ILLUSTRATIVE CASE
Primary Hyperparathyroidism: An Uncommon Cause of Hip Pain Muhammad Waseem, MD,*†‡ Evelyn Erickson, MD,‡ Samuel Agyare, MD,* and Mushtaq A. Godil, MD§ Abstract: Hip pain is a common complaint in a pediatric emergency department. The causes of hip pain are diverse and generally include traumatic and infectious causes. We report a case of hip pain caused by deep soft tissue infection associated with hypercalcemia and primary hyperparathyroidism. Atypical presentation of primary hyperparathyroidism may result in a delay in diagnosis. Key Words: hypercalcemia, hyperparathyroidism, hip pain (Pediatr Emer Care 2015;31: 272–273)
CASE A previously healthy 12-year-old boy presented with a 5-day history of fever and 1 day of left inguinal and hip pain. He vomited twice before presentation to the emergency department (ED). He denied headache, neck pain, or abdominal pain. He had a previous ED visit 3 days prior, when he twisted his right ankle while playing basketball. He was discharged home after obtaining an ankle radiograph, which was negative for fracture. His medical history was significant for mild intermittent asthma and constipation; he was being treated with stool softeners. He denied any recent change in bowel habit, recurrent abdominal pain, polyuria, or mood swings. In the ED, the patient was limping. His vital signs were as follows: temperature, 103°F; heart rate, 114 beats per minute; respiratory rate, 22 breaths per minute; blood pressure, 124/79 mm Hg; and oxygen saturation, 99%. Physical examination revealed mild tenderness over the left groin. No erythema or induration was present over the hip joint. There was no pain on internal or external rotation of the left hip. Range of movement was not limited. The remainder of his physical examination was unremarkable. Initial complete blood count showed a white blood cell count of 9.4 103/μL, hemoglobin level of 13.4 g/dL, and platelet count of 197,000 103/μL, with 82% neutrophils and 9% lymphocytes. His erythrocyte sedimentation rate was borderline elevated at 27 mm/hour (0-10) but C-reactive protein was significantly elevated at 83.26 mg/L (0.25-3.0). Radiograph of the pelvis was normal. Serum electrolytes were as follows: serum sodium, 135 mmol/L; potassium, 4.8 mmol/L; chloride, 100 mmol/L; bicarbonate, 28 mmol/L; glucose, 129 mg/dL; blood urea nitrogen, 15 mg/dL; creatinine, 1.0 mg/dL; and calcium, 12.4 mg/dL (8.010.4). Ultrasound of the hip showed no joint effusion. Because of fever, hip pain, and limping, a diagnosis of septic arthritis was considered and an orthopedic consultation was obtained. The patient was admitted to the pediatric service for intravenous antibiotics. From the *Department of Emergency Medicine, Lincoln Medical & Mental Health Center, Bronx, NY; †St. Georges University Grenada West Indies, ‡Department of Pediatrics, Lincoln Medical & Mental Health Center, Bronx, NYand § Department of Pediatric Endocrinology, Geisinger Health System, Danville, PA Disclosure: The authors declare no conflict of interest. Reprints: Muhammad Waseem, MD, Lincoln Medical & Mental Health Center, 234 East 149th St, Bronx, NY 10451. (e‐mail: [email protected]). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0749-5161
272
www.pec-online.com
Magnetic resonance imaging of the left hip was normal. Subsequently, a gallium scan was obtained, which showed a small area of increased uptake in the soft tissue anterior to the left hip. This was interpreted as consistent with deep soft tissue infection. Methicillin susceptible Staphylococcus aureus bacteremia was reported in the blood culture obtained in the ED. The patient did not have any history of sickle cell disease, human immunodeficiency virus, or other immunodeficiency states. He received intravenous antibiotics for suspected septic arthritis. Further laboratory evaluation revealed the following: calcium, 14.4 mg/dL; phosphorus, 2.9 mg/dL (2.7-4.5); magnesium, 1.8 mg/dL (1.6-2.5); ionized calcium, 7.4 mg/dL (4.5-5.3); parathyroid hormone, 43 pg/mL (10-65); 25 (OH) vitamin D, 35 ng/mL; 1, 25 (OH)2 vitamin D, 30 pg/mL; calcitonin, less than 2; alkaline phosphatase, 161 IU/L; urinary calcium, 20.77 mg/dL; and urinary creatinine, 29.5 mg/dL. His calcium creatinine clearance ratio was 0.049, which was greater than 0.01 ruling out hypocalciuric hypercalcemia. Subsequently, a parathyroid radionuclide scan was obtained, which showed a parathyroid adenoma. Medical management, including hydration, hydrocortisone, calcitonin, and bisphosphonate supplementation, was initiated before surgical excision of the tumor.
