid serum. We managed our patient conservatively in postoperative period. Oral intake of the patient was stopped; intravenous fluid replacement therapy, antibiotherapy, proton pump inhibitor, insulin, and heparin therapy were started. The patient’s clinical condition subsequently improved.

Cases of acute pancreatitis induced by hypertrigliceridemia during pregnancy published in the literature are listed in Table 1. In the majority of published case, medical treatment was first tired. Oral intake was closed, supportive treatment started. However, pregnancy-induced pancreatitis has been mortal in some cases and has gone as far as maternal death.

Table 1: Case literatures of acute pancreatitis induced by hypertriglyceridemia during pregnancy.

First Author
Year
Age
G/P
Birth
Medication
Other
Mode BW
Indication
Laboratory
After Treatment

Billion JM [3]
1991
32

35
TPN

Achard JM [4]
1991

Two
Lipaphereses

Perrone G [5]
1996
37

35
Diet,
Gemfibrozil

İbrahim Bildirici [6]
2002
26
G2P2
24
Insulin,
Plasmapheresis

C/S
Fetal Distress (750 g)
Serum Amylase: 487
Panc. Amylase: 184
Panc Lipase:786
TG: 2316

Chee-Chuen Loo [7]
2002
37
G3P2
37
Ranitidine,
Heparin,
Insulin

SVD

Serum Amylase: 956 TG: 2066
Serum Amylase: 39 TG: 492

J.C. Sleth [8]
2004
28
G2P1
37
Heparin

C/S
Unstable Condition of the Mother
TG: 2316
Cholesterol: 1000
Panc. Amylase: 574
Panc. Lipase: 1310
TG: 100

A. Abu Musa [9]
2006
39
G2P1
28
Plasmapheresis

C/S
A Repeat C/S Delivery
TG: 3810
Panc. Amylase: 525
Panc. Lipase: 3524
TG: 591
Panc. Amylase: 79
Panc. Lipase: 396

Shih-Chang Chuang [10]
2006
28
G1P0
34
Antibiotics,
TPN
Pancreatic Necrosectomy,
Right Hemicolectomy
Ileostomy,
Cholecystostomy,
Gastrostomy,
Feeding Jejunostomy

Unstable Condition of the Mother
TG: 2184
Panc. Amylase: 1365
Panc. Lipase: 533
TG: 319

Alptekin Gürsoy [11]
2006
24
G1P0
37

C/S
(3230 g)
Fetal Distress
TG: 10092
Cholesterol: 1159
Panc. Amylase: 367
Panc. Lipase: 797
TG: 143
Cholesterol: 274
Panc Amylase: 23
Panc Lipase: 41

V. Exbrayat [12]
2007
31

33
Plasmapheresis, Heparin

C/S
Fetal Distress
TG: 11300
Cholesterol: 2500
Panc Amylase: 334
Panc Lipase: 168
TG: 1000

Luminita S. Crisan [13] - 1
2008
27
G2P0
35
TPN, Analgesics, Bowel Rest
ARDS
C/S
(2653 g)
Fetal Distress

Luminita S. Crisan [13] - 2
2008
29
G3P1
30
TPN, Analgesics, Bowel Rest
Acute Myocardial Infarction
Forceps–
Assisted
Vaginal
Delivery
(1854 g)

Luminita S. Crisan [13] - 3
2008
34
G3P0
33
TPN, Analgesics, Bowel Rest
ARDS
SVD
(2147 g)

Luminita S. Crisan [13] - 4
2008
23
G1P0
35
TPN, Analgesics, Bowel Rest

C/S (2498 g)
Low BPP

L. Vandenbroucke [14]
2009
34

37
Heparin,
A Low-Fat Diet

C/S (3940 g)
Fetal Distress
TG: 8447
TG: 240

Dilek Altun [15] - 1
2012
27
G1P0
5
Plasmapheresis, Heparin

Termination
TG: 2225
Cholesterol: 470
Panc. Amylase: 959
TG: 278
Cholesterol: 181

Dilek Altun [15] - 2
2012
24
G1P0
34
Plasmapheresis, A Low-Fat Diet

C/S (3100 g)

TG: 2699
Cholesterol: 230
Panc. Amylase: 956
Panc. Lipase: 2580
TG: 570
Cholesterol: 2500
Panc. Amylase: 208
Panc. Lipase: 208

