Acute Pancreatitis In Pregnancy Research Articles

Recurrent Acute Pancreatitis in Pregnancy Caused by Parathyroid Hyperplasia: A Case Report and Literature Review

Background: Hypercalcemia during pregnancy leads to multiple maternal and fetal complications. To date, fewer than 30 cases of primary hyperparathyroidism (PHPT)-induced pancreatitis have been diagnosed during pregnancy. Most cases have been caused by a parathyroid adenoma. In the present report, the author described the first case of PHPT due to parathyroid hyperplasia presented with recurrent, acute pancreatitis during pregnancy. Case Report: A 38-year-old female, with a history of acute pancreatitis during her first pregnancy, presented with severe epigastric pain, nausea, and vomiting for three days at 24 weeks of gestation. Parathyroid-dependent, hypercalcemia-induced recurrence of pancreatitis was diagnosed based on the clinical presentation and laboratory investigations. An ultrasound on her neck revealed a possible parathyroid adenoma located on the inferior pole of the left thyroid gland. She underwent an uneventful left-lower parathyroidectomy. The pathological examination revealed parathyroid hyperplasia. Her serum calcium and parathyroid hormone levels returned to normal after surgery. She delivered a healthy male newborn at gestational age 38 weeks without any complications. Conclusion: PHPT-induced acute pancreatitis during pregnancy is rare. Hypercalcemia, involving both total and ionized calcium, should be investigated in pregnant women who present with acute pancreatitis. Early diagnosis and appropriate management can significantly improve the maternal, fetal, and pregnancy outcomes. Keywords: Hypercalcemia, Recurrent pancreatitis, Pregnancy, Primary hyperparathyroidism, Parathyroid hyperplasia

Acute Pancreatitis in Pregnancy: Three Case Reports

Acute pancreatitis is a rare condition during pregnancy, with peculiar specificities and particular findings. We report a series of 03 cases of pregnant women, treated for acute pancreatitis from 2016 to 2020. Their average age was 34.33 years and the diagnosis was based on clinical-biological clues: epigastric pain with strong elevation of lipasemia. Biliary etiology was confirmed in all patients initially by ultrasounds. Two patients had benign pancreatitis of favorable evolution. The third patient presented with a clinically severe pancreatitis and systemic inflammatory response syndrome, multiple organ failure syndrome with maternal and fetal deaths. Treatment was mainly symptomatic (medical), followed by cholecystectomy after delivery. Acute pancreatitis during pregnancy is a real threat for both the maternal and fetal prognosis and is a differential diagnosis that must be kept in mind for prompt management.

The early predictive value of routine laboratory tests on the severity of acute pancreatitis patients in pregnancy: a retrospective study

Acute pancreatitis in pregnancy (APIP) varies in severity from a self-limiting mild condition to a severe life-threatening condition, and its severity is significantly correlated with higher risks of maternal and foetal death. This study evaluated the early predictive value of routine laboratory tests on the severity of APIP patients. We enrolled 100 patients with APIP in West China Hospital. Initial routine laboratory tests, including the biochemistry and hematologic tests were collected within 48 hours after the onset of APIP. For predicting SAP in AP, LDH had the highest specificity of 0.879. RDW was a suitable predictive marker as it had the sensitivity of 0.882. Lower levels of triglycerides (<4.72 mmol/L) predicted mild AP of APIP, with an area under the curve (AUC) of 0.724, and a negative predictive value of 0.80. Furthermore, a risk score was calculated based on white blood cells, neutrophils, RDW, LMR and LDH, as an independent marker (adjusted odds ratio = 3.013, 95% CI 1.893 to 4.797, P < 0.001), with the highest AUC of 0.906, a sensitivity of 0.875 and a specificity of 0.828. In conclusion, the risk score we recommended was the powerful marker to aid in the early prediction of the severity of APIP patients.