DISCUSSION Hypercalcemia is a well-recognized complication of infectious and noninfectious granulomatous diseases1 but is usually not considered a predisposing factor to infection. Although our patient presented with left inguinal and hip pain and he was subsequently diagnosed with deep soft tissue infection, he did not have any risk factor predisposing him to infection except for hypercalcemia and hyperparathyroidism. It is difficult to say how much hypercalcemia and hyperparathyroidism contributed to his pain and infection, but in the absence of any other risk factor; we believe it was not an incidental finding. We speculated that hypercalcemia or hyperparathyroidism increased the risk of soft tissue infection by an unknown mechanism, yet to be elucidated. One such explanation can be ectopic calcification in the short tissue predisposing it to infection. We found only 1 report in which a patient presented with unexplained splenic abscess without evidence of an underlying cause except for primary hyperparathyroidism.2 When severe, hypercalcemia can represent a medical emergency. Severe hypercalcemia may result in frank confusion, delirium, or obtundation. Total calcium level measurement may be influenced by changes in plasma proteins, particularly albumin; therefore, an ionized calcium level should be obtained in a child with hypercalcemia. In an asymptomatic child, it is also prudent to confirm the presence of hypercalcemia by obtaining a repeat sample to exclude falsely elevated calcium, such as is found in excessive tourniquet use or laboratory error. In the evaluation of hypercalcemia, one of the most important tests to obtain is serum parathyroid hormone level.3 Parathyroid hormone (PTH) can cause hypercalcemia through various mechanisms. It directly stimulates bone resorption, increases renal calcium reabsorption, and indirectly stimulates the production of active vitamin D that promotes intestinal calcium absorption. Dehydration often Pediatric Emergency Care • Volume 31, Number 4, April 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Pediatric Emergency Care • Volume 31, Number 4, April 2015
exacerbates underlying hypercalcemia by reducing renal calcium clearance. Identifying the etiology of hypercalcemia is important because the subsequent management depends on the underlying cause. The possible causes of hypercalcemia in children include primary hyperparathyroidism, familial hypocalciuric hypercalcemia, vitamin D intoxication, malignancy, drugs (such as lithium and thiazide diuretics), immobilization, tuberculosis, sarcoidosis, infantile idiopathic hypercalcemia (variation in CYP24A1), and William syndrome. Thyrotoxicosis can also cause hypercalcemia. High plasma T3 levels may have a direct effect by increasing osteoclast activity, thus resulting in hypercalcemia. Management depends on the severity of hypercalcemia, and the presence or absence of symptoms. The goals of treatment are to relieve the symptoms, establish the underlying cause, and lower the plasma calcium concentration to prevent further end organ damage. Because a majority of children with hypercalcemia are dehydrated, aggressive hydration couple with forced diuresis with loop diuretics should be used if the patient is symptomatic. Hypercalcemia resolves as intravascular calcium is diluted and calciuresis is promoted by increasing fractional excretion of calcium. In the presence of extrarenal synthesis of 1,25-dihydroxyvitamin D, glucocorticoids can be helpful by inhibiting synthesis of 1,25dihydroxyvitamin D from 25-hydroxyvitamin D. Calcitonin inhibits bone resorption but it action is short lived. If hypercalcemia is severe or does not improve with these measures, bisphosphonate agents, such as pamidronate, should be considered. These agents inhibit bone resorption by inhibiting osteoclast function. Primary hyperparathyroidism is a rare cause of hypercalcemia in children, which may account for up to 1% of hypercalcemia.4 It results from PTH overproduction by one or more hyperfunctioning parathyroid glands. In primary hyperparathyroidism, autonomous PTH secretion occurs, independent