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

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.

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 maybe 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.


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[25] F. Gok, S. Koker, A. Kilicaslan, G. Sarkilar, A. Yosunkaya, and S. Otelcioglu, "Acute pancreatitis due to hypertriglyceridaemia in pregnancy," Turk Anesteziyoloji ve Reanimasyon Dernegi Dergisi, vol. 43, no. 2, pp. 116-118, 2015.

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[27] 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.

[28] 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.

[29] 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.

[30] R. Klingel, B. Gohlen, A. Schwarting, F. Himmelsbach, and R. Straube, "Differential indication of lipoprotein apheresis during pregnancy," Therapeutic Apheresis, vol. 7, no. 3, pp. 359-364, 2003.

[31] 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.

[32] 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.

[33] 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.

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[36] 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.

[37] 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.

[38] 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.

Pinar Yalcin Bahat (iD), Gokce Turan (iD), 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 Pinar Yalcin Bahat;

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

Academic Editor: Erich Cosmi
Table 1: Case literatures of acute pancreatitis induced
by hypertriglyceridemia during pregnancy.

Author            Year   Age   G/P    Birth      Medication

Billion           1991   32            35            TPN
JM [3]

Achard            1991                              Two
JM [4]                                          Lipaphereses

Perrone           1996   37            35          Diet,
G [5]                                            Gemfibrozil

Ibrahim           2002   26    G2P2    24         Insulin,
Bildirici                                      Plasmapheresis

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

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

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

Shih-Chang        2006   28    G1P0    34       Antibiotics,
Chuang [10]                                          TPN

Alptekin          2006   24    G1P0    37
Gursoy [11]

V.                2007   31            33     Plasmapheresis,
Exbrayat                                           Heparin

Luminita S.       2008   27    G2P0    35           TPN,
Crisan                                          Analgesics,
[13]-1                                           Bowel Rest

Luminita S.       2008   29    G3P1    30           TPN,
Crisan                                          Analgesics,
[13]-2                                           Bowel Rest

Luminita S.       2008   34    G3P0    33           TPN,
Crisan                                          Analgesics,
[13]-3                                           Bowel Rest

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

L. Vanden-        2009   34            37        Heparin, A
broucke [14]                                    Low-Fat Diet

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

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

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

Kumar             2013   37    G3P0    14         Insulin,
Thulasi-dass                                     Metformin,
[17]-1                                            Fish Oil

Kumar             2013   24    G1P0     8

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

Rafet Basar              30    G2P1    36         Heparin,
[18]-2                                          Fatty Acids,

Ying              2013   31    G2P0    27
Hang [19]

Bahiyah           2014   25    G4P3     8

Tejal             2014   40    G5P4    18          Insulin
Amin [21]

Natasha           2014   32    G5P4    38      Plasmapheresis
Gupta [22]

Fadi              2014   24    G9P8    35      Plasmapheresis
Safi [23]

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

Ying              2015   30    G1P0    32      Plasmapheresis
Liu [24]

Funda             2015   37            31        Insulin, DF
Gok [25]

Hae Rin           2016   28    G1P0    23
Jeon [26]

Ioanna            2017   38    G2P1    30         Heparin,
Poly-pathelli                                   Fatty Acids,
[27]                                             Antibiotics

Tamanna           2017   38            11

Author                   Other            Mode BW

JM [3]

JM [4]

G [5]

Ibrahim                                     C/S

Chee-Chuen                                  SVD
Loo [7]

J.C.                                        C/S
Sleth [8]

A.Abu                                       C/S
Musa [9]

Shih-Chang            Pancreatic
Chuang [10]         Necrosectomy,

Alptekin                                    C/S
Gursoy [11]                               (3230 g)

V.                                          C/S

Luminita S.              ARDS               C/S
Crisan                                    (2653 g)

Luminita S.             Acute             Forceps-
Crisan                Myocardial         Assisted
[13]-2                Infarction          Vaginal
                                          (1854 g)

Luminita S.              ARDS               SVD
Crisan                                    (2147 g)

Luminita S.                                 C/S
Crisan                                    (2498 g)

L. Vanden-                                  C/S
broucke [14]                              (3940 g)

Dilek Altun

Dilek Altun                                 C/S
[15]-2                                    (3100 g)

Serpytis [16]

Kumar                 Termination

Kumar                    ARDS           Spontaneous
Thulasi-dass                              Abortion

Rafet Basar                                 C/S

Rafet Basar                                 C/S

Ying                 Noninvasive            C/S
Hang [19]              Positive           (1180 g)
                     Drainage of
                     Lavage, ARDS

Bahiyah               Diagnostic        Spontaneous
Abdullah             Laparoscopy,         Abortion
[20]                    Acute

Tejal                    IUMF
Amin [21]

Natasha             Preeclampsia,           C/S
Gupta [22]             Pleural

Fadi                                        C/S
Safi [23]                                (1720 gr)

Rachel                Placental             SVD
Lim [24]               Abruption

Ying                   Compound          C/S Fetal
Liu [24]            Heterozygosity        Distress
                    and Leu252VaL)

Funda                    IUMF               SVD
Gok [25]

Hae Rin                  IUMF,
Jeon [26]             Pancreatic
                      Arrest, EX

Ioanna                                      C/S

Tamanna                Cardiac
Chibber               Arrest, EX

Author                 Indication             Laboratory *

JM [3]

JM [4]

G [5]