Mindaugas Serpytis [16]
2012
31
G2P0
33
Heparin, Insulin, Plasmapheresis

TG: 1576
TG:183

Kumar Thulasidass [17] - 1
2013
37
G3P0
14
Insulin,
Metformin,
Fish Oil Therapy
Termination

TG: 1421
Cholesterol: 481
Serum Amylase: 1464
TG: 111
Cholesterol:93

Kumar Thulasidass [17] - 2
2013
24
G1P0
8

ARDS
Spontaneous Abortion

TG: 839
Cholesterol: 300
Serum Amylase: 8962
TG: 57
Cholesterol:77

Rafet Basar [18] - 1
2013
32
G3P0
37
Heparin,
Fatty Acids, DF

C/S
Elective
TG: 1400
TG: 380

Rafet Basar [18] - 2

30
G2P1
36
Heparin,
Fatty Acids,
DF, Plasmapheresis

C/S
Elective
TG: 12000
TG: 758

Ying Hang [19]
2013
31
G2P0
27

Noninvasive Positive
Pressure Ventilation
(NPPV), Drainage of
Chylous Ascites,
Peritoneal Lavage, ARDS
C/S
(1180 g)
Fetal Distress
TG: 523
Cholesterol:325
Panc. Amylase: 178
TG: Normal
Cholesterol: Normal

Bahiyah Abdullah [20]
2014
25
G4P3
8

Diagnostic Laparoscopy,
Acute Hemorrhagic Pancreatitis
Spontaneous Abortion

Serum Amylase: 1273
Serum Amylase: 147

Tejal Amin [21]
2014
40
G5P4
18
Insulin
IUMF

TG: 836
Cholesterol: 300
TG: 90

Natasha Gupta [22]
2014
32
G5P4
38
Plasmapheresis
Preeclampsia,
Pleural Effusion,
Chronic Pericarditis,
Retinal Detachment
C/S
Unstable Condition of the Mother
TG: 12.570
Cholesterol: 1067
Panc. Amylase: 1617
Panc. Lipase: 1330
TG: 295
Cholesterol: 179

Fadi Safi [23]
2014
24
G9P8
35
Plasmapheresis

C/S
(1720 gr)
Unresponsiveness to Treatment
TG: 2661
Cholesterol: 683
Serum Amylase: 802
TG: 425

Rachel Lim [24]
2015
27
G1P0
33
Insulin,
Plasmapheresis
Placental Abruption
SVD

TG: 720
Cholesterol: 90
Panc. Lipase: 504
TG: 41

Ying Liu [24]
2015
30
G1P0
32
Plasmapheresis
Compound Heterozygosity
(Glu242Lys and
Leu252VaL)
C/S
Fetal Distress
TG: 2160
Cholesterol: 670
Panc. Amylase: 132
TG: 420

Funda Gok [25]
2015
37

31
Insulin,
DF
IUMF
SVD

TG: 9742
Cholesterol: 705
Panc. Amylase: 570
Panc. Lipase: 319
TG: 556
Panc. Amylase: 107
Panc. Lipase: 77

Hae Rin Jeon [26]
2016
28
G1P0
23

IUMF,
Pancreatic Cells Necrotized,
Diabetic Ketoacidosis,
Metabolic Acidosis,
Cardiac Arrest, EX

TG: 10392
Cholesterol: 1006
Panc. Amylase: 1833
Panc. Lipase: 1863

Ioanna Polypathelli [27]
2017
38
G2P1
30
Heparin,
Fatty Acids,
Antibiotics

C/S
Resistant
Exaggerated
Thrombocytosis
TG: 14440
Cholesterol: 1600
Serum Amylase: 540
TG: 521

Tamanna Chibber [28]
2017
38

11

Cardiac Arrest, EX

TG: >1254
Cholesterol: 648
Panc. Lipase: 1079

BW: birth weight, G: gravida, P: parity, SVD: spontaneous vaginal delivery, BPP: biophysical profile, TPN: total parenteral nutrition, DF: double filtration apheresis, C/S: cesarean section, TG: triglyceride, ARDS: Adult Respiratory Distress Syndrome, and IUMF: Intra-Uterine Mort Fetus.

Triglyceride and total cholesterol units are calculated in mg/dL. Other units are converted to mg/dL.

Serum Amylase: normal range is between 30 and 110 (U/L) [11].

Pancreatic Amylase: normal range is between 17 and 115 (U/L) [11].

Pancreatic Lipase: normal range is between 13 and 60 U/L (U/L) [11].