Hypertriglyceridemia Induced Acute Pancreatitis in Pregnancy: A Case Report

Introduction: Acute pancreatitis is a rare event in pregnancy. Hypertriglyceridemia induced acute pancreatitis accounts for the second most common cause in pregnancy. This rare event has a high maternal and fetal mortality of 20% and 50% respectively. Case report: A 21-year-old woman, G2P0+1 at 26 weeks period of gestation presented to OBGYN emergency in a state of shock with history of sudden onset of severe epigastric pain and multiple episodes of vomiting for one day and absent fetal movement for six hours. Immediate fluid resuscitation was done. Her reports showed increased hematocrit, leukocytosis, serum lipase and amylase elevated to > 200U/L. Ultrasonography showed bulky pancreas with intrauterine fetal death. With the diagnosis of acute pancreatitis with fetal demise, she was managed conservatively in intensive care unit by fasting, nasogastric aspiration, intravenous fluids, antibiotics, analgesics and heparin. She was intubated on the third day for increasing tachypnea. Her lipid profile showed elevated triglyceride> 1000 mg/dl and was started on oral hypolipidemic drugs. Pregnancy was terminated vaginally by misoprostol and was discharged on 19th day. Conclusion: Hypertriglyceridemia induced acute pancreatitis in pregnancy has an increased maternal and fetal complication.

A Retrospective Cohort Study of Maternal and Fetal Outcomes in Pregnancies Complicated by Acute Pancreatitis [02N

INTRODUCTION: Acute pancreatitis is a rare condition that can be associated with significant complications. In pregnancy, pancreatitis can be linked with poor maternal and fetal outcomes. The objective of this study is to better understand the complications associated with acute pancreatitis (AP) in pregnancy. METHODS: A retrospective cohort study using the Healthcare Cost and Utilization Project – National Inpatient Sample from the United States was performed. All pregnant women admitted with AP were identified using International Classification of Disease-9 coding from 1999 to 2015. The maternal and neonatal outcomes among women diagnosed with AP in pregnancy were compared to women without acute pancreatitis who delivered using multivariate logistic regression adjusting for baseline maternal characteristics. RESULTS: There were 14,258 admissions for AP in pregnancy among 13,815,919 births in our study period for an overall incidence of 10.3 cases per 10,000 births. Women admitted with AP in pregnancy were more likely to require transfusions, OR 2.58 (95% CI 2.32–2.87), develop pre-eclampsia, 3.81 (3.33–4.36), deliver prematurely, 4.27 (3.83–4.77), develop venous thromboembolisms, 3.97 (3.30–4.78), develop acute respiratory failure, 21.99 (19.08–25.34), develop disseminated intravascular coagulation, 7.66 (5.48–10.69), and to suffer from maternal death, 9.15 (6.05–13.85) as compared to women without AP. Acute pancreatitis in pregnancy was also associated with an increased risk of intrauterine fetal demise, 2.60 (1.86–3.62). CONCLUSION: Acute pancreatitis in pregnancy is associated with severe maternal and newborn complications and thus should be managed in tertiary level centers capable of providing with adequate maternal care for this condition as well and appropriate fetal and premature neonatal care.

Naringin Attenuated Acute Lung Injury in Rat Model with Acute Pancreatitis in Pregnancy through Inactivation of p38 MAPK Pathway

Acute pancreatitis in pregnancy can cause fetal lung injury. Naringin exhibits ant-inflammation effect against pulmonary injuries. However, whether naringin can alleviate lung injury associated with acute pancreatitis in pregnancy has not been elucidated. Establishment of acute pancreatitis in pregnancy model by sodium taurocholate showed that sodium taurocholate induced obvious pathological changes in pancreas. Histopathological changes in lungs were also aggravated post sodium taurocholate treatment with enhanced inflammation of neutrophils, thickened alveolar walls and alveolus collapse. Diagnostic blood tests for acute pancreatitis in pregnancy indicated that serum amylase and lipase were increased post sodium taurocholate treatment. Sodium taurocholate-induced rats were intragastrically administered with naringin to investigate the protective effect of naringin on acute lung injury induced by acute pancreatitis in pregnancy. Results revealed that administration of naringin could attenuate pathological changes in pancreas and lungs and decrease amylase and lipase. Moreover, naringin treatment attenuated sodium taurocholate-induced increase in inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-6/1β in lungs. Sodium taurocholate-induced increase in phosphorylation of p38 was also reduced post naringin treatment. In conclusion, naringin could ameliorate acute lung injury and inflammation induced by acute pancreatitis in pregnancy by inhibiting the p38 pathway.

