eMedicine Specialties > Endocrinology > Multiple Endocrine Disease and Miscellaneous Endocrine Disease

Wermer Syndrome (MEN Type 1): Differential Diagnoses & Workup

Author: Irina Lendel, MD, Clinical Instructor in Endocrinology, Division of Endocrinology, Diabetes, and Metabolism, Milton S Hershey Medical Center
Coauthor(s): James M Hammond, MD, Distinguished Professor of Medicine, Penn State University College of Medicine, Milton S Hershey Medical Center; Klaus Radebold, MD, PhD, Research Associate, Department of Surgery, Yale University School of Medicine
Contributor Information and Disclosures

Updated: May 14, 2009

Differential Diagnoses

Achlorhydria
Insulinoma
Adrenal Adenoma
Prolactinoma
Carcinoid Lung Tumors
VIPomas
Carcinoid Tumor, Intestinal
Zollinger-Ellison Syndrome
Duodenal Ulcers

Other Problems to Be Considered

Pancreatic islet cell tumor should also be considered.

Hyperparathyroidism in MEN 1 must be separated from other familial forms of hypercalcemia, including familial parathyroid hyperplasia and familial adenomatous hyperparathyroidism. Familial hypocalciuric hypercalcemia may also have a similar presentation. These latter 2 have no pancreatic or pituitary manifestations.

Conditions other than ZES that are associated with elevated serum gastrin levels include retained gastric antrum, gastric outlet obstruction, hypercalcemia, massive small bowel resection, atrophic gastritis, and treatment with proton pump inhibitors.

Workup

Laboratory Studies

  • Lab studies in known MEN 1 carriers screen for the different syndromes expressed by tumors expressed in multiple endocrine adenopathy (MEA) type 1.
  • Gastrinomas
    • Combination of elevated gastrin levels and increased gastric acid output. Gastric acid output is measured if gastrin is high (measured by pH probe).
    • If serum gastrin is high (normal is <115 ng/mL) or if gastric acid output is high, then gastrin levels could be evaluated after secretin stimulation. An increase of gastrin level by more than 200 ng/mL after an intravenous injection of secretin at 2 IU/kg of body weight is abnormal.
    • The secretin test is necessary to exclude other diseases associated with pathologically increased serum gastrin levels.
  • Insulinomas
    • Perform a fasting hypoglycemia test when inappropriately elevated serum insulin, C peptide, or proinsulin concentrations are present.
    • A supervised 72-hour fast often is required if elevated fasted insulin (>72 pmol/L) and low fasted blood sugar (45 mg/dL) cannot be documented in the setting of suspected hypoglycemia.
  • Glucagonoma: Elevated serum glucagon levels and hyperglycemia are present.
  • Watery diarrhea syndrome: Elevated serum levels of vasoactive intestinal polypeptide are present.
  • Carcinoids: Elevated levels of serotonin, chromogranin A, calcitonin, and corticotropin are present. Elevated urinary levels of 5-hydroxyindoleacetic acid also are present.
  • Pituitary tumors: Assess growth hormone levels (IGF-1) and prolactin.
  • Hyperparathyroidism
    • Calcium and intact parathyroid hormone (PTH) levels are outside of the normogram range for the specific laboratory concurrent calcium/PTH determinations.
    • Dual-energy x-ray absorptiometry may be useful in assessing chronic bone mineral loss. Significant bone loss — absolute (T score) and for age (Z score) — may be an indicator for parathyroid surgery even in the absence of other clinical symptoms or marked hypercalcemia.