TG: normal range is between 50 and 160 mg/dL (mg/dL) [11].

Cholesterol: normal range is between 130 and 230 (mg/dL) [11].

Highest values.

Lowest values.

Ihuang et al. performed a retrospective study on 21 pregnant women diagnosed with acute pancreatitis (AP). Patients were divided into acute biliary pancreatitis (A BP), hypertriglyceridemia-induced acute pancreatitis (HTG P), and idiopathic groups according to etiology. 95% of the patients were in the third trimester of gestation. The percentage of patients with HTGP was higher than that of ABP (48% versus 14%). The percentage of severe acute pancreatitis (SAP) in the HTGP group was higher than that in the ABP group (40.0% versus 0%). In the HTGP group, five patients given were plasma exchange therapy and five were not. According to the results of this study it was found that plasma exchange may be safe and effectively administered for HTGP patients during pregnancy with SIRS or multiple organ dysfunction syndrome (MODS) [36].

In a study by Lingyu Luo et al., they retrospectively reviewed 121 acute pancreatitis in pregnancy (APIP) cases. The correlation between APIP types, severity, biochemical parameters, and mortality was analyzed. The most common causes of APIP were gallstone and hypertriglyceridemia. Lower level of serum calcium could be used as an indicator for the severity of the APIP. According to the result s of this study it was found that the severity of APIP was associated with higher risk for neonate asphyxia and maternal and fetal death [37].

In a prospective study performed by Athyros VG et al., 17 cases of acute pancreatitis induced by hypertriglyceridemia were included in the study. These patients were followed for 42 months. In the content of the study causative conditions of HTG-induced A P were familial HTG in eight patients, HTG caused by uncontrolled diabetes mellitus in five, HTG aggravated by drugs in two (one by tamoxifen and one by fluvastatin), familial hyperchylomicronemia (HCM) in one, and lipemia of pregnancy in one. During the acute phase of pancreatitis, patients underwent standard treatment. After that, HTG was efficiently controlled with high dosages of fibrates or a fibrate plus acipimox, except for the patient with H CM, who was on a specific diet (the only source of fat was a special oil consisting of medium chain triglyceride) and taking a high dosage of acipimox. One of the patients died during the acute phase of pancreatitis with acute respiratory distress syndrome. According to the results of the study it was found that appropriate diet and drug treatment, including dose titration, of severe HTG are very effective in preventing relapses of HTG-induced AP [38].

As a result, pancreatitis can be seen in pregnancy in cases with uncontrolled hypertriglyceridemia. Patients with known hypertriglyceridemia or family history should be followed up more closely. Acute pancreatitis should be considered in pregnant women who have sudden onset, severe, persistent epigastric pain and who have a risk factor for acute pancreatitis.

Conflicts of Interest

The authors declare that there are no conflicts of interest regarding the publication of this paper.

References

J. J. Eddy, M. D. Gideonsen, J. Y. Song, W. A. Grobman, and P. O'Halloran, “Pancreatitis in pregnancy,” Obstetrics & Gynecology, vol. 112, no. 5, pp. 1075–1081, 2008.

K. D. Ramin, S. M. Ramin, S. D. Richey, and F. G. Cunningham, “Acute pancreatitis in pregnancy,” American Journal of Obstetrics & Gynecology, vol. 173, no. 1, pp. 187–191, 1995.

K. Ohmoto, Y. Neishi, I. Miyake, and S. Yamamoto, “Severe acute pancreatitis associated with hyperlipidemia: Report of two cases and review of the literature in Japan,” Hepato-Gastroenterology, vol. 46, no. 29, pp. 2986–2990, 1999.

J. M. Achard, P. F. Westeel, P. Moriniere, J. D. Lalau, B. de Cagny, and A. Fournier, “Pancreatitis related to severe acute hypertriglyceridemia during pregnancy: Treatment with lipoprotein apheresis,” Intensive Care Medicine, vol. 17, no. 4, pp. 236-237, 1991.

G. Perrone and C. Critelli, “Severe hypertriglyceridemia during pregnancy. A case report,” Minerva Ginecologica, vol. 48, no. 12, pp. 573–576, 1996.

I. Bildirici, I. Esinler, O. Deren, T. Durukan, B. Kabay, and L. Onderoglu, “Hyperlipidemic pancreatitis during pregnancy,” Acta Obstetricia et Gynecologica Scandinavica, vol. 81, no. 5, pp. 468–470, 2002.

