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A life-threatening duodenal ulcer hemorrhage due to previously unknown primary hyperparathyroidism

A life-threatening duodenal ulcer hemorrhage due to previously unknown primary hyperparathyroidism Peptic ulcer bleeding due to primary hyperparathyroidism is extremely rare. We report a case of a 42-year-old male with life-threatening acute upper gastrointestinal bleeding secondary to a duodenal ulcer and a history of kidney stones. Gastroscopic therapy, Billroth II gastrointestinal anastomosis and angiographic embolization were sequentially conducted to arrest the hemorrhage. A complete investigative work-up revealed that the duodenal ulcer bleeding was due to primary hyperparathyroidism coexisting with a parathyroid adenoma. Following this event, the patient developed a severe abdomi- nal cavity infection and sepsis. An elective parathyroidectomy was performed, and the histology was confirmed to be a typi- cal parathyroid adenoma. Postoperatively, the patient’s calcium and parathyroid levels were normalized. Attention should be paid to patients with an upper gastrointestinal ulcer, especially when it is accompanied by kidney stones. Key words: primary hyperparathyroidism; peptic ulcer hemorrhage; hypercalcemia threatening duodenal ulcer hemorrhage due to primary hyper- Introduction parathyroidism coexisting with a parathyroid adenoma. Upper gastrointestinal (UGI) bleeding is the most common com- plication of peptic ulcer disease. Helicobacter pylori infection and nonsteroidal anti-inflammatory drug administration are two Case Report independent risk factors for peptic ulcerbleeding. However, there are still some less common causes for UGI bleeding such A 42-year-old male presented to the emergency department as primary hyperparathyroidism (PHPT). Peptic ulcer disease is complaining of an upper abdomen paroxysmal cramp for one usually a manifestation of primary hyperparathyroidism [1–5], week. He had a five-year history of multiple kidney stones and although the complete pathophysiological mechanism has not had been consistently treated for these without any further yet been established [6–14]. However, only a few cases of peptic work-up. The patient was admitted to the Department of ulcer bleeding, due to primary hyperparathyroidism have been Urology Surgery with the suspicion of renal colic. On day two, reported [14–17]. In this article, we report the case of a life- he excreted a large amount of tarry stool accompanied by Submitted: 16 June 2016; Revised: 24 July 2016; Accepted: 1 August 2016 V C The Author(s) 2016. Published by Oxford University Press and Sixth Affiliated Hospital of Sun Yat-Sen University This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/ licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com Downloaded from https://academic.oup.com/gastro/article-abstract/6/3/231/2909372 by Ed 'DeepDyve' Gillespie user on 22 August 2018 232 | D. Xie et al. coffee-ground emesis. The patient’s blood pressure dropped, metabolic toxin products. On day 19, the patient underwent and he received a blood transfusion and rehydration. The pa- elective surgical exploration with excision of the parathyroid tient was then transferred to the Intensive Care Unit for further adenoma. Histology of the two parathyroid glands revealed a treatment. A bedside upper gastrointestinal endoscopy was per- typical parathyroid adenoma (Figure 3). formed, revealing a duodenal ulcer with an adherent clot that After surgery, the patient’s PTH level was normalized was freely oozing (Forrest-Ib, Figure 1). An intragastric local in- (6.29 pg/ml), and his calcium level decreased rapidly (2.24 mmol/ stillation of norepinephrine and epinephrine was administered l). On day 22, he was transferred to the general ward. Three to stop the bleeding. However, eight hours later, the patient months after