Imaging Studies

  • Pituitary tumors: Magnetic resonance imaging (MRI), with attention to the sella turcica region, is the test of choice when biochemical evidence of pituitary disease is found.
  • Some tumors may not be functioning; however, asymptomatic patients should also be screened regularly (every 3-5 y).
  • Gastrinomas
    • Somatostatin receptor scintigraphy is the imaging procedure of choice for gastrinomas. Its sensitivity range is 70-90%.
    • Somatostatin receptor scintigraphy can be enhanced by selective arterial secretagogue test with secretin or calcium infusion (in 10% of cases of gastrinomas secretin is not diagnostically useful).
    • Operative intervention should be preceded by a computed tomography (CT) or MRI scan. Evidence from a study of adrenal CT scans from 28 patients with MEN 1 indicated that the frequency of adrenal limb hyperplasia and adrenal nodules in patients with the syndrome is significantly increased.5
    • Endoscopic ultrasonography detects tumors in the pancreatic head but rarely in the duodenal wall. It is more sensitive than CT or transabdominal ultrasound.
  • Insulinomas
    • CT scan and MRI are recommended first.
    • Somatostatin receptor scintigraphy findings may be positive in up to 50% of patients with insulinomas. It is best used in conjunction with SPECT (single-photon emission CT).
    • Endoscopic ultrasonography (see image below) has a reported detection sensitivity of up to 94%.

      • Endoscopic ultrasonogram in a patient with an ins...

        Endoscopic ultrasonogram in a patient with an insulinoma. The hypoechoic neoplasm (arrows) is seen in the body of the pancreas anterior to the splenic vein (SV). (From: Rosch T, Lightdale CJ, Botet JF, et al. Localization of pancreatic endocrine tumors by endoscopic ultrasonography. N Engl J Med. Jun 25 1992;326(26):1721-6.)

        Endoscopic ultrasonogram in a patient with an ins...

        Endoscopic ultrasonogram in a patient with an insulinoma. The hypoechoic neoplasm (arrows) is seen in the body of the pancreas anterior to the splenic vein (SV). (From: Rosch T, Lightdale CJ, Botet JF, et al. Localization of pancreatic endocrine tumors by endoscopic ultrasonography. N Engl J Med. Jun 25 1992;326(26):1721-6.)

    • Selective arterial calcium stimulation with hepatic venous sampling is often required as in patients with MEN 1 multiple lesions are likely to be present. The imaged lesion may not be the one causing the symptoms.
    • Intraoperative ultrasonography can be helpful.
  • Parathyroid tumors
    • Sestamibi scans of the parathyroids may be useful for localization if surgery is anticipated (see image below).

      • Technetium-99m sestamibi scan (<SUP><FONT size=-1...

        Technetium-99m sestamibi scan (99mTc MIBI) in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1). These images demonstrate persistent abnormal activity of the inferior right parathyroid gland that is consistent with an adenoma.

        Technetium-99m sestamibi scan (<SUP><FONT size=-1...

        Technetium-99m sestamibi scan (99mTc MIBI) in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1). These images demonstrate persistent abnormal activity of the inferior right parathyroid gland that is consistent with an adenoma.

    • This is particularly true for identifying adenomas, although most patients with MEN 1 have hyperplasia.
  • Nonfunctioning pancreatic tumors: Endoscopic ultrasonography can identify tumors in 55% of asymptomatic patients.

Other Tests

Genetic testing

  • Sequence analysis of the MEN gene for menin by polymerase chain reaction techniques provides best evidence of gene carrier status. This test is performed in several commercial laboratories and is recommended in asymptomatic first-degree relatives of affected individuals who are younger than 35 years.6
  • If test findings are normal on 3 occasions and patients are older than 35 years, patients are declared noncarriers. Offspring testing is not necessary.
  • Nongenetic screening for investigation of MEN 1 gene carrier status can be conducted by measuring serum calcium, PTH, and serum prolactin every 3 years starting after age 5 years. Other tests include glucose, gastrin, insulin, proinsulin, and glucagon. Chromogranin A may be added where resources allow. Although these individual tests are less expensive than genetic testing, they are more expensive in the aggregate.