C.-C. Loo and J. Y. L. Tan, “Decreasing the plasma triglyceride level in hypertriglyceridemia-induced pancreatitis in pregnancy: A case report,” American Journal of Obstetrics & Gynecology, vol. 187, no. 1, pp. 241-242, 2002.

J. C. Sleth, E. Lafforgue, R. Servais et al., “A case of hypertriglycideremia-induced pancreatitis in pregnancy: Value of heparin,” Annales Françaises d’Anesthésie et de Réanimation, vol. 23, no. 8, pp. 835–837, 2004.

A. A. Abu Musa, I. M. Usta, J. B. Rechdan, and A. H. Nassar, “Recurrent hypertriglyceridemia-induced pancreatitis in pregnancy: A management dilemma [5],” Pancreas, vol. 32, no. 2, pp. 227-228, 2006.

S.-C. Chuang, K.-T. Lee, S.-N. Wang, K.-K. Kuo, and J.-S. Chen, “Hypertriglyceridemia-associated acute pancreatitis with chylous ascites in pregnancy,” Journal of the Formosan Medical Association, vol. 105, no. 7, pp. 583–587, 2006.

A. Gürsoy, M. Kulaksizoglu, M. Sahin et al., “Severe hypertriglyceridemia-induced pancreatitis during pregnancy,” Journal of the National Medical Association, vol. 98, no. 4, pp. 655–657, 2006.

V. Exbrayat, J. Morel, J. P. De Filippis, G. Tourne, R. Jospe, and C. Auboyer, “Pancréatite aiguë secondaire à une hypertriglycéridémie majeure dorigine gestationnelle. À propos dun cas,” in In Annales françaises danesthésie et de réanimation, vol. 26, pp. 677–679, Elsevier Masson, 2007.

L. S. Crisan, E. T. Steidl, and M. E. Rivera-Alsina, “Acute hyperlipidemic pancreatitis in pregnancy,” American Journal of Obstetrics & Gynecology, vol. 198, no. 5, pp. e57–e59, 2008.

L. Vandenbroucke, S. Seconda, L. Lassel, G. Le Bouar, and P. Poulain, “Pancréatite aiguë secondaire à une hypertriglycéridémie majeure au cours de la grossesse. À propos dun cas,” Journal de Gynécologie Obstétrique et Biologie de la Reproduction, vol. 38, no. 5, pp. 436–439, 2009.

D. Altun, G. Eren, Z. Cukurova, O. Hergünsel, and L. Yasar, “An alternative treatment in hypertriglyceridemia-induced acute pancreatitis in pregnancy: plasmapheresis,” Journal of Anaesthesiology Clinical Pharmacology, vol. 28, no. 2, pp. 252–254, 2012.

M. Serpytis, V. Karosas, R. Tamosauskas et al., “Hypertriglyceridemia-induced acute pancreatitis in pregnancy,” Journal of the Pancreas, vol. 13, no. 6, pp. 677–680, 2012.

K. Thulasidass and T. A. Chowdhury, “Hypertriglyceridemic pancreatitis in pregnancy: case reports and review of the literature,” JRSM Short Reports, vol. 4, no. 8, pp. 1–3, 2013.

R. Basar, A. K. Uzum, B. Canbaz et al., “Therapeutic apheresis for severe hypertriglyceridemia in pregnancy,” Archives of Gynecology and Obstetrics, vol. 287, no. 5, pp. 839–843, 2013.

S. Gupta, M. Jayant, and R. Kaushik, “Acute hyperlipidemic pancreatitis in a pregnant woman,” World Journal of Emergency Medicine, vol. 4, no. 3, p. 311, 2013.

B. Abdullah, T. K. Pillai, L. H. Cheen, and R. J. Ryan, “Severe acute pancreatitis in pregnancy,” Case reports in obstetrics and gynecology, 2015.

T. Amin, L. C. Y. Poon, T. G. Teoh et al., “Management of hypertriglyceridaemia-induced acute pancreatitis in pregnancy,” The Journal of Maternal-Fetal and Neonatal Medicine, vol. 28, no. 8, pp. 954–958, 2015.

N. Gupta, S. Ahmed, L. Shaffer, P. Cavens, and J. Blankstein, “Severe hypertriglyceridemia induced pancreatitis in pregnancy,” Case Reports in Obstetrics and Gynecology, 2014.