parathyroidectomy, the patient’s PTH and calcium again excreted a large amount of tarry stools and vomited a co- levels were 74.97 pg/ml and 2.05 mmol/l, respectively. The se- pious amount of coffee-ground material. An emergent subtotal rum creatinine level also decreased to 175 mmol/L. At 8 months gastrectomy and Billroth II gastrointestinal anastomosis were follow-up, the patient’s PTH and calcium levels were 101.84 pg/ performed to arrest the bleeding. On day four, his heart rate be- ml and 2.17 mmol/l, respectively. The patient denied any diges- came rapid (132–144 beats per minute), his central venous pres- tive tract symptoms such as abdominal pain and diarrhea. sure dropped, his blood hemoglobin decreased, and his abdominal circumference increased. An ultrasound examina- Discussion tion detected a hematocele in the left upper quadrant. There was still active bleeding. Finally, gastroduodenal artery emboli- Primary hyperparathyroidismis a disorder in which the para- zation was carried out to stop the hemorrhage. thyroid gland inappropriately secretes high PTH levels, which During the process, we noted that the patient’s serum cal- leads to hypercalcinemia,, and kidney stone is a classical clini- cium level was elevated (2.98 mmol/L, normal range 2.03– cal symptom of primary hyperparathyroidism. Solitary parathy- 2.65 mmol/L) and that he had a low serum phosphorus level roid adenomas are responsible for primary (0.5 mmol/L, normal range 0.74–1.52 mmol/L), which is uncom- hyperparathyroidism in 80–85% of such cases. Definitive treat- mon in a patient with renal dysfunction (serum creatinine level ment is achieved by surgical resection. However, the disease was 286 mmol/L, normal range 31.8–116 mmol/L). His plasma has no specific symptoms. The diagnosis of PTPH is usually parathyroid hormone (PTH) level was found to be elevated in a made incidentally with an initial finding of hypercalcemia on subsequent test (468.67 pg/ml, normal range 12–65 pg/ml). A routine laboratory studies, which leads to further investigation. neck computed tomography (CT) scan with contrast showed In this report, the patient was initially managed for an upper two enhancing masses (larger mass size 10 9 mm) in the rear gastrointestinal hemorrhage. A high index of suspicion for hy- of the right lobe of his thyroid gland (Figure 2). To exclude mul- perparathyroidism developed when we noted an elevated se- tiple endocrine neoplasia I (MEN I) and Zollinger-Ellison syn- rum calcium level and a low serum phosphorus level, which are drome, CT imaging studies of the head and abdomen were abnormal in a renal failure patient. Upon further testing, the pa- performed and did not indicate any abnormalities. All of these tient’s plasma parathyroid hormone level was found to be ele- findings suggested a diagnosis of primary hyperparathyroidism. vated. A neck CT scan with contrast showed two solitary Unfortunately, in the next period, the patient developed se- parathyroid adenomas, which were subsequently managed sur- vere abdominal pain, tenderness, guarding and rebound pain gically and confirmed histologically. In some cases, primary hy- upon abdominal palpation. Heart rate was rapid (150–160 beats perparathyroidism is a manifestation of multiple endocrine per minute), and his leucocyte count in blood was high neoplasia I and usually occurs in combination with Zollinger- (18.57 10 /L). White blood cell count of the peritoneal drainage Ellison syndrome. Gastrointestinal bleeding is the initial presen- fluid was 111005 106. These signs indicated a severe abdomi- tation in a quarter of patients with Zollinger-Ellison syndrome nal cavity infection, peritonitis and sepsis. Intravenous antibi- [18]. In this case, CT imaging studies of the head and abdomen otics (imipenem 1 g every 8 hours; tigecycline 50 mg every did not exhibit any abnormalities of the pituitary gland or pan- 