A Curious Case of Acute Pancreatitis in Pregnancy

Hypercalcaemia is rare in pregnancy and is under diagnosed owing to its non-specific presentation which is frequently attributed to the pregnancy itself. Severe hypercalcaemia presents a therapeutic challenge, especially during pregnancy. The present case of a 26-year-old primigravida who presented with acute pancreatitis is described here. The pancreatitis was found to be secondary to parathyroid adenoma- induced hypercalcaemia. After initial conservative medical management with subcutaneous and intranasal calcitonin, she underwent a small-incision adenoma excision. This unusual cause and presentation of hypercalcaemia and its management is reviewed thereof.

Acute pancreatitis in third trimester of pregnancy: A case report

Acute pancreatitis in third trimester of pregnancy: A case report - IJOGR- Print ISSN No: - 2394-2746 Online ISSN No:- 2394-2754 Article DOI No:- 10.18231/j.ijogr.2019.116, Indian Journal of Obstetrics and Gynecology Research-Indian J Obstet Gynecol Res

Acute pancreatitis in pregnancy – a case report and literature review

Acute pancreatitis in pregnancy – a case report and literature review

Challenges encountered in the management of gall stones induced pancreatitis in pregnancy.

Though uncommon, acute biliary pancreatitis in pregnancy carries a potential of serious and life threatening complications to mother and foetus. The management of acute pancreatitis in pregnancy is challenging due to the complexity of physiological and anatomical changes. This becomes even more challenging when invasive interventions are urgently needed. Therefore, there have been various debates among clinicians on the type and timing of these interventions. We systematically reviewed the evidences that looked into these debates to formulate a list of recommendations for clinical practice. An electronic literature search of the databases (Medline/Pubmed, EMBASE, Cochrane database, NICE guidelines and Google Scholar) using the keywords "pancreatitis, pancreatitis in pregnancy, biliary pancreatitis, laparoscopy in pregnancy, and gall stones in pregnancy" was conducted. The relevant studies were screened and full text versions were retrieved. The references to all the retrieved texts were searched for further relevant studies. All studies were systematically reviewed and critically analysed. The available published literature on management of gall stones induced acute pancreatitis in pregnancy was solely based on retrospective studies and case series. The management of biliary induced pancreatitis in pregnant patients is challenging and complex, and it should involve the input of highly skilled clinicians from different specialities. Each case should be individually and thoroughly assessed by weighing the risks against the benefits. The authors have formulated a list of recommendations for clinical practice that is based on this comprehensive review of the literature.

Continuous plasma filtration adsorption for treatment of acute pancreatitis in pregnancy: analysis of 18 cases

Continuous plasma filtration adsorption for treatment of acute pancreatitis in pregnancy: analysis of 18 cases

Hypertriglyceridemia induced acute pancreatitis in pregnancy: Learning experiences and challenges of a Case report

Hypertriglyceridemia induced acute pancreatitis in pregnancy: Learning experiences and challenges of a Case report

Inhibition of macrophage migration inhibitory factor attenuates inflammation and fetal kidney injury in a rat model of acute pancreatitis in pregnancy

