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Table of Contents
CASE REPORT
Year : 2020  |  Volume : 17  |  Issue : 2  |  Page : 105-107

Hypertriglyceridemia-induced pancreatitis in pregnancy and its management issues: A case-based study


1 Elite Endocrinology and Diabetes Super Specialty Clinic, Secunderabad, Telangana, India
2 Department of Endocrinology, Krishna Institute of Medical Sciences, Secunderabad, Telangana, India
3 Department of Biochemistry, Maheshwara Medical College, Patancheru, Hyderabad, Telangana, India
4 Department of Gastroenterology, Krishna Institute of Medical Sciences, Kondapur, Hyderabad, Telangana, India

Date of Submission25-Mar-2020
Date of Acceptance16-Apr-2020
Date of Web Publication18-Jun-2020

Correspondence Address:
Babul Reddy Hanmayyagari
Flat No. A 904, Sri Sairam Towers, Hafeezpet, Hyderabad - 500 049, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/am.am_18_20

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  Abstract 


Hyperlipidemia in pregnancy has grave complications; lipid levels in pregnancy are influenced by genetic and hormonal factors, primarily due to estrogen. Here, we present a case of acute pancreatitis with hypertriglyceridemia presenting during the second trimester of pregnancy. We also discuss the management issues of this entity during pregnancy.

Keywords: Hypertriglyceridemia, pancreatitis, pregnancy


How to cite this article:
Hanmayyagari BR, Wadwa J, Guntaka M, Krishna B. Hypertriglyceridemia-induced pancreatitis in pregnancy and its management issues: A case-based study. Apollo Med 2020;17:105-7

How to cite this URL:
Hanmayyagari BR, Wadwa J, Guntaka M, Krishna B. Hypertriglyceridemia-induced pancreatitis in pregnancy and its management issues: A case-based study. Apollo Med [serial online] 2020 [cited 2020 Jul 11];17:105-7. Available from: http://www.apollomedicine.org/text.asp?2020/17/2/105/287081




  Introduction Top


Serum lipid levels during pregnancy are influenced by genetic and environmental factors further modulated by estrogen. Undiagnosed and untreated hyperlipidemia in pregnancy can have grave complications. Physiological changes in lipid metabolism during pregnancy are caused by several hormones, predominantly due to estrogen. The mechanism to explain the increase in cholesterol during pregnancy is thought to be secondary to increased cholesterol synthesis in the liver under the influence of estrogen.[1] Cholesterol synthesis upregulation during pregnancy may be attributable to an increased need for sex steroid production and to possibly help to maintain adequate nutrition for the mother and fetus.[2] Serum cholesterol levels can increase by as much as 25%–50%, and triglyceride (TG) levels can double during the third trimester of pregnancy. In addition, the levels of low-density lipoprotein (LDL) and very-low-density lipoproteins (VLDL) increase from thefirst to the third trimester; the levels of high-density lipoproteins (HDL) increase only during thefirst half of the pregnancy.[3] Here, we present a case of acute pancreatitis with hypertriglyceridemia (HTG) presenting during the second trimester of pregnancy.


  Case Report Top


A 28-year-old female patient with 25 weeks of gestational age presented to the emergency department with complaints of acute pain abdomen and vomiting for 1 day. She also complained of difficulty in breathing. There was no history of fever, jaundice, cough, and expectoration. There was not a known diabetic, hypertensive, or hypothyroidism in the past. There was no family history of dyslipidemia or premature coronary artery disease. There was a history of previous one miscarriage at 42 days, 1 year back. During the present pregnancy, she had conceived followingin vitro fertilization treatment with twin pregnancy with a history of single fetal demise during thefirst trimester. On examination, she was tachypneic and appeared dehydrated with a heart rate of 120/min, and her blood pressure was 100/70 mmHg with a respiratory rate of 28/min. On examination, she has no eruptive xanthomas. She has distended abdomen due to gravid uterus with 24-week fundal height. Systemic examination was otherwise normal. On investigation, glucometer random blood sugar on presentation was 212 mg% and urine ketones 3+, and arterial blood gas (ABG) analysis showed pH of 7.26, HCO3 of 16, pCO2 of 32, and lactate of 1mmol/L. Serum beta-hydroxybutyric acid was 2.11 mmol/L. HbA1c was found to be 5.7%. Her lipid profile showed that total cholesterol was 495 mg/dL, LDL: 175 mg/dL, VLDL: 280 mg/dL, HDL: 40 mg/dL, and TGs: 1400 mg/dL. Her amylase and lipase were found to be elevated. Ultrasound of the abdomen confirmed the presence of pancreatitis with mild gallbladder sludge. There was no evidence of necrosis or peripancreatic collection. Single live fetus of 24-week size in cephalic position was noted.