12 hours) were used to control infection. Additionally, the pa- creas. After excision of the parathyroid adenomas, the patient’s tient’s creatinine level increased to 560 mmol/L. Continuous re- nal replacement therapy (CRRT) was used to treat the hypercalcemia and remove the inflammatory mediators and Figure 1. Endoscopy demonstrated a duodenal ulcer bleeding. Figure 2. Two enhanced masses in the rear of the right lobe of thyroid gland. Downloaded from https://academic.oup.com/gastro/article-abstract/6/3/231/2909372 by Ed 'DeepDyve' Gillespie user on 22 August 2018 Hyperparathyroidism and peptic ulcer bleeding | 233 Figure 3. Histology of parathyroid gland. PTH and calcium levels normalized. No pancreatic tumor-like 7. Barreras RF. Calcium and gastric secretion. Gastroenterology symptoms such as diarrhea or hypokalemia were observed. 1973;64:1168–84. Additionally, no regular upper abdominal pain was observed. 8. Stremple JF and Watson CG. Serum calcium, serum gastrin, and gastric acid secretion before and after parathyroidec- These results support the diagnosis of primary hyperparathy- roidism caused by a parathyroid adenoma. tomy for hyperparathyroidism. Surgery 1974;75:841–52. Due to severe sepsis and renal dysfunction, CRRT was used 9. Patterson M, Wolma F, Drake A, et al. Gastric secretion and to remove inflammatory mediators and metabolic toxin prod- chronic hyperparathyroidism. Arch Surg 1969;99:9–14. 10. Wise SR, Quigley M, Saxe AW, et al. Hyperparathyroidism and ucts with the advantage of potentially avoiding the development of hypotension in a hemodynamically unstable and critically ill cellular mechanisms of gastric acid secretion. Surgery patient. It also decreased the serum calcium level to prevent a 1990;108:1058–63. calcium crisis. There are few case reports in the current litera- 11. Geibel JP, Wagner CA, Caroppo R, et al. The stomach divalent ion-sensing receptor scar is a modulator of gastric acid secre- ture documenting effective treatment of hypercalcemia with CRRT [20–22]. We considered CRRT to be a good therapeutic tion. J Biol Chem 2001;276:39549–52. choice for preventing a calcium crisis in this patient. 12. Corleto VD, Minisola S, Moretti A, et al. Prevalence and causes In conclusion, peptic ulcer bleeding due to primary hyper- of hypergastrinemia in primary hyperparathyroidism: a pro- parathyroidism is extremely rare. The serum calcium level and spective study. J Clin Endocrinol Metab 1999;84:4554–8. PTH level must be considered routine tests in patients with a 13. Do ¨ kmetas ¸ HS, Tu ¨ rkay C, Aydin C, et alet al. Prevalence of Helicobacter pylori in patients with primary hyperparathy- peptic ulcer, especially when it is accompanied by a history of kidney stones with hypercalcemia. Parathyroidectomy is rec- roidism. J Bone Miner Metab 2001;19:373–7. ommended in patients with primary hyperparathyroidism that 14. Sato H, Abe K, Oshima N, et al. Primary hyperparathyroidism are clinically symptomatic. The CRRT could be considered a with duodenal ulcer and H. pylori infection. Intern Med 2002;41:377–80. good therapy choice for preventing a calcium crisis in septic pa- tients with renal dysfunction. 15. Goretzki PE, Becker H, Dotzenrath C, et al. Acute abdomen in unrecognized hyperparathyroidism. Wien Klin Wochenschr 1988;100:373–5 16. Sarter S and Pier A. Forrest 1b duodenal hemorrhage in previ- Funding ously undiagnosed primary hyperparathyroidism. Zentralbl Supported by Science and Technology Planning Project of Chir 1996;121:869–71 Guangdong Province, China (2014A020212715) 17. Sawa TE and Safar SB. Pathological fracture: a common pre- sentation of primary hyperparathyroidism in Iraq. Eur J Surg Conflicts of interest statement: none declared. 1996:162:777–81. 18. Roy PK, Venzon DJ, Shojamanesh H, et al. Zollinger-Ellison References syndrome. Clinical presentation in 261 patients. Medicine (Baltimore) 2000;79:379–411. 