of circulating calcium levels. Diagnosis of primary hyperparathyroidism is made by demonstrating elevated total serum or ionized calcium levels and an unsuppressed intact PTH level in the presence of normal renal function. In our patient, the PTH level was unsuppressed with significant hypercalcemia, consistent with the diagnosis of primary hyperparathyroidism. Many patients with primary hyperparathyroidism may have a delay in diagnosis.5,6 Primary hyperparathyroidism is frequently recognized after the incidental discovery of hypercalcaemia7 because many patients with hypercalcemia are asymptomatic.8 A wide range of nonspecific symptoms however may be present. These include headache, abdominal pain, polyuria, polydipsia, constipation, vomiting, joint or bone pain, fatigue, and anorexia. Muscle weakness may be present in minimally symptomatic patients. Many of these nonspecific symptoms are common in children,9 but bone or joint pain is an uncommon presentation of hyperparathyroidism in children.10 It is also suggested that children with symptoms of fatigue, headache, nausea, abdominal pain, emesis, polydipsia, diarrhea, depression, or joint pain in the absence of specific diagnosis should be screened for primary hyperparathyroidism by obtaining a serum calcium and PTH level.11 Parathyroid adenoma is the most common cause of primary hyperparathyroidism12 although hyperplasia of multiple
Primary Hyperparathyroidism
parathyroid glands can also cause hypercalcemia. It can be sporadic or associated with multiple endocrine neoplasia type 1 and type 2A. A nuclear medicine sestamibi scan should be obtained to establish a diagnosis of parathyroid adenoma.13 Surgical removal of the tumor is the treatment of choice and generally is curative. In our patient, there was no family history of an underlying multiple endocrine neoplasia. Although he could represent a new mutation, in the absence of family history and other endocrine tumors, genetic testing was not performed.
CONCLUSIONS Primary hyperparathyroidism, although uncommon in children, should be suspected in the differential diagnosis of nonspecific musculoskeletal symptoms. REFERENCES 1. Fuss M, Pepersack T, Gillet C, et al. Calcium and vitamin D metabolism in granulomatous diseases. Clin Rheumatol. 1992;11:28–36. 2. Nadarajah CV, Saif I, Asghar SA. An unusual cause of septicaemia. Acute Med. 2011;10:26–28. 3. Joshi D, Center JR, Eisman JA. Investigation of incidental hypercalcaemia. BMJ. 2009;339:b4613. 4. Kauffmann C, Leroy B, Sinnassamy P, et al. A rare cause of bone pain in children: primary hyperparathyroidism caused by adenoma. Arch Fr Pediatr. 1993;50:771–774. 5. Colognesi A, de Tullio D, Messina F, et al. Primary hyperparathyroidism related to a parathyroid adenoma: the dramatic clinical evolution of a misdiagnosed patient and its surgical solution. Minerva Chir. 2006;61: 51–56. 6. Makhdoomi KR, Chalmers J, Campbell IW, et al. Delayed diagnosis of juvenile primary hyperparathyroidism. J R Coll Surg Edinb. 1996;41: 351–353. 7. Mischis-Troussard C, Goudet P, Verges B, et al. Primary hyperparathyroidism with normal serum intact parathyroid hormone levels. QJM. 2000;93:365–367. 8. Koh LK. The diagnosis and management of hypercalcaemia. Ann Acad Med Singapore. 2003;32:129–139. 9. Venail F, Nicollas R, Morin D, et al. Solitary parathyroid adenoma: a rare cause of primary hyperparathyroidism in children. Laryngoscope. 2007; 117:946–949. 10. Krishnamoorthy P, Alyaarubi S, Abish S, et al. Primary hyperparathyroidism mimicking vaso-occlusive crises in sickle cell disease. Pediatrics. 2006;118:e537–539. 11. Kollars J, Zarroug AE, van Heerden J, et al. Primary hyperparathyroidism in pediatric patients. Pediatrics. 2005;115:974–980. 12. Gurrado A, Marzullo A, Lissidini G, et al. Substernal oxyphil parathyroid adenoma producing PTHrP with hypercalcemia and normal PTH level. World J Surg Oncol. 2008;6:24. 13. Hindie E, Urena P, Jeanguillaume C, et al. Preoperative imaging of parathyroid glands with technetium-99 m-labelled sestamibi and iodine-123 subtraction scanning in secondary hyperparathyroidism. Lancet. 1999;353:2200–2204.