Screening for tumor expression

  • Screening for tumor expression after MEN 1 gene carrier status is established includes biochemical studies on a yearly basis and imaging every 3-5 years.7
  • Biochemical screening involves performing fasting glucose, insulin, prolactin, and IGF-1 levels starting after age 5 years; calcium (preferably ionized) and intact PTH starting after age 8 years; and gastrin (with gastric acid output and secretin stimulation test if gastrin is high), chromogranin A, glucagon, and proinsulin starting after age 20 years, on an annual basis.
  • Imaging studies include brain MRI starting after age 5 years and chest/abdominal CT or MRI for foregut carcinoids and enteropancreatic tumors starting after age 20 years, every 3-5 years.

Histologic Findings

In the parathyroids, the glands show diffuse or nodular proliferations of chief cells, admixed with some oncocytic cells. Usually, all 4 glands are involved and show signs of hyperplasia.

In the pancreas, numerous microadenomas, usually in the pancreatic tail, are present. The tumors display a trabecular pattern and may show conspicuous connective tissue stroma. Immunohistochemically, expression of multiple hormones is found. Pancreatic polypeptide and glucagon are expressed most often, followed by insulin and, rarely, gastrin. Nesidioblastosis and islet cell hyperplasia are not features of MEN 1, as previously thought.

In the duodenum, most tumors are found in the first part of the duodenum. They all stain positive for gastrin and metastasize to regional lymph nodes.

In the stomach, diffuse hyperplasia of enterochromaffinlike (ECL) cells is found and is often associated with carcinoid tumors of considerable size (rarely metastases).

In the pituitary, most tumors that produce growth hormone are found in the anterior part of the gland and usually are single.

More on Wermer Syndrome (MEN Type 1)

Overview: Wermer Syndrome (MEN Type 1)
Differential Diagnoses & Workup: Wermer Syndrome (MEN Type 1)
Treatment & Medication: Wermer Syndrome (MEN Type 1)
Follow-up: Wermer Syndrome (MEN Type 1)
Multimedia: Wermer Syndrome (MEN Type 1)
References
Further Reading

References

  1. Eller-Vainicher C, Chiodini I, Battista C, et al. Sporadic and MEN 1 related primary hyperparathyroidism: differences in clinical expression and severity. J Bone Miner Res. Mar 23 2009;[Medline].

  2. Anlauf M, Perren A, Meyer CL, et al. Precursor lesions in patients with multiple endocrine neoplasia type 1-associated duodenal gastrinomas. Gastroenterology. May 2005;128(5):1187-98. [Medline].

  3. Ferolla P, Falchetti A, Filosso P, et al. Thymic neuroendocrine carcinoma (carcinoid) in multiple endocrine neoplasia type 1 syndrome: the Italian series. J Clin Endocrinol Metab. May 2005;90(5):2603-9. [Medline][Full Text].

  4. Yip L, Ogilvie JB, Challinor SM, et al. Identification of multiple endocrine neoplasia type 1 in patients with apparent sporadic primary hyperparathyroidism. Surgery. Dec 2008;144(6):1002-6; discussion 1006-7. [Medline].

  5. Whitley SA, Moyes VJ, Park KM, et al. The appearance of the adrenal glands on computed tomography in multiple endocrine neoplasia type 1. Eur J Endocrinol. Dec 2008;159(6):819-24. [Medline].

  6. Tsukada T, Nagamura Y, Ohkura N. MEN1 gene and its mutations: basic and clinical implications. Cancer Sci. Dec 8 2008;[Medline].

  7. Waldmann J, Fendrich V, Habbe N, et al. Screening of patients with multiple endocrine neoplasia type 1 (MEN-1): a critical analysis of its value. World J Surg. Jun 2009;33(6):1208-18. [Medline].

  8. Hebert SC. Therapeutic use of calcimimetics. Annu Rev Med. 2006;57:349-64. [Medline].

  9. Tucker ON, Crotty PL, Conlon KC. The management of insulinoma. Br J Surg. Mar 2006;93(3):264-75. [Medline].

  10. Wilson SD, Krzywda EA, Zhu YR, et al. The influence of surgery in MEN-1 syndrome: observations over 150 years. Surgery. Oct 2008;144(4):695-701; discussion 701-2. [Medline].