1. Gasparoni P, Caroli A, Sardeo G, et al. Primary hyperparathy- 19. Silverberg SJ, Shane E, Jacobs TP, et al. A 10-year prospective roidism and peptic ulcer. Minerva Med 1989;80:1327–30. study of primary hyperparathyroidism with or without para- 2. Clark CG, Chowcat NL, Lewin MR, et al. Surgery for peptic ul- thyroid surgery. N Engl J Med 1999;341:1249–55. ceration associated with hypergastrinaemia. Br J Surg 20. Sramek  V, Novak  I, Matejovic  M, et al. Continuous venove- 1986;73:248–52. nous hemodiafiltration (CVVHDF) with citrate anticoagula- 3. Corlew DS, Bryda SL,2Bradley EL 3rd, et alet al. Observations tion in the treatment of a patient with acute renal failure, on the course of untreated primary hyperparathyroidism. hypercalcemia, and thrombocytopenia. Intensive Care Med Surgery 1985;98:1064–71. 1998;24:262–4. 4. Mowat E, Gunn A, Paterson CR. Hyperparathyroidism in pep- 21. Kindgen-Milles D, Kram R, Kleinekofort W, et al. Treatment of tic ulcer patients. Br J Surg 1981;68:455–8. severe hypercalcemia using continuous renal replacement 5. Gardner EC Jr and Hersh T. Primary hyperparathyroidism and therapy with regional citrate anticoagulation. ASAIO J the gastrointestinal tract. South Med J 1981;74:197–9. 2008;54:442–4. 6. Reeder DD, Jackson BM, Ban J, et al. Influence of hypercalce- 22. Au S, Dunham M, Godinez T. Treatment of medically refrac- mia on gastric secretion and serum gastrin concentrations in tory hypercalcemic crisis. Int J Artif Organs 2012;35:538–41. man. Ann Surg 1970;172:540–6. Downloaded from https://academic.oup.com/gastro/article-abstract/6/3/231/2909372 by Ed 'DeepDyve' Gillespie user on 22 August 2018 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Gastroenterology Report Oxford University Press

A life-threatening duodenal ulcer hemorrhage due to previously unknown primary hyperparathyroidism

Gastroenterology Report , Volume 6 (3) – Aug 1, 2018
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Oxford University Press
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© The Author(s) 2016. Published by Oxford University Press and Sixth Affiliated Hospital of Sun Yat-Sen University
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10.1093/gastro/gow029
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Abstract

Peptic ulcer bleeding due to primary hyperparathyroidism is extremely rare. We report a case of a 42-year-old male with life-threatening acute upper gastrointestinal bleeding secondary to a duodenal ulcer and a history of kidney stones. Gastroscopic therapy, Billroth II gastrointestinal anastomosis and angiographic embolization were sequentially conducted to arrest the hemorrhage. A complete investigative work-up revealed that the duodenal ulcer bleeding was due to primary hyperparathyroidism coexisting with a parathyroid adenoma. Following this event, the patient developed a severe abdomi- nal cavity infection and sepsis. An elective parathyroidectomy was performed, and the histology was confirmed to be a typi- cal parathyroid adenoma. Postoperatively, the patient’s calcium and parathyroid levels were normalized. Attention should be paid to patients with an upper gastrointestinal ulcer, especially when it is accompanied by kidney stones. Key words: primary hyperparathyroidism; peptic ulcer hemorrhage; hypercalcemia threatening duodenal ulcer hemorrhage due to primary hyper- Introduction parathyroidism coexisting with a parathyroid adenoma. Upper gastrointestinal (UGI) bleeding is the most common com- plication of peptic ulcer disease. Helicobacter pylori infection and nonsteroidal anti-inflammatory drug administration are two Case Report independent risk factors for peptic ulcerbleeding. However, there are still some less common causes for UGI bleeding such A 42-year-old male presented to the emergency department as primary hyperparathyroidism (PHPT). Peptic ulcer disease