Acute pancreatitis in pregnancy (APIP) is a severe disease during pregnancy that mostly occurs during the third trimester. It can lead to additional complications including preterm delivery and high fetal mortality. In this study, we investigated the protective effects of (S, R)-3-(4-hydroxyphenyl)-4, 5dihydro-5-isoxazole acetic methyl ester (ISO-1), an inhibitor of macrophage migration inhibitory factor (MIF), on fetal kidney injury associated with the maternal acute necrotizing pancreatitis (ANP) and its potential mechanisms in a rat model. The APIP rat model was induced by retrograde infusion of sodium taurocholate saline solution into biliopancreatic duct. ISO-1 was given by intraperitoneally injection 30 min before the model was induced. The levels of maternal serum amylase, lipase, tumor necrosis factor-α (TNF-α) and interleukins (IL)-1β were measured. Maternal pancreas and fetal kidney injury were evaluated, and the expressions of MIF, phospho-p38MAPK (p-p38), nuclear factor-κB (NF-κB), TNF-α, IL-1β in fetal kidneys were detected. The results showed that fetal rats exhibited obvious acute kidney injury during APIP, and pregnant rats pretreated with ISO-1 notably attenuated the lesions. ISO-1 also significantly reduced the expression of MIF and the activations of p38MAPK, NF-κB, as well as the levels of TNF-α and IL-1β. These results indicated that ISO-1 could attenuate fetal kidney injury in pregnant rats with ANP by inhibiting MIF mediated p38MAPK/NF-κB signal pathways to reduce inflammatory response.

Serum thyroid hormones levels are significantly decreased in pregnant rats with acute pancreatitis

Acute pancreatitis in pregnancy (APIP), which was thought to be a rare but severe disease, with a high perinatal mortality among maternal-fetuses. Our research aimed to study and assess thyroid injury in a rat model of APIP and its possible mechanisms. The APIP model was established by retrograde injection with sodium taurocholate. Sham-operated (SO) and APIP groups were performed at 3 time-points. Histological changes in the maternal thyroid and pancreas were assessed. The activities of serum amylase, lipase and levels of FT3, FT4, MDA, TNF-α and IL-1β were detected in maternal rats, and the expression of MIF, ICAM-1 and CD68 in the maternal thyroids were determined. In this study, maternal thyroid injury as well as pancreas injury occurred in a time-dependent manner. The activities of serum amylase, lipase and levels of MDA, TNF-α and IL-1β were markedly increased in acute pancreatitis rats, the levels of serum FT3 and FT4 were obviously decreased in APIP groups, and the expressions of MIF, ICAM-1 and CD68 were significantly increased in the thyroid of the APIP group. Ultrastructural thyroid injuries were observed in the APIP group. Our research suggests that thyroid injury is involved in the rat experimental model of APIP. The degree of thyroid dysfunction is associated with APIP, which may affect the prognosis of acute pancreatitis.

SB203580 attenuates acute lung injury and inflammation in rats with acute pancreatitis in pregnancy

Acute pancreatitis in pregnancy (APIP) can lead to multiple maternal and fetal organ injury and mitogen-activated protein kinase (MAPK) signaling pathway may be involved in it; however, whether APIP can result in acute lung injury and P38MAPK signaling pathway is involved in the pathogenesis has not been elucidated. The present study was undertaken to investigate the participation of P38MAPK signaling pathway and the protective effect of SB203580, an inhibitor of P38MAPK on acute lung injury induced by APIP. Twenty-four late-gestation SD rats were randomly assigned to four groups: Sham operation (SO) group, SB302580 (SB) group, APIP group, and SB + APIP group. All the rats were killed 6h after modeling. The severity of pancreatitis was evaluated by serum amylase (AMY) and lipase (LIPA) and histopathological changes. Histological assessment of the lung and inflammatory cell infiltration was performed by H&E and immunofluorescence assay. The lung wet/dry (W/D) weight ratio was determined, and the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 were detected by enzyme-linked immunosorbent assay (ELISA). Western blot analysis was used to detect the protein expression of phosphorylated and total P38, tumor necrosis factor (TNF)-α, and intercellular adhesion molecules 1 (ICAM-1) in lung tissues. Obvious pathological changes existed in pancreas and lung after the induction of APIP, and their pathological scores were significantly higher than that of control group. The results showed that the phosphorylation of P38MAPK was elevated in the lung of APIP rats. Compared with APIP group, the intervention of SB203580 alleviated the pathological injury of the pancreas and lungs, decreased serum AMY and LIPA, attenuated the secretion of TNF-α, IL-1β, and IL-6 in lung, reduced the inflammatory cells' infiltration and lung W/D ratio and inhibited the activation of P38MAPK signaling pathway. These results suggest that APIP can lead to acute lung injury and inflammation and SB203580 can inhibit the lung injury by inhibiting the P38MAPK signaling pathway and blocking the inflammatory responses.