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.pec-online.com
273
Primary Hyperparathyroidism: An Uncommon Cause of Hip Pain Muhammad Waseem, MD,*†‡ Evelyn Erickson, MD,‡ Samuel Agyare, MD,* and Mushtaq A. Godil, MD§ Abstract: Hip pain is a common complaint in a pediatric emergency department. The causes of hip pain are diverse and generally include traumatic and infectious causes. We report a case of hip pain caused by deep soft tissue infection associated with hypercalcemia and primary hyperparathyroidism. Atypical presentation of primary hyperparathyroidism may result in a delay in diagnosis. Key Words: hypercalcemia, hyperparathyroidism, hip pain (Pediatr Emer Care 2015;31: 272–273)
CASE A previously healthy 12-year-old boy presented with a 5-day history of fever and 1 day of left inguinal and hip pain. He vomited twice before presentation to the emergency department (ED). He denied headache, neck pain, or abdominal pain. He had a previous ED visit 3 days prior, when he twisted his right ankle while playing basketball. He was discharged home after obtaining an ankle radiograph, which was negative for fracture. His medical history was significant for mild intermittent asthma and constipation; he was being treated with stool softeners. He denied any recent change in bowel habit, recurrent abdominal pain, polyuria, or mood swings. In the ED, the patient was limping. His vital signs were as follows: temperature, 103°F; heart rate, 114 beats per minute; respiratory rate, 22 breaths per minute; blood pressure, 124/79 mm Hg; and oxygen saturation, 99%. Physical examination revealed mild tenderness over the left groin. No erythema or induration was present over the hip joint. There was no pain on internal or external rotation of the left hip. Range of movement was not limited. The remainder of his physical examination was unremarkable. Initial complete blood count showed a white blood cell count of 9.4 103/μL, hemoglobin level of 13.4 g/dL, and platelet count of 197,000 103/μL, with 82% neutrophils and 9% lymphocytes. His erythrocyte sedimentation rate was borderline elevated at 27 mm/hour (0-10) but C-reactive protein was significantly elevated at 83.26 mg/L (0.25-3.0). Radiograph of the pelvis was normal. Serum electrolytes were as follows: serum sodium, 135 mmol/L; potassium, 4.8 mmol/L; chloride, 100 mmol/L; bicarbonate, 28 mmol/L; glucose, 129 mg/dL; blood urea nitrogen, 15 mg/dL; creatinine, 1.0 mg/dL; and calcium, 12.4 mg/dL (8.010.4). Ultrasound of the hip showed no joint effusion. Because of fever, hip pain, and limping, a diagnosis of septic arthritis was considered and an orthopedic consultation was obtained. The patient was admitted to the pediatric service for intravenous antibiotics. From the *Department of Emergency Medicine, Lincoln Medical & Mental Health Center, Bronx, NY; †St. Georges University Grenada West Indies, ‡Department of Pediatrics, Lincoln Medical & Mental Health Center, Bronx, NYand § Department of Pediatric Endocrinology, Geisinger Health System, Danville, PA Disclosure: The authors declare no conflict of interest. Reprints: Muhammad Waseem, MD, Lincoln Medical & Mental Health Center, 234 East 149th St, Bronx, NY 10451. (e‐mail: [email protected]). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0749-5161
272
www.pec-online.com
Magnetic resonance imaging of the left hip was normal. Subsequently, a gallium scan was obtained, which showed a small area of increased uptake in the soft tissue anterior to the left hip. This was interpreted as consistent with deep soft tissue infection. Methicillin susceptible Staphylococcus aureus bacteremia was reported in the blood culture obtained in the ED. The patient did not have any history of sickle cell disease, human immunodeficiency virus, or other immunodeficiency states. He received intravenous antibiotics for suspected septic arthritis. Further laboratory evaluation revealed the following: calcium, 14.4 mg/dL; phosphorus, 2.9 mg/dL (2.7-4.5); magnesium, 1.8 mg/dL (1.6-2.5); ionized calcium, 7.4 mg/dL (4.5-5.3); parathyroid hormone, 43 pg/mL (10-65); 25 (OH) vitamin D, 35 ng/mL; 1, 25 (OH)2 vitamin D, 30 pg/mL; calcitonin, less than 2; alkaline phosphatase, 161 IU/L; urinary calcium, 20.77 mg/dL; and urinary creatinine, 29.5 mg/dL. His calcium creatinine clearance ratio was 0.049, which was greater than 0.01 ruling out hypocalciuric hypercalcemia. Subsequently, a parathyroid radionuclide scan was obtained, which showed a parathyroid adenoma. Medical management, including hydration, hydrocortisone, calcitonin, and bisphosphonate supplementation, was initiated before surgical excision of the tumor.