Since her serum lactic acid was found to be normal, the reason for acidosis was thought of possibly as euglycemic ketoacidosis or starvation ketoacidosis. Serum beta-hydroxybutyrate levels of 2.11 favored the presence of latter. She was kept nil by mouth (NBM) and initially managed with insulin infusion with dextrose. Her blood sugars ranged between 140 and 170 mg%. Serum TGs were repeated on the next day which showed consistently elevated value of 1400mg%. Despite normal sugars and lactate, her ABG done on the next day showed worsening of acidosis pH 7.22 and HCO3 was 14 meq/L. She had continuous pain in the abdomen which was managed with epidural anesthesia. The patient was managed initially with NBM for pancreatitis, but in view of her pregnancy status and worsening ABG, it was decided to start her on total parenteral nutrition. Insulin infusion was being continued. For elevated TGs, she was being started on tablet gemfibrozil 300 mg twice daily with omega-3 fatty acids 1000 mg/day for rapid lowering of TGs. Her TG levels reduced to 849 mg% by the next day, reaching 545 mg% by the 5th day. The patient was diagnosed to have gestational diabetes mellitus with dyslipidemia, with treatment her acidosis gradually resolved by the 3rd day and she was switched to subcutaneous insulin. The patient was discharged after 12 days of hospitalization.

The patient was followed up regularly until delivery, with insulin for her diabetes and gemfibrozil 300 mg twice a day along with omega-3 fatty acids 1000 mg/day. She delivered a baby boy with 2.8 kg birth weight at 38 weeks of gestation through cesarean section. In the postpartum period, the patient was advised to continue anti lipid medication and to stop insulin, as blood sugars were normalized. She returned at 3 months of postpartum period where her 75 g glucose tolerance test values were fasting sugar of 120mg/dl and 2 h postglucose of 204 mg/dl with a total cholesterol of 190 mg/dl, TGs of 220 mg/dl, and LDL of 128 mg/dl; she could not feed her baby at this time because of insufficient breast milk. She was doing well at follow-up with metformin 500 mg twice a day and saroglitazar 4 mg/day with optimal control of both diabetes and lipids.


  Discussion Top


Hypertriglyceridemia can be of primary or secondary subtypes. Primary HTG may result due to the deficiency of inactivity of LPL or Apo-CII. It is usually seen in childhood with high fasting TG levels (often >1000 mg/dL), hepatosplenomegaly, lipemia retinalis, and eruptive xanthomas with recurrent episodes of pain in the abdomen due to pancreatitis. Secondary causes of HTG usually include obesity, alcohol, Type 2 Diabetes, antiretroviral drugs, corticosteroids, tamoxifen, estrogens, and pregnancy. Mild-to-moderate HTG acts as a risk factor for premature cardiovascular disease, while severe HTG is predominantly a risk factor for pancreatitis.[4] The National Cholesterol Education Program (NCEP) Adult Treatment Panel III) and the Endocrine Society 2010 proposed criteria for the clinical diagnosis of elevated TG levels under fasting conditions.[5]

Normally, dietary TGs are hydrolyzed by lipases within intestinal lumen and emulsified with bile acids to form micelles. Long chain fatty acids (>12 carbon) are incorporated into TGs and packaged with apoB48, cholesteryl, and retinyl esters with phospholipids to form chylomicrons. These are delivered through the thoracic duct into the systemic circulation, where they are hydrolyzed by lipoprotein lipase (LPL) attached to the endothelial surfaces of capillaries. LPL is present in the adipose tissue, heart, and skeletal muscle. Apo-CII is required as a cofactor in this enzymatic reaction. The released free fatty acids are taken up by myocytes or adipocytes and either oxidized or re-esterified to form TG. The removal of chylomicron remnants by the liver is mediated by apoE.

During pregnancy, in thefirst two trimesters, the effect of the hormonal changes is to direct lipids toward storage depots for use in later gestation. In the third trimester, estrogen stimulates the production of hepatic VLDL, reduces removal of TG by LPL in the liver and adipose tissue, and reduces postheparin lipolytic activity. During the third trimester of pregnancy, plasma TG levels normally rise to as much as threefold,[6] but this physiologic TG increase has little clinical consequence. Marked TG increase may result, however, when LPL activity is genetically compromised. HTG during pregnancy poses complications, namely acute pancreatitis, hyper viscosity syndrome, and possibly preeclampsia.[7] The risk for pancreatitis is highly increased when fasting TG >1000 mg/dL, the level at which chylomicrons are present in the blood. These particles are thought to obstruct capillaries producing local ischemia. This can activate pancreatic lipases which, in turn, may cause the degradation of TG. TG-induced pancreatitis can be preceded by episodic nausea and epigastric pain, during which serum amylase may not exceed common diagnostic cutoffs.

