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Acute Pancreatitis as an Initial Presentation of Primary Hyperparathyroidism
Background: Acute pancreatitis secondary to hypercalcemia is may be the initial presentation of a patient with primary hyperparathyroidism. However, because of its infrequency as a cause of pancreatitis, it can be easily missed during clinical management. Clinical Case: A 56-year old woman initially...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8089631/ http://dx.doi.org/10.1210/jendso/bvab048.363 |
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author | Yamane Laforteza, Alexis Roberto Villa, Michael Lim |
author_facet | Yamane Laforteza, Alexis Roberto Villa, Michael Lim |
author_sort | Yamane Laforteza, Alexis Roberto |
collection | PubMed |
description | Background: Acute pancreatitis secondary to hypercalcemia is may be the initial presentation of a patient with primary hyperparathyroidism. However, because of its infrequency as a cause of pancreatitis, it can be easily missed during clinical management. Clinical Case: A 56-year old woman initially presented with epigastric pain with radiation to the back. She had no previous comorbidities, did not drink alcohol, and had no previous history of cholelithiasis, nephrolithiasis nor pathologic fractures. The diagnosis was confirmed by an elevated serum lipase level (59117 U/L, reference interval (RI): 73–393 U/L) and contrast-enhanced MRI findings suggestive of acute pancreatitis with hemorrhagic component in the pancreatic body and tail. Hypercalcemia was documented on two separate occasions during her confinement with a serum total calcium level of 10.5 mg/dL (RI: 8.5–10.1 mg/dL) and an ionized calcium level of 1.45 mmol/L (RI: 1.09–130 mmol/L), however, no further workup was done at that time. She was managed conservatively and was sent home with plans to do an ERCP and possible laparoscopic cholecystectomy once her condition had stabilized. However, she had recurrence of the epigastric pain about one month after her initial episode. Her serum lipase showed an interval increase from her last result (1426 U/L from 933 U/L) and contrast-MRI now showed the development of areas of walled-off necrosis in the body and tail of the pancreas. Serum ionized calcium was again elevated (2.17 mmol/L); she also had an elevated intact PTH level (780.6 pg/ml, RI: 18.5–88.0 pg/ml). Parathyroid SPECT-CT showed a sestamibi-avid lesion inferoposterior to the right thyroid lobe, indicating a probable parathyroid adenoma. She was given 1 dose of Denusomab 120 mg subcutaneously and started on Calcitonin nasal spray 200 IU twice a day. She underwent ultrasound-guided drainage of the pancreatic necrosis and was subsequently discharged. Due to difficulty in procurement of the Calcitonin nasal spray, she was maintained on Cinacalcet 30 mg/tablet, 1 tablet once a day upon discharge with plans to undergo parathyroidectomy once she was had fully recovered from her pancreatitis. Conclusion: Primary hyperparathyroidism should always be considered when hypercalcemia is noted during the clinical management of acute pancreatitis. Reference: Misgar RA, Bhat MH, Rather TA, Masoodi SR, Wani AI, Bashir MI, Wani MA, Malik AA. Primary hyperparathyroidism and pancreatitis. J Endocrinol Invest. 2020 Oct;43(10):1493–1498. |
format | Online Article Text |
id | pubmed-8089631 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-80896312021-05-06 Acute Pancreatitis as an Initial Presentation of Primary Hyperparathyroidism Yamane Laforteza, Alexis Roberto Villa, Michael Lim J Endocr Soc Bone and Mineral Metabolism Background: Acute pancreatitis secondary to hypercalcemia is may be the initial presentation of a patient with primary hyperparathyroidism. However, because of its infrequency as a cause of pancreatitis, it can be easily missed during clinical management. Clinical Case: A 56-year old woman initially presented with epigastric pain with radiation to the back. She had no previous comorbidities, did not drink alcohol, and had no previous history of cholelithiasis, nephrolithiasis nor pathologic fractures. The diagnosis was confirmed by an elevated serum lipase level (59117 U/L, reference interval (RI): 73–393 U/L) and contrast-enhanced MRI findings suggestive of acute pancreatitis with hemorrhagic component in the pancreatic body and tail. Hypercalcemia was documented on two separate occasions during her confinement with a serum total calcium level of 10.5 mg/dL (RI: 8.5–10.1 mg/dL) and an ionized calcium level of 1.45 mmol/L (RI: 1.09–130 mmol/L), however, no further workup was done at that time. She was managed conservatively and was sent home with plans to do an ERCP and possible laparoscopic cholecystectomy once her condition had stabilized. However, she had recurrence of the epigastric pain about one month after her initial episode. Her serum lipase showed an interval increase from her last result (1426 U/L from 933 U/L) and contrast-MRI now showed the development of areas of walled-off necrosis in the body and tail of the pancreas. Serum ionized calcium was again elevated (2.17 mmol/L); she also had an elevated intact PTH level (780.6 pg/ml, RI: 18.5–88.0 pg/ml). Parathyroid SPECT-CT showed a sestamibi-avid lesion inferoposterior to the right thyroid lobe, indicating a probable parathyroid adenoma. She was given 1 dose of Denusomab 120 mg subcutaneously and started on Calcitonin nasal spray 200 IU twice a day. She underwent ultrasound-guided drainage of the pancreatic necrosis and was subsequently discharged. Due to difficulty in procurement of the Calcitonin nasal spray, she was maintained on Cinacalcet 30 mg/tablet, 1 tablet once a day upon discharge with plans to undergo parathyroidectomy once she was had fully recovered from her pancreatitis. Conclusion: Primary hyperparathyroidism should always be considered when hypercalcemia is noted during the clinical management of acute pancreatitis. Reference: Misgar RA, Bhat MH, Rather TA, Masoodi SR, Wani AI, Bashir MI, Wani MA, Malik AA. Primary hyperparathyroidism and pancreatitis. J Endocrinol Invest. 2020 Oct;43(10):1493–1498. Oxford University Press 2021-05-03 /pmc/articles/PMC8089631/ http://dx.doi.org/10.1210/jendso/bvab048.363 Text en © The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Bone and Mineral Metabolism Yamane Laforteza, Alexis Roberto Villa, Michael Lim Acute Pancreatitis as an Initial Presentation of Primary Hyperparathyroidism |
title | Acute Pancreatitis as an Initial Presentation of Primary Hyperparathyroidism |
title_full | Acute Pancreatitis as an Initial Presentation of Primary Hyperparathyroidism |
title_fullStr | Acute Pancreatitis as an Initial Presentation of Primary Hyperparathyroidism |
title_full_unstemmed | Acute Pancreatitis as an Initial Presentation of Primary Hyperparathyroidism |
title_short | Acute Pancreatitis as an Initial Presentation of Primary Hyperparathyroidism |
title_sort | acute pancreatitis as an initial presentation of primary hyperparathyroidism |
topic | Bone and Mineral Metabolism |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8089631/ http://dx.doi.org/10.1210/jendso/bvab048.363 |
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