  11. Hubbard JG, Sebag F, Maweja S, et al. Subtotal parathyroidectomy as an adequate treatment for primary hyperparathyroidism in multiple endocrine neoplasia type 1. Arch Surg. Mar 2006;141(3):235-9. [Medline][Full Text].

  12. Asgharian B, Turner ML, Gibril F, Entsuah LK, Serrano J, Jensen RT. Cutaneous tumors in patients with multiple endocrine neoplasm type 1 (MEN1) and gastrinomas: prospective study of frequency and development of criteria with high sensitivity and specificity for MEN1. J Clin Endocrinol Metab. Nov 2004;89(11):5328-36. [Medline].

  13. Brandi ML, Gagel RF, Angeli A, Bilezikian JP, Beck-Peccoz P, Bordi C. Guidelines for diagnosis and therapy of MEN type 1 and type 2. J Clin Endocrinol Metab. Dec 2001;86(12):5658-71. [Medline].

  14. Doherty GM, Olson JA, Frisella MM. Lethality of multiple endocrine neoplasia type I. World J Surg. Jun 1998;22(6):581-6; discussion 586-7. [Medline].

  15. Donow C, Pipeleers-Marichal M, Schroder S. Surgical pathology of gastrinoma. Site, size, multicentricity, association with multiple endocrine neoplasia type 1, and malignancy. Cancer. Sep 15 1991;68(6):1329-34. [Medline].

  16. Eriksson B, Bergstrom M, Orlefors H. Use of PET in neuroendocrine tumors. In vivo applications and in vitro studies. Q J Nucl Med. Mar 2000;44(1):68-76. [Medline].

  17. Eriksson B, Oberg K, Stridsberg M. Tumor markers in neuroendocrine tumors. Digestion. 2000;62 Suppl 1:33-8. [Medline].

  18. Granberg D, Stridsberg M, Seensalu R. Plasma chromogranin A in patients with multiple endocrine neoplasia type 1. J Clin Endocrinol Metab. Aug 1999;84(8):2712-7. [Medline].

  19. Hausman MS Jr, Thompson NW, Gauger PG, Doherty GM. The surgical management of MEN-1 pancreatoduodenal neuroendocrine disease. Surgery. Dec 2004;136(6):1205-11.

  20. Katai M, Sakurai A, Inaba H, Ikeo Y, Yamauchi K, Hashizume K. Octreotide as a rapid and effective painkiller for metastatic carcinoid tumor. Endocr J. Apr 2005;52(2):277-80.

  21. Lairmore TC, Chen VY, DeBenedetti MK. Duodenopancreatic resections in patients with multiple endocrine neoplasia type 1. Ann Surg. Jun 2000;231(6):909-18. [Medline].

  22. Lairmore TC, Piersall LD, DeBenedetti MK, Dilley WG, Mutch MG, Whelan AJ. Clinical genetic testing and early surgical intervention in patients with multiple endocrine neoplasia type 1 (MEN 1). Ann Surg. May 2004;239(5):637-45; discussion 645-7.

  23. Lambert LA, Shapiro SE, Lee JE, Perrier ND, Truong M, Wallace MJ. Surgical treatment of hyperparathyroidism in patients with multiple endocrine neoplasia type 1. Arch Surg. Apr 2005;140(4):374-82.

  24. Lowney JK, Frisella MM, Lairmore TC. Pancreatic islet cell tumor metastasis in multiple endocrine neoplasia type 1: correlation with primary tumor size. Surgery. Dec 1998;124(6):1043-8, discussion 1048-9. [Medline].

  25. MacFarlane MP, Fraker DL, Alexander HR. Prospective study of surgical resection of duodenal and pancreatic gastrinomas in multiple endocrine neoplasia type 1. Surgery. Dec 1995;118(6):973-9; discussion 979-80. [Medline].