is complaining of an upper abdomen paroxysmal cramp for one usually a manifestation of primary hyperparathyroidism [1–5], week. He had a five-year history of multiple kidney stones and although the complete pathophysiological mechanism has not had been consistently treated for these without any further yet been established [6–14]. However, only a few cases of peptic work-up. The patient was admitted to the Department of ulcer bleeding, due to primary hyperparathyroidism have been Urology Surgery with the suspicion of renal colic. On day two, reported [14–17]. In this article, we report the case of a life- he excreted a large amount of tarry stool accompanied by Submitted: 16 June 2016; Revised: 24 July 2016; Accepted: 1 August 2016 V C The Author(s) 2016. Published by Oxford University Press and Sixth Affiliated Hospital of Sun Yat-Sen University This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/ licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com Downloaded from https://academic.oup.com/gastro/article-abstract/6/3/231/2909372 by Ed 'DeepDyve' Gillespie user on 22 August 2018 232 | D. Xie et al. coffee-ground emesis. The patient’s blood pressure dropped, metabolic toxin products. On day 19, the patient underwent and he received a blood transfusion and rehydration. The pa- elective surgical exploration with excision of the parathyroid tient was then transferred to the Intensive Care Unit for further adenoma. Histology of the two parathyroid glands revealed a treatment. A bedside upper gastrointestinal endoscopy was per- typical parathyroid adenoma (Figure 3). formed, revealing a duodenal ulcer with an adherent clot that After surgery, the patient’s PTH level was normalized was freely oozing (Forrest-Ib, Figure 1). An intragastric local in- (6.29 pg/ml), and his calcium level decreased rapidly (2.24 mmol/ stillation of norepinephrine and epinephrine was administered l). On day 22, he was transferred to the general ward. Three to stop the bleeding. However, eight hours later, the patient months after parathyroidectomy, the patient’s PTH and calcium again excreted a large amount of tarry stools and vomited a co- levels were 74.97 pg/ml and 2.05 mmol/l, respectively. The se- pious amount of coffee-ground material. An emergent subtotal rum creatinine level also decreased to 175 mmol/L. At 8 months gastrectomy and Billroth II gastrointestinal anastomosis were follow-up, the patient’s PTH and calcium levels were 101.84 pg/ performed to arrest the bleeding. On day four, his heart rate be- ml and 2.17 mmol/l, respectively. The patient denied any diges- came rapid (132–144 beats per minute), his central venous pres- tive tract symptoms such as abdominal pain and diarrhea. sure dropped, his blood hemoglobin decreased, and his abdominal circumference increased. An ultrasound examina- Discussion tion detected a hematocele in the left upper quadrant. There was still active bleeding. Finally, gastroduodenal artery emboli- Primary hyperparathyroidismis a disorder in which the para- zation was carried out to stop the hemorrhage. thyroid gland inappropriately secretes high PTH levels, which During the process, we noted that the patient’s serum cal- leads to hypercalcinemia,, and kidney stone is a classical clini- cium level was elevated (2.98 mmol/L, normal range 2.03– cal symptom of primary hyperparathyroidism. Solitary parathy- 2.65 mmol/L) and that he had a low serum phosphorus level roid adenomas are responsible for primary (0.5 mmol/L, normal range 0.74–1.52 mmol/L), which is uncom- hyperparathyroidism in 80–85% of such cases. Definitive treat- mon in a patient with renal dysfunction (serum creatinine level ment is achieved by surgical resection. However, the disease was 286 mmol/L, normal range 31.8–116 mmol/L). His plasma has no specific symptoms. The diagnosis of PTPH is usually parathyroid hormone (PTH) level was found to