Neutrophil-lymphocyte ratio, gamma-glutamyl transpeptidase, lipase, high-density lipoprotein as a panel of factors to predict acute pancreatitis in pregnancy.

Acute pancreatitis in pregnancy (APIP) is a rare but dangerous complication. APIP has common symptoms with acute abdomen. Assessment of an acute abdomen is more complicated during pregnancy because the gravid uterus could mask most of symptomatic signs. It has been a challenge to diagnose APIP by physical examination or diagnostic imaging. Case studies on APIP are also limited for analysis on the risk factors associated with the disease. This retrospective study evaluated a series of risk factors from a relatively substantial number of APIP cases to determine early predictors or prognosis markers for APIP.Fifty-nine APIP patients together with 179 random normal pregnant women in Shengjing Affiliated Hospital of China Medical University were included for this retrospective study. Medical parameters of blood test in biochemistry and hematology were compared between 2 groups using t test. Multivariate logistic regression analysis was performed to investigate the relationship between various factors and APIP using Statistical Applied Software (SAS student version).Compared with normal pregnant women, APIP patients have elevated values in alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen, creatinine, C-reactive protein, direct bilirubin, fibrin degradation products, gamma-glutamyl transpeptidase (GGT), glucose, lipase, pH and decreased values in albumin, fibrinogen, high-density lipoprotein (HDL), hemoglobin, low-density lipoprotein cholesterol (LDL-D), and total proteins from their blood tests. In addition, APIP patients have decreased numbers in red cells but increased numbers in white blood cells and increased ratio of neutrophil/lymphocyte (N/L). Among these factors, N/LR, GGT, lipase, and HDL are significantly associated with APIP. This study suggests that the combination of those factors serve as a panel of indicators for early-onset prognosis of APIP.GGT, lipase, HDL, and N/LR can serve as a panel of factors to predict APIP. More case studies are important to further evaluate the predicting power of this panel factors in APIP.

Macrophage migration inhibitory factor antagonist (S,R)3‑(4‑hydroxyphenyl)‑4,5‑dihydro‑5‑isoxazole acetic acid methyl ester attenuates inflammation and lung injury in rats with acute pancreatitis in pregnancy.

Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine involved in many acute and chronic inflammatory diseases. However, its role in acute lung injury associated with acute pancreatitis in pregnancy (APIP) has not yet been elucidated. The present study was undertaken to clarify the effect and potential mechanism of MIF antagonist (S,R)3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1) in the development of acute lung injury in rats with APIP. Eighteen late-gestation SD rats were randomly assigned to three groups: Sham operation (SO) group, APIP group, and ISO-1 group. All the rats were sacrificed 6 h after modeling. The severity of pancreatitis was evaluated by serum amylase (AMY), lipase (LIPA), tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 and assessing the histopathological score. Lung injury was determined by performing histology and inflammatory cell infiltration investigations. Western blot analysis was used to detect the protein expression of MIF, phosphorylated and total P38 and nuclear factor-κB (NF-κB) protein in lungs. The results showed that MIF was upregulated in the lung of APIP rats. Compared with APIP group, the intervention of ISO-1 alleviated the pathological injury of the pancreas and lungs, decreased serum AMY and LIPA, attenuated serum concentrations of TNF-α, IL-1β, and IL-6, reduced the number of MPO-positive cells in the lung and inhibited the activation of P38MAPK and NF-κB. These results suggest that MIF is activated in lung injury induced by APIP. Furhtermore, the present findings indicate that the MIF antagonist ISO-1 has a protective effect on lung injury and inflammation, which may be associated with deactivating the P38MAPK and NF-κB signaling pathway.

Differential JNK, p38 and ERK response to renal injury in a rat model of acute pancreatitis in pregnancy.