  26. Mailman MD, Muscarella P, Schirmer WJ. Identification of MEN1 mutations in sporadic enteropancreatic neuroendocrine tumors by analysis of paraffin-embedded tissue. Clin Chem. Jan 1999;45(1):29-34. [Medline].

  27. Norton JA, Cornelius MJ, Doppman JL. Effect of parathyroidectomy in patients with hyperparathyroidism, Zollinger-Ellison syndrome, and multiple endocrine neoplasia type I: a prospective study. Surgery. Dec 1987;102(6):958-66. [Medline].

  28. Norton JA, Melcher ML, Gibril F, Jensen RT. Gastric carcinoid tumors in multiple endocrine neoplasia-1 patients with Zollinger-Ellison syndrome can be symptomatic, demonstrate aggressive growth, and require surgical treatment. Surgery. Dec 2004;136(6):1267-74.

  29. Oberg K. Interferon in the management of neuroendocrine GEP-tumors. a review. Digestion. 2000;62 Suppl 1:92-7. [Medline].

  30. Phan GQ, Yeo CJ, Hruban RH. Surgical experience with pancreatic and peripancreatic neuroendocrine tumors: review of 125 patients. J Gastrointest Surg. Sep-Oct 1998;2(5):472-82. [Medline].

  31. Proye CA, Nguyen HH. Current perspectives in the surgery of multiple endocrine neoplasias. Aust N Z J Surg. Feb 1999;69(2):106-16. [Medline].

  32. Rosch T, Lightdale CJ, Botet JF, et al. Localization of pancreatic endocrine tumors by endoscopic ultrasonography. N Engl J Med. Jun 25 1992;326(26):1721-6. [Medline].

  33. Ruszniewski P, Podevin P, Cadiot G. Clinical, anatomical, and evolutive features of patients with the Zollinger-Ellison syndrome combined with type I multiple endocrine neoplasia. Pancreas. May 1993;8(3):295-304. [Medline].

  34. Shan L, Nakamura Y, Nakamura M. Somatic mutations of multiple endocrine neoplasia type 1 gene in the sporadic endocrine tumors. Lab Invest. Apr 1998;78(4):471-5. [Medline].

  35. Silverberg SJ, Bone HG 3rd, Marriott TB, Locker FG, Thys-Jacobs S, Dziem G. Short-term inhibition of parathyroid hormone secretion by a calcium-receptor agonist in patients with primary hyperparathyroidism. N Engl J Med. Nov 20 1997;337(21):1506-10. [Medline].

  36. Skogseid B, Doherty GM. Multiple endocrine neoplasia type 1: clinical and genetic features. Ital J Gastroenterol Hepatol. Oct 1999;31 Suppl 2:S131-4. [Medline].

  37. Thompson NW. Current concepts in the surgical management of multiple endocrine neoplasia type 1 pancreatic-duodenal disease. Results in the treatment of 40 patients with Zollinger-Ellison syndrome, hypoglycaemia or both. J Intern Med. Jun 1998;243(6):495-500. [Medline].

  38. Thompson NW. Management of pancreatic endocrine tumors in patients with multiple endocrine neoplasia type 1. Surg Oncol Clin N Am. Oct 1998;7(4):881-91. [Medline].

  39. Triponez F, Dosseh D, Goudet P, et al. Epidemiology data on 108 MEN 1 patients from the GTE with isolated nonfunctioning tumors of the pancreas. Ann Surg. Feb 2006;243(2):265-72. [Medline].

  40. Wang EH, Ebrahimi SA, Wu AY. Mutation of the MENIN gene in sporadic pancreatic endocrine tumors. Cancer Res. Oct 1 1998;58(19):4417-20. [Medline].

  41. Yano M, Fukai I, Kobayashi Y, et al. ACTH-secreting thymic carcinoid associated with multiple endocrine neoplasia type 1. Ann Thorac Surg. Jan 2006;81(1):366-8. [Medline].

