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Pancreatic enlargement in a patient receiving therapy with vasodilators for pulmonary arterial hypertension: a case report

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Epoprostenol is a prostacyclin (prostaglandin I2) analog that causes vasodilation and inhibits platelet aggregation and is used in the management of severe pulmonary arterial hypertension (PAH). We herein report a patient with PAH who developed pancreatic enlargement after the initiation of therapy including epoprostenol. Although it is well known that thyroid enlargement occurs in patients with PAH receiving epoprostenol therapy, the pancreatic findings associated with epoprostenol therapy have not been well described. Although the size of the pancreas was clearly increased, there was no blood data or symptoms suggestive of abnormal pancreatic function and pancreatitis, and the patient’s abdominal complaints improved quickly, despite the continuation of epoprostenol therapy. Eleven months after the start of continuous intravenous epoprostenol infusion therapy, the pancreatic enlargement was still evident on imaging, but there were no abdominal symptoms or elevated pancreatic enzymes. This case highlights the fact that epoprostenol therapy may cause pancreatic changes that mimic acute or autoimmune pancreatitis.

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  1. McLaughlin VV, McGoon MD (2006) Pulmonary arterial hypertension. Circulation 114:1417–1431

    Article  Google Scholar 

  2. Prins KW, Thenappan T (2016) World health organization group I pulmonary hypertension: Epidemiology and pathophysiology. Cardiol Clin 34:363–374

    Article  Google Scholar 

  3. Galiè N, Humbert M, Vachiery J-L, et al (2015) 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Respir J 46:903–975

    Article  Google Scholar 

  4. Fukuda K, Date H, Doi S, et al (2019) Guidelines for the Treatment of Pulmonary Hypertension (JCS 2017/JPCPHS 2017). Circ J 83:842–945

    Article  Google Scholar 

  5. Barst RJ, Rubin LJ, Long WA, et al (1996) A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. N Engl J Med 334:296–301

    Article  CAS  Google Scholar 

  6. Chadha C, Pritzker M, Mariash CN (2009) Effect of epoprostenol on the thyroid gland: enlargement and secretion of thyroid hormone. Endocr Pract 15:116–121

    Article  Google Scholar 

  7. Satoh M, Aso K, Nakayama T, Saji T (2017) Effect of treatment with epoprostenol and endothelin receptor antagonists on the development of thyrotoxicosis in patients with pulmonary arterial hypertension. Endocr J 64:1173–1180

    Article  CAS  Google Scholar 

  8. Menon AA, Sahay S, Braverman LE, Farber HW (2019) Thyroid Dysfunction in Patients with Pulmonary Artery Hypertension (PAH): The Effect of Therapies Affecting the Prostanoid Pathway. Lung 197:761–768

    Article  CAS  Google Scholar 

  9. Saisho Y, Butler AE, Meier JJ, et al (2007) Pancreas volumes in humans from birth to age one hundred taking into account sex, obesity, and presence of type-2 diabetes. Clin Anat 20:933–942

    Article  CAS  Google Scholar 

  10. Shirai Y, Tamura Y, Yasuoka H, et al (2014) IgG4-related disease in pulmonary arterial hypertension on long-term epoprostenol treatment. Eur Respir J 43:1516–1519

    Article  Google Scholar 

  11. Majed BH, Khalil RA (2012) Molecular mechanisms regulating the vascular prostacyclin pathways and their adaptation during pregnancy and in the newborn. Pharmacol Rev 64:540–582

    Article  CAS  Google Scholar 

  12. Beswick IP, Pirola RC, Bouchier IA (1971) The cause of pancreatic enlargement in rats fed raw soybean. Br J Exp Pathol 52:252–255

    CAS  PubMed  PubMed Central  Google Scholar 

  13. Kato M, Ohkuma S, Kataoka K, et al (1994) Mechanisms for pancreatic hypertrophy induced by long-term administration of bethanechol. Eur J Pharmacol (Environ Toxicol Pharmacol Sect) 292:47–55

    Article  CAS  Google Scholar 

  14. Homma T, Malik KU (1982) Effect of prostaglandins on pancreatic circulation in anesthetized dogs. J Pharmacol Exp Ther 222:623–628

    CAS  PubMed  Google Scholar 

  15. Dolenšek J, Pohorec V, Rupnik MS, Stožer A (2017) Pancreas Physiology. In: Seicean A (ed) Challenges in Pancreatic Pathology. IntechOpen, Rijeka

  16. Glasbrenner B, Adler G (1993) Pathophysiology of acute pancreatitis. Hepatogastroenterology 40:517–521

    CAS  PubMed  Google Scholar 

  17. Zhang X-M, Feng Z-S, Zhao Q-H, et al (2006) Acute interstitial edematous pancreatitis: Findings on non-enhanced MR imaging. World J Gastroenterol 12:5859–5865

    Article  Google Scholar 

  18. Notohara Kenji ZL (2013) Histology of autoimmune pancreatitis. The Pancreapedia: Exocrine Pancreas Knowledge Base

  19. Takahashi M, Fujinaga Y, Notohara K, et al (2020) Diagnostic imaging guide for autoimmune pancreatitis. Jpn J Radiol 38:591–612

    Article  Google Scholar 

  20. Kamisawa T, Takuma K, Anjiki H, et al (2010) Differentiation of autoimmune pancreatitis from pancreatic cancer by diffusion-weighted MRI. Am J Gastroenterol 105:1870–1875

    Article  Google Scholar 

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We thank Kelly Zammit, BVSc, from Edanz ( for editing a draft of this manuscript.


This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

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Correspondence to Yuko Someya.

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Someya, Y., Koyasu, S., Ohnishi, Y. et al. Pancreatic enlargement in a patient receiving therapy with vasodilators for pulmonary arterial hypertension: a case report. Abdom Radiol 47, 1948–1953 (2022).

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