Management of hyperlipidemia during pregnancy needs involvement of multidisciplinary approach, with collaboration between the obstetric, endocrinology, and specialist dietician teams. The NCEP advises a carbohydrate intake of 55%–60% and a protein intake of 15%–20% of daily dietary intake, whereas total and saturated fat should not surpass 30% and 7%, respectively.[7] Plasma TG response to diet and weight loss is about 25%,[8] with a marked variation among patients.[9] Daily consumption of 4 g of omega-3 fatty acids, along with restricted energy and saturated-fat intakes, can reduce plasma TG levels by as much as 20%. However, omega-3 fatty acids are rarely effective when used as the sole TG-lowering therapy. Fibrates are the drug of choice for patients with HTG, but safety in pregnancy is not known. Nevertheless, no teratogenic effects have been observed in the various case reports mentioned so far with gemfibrozil.[10] Therapeutic plasma exchange has also been reported as a treatment option for HTG in pregnancy with no untoward effects reported.[11] Pancreatitis is a rare but potentially lethal complication of HTG and poses a serious threat to the mother and fetus during pregnancy.[12] Early intervention for HTG may prevent this deadly complication during pregnancy. Limitation in this case report was we could not carried out genetic analysis in this patient.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Amundsen AL, Khoury J, Iversen PO, Bergei C, Ose L, Tonstad S, et al. Marked changes in plasma lipids and lipoproteins during pregnancy in women with familial hypercholesterolemia. Atherosclerosis 2006;189:451-7.  Back to cited text no. 1
    
2.
Kusters DM, Homsma SJ, Hutten BA, Twickler MT, Avis HJ, van der Post JA, et al. Dilemmas in treatment of women with familial hypercholesterolaemia during pregnancy. Neth J Med 2010;68:299-303.  Back to cited text no. 2
    
3.
Knopp RH, Bergelin RO, Wahl PW, Walden CE, Chapman M, Irvine S. Population-based lipoprotein lipid reference values for pregnant women compared to non-pregnant women classified by sex hormone usage. Am J Obstet Gynecol 1982;143:626-37.  Back to cited text no. 3
    
4.
Berglund L, Brunzell JD, Goldberg AC, Goldberg IJ, Sacks F, Murad MH, et al. Evaluation and treatment of hypertriglyceridemia: An endocrine society clinical practice guideline. J Clin Endocrinol Metab 2012;97:2969-89.  Back to cited text no. 4
    
5.
National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third Report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel iii) final report. Circulation 2002;106:3143-421.  Back to cited text no. 5
    
6.
Warth MR, Arky RA, Knopp RH. Lipid metabolism in pregnancy. II. Altered lipid composition in intermediage, very low, low and high-density lipoprotein fractions. J Clin Endocrinol Metab 1975;41:649-55.  Back to cited text no. 6
    
7.
Ray JG, Diamond P, Singh G, Bell CM. Brief overview of maternal triglycerides as a risk factor for pre-eclampsia. BJOG 2006;113:379-86.  Back to cited text no. 7
    
8.
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA 2001;285:2486-97.  Back to cited text no. 8
    
9.
Gerhard GT, Ahmann A, Meeuws K, McMurry MP, Duell PB, Connor WE. Effects of a low-fat diet compared with those of a high-monounsaturated fat diet on body weight, plasma lipids and lipoproteins, and glycemic control in type 2 diabetes. Am J Clin Nutr 2004;80:668-73.  Back to cited text no. 9
    
10.
Goldberg AS, Hegele RA. Severe hypertriglyceridemia in pregnancy. J Clin Endocrinol Metab 2012;97:2589-96.  Back to cited text no. 10
    
11.
Sivakumaran P, Tabak SW, Gregory K, Pepkowitz SH, Klapper EB. Management of familial hypertriglyceridemia during pregnancy with plasma exchange. J Clin Apher 2009;24:42-6.  Back to cited text no. 11
    
12.
Hsia SH, Connelly PW, Hegele RA. Successful outcome in severe pregnancy-associated hyperlipemia: A case report and literature review. Am J Med Sci 1995;309:213-8.  Back to cited text no. 12
    




 

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