DISCUSSION Hypercalcemia is a well-recognized complication of infectious and noninfectious granulomatous diseases1 but is usually not considered a predisposing factor to infection. Although our patient presented with left inguinal and hip pain and he was subsequently diagnosed with deep soft tissue infection, he did not have any risk factor predisposing him to infection except for hypercalcemia and hyperparathyroidism. It is difficult to say how much hypercalcemia and hyperparathyroidism contributed to his pain and infection, but in the absence of any other risk factor; we believe it was not an incidental finding. We speculated that hypercalcemia or hyperparathyroidism increased the risk of soft tissue infection by an unknown mechanism, yet to be elucidated. One such explanation can be ectopic calcification in the short tissue predisposing it to infection. We found only 1 report in which a patient presented with unexplained splenic abscess without evidence of an underlying cause except for primary hyperparathyroidism.2 When severe, hypercalcemia can represent a medical emergency. Severe hypercalcemia may result in frank confusion, delirium, or obtundation. Total calcium level measurement may be influenced by changes in plasma proteins, particularly albumin; therefore, an ionized calcium level should be obtained in a child with hypercalcemia. In an asymptomatic child, it is also prudent to confirm the presence of hypercalcemia by obtaining a repeat sample to exclude falsely elevated calcium, such as is found in excessive tourniquet use or laboratory error. In the evaluation of hypercalcemia, one of the most important tests to obtain is serum parathyroid hormone level.3 Parathyroid hormone (PTH) can cause hypercalcemia through various mechanisms. It directly stimulates bone resorption, increases renal calcium reabsorption, and indirectly stimulates the production of active vitamin D that promotes intestinal calcium absorption. Dehydration often Pediatric Emergency Care • Volume 31, Number 4, April 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Pediatric Emergency Care • Volume 31, Number 4, April 2015
exacerbates underlying hypercalcemia by reducing renal calcium clearance. Identifying the etiology of hypercalcemia is important because the subsequent management depends on the underlying cause. The possible causes of hypercalcemia in children include primary hyperparathyroidism, familial hypocalciuric hypercalcemia, vitamin D intoxication, malignancy, drugs (such as lithium and thiazide diuretics), immobilization, tuberculosis, sarcoidosis, infantile idiopathic hypercalcemia (variation in CYP24A1), and William syndrome. Thyrotoxicosis can also cause hypercalcemia. High plasma T3 levels may have a direct effect by increasing osteoclast activity, thus resulting in hypercalcemia. Management depends on the severity of hypercalcemia, and the presence or absence of symptoms. The goals of treatment are to relieve the symptoms, establish the underlying cause, and lower the plasma calcium concentration to prevent further end organ damage. Because a majority of children with hypercalcemia are dehydrated, aggressive hydration couple with forced diuresis with loop diuretics should be used if the patient is symptomatic. Hypercalcemia resolves as intravascular calcium is diluted and calciuresis is promoted by increasing fractional excretion of calcium. In the presence of extrarenal synthesis of 1,25-dihydroxyvitamin D, glucocorticoids can be helpful by inhibiting synthesis of 1,25dihydroxyvitamin D from 25-hydroxyvitamin D. Calcitonin inhibits bone resorption but it action is short lived. If hypercalcemia is severe or does not improve with these measures, bisphosphonate agents, such as pamidronate, should be considered. These agents inhibit bone resorption by inhibiting osteoclast function. Primary hyperparathyroidism is a rare cause of hypercalcemia in children, which may account for up to 1% of hypercalcemia.4 It results from PTH overproduction by one or more hyperfunctioning parathyroid glands. In primary hyperparathyroidism, autonomous PTH secretion occurs, independent of circulating calcium levels. Diagnosis of primary hyperparathyroidism is made by