F. Safi, A. Toumeh, M. A. A. Qadan, R. Karaz, B. AlAkdar, and R. Assaly, “Management of familial hypertriglyceridemia-induced pancreatitis during pregnancy with therapeutic plasma exchange: A case report and review of literature,” American Journal of Therapeutics, vol. 21, no. 5, pp. e134–e136, 2014.

Y. Liu, Y. Lun, W. Lv, X. Hou, and Y. Wang, “A Chinese patient with recurrent pancreatitis during pregnancy induced by hypertriglyceridemia associated with compound heterozygosity (Glu242Lys and Leu252VaL) in the lipoprotein lipase gene,” Journal of Clinical Lipidology, vol. 10, no. 1, pp. 199–203e1, 2016.

F. Gök, S. Köker, A. Kılıçaslan, G. Sarkılar, A. Yosunkaya, and Ş. Otelcioğlu, “Acute pancreatitis due to hypertriglyceridaemia in pregnancy,” Turk Anesteziyoloji ve Reanimasyon Dernegi Dergisi, vol. 43, no. 2, pp. 116–118, 2015.

H. R. Jeon, S. Y. Kim, Y. J. Cho, and S. J. Chon, “Hypertriglyceridemia-induced acute pancreatitis in pregnancy causing maternal death,” Obstetrics gynecology science, vol. 59, no. 2, pp. 148–151, 2016.

I. Polypathelli, C. Demosthenous, M. Gavra, E. Matsaridou, and G. Tzatzagou, “Hypertriglyceridemia-induced acute pancreatitis in third trimester of pregnancy: A case report,” Atherosclerosis, vol. 263, pp. e203–e204, 2017.

T. Chibber and P. S. Gibson, “Fatal Abdominal Compartment Syndrome Due to Severe Triglyceride-Induced Pancreatitis in Early Pregnancy,” Journal of Obstetrics and Gynaecology Canada, 2017.

G. Lippi, A. Albiero, M. Montagnana et al., “Lipid and lipoprotein profile in physiological pregnancy,” Clinical Laboratory, vol. 53, no. 3-4, pp. 173–177, 2007.

R. Klingel, B. Göhlen, A. Schwarting, F. Himmelsbach, and R. Straube, “Differential indication of lipoprotein apheresis during pregnancy,” Therapeutic Apheresis, vol. 7, no. 3, pp. 359–364, 2003.

R. H. Knopp, M. R. Warth, D. Charles et al., “Lipoprotein metabolism in pregnancy, fat transport to the fetus, and the effects of diabetes,” Biology of the Neonate, vol. 50, no. 6, pp. 297–317, 1986.

J. H. Bae, S. H. Baek, and H. S. Choi, “Acute pancreatitis due to hypertriglyceridemia: report of 2 cases,” The Korean Journal of Gastroenterology, vol. 46, no. 6, pp. 475–480, 2005.

E.-Q. Mao, Y.-Q. Tang, and S.-D. Zhang, “Formalized therapeutic guideline for hyperlipidemic severe acute pancreatitis,” World Journal of Gastroenterology, vol. 9, no. 11, pp. 2622–2626, 2003.

A. Monga, A. Arora, R. P. S. Makkar, and A. K. Gupta, “Hypertriglyceridemia-induced acute pancreatitis—treatment with heparin and insulin,” Indian Journal of Gastroenterology, vol. 22, no. 3, pp. 102-103, 2003.

S. B. Iskandar and K. E. Olive, “Plasmapheresis as an adjuvant therapy for hypertriglyceridemia-induced pancreatitis,” The American Journal of the Medical Sciences, vol. 328, no. 5, pp. 290–294, 2004.

C. Huang, J. Liu, Y. Lu et al., “Clinical features and treatment of hypertriglyceridemia-induced acute pancreatitis during pregnancy: A retrospective study,” Journal of Clinical Apheresis, vol. 31, no. 6, pp. 571–578, 2016.

L. Luo, H. Zen, H. Xu et al., “Clinical characteristics of acute pancreatitis in pregnancy: experience based on 121 cases,” Archives of gynecology and obstetrics, pp. 1–7, 2017.

V. G. Athyros, O. I. Giouleme, N. L. Nikolaidis et al., “Long-term follow-up of patients with acute hypertriglyceridemia-induced pancreatitis,” Journal of Clinical Gastroenterology, vol. 34, no. 4, pp. 472–475, 2002.