Ibrahim                  Fetal               Serum Amylase:
Bildirici               Distress               487 Pane.
[6]                      (750 g)              Amylase: 184
                                            Pane Lipase: 786
                                                TG: 2316

Chee-Chuen                                   Serum Amylase:
Loo [7]                                       956 TG: 2066

J.C.                    Unstable                TG: 2316
Sleth [8]              Condition           Cholesterol: 1000
                      of the Mother        Pane. Amylase: 574
                                           Pane. Lipase: 1310

A.Abu                 A Repeat C/S           TG: 3810 Pane.
Musa [9]                Delivery           Amylase: 525 Pane.
                                              Lipase: 3524

Shih-Chang              Unstable                TG: 2184
Chuang [10]            Condition          Pane. Amylase: 1365
                         of the             Pane. Lipase: 533

Alptekin                 Fetal                 TG: 10092
Gursoy [11]             Distress           Cholesterol: 1159
                                           Pane. Amylase: 367
                                            Pane. Lipase: 797

V.                       Fetal                 TG: 11300
Exbrayat                Distress           Cholesterol: 2500
[12]                                       Pane Amylase: 334
                                            Pane Lipase: 168

Luminita S.              Fetal
Crisan                  Distress

Luminita S.

Luminita S.

Luminita S.              Low BPP

L. Vanden-               Fetal                  TG: 8447
broucke [14]            Distress

Dilek Altun            Termination              TG: 2225
[15]-1                                      Cholesterol: 470
                                           Pane. Amylase: 959

Dilek Altun                                     TG: 2699
[15]-2                                      Cholesterol: 230
                                           Pane. Amylase: 956
                                           Pane. Lipase: 2580

Mindaugas                                       TG: 1576
Serpytis [16]

Kumar                                           TG: 1421
Thulasi-dass                                Cholesterol: 481
[17]-1                                     Serum Amylase: 1464

Kumar                                           TG: 839
Thulasi-dass                                Cholesterol: 300
[17]-2                                     Serum Amylase: 8962

Rafet Basar             Elective                TG: 1400

Rafet Basar             Elective                TG: 12000

Ying                     Fetal                  TG: 523
Hang [19]               Distress            Cholesterol:325
                                           Pane. Amylase: 178

Bahiyah                                          Serum
Abdullah                                      Amylase: 1273

Tejal                                           TG: 836
Amin [21]                                   Cholesterol: 300

Natasha                 Unstable               TG: 12.570
Gupta [22]             Condition           Cholesterol: 1067
                         of the           Pane. Amylase: 1617
                         Mother            Pane. Lipase: 1330

Fadi                Unresponsiveness            TG: 2661
Safi [23]             to Treatment          Cholesterol: 683
                                           Serum Amylase: 802

Rachel                  TG: 720                  TG: 41
Lim [24]            Cholesterol: 90
                    Pane. Lipase: 504

Ying                    TG: 2160                 TG: 420
Liu [24]            Cholesterol: 670
                   Pane. Amylase: 132

Funda                   TG: 9742             TG: 556 Pane.
Gok [25]            Cholesterol: 705          Amylase: 107
                   Pane. Amylase: 570       Pane. Lipase: 77
                    Pane. Lipase: 319

Hae Rin                TG: 10392
Jeon [26]           Cholesterol: 1006
                  Pane. Amylase: 1833
                   Pane. Lipase: 1863

Ioanna                 Resistant               TG: 14440
Poly-pathelli         Exaggerated          Cholesterol: 1600
[27]                 Thrombocytosis        Serum Amylase: 540

Tamanna                                        TG: >1254
Chibber                                     Cholesterol: 648
[28]                                       Pane. Lipase: 1079

First                    After
Author                Treatment **

JM [3]

JM [4]

G [5]


Chee-Chuen          Serum Amylase:
Loo [7]                39 TG: 492

J.C.                    TG: 100
Sleth [8]

A.Abu                   TG: 591
Musa [9]           Pane. Amylase: 79
                   Pane. Lipase: 396

Shih-Chang              TG: 319
Chuang [10]

Alptekin                TG: 143
Gursoy [11]        Cholesterol: 274
                   Pane Amylase: 23
                    Pane Lipase: 41

V.                      TG: 1000

Luminita S.

Luminita S.

Luminita S.

Luminita S.

L. Vanden-              TG: 240
broucke [14]

Dilek Altun             TG: 278
[15]-1              Cholesterol: 181

Dilek Altun             TG: 570
[15]-2             Cholesterol: 2500
                  Pane. Amylase: 208
                   Pane. Lipase: 208

Mindaugas                TG:183
Serpytis [16]

Kumar                   TG: 111
Thulasi-dass        Cholesterol: 93

Kumar                   TG: 57
Thulasi-dass         Cholesterol:77

Rafet Basar             TG: 380

Rafet Basar             TG: 758

Ying                  TG: Normal
Hang [19]            Cholesterol:

Bahiyah                  Serum
Abdullah              Amylase: 147

Tejal                    TG: 90
Amin [21]

Natasha                 TG: 295
Gupta [22]          Cholesterol: 179

Fadi                    TG: 425
Safi [23]

Lim [24]

Liu [24]

Gok [25]

Hae Rin
Jeon [26]

Ioanna                  TG: 521


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.
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Title Annotation:Case Report
Author:Bahat, Pinar Yalcin; Turan, Gokce; Cetin, Berna Aslan
Publication:Case Reports in Obstetrics and Gynecology
Date:Jan 1, 2018
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