demonstrating elevated total serum or ionized calcium levels and an unsuppressed intact PTH level in the presence of normal renal function. In our patient, the PTH level was unsuppressed with significant hypercalcemia, consistent with the diagnosis of primary hyperparathyroidism. Many patients with primary hyperparathyroidism may have a delay in diagnosis.5,6 Primary hyperparathyroidism is frequently recognized after the incidental discovery of hypercalcaemia7 because many patients with hypercalcemia are asymptomatic.8 A wide range of nonspecific symptoms however may be present. These include headache, abdominal pain, polyuria, polydipsia, constipation, vomiting, joint or bone pain, fatigue, and anorexia. Muscle weakness may be present in minimally symptomatic patients. Many of these nonspecific symptoms are common in children,9 but bone or joint pain is an uncommon presentation of hyperparathyroidism in children.10 It is also suggested that children with symptoms of fatigue, headache, nausea, abdominal pain, emesis, polydipsia, diarrhea, depression, or joint pain in the absence of specific diagnosis should be screened for primary hyperparathyroidism by obtaining a serum calcium and PTH level.11 Parathyroid adenoma is the most common cause of primary hyperparathyroidism12 although hyperplasia of multiple
Primary Hyperparathyroidism
parathyroid glands can also cause hypercalcemia. It can be sporadic or associated with multiple endocrine neoplasia type 1 and type 2A. A nuclear medicine sestamibi scan should be obtained to establish a diagnosis of parathyroid adenoma.13 Surgical removal of the tumor is the treatment of choice and generally is curative. In our patient, there was no family history of an underlying multiple endocrine neoplasia. Although he could represent a new mutation, in the absence of family history and other endocrine tumors, genetic testing was not performed.
CONCLUSIONS Primary hyperparathyroidism, although uncommon in children, should be suspected in the differential diagnosis of nonspecific musculoskeletal symptoms. REFERENCES 1. Fuss M, Pepersack T, Gillet C, et al. Calcium and vitamin D metabolism in granulomatous diseases. Clin Rheumatol. 1992;11:28–36. 2. Nadarajah CV, Saif I, Asghar SA. An unusual cause of septicaemia. Acute Med. 2011;10:26–28. 3. Joshi D, Center JR, Eisman JA. Investigation of incidental hypercalcaemia. BMJ. 2009;339:b4613. 4. Kauffmann C, Leroy B, Sinnassamy P, et al. A rare cause of bone pain in children: primary hyperparathyroidism caused by adenoma. Arch Fr Pediatr. 1993;50:771–774. 5. Colognesi A, de Tullio D, Messina F, et al. Primary hyperparathyroidism related to a parathyroid adenoma: the dramatic clinical evolution of a misdiagnosed patient and its surgical solution. Minerva Chir. 2006;61: 51–56. 6. Makhdoomi KR, Chalmers J, Campbell IW, et al. Delayed diagnosis of juvenile primary hyperparathyroidism. J R Coll Surg Edinb. 1996;41: 351–353. 7. Mischis-Troussard C, Goudet P, Verges B, et al. Primary hyperparathyroidism with normal serum intact parathyroid hormone levels. QJM. 2000;93:365–367. 8. Koh LK. The diagnosis and management of hypercalcaemia. Ann Acad Med Singapore. 2003;32:129–139. 9. Venail F, Nicollas R, Morin D, et al. Solitary parathyroid adenoma: a rare cause of primary hyperparathyroidism in children. Laryngoscope. 2007; 117:946–949. 10. Krishnamoorthy P, Alyaarubi S, Abish S, et al. Primary hyperparathyroidism mimicking vaso-occlusive crises in sickle cell disease. Pediatrics. 2006;118:e537–539. 11. Kollars J, Zarroug AE, van Heerden J, et al. Primary hyperparathyroidism in pediatric patients. Pediatrics. 2005;115:974–980. 12. Gurrado A, Marzullo A, Lissidini G, et al. Substernal oxyphil parathyroid adenoma producing PTHrP with hypercalcemia and normal PTH level. World J Surg Oncol. 2008;6:24. 13. Hindie E, Urena P, Jeanguillaume C, et al. Preoperative imaging of parathyroid glands with technetium-99 m-labelled sestamibi and iodine-123 subtraction scanning in secondary hyperparathyroidism. Lancet. 1999;353:2200–2204.
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.pec-online.com
273
![[Epiploic appendagitis: an uncommon cause of abdominal pain in primary care].](/assets/img/hold.png)