  42. Yeo CJ. Islet cell tumors of the pancreas. In: Niederhuber JE, ed. Current Therapy in Oncology. St Louis, Mo: Mosby-Year Book; 1993:272.

  43. Yim JH, Siegel BA, DeBenedetti MK. Prospective study of the utility of somatostatin-receptor scintigraphy in the evaluation of patients with multiple endocrine neoplasia type 1. Surgery. Dec 1998;124(6):1037-42. [Medline].

Further Reading

Related eMedicine topics:
Gastrinoma
Glucagonoma
Hyperparathyroidism [Emergency Medicine]
Hyperparathyroidism [Endocrinology]
Hyperparathyroidism [Otolaryngology and Facial Plastic Surgery]
Hyperparathyroidism [Pediatrics: General Medicine]
Hyperparathyroidism, Primary
Insulinoma
Multiple Endocrine Neoplasia

Multiple Endocrine Neoplasia Type 1
Multiple Endocrine Neoplasia, Type 2
Neoplasms of the Endocrine Pancreas
Pancreas, Islet Cell Tumors
Prolactinoma
Zollinger-Ellison Syndrome [Gastroenterology]
Zollinger-Ellison Syndrome [Pediatrics: General Medicine]
Zollinger-Ellison Syndrome [Radiology]

Clinical guidelines:
Intraoperative parathyroid hormone. Laboratory medicine practice guidelines: evidence-based practice for point-of-care testing. National Academy of Clinical Biochemistry - Professional Association.  2006.  15 pages.  NGC:005645

Procedure guideline for parathyroid scintigraphy. Society of Nuclear Medicine, Inc - Medical Specialty Society.  1999 Feb (revised 2004 Jun).  6 pages.  NGC:004256

Clinical studies:
Studies of Inherited Diseases of Metabolism

Treatment of Zollinger-Ellison Syndrome With Prevacid

Keywords

multiple endocrine neoplasia type 1, MEN 1, parathyroidhyperparathyroidism, pituitary tumor, MEN 1 syndrome, MEN 2 syndrome, MEN 2a, MEN 2b, prolactinoma, insulinoma, pituitary tumors, pancreatic tumor, pancreatic tumors, endocrine disorder, endocrine disease, endocrine diseases, glucagonoma, islet cell tumor, pluriglandular syndrome, multiple endocrine adenopathy, MEA, Wermer's syndrome, parathyroid tumor, pancreatic islet cell tumor, pituitary hyperplasia, pituitary tumor formation, pancreas tumor, pancreatic polypeptide tumors, PPomas, gastrinomas, VIPoma, vasoactive intestinal polypeptide tumor, Zollinger-Ellison syndrome, ZES, Cushing syndrome, Cushing’s syndrome, Sipple syndrome

Contributor Information and Disclosures

Author

Irina Lendel, MD, Clinical Instructor in Endocrinology, Division of Endocrinology, Diabetes, and Metabolism, Milton S Hershey Medical Center
Disclosure: Nothing to disclose.

Coauthor(s)

James M Hammond, MD, Distinguished Professor of Medicine, Penn State University College of Medicine, Milton S Hershey Medical Center
James M Hammond, MD is a member of the following medical societies: Alpha Omega Alpha, American Diabetes Association, American Federation for Clinical Research, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Phi Beta Kappa, and Society for the Study of Reproduction
Disclosure: Nothing to disclose.

Klaus Radebold, MD, PhD, Research Associate, Department of Surgery, Yale University School of Medicine
Klaus Radebold, MD, PhD is a member of the following medical societies: American Gastroenterological Association and New York Academy of Sciences
Disclosure: Nothing to disclose.

Medical Editor

Frederick H Ziel, MD, Associate Professor of Medicine, David Geffen School of Medicine at UCLA; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group
Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, and International Society for Clinical Densitometry
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS, Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC
Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, American Society of Law, Medicine & Ethics, Endocrine Society, and International Society for Clinical Densitometry
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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