be elevated in a made incidentally with an initial finding of hypercalcemia on subsequent test (468.67 pg/ml, normal range 12–65 pg/ml). A routine laboratory studies, which leads to further investigation. neck computed tomography (CT) scan with contrast showed In this report, the patient was initially managed for an upper two enhancing masses (larger mass size 10 9 mm) in the rear gastrointestinal hemorrhage. A high index of suspicion for hy- of the right lobe of his thyroid gland (Figure 2). To exclude mul- perparathyroidism developed when we noted an elevated se- tiple endocrine neoplasia I (MEN I) and Zollinger-Ellison syn- rum calcium level and a low serum phosphorus level, which are drome, CT imaging studies of the head and abdomen were abnormal in a renal failure patient. Upon further testing, the pa- performed and did not indicate any abnormalities. All of these tient’s plasma parathyroid hormone level was found to be ele- findings suggested a diagnosis of primary hyperparathyroidism. vated. A neck CT scan with contrast showed two solitary Unfortunately, in the next period, the patient developed se- parathyroid adenomas, which were subsequently managed sur- vere abdominal pain, tenderness, guarding and rebound pain gically and confirmed histologically. In some cases, primary hy- upon abdominal palpation. Heart rate was rapid (150–160 beats perparathyroidism is a manifestation of multiple endocrine per minute), and his leucocyte count in blood was high neoplasia I and usually occurs in combination with Zollinger- (18.57 10 /L). White blood cell count of the peritoneal drainage Ellison syndrome. Gastrointestinal bleeding is the initial presen- fluid was 111005 106. These signs indicated a severe abdomi- tation in a quarter of patients with Zollinger-Ellison syndrome nal cavity infection, peritonitis and sepsis. Intravenous antibi- [18]. In this case, CT imaging studies of the head and abdomen otics (imipenem 1 g every 8 hours; tigecycline 50 mg every did not exhibit any abnormalities of the pituitary gland or pan- 12 hours) were used to control infection. Additionally, the pa- creas. After excision of the parathyroid adenomas, the patient’s tient’s creatinine level increased to 560 mmol/L. Continuous re- nal replacement therapy (CRRT) was used to treat the hypercalcemia and remove the inflammatory mediators and Figure 1. Endoscopy demonstrated a duodenal ulcer bleeding. Figure 2. Two enhanced masses in the rear of the right lobe of thyroid gland. Downloaded from https://academic.oup.com/gastro/article-abstract/6/3/231/2909372 by Ed 'DeepDyve' Gillespie user on 22 August 2018 Hyperparathyroidism and peptic ulcer bleeding | 233 Figure 3. Histology of parathyroid gland. PTH and calcium levels normalized. No pancreatic tumor-like 7. Barreras RF. Calcium and gastric secretion. Gastroenterology symptoms such as diarrhea or hypokalemia were observed. 1973;64:1168–84. Additionally, no regular upper abdominal pain was observed. 8. Stremple JF and Watson CG. Serum calcium, serum gastrin, and gastric acid secretion before and after parathyroidec- These results support the diagnosis of primary hyperparathy- roidism caused by a parathyroid adenoma. tomy for hyperparathyroidism. Surgery 1974;75:841–52. Due to severe sepsis and renal dysfunction, CRRT was used 9. Patterson M, Wolma F, Drake A, et al. Gastric secretion and to remove inflammatory mediators and metabolic toxin prod- chronic hyperparathyroidism. Arch Surg 1969;99:9–14. 10. Wise SR, Quigley M, Saxe AW, et al. Hyperparathyroidism and ucts with the advantage of potentially avoiding the development of hypotension in a hemodynamically unstable and critically ill cellular mechanisms of gastric acid secretion. Surgery patient. It also decreased the serum calcium level to prevent a 1990;108:1058–63. calcium crisis. There are few case reports in the current litera- 11. Geibel JP, Wagner CA, Caroppo R, et al. The stomach divalent ion-sensing receptor scar is a modulator of gastric acid secre- ture documenting effective treatment of hypercalcemia with CRRT [20–22]. We considered CRRT to be a good therapeutic tion. J Biol Chem 2001;276:39549–52. choice for preventing a calcium crisis in this patient. 