The objective of this study was to determine the mechanism of acute renal injury (ARI) in acute necrotizing pancreatitis in late pregnancy (ANPIP). Pregnant Sprague-Dawley rats in the third trimester were used for this study, and an ANPIP model was induced by injecting 5% sodium taurocholate into the biliary pancreatic duct. The rats were randomly divided into three groups: the normal, sham-operated (SO) and acute necrotizing pancreatitis (ANP) groups. Rats were killed at 3, 6, 12h after the operation, and blood, pancreatic and renal tissue samples were harvested. Differences were detected in the physiology, pathology and cellular and molecular responses among the different groups. Serum amylase, lipase, urea and Cr levels were increased in rats with ANPIP. Additionally, expression of phosphorylation p38 and JNK as well as TNF-α and NF-κB were increased in the renal tissues of rats with ANPIP. The expression of phosphorylation ERK was decreased in the renal tissues of rats with ANPIP. Mitogen-activated protein kinases may play an important role in renal injury in rat models of ANPIP.

Management of Gallstone-Induced Acute Pancreatitis in Pregnancy: A Tertiary-Center Experience.

Objectives:Gallbladder stones are the most frequently reported etiology of acute pancreatitis in pregnancy and are often diagnosed in the third trimester. This condition is associated with both mother and infant morbidity and mortality, and its treatment remains controversial.Methods:Relevant patient data between September 2010 and April 2017 from the Kanuni Sultan Suleyman Training and Research Hospital were analyzed regarding etiology (of gallstone pancreatitis), trimester of pregnancy, diagnostic tools, pancreatitis stage, clinical status, medical treatment, surgical interventions, and pregnancy status.Results:We included 68 patients recorded with acute pancreatitis due to biliary gallstones. Pancreatitis symptoms developed in most (n=38) (55.8%) patients during the third trimester. Of 24 patients who had their first episode of pancreatitis in the first trimester of pregnancy, 12 (50%) were readmitted due to recurrence. Seven (11.3%) patients whose Ranson scale score was 3 underwent computed tomography evaluation. The number of patients with acute cholecystitis with pancreatitis was 5 (7.3%), whereas the number of patients with choledocholithiasis was 4 (5.8%). Sphincterotomy with endoscopic retrograde cholangiopancreatography was performed in 2 (2.9%) patients. Laparoscopic cholecystectomy was performed in 9 (13.2%) patients during pregnancy. No fetal and maternal morbidity and mortality was found in all periods.Conclusion:Developments in supportive care, wide-spread use of imaging methods, and a multidisciplinary approach with better antenatal care of pregnant patients with acute pancreatitis can help prevent fetal and maternal morbidity and mortality in such cases. Early laparoscopic cholecystectomy should be considered especially in pregnant patients with acute pancreatitis due to gallstones in the first trimester.

Fetal liver injury ameliorated by migration inhibitory factor inhibition in a rat model of acute pancreatitis in pregnancy.

This study was designed to investigate and assess fetal liver injury in a rat model of acute pancreatitis in pregnancy (APIP) as well as its possible mechanisms and potential therapeutic targets. The APIP model was induced by sodium taurocholate in Sprague-Dawley rats during the third trimester. ISO-1, a macrophage migration inhibitory factor (MIF) antagonist, was given before the induction of APIP. In addition, sham-operated rats at later gestation were set as controls. Histological changes in the fetal liver and maternal pancreas were assessed. Amylase and lipase activity as well as the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1β were examined. The expression of MIF in fetal liver was determined by immunochemistry and the expression of NF-κB, IκBα, high mobility group box-1 protein (HMGB1), TNF-α, and IL-1β in fetal liver was determined by Western blot analysis. Ultrastructures of hepatic cells in fetal rats were observed under transmission electron microscopy. ISO-1 ameliorated the following: (i) pathological injuries in maternal pancreas and fetal liver; (ii) levels of TNF-α and IL-1β in maternal serum; and (iii) levels of MIF, myeloperoxidase, NF-κB, HMGB1, TNF-α, and IL-1β in fetal liver. Pathological damage and an inflammatory response in fetal liver were induced by APIP, and MIF inhibition ameliorated fetal liver injury by inhibiting the inflammatory cascade.