12. Corleto VD, Minisola S, Moretti A, et al. Prevalence and causes In conclusion, peptic ulcer bleeding due to primary hyper- of hypergastrinemia in primary hyperparathyroidism: a pro- parathyroidism is extremely rare. The serum calcium level and spective study. J Clin Endocrinol Metab 1999;84:4554–8. PTH level must be considered routine tests in patients with a 13. Do ¨ kmetas ¸ HS, Tu ¨ rkay C, Aydin C, et alet al. Prevalence of Helicobacter pylori in patients with primary hyperparathy- peptic ulcer, especially when it is accompanied by a history of kidney stones with hypercalcemia. Parathyroidectomy is rec- roidism. J Bone Miner Metab 2001;19:373–7. ommended in patients with primary hyperparathyroidism that 14. Sato H, Abe K, Oshima N, et al. Primary hyperparathyroidism are clinically symptomatic. The CRRT could be considered a with duodenal ulcer and H. pylori infection. Intern Med 2002;41:377–80. good therapy choice for preventing a calcium crisis in septic pa- tients with renal dysfunction. 15. Goretzki PE, Becker H, Dotzenrath C, et al. Acute abdomen in unrecognized hyperparathyroidism. Wien Klin Wochenschr 1988;100:373–5 16. Sarter S and Pier A. Forrest 1b duodenal hemorrhage in previ- Funding ously undiagnosed primary hyperparathyroidism. Zentralbl Supported by Science and Technology Planning Project of Chir 1996;121:869–71 Guangdong Province, China (2014A020212715) 17. Sawa TE and Safar SB. Pathological fracture: a common pre- sentation of primary hyperparathyroidism in Iraq. Eur J Surg Conflicts of interest statement: none declared. 1996:162:777–81. 18. Roy PK, Venzon DJ, Shojamanesh H, et al. Zollinger-Ellison References syndrome. Clinical presentation in 261 patients. Medicine (Baltimore) 2000;79:379–411. 1. Gasparoni P, Caroli A, Sardeo G, et al. Primary hyperparathy- 19. Silverberg SJ, Shane E, Jacobs TP, et al. A 10-year prospective roidism and peptic ulcer. Minerva Med 1989;80:1327–30. study of primary hyperparathyroidism with or without para- 2. Clark CG, Chowcat NL, Lewin MR, et al. Surgery for peptic ul- thyroid surgery. N Engl J Med 1999;341:1249–55. ceration associated with hypergastrinaemia. Br J Surg 20. Sramek  V, Novak  I, Matejovic  M, et al. Continuous venove- 1986;73:248–52. nous hemodiafiltration (CVVHDF) with citrate anticoagula- 3. Corlew DS, Bryda SL,2Bradley EL 3rd, et alet al. Observations tion in the treatment of a patient with acute renal failure, on the course of untreated primary hyperparathyroidism. hypercalcemia, and thrombocytopenia. Intensive Care Med Surgery 1985;98:1064–71. 1998;24:262–4. 4. Mowat E, Gunn A, Paterson CR. Hyperparathyroidism in pep- 21. Kindgen-Milles D, Kram R, Kleinekofort W, et al. Treatment of tic ulcer patients. Br J Surg 1981;68:455–8. severe hypercalcemia using continuous renal replacement 5. Gardner EC Jr and Hersh T. Primary hyperparathyroidism and therapy with regional citrate anticoagulation. ASAIO J the gastrointestinal tract. South Med J 1981;74:197–9. 2008;54:442–4. 6. Reeder DD, Jackson BM, Ban J, et al. Influence of hypercalce- 22. Au S, Dunham M, Godinez T. Treatment of medically refrac- mia on gastric secretion and serum gastrin concentrations in tory hypercalcemic crisis. Int J Artif Organs 2012;35:538–41. man. Ann Surg 1970;172:540–6. Downloaded from https://academic.oup.com/gastro/article-abstract/6/3/231/2909372 by Ed 'DeepDyve' Gillespie user on 22 August 2018

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Gastroenterology Report – Oxford University Press

Published: Aug 1, 2018

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