eMedicine Specialties > Endocrinology > Pituitary Gland

Kallmann Syndrome and Idiopathic Hypogonadotropic Hypogonadism: Treatment & Medication

Author: Nicholas A Tritos, MD, DSc, MMSc, FACE, FACP, Assistant Professor of Medicine, Tufts University School of Medicine; Senior Staff Physician, Department of Endocrinology, Lahey Clinic Medical Center
Contributor Information and Disclosures

Updated: Nov 26, 2008

Treatment

Medical Care

  • Evaluation and therapy can usually be implemented on an outpatient basis. Inpatient evaluation and treatment may be necessary for patients with congenital heart disease or acute adrenocortical insufficiency.
  • All postpubertal-age patients with Kallmann syndrome and idiopathic hypogonadotropic hypogonadism are candidates for gonadal steroid replacement therapy in the absence of specific contraindications. Additional therapies to restore fertility can be implemented on request.
  • Behavioral modification and psychological counseling may benefit individuals with hypothalamic amenorrhea. Such approaches should be offered before estrogen replacement therapy.
  • Medical therapies are used to treat associated conditions, including osteoporosis, adrenocortical insufficiency, congenital heart disease, and neurologic disorders.

Surgical Care

  • Assisted reproductive technologies, including in vitro fertilization (IVF), zygote intrafallopian transfer (ZIFT), and gamete intrafallopian transfer (GIFT), have been used successfully when male patients with Kallmann syndrome or idiopathic hypogonadotropic hypogonadism do not achieve adequate sperm counts on either GnRH or gonadotropin therapy.
  • Patients with Kallmann syndrome and congenital heart disease may need corrective surgery. A detailed description of the pertinent procedures is beyond the scope of this review.
  • Patients with cleft lip or palate also need surgical correction.

Consultations

  • Adult or pediatric specialists should be consulted, depending on the patient's age.
  • Consultations include the following:
    • Endocrinologist and reproductive endocrinologist
    • Cardiologist
    • Cardiothoracic surgeon and pediatric surgeon
    • Neurologist and psychiatrist
    • Otolaryngologist
    • Dermatologist

Diet

  • No dietary restrictions are required in the absence of congenital heart disease. Salt restriction (adult Na+ intake <2 g/d) is advised for patients with congestive heart failure.
  • All patients must ensure an adequate calcium (1200-1500 mg/d) and vitamin D (800-1000 U/d) intake, especially if they are osteopenic. Dietary supplements may be necessary for patients to achieve these goals.

Activity

  • Routine activity restrictions are not necessary; however, patients with osteoporosis need to avoid high-impact sports and situations conducive to falls.
  • Activity restrictions are also appropriate in patients with certain forms of congenital heart disease or seizures.

Medication

Patients with Kallmann syndrome or idiopathic hypogonadotropic hypogonadism who do not desire fertility should have gonadal steroid replacement therapy, including testosterone in males and estrogen-progestin in females, unless contraindicated. Fertility options include either GnRH (gonadorelin [no longer commercially available in the US]) or gonadotropin-based regimens. Clomiphene may also be used in women with hypothalamic amenorrhea.

Androgens

Androgen replacement in males with Kallmann syndrome or idiopathic hypogonadotropic hypogonadism restores libido, erectile function, and well-being. In addition, androgen replacement promotes the development of secondary sex characteristics (eg, facial, axillary, and pubic hair) and increases muscle strength. A short course of androgens in infancy leads to penile growth in infants with micropenis. Androgen replacement also improves bone density and may prevent osteoporosis. Either parenteral or transdermal testosterone is the drug of choice for androgen replacement. Orally administered alkylated androgens should be avoided because of the risk of serious hepatic toxicity, including peliosis hepatitis, cholestasis, and hepatocellular carcinoma.


Testosterone (Andro-L.A., dep-Andro, Androderm, Androgel, Testim)

Promotes and maintains secondary sex characteristics in males who are androgen deficient.

Adult

75-150 mg IM q7-10d or 100-200 mg IM q2wk
Alternatively, apply a nonscrotal (5-mg) skin patch every pm or 2.5-7.5 g of 1% testosterone gel every morning

Pediatric

<12 years: Not established
>12 years: 50-100 mg IM every mo initially followed by 50-100 mg IM q2wk after 1 y of treatment, with gradual increase to adult dose

May increase effects of anticoagulants

Documented hypersensitivity; severe cardiac or renal disease; benign prostatic hypertrophy with obstruction; males with breast cancer; untreated sleep apnea

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Lower doses (such as 50-100 mg IM q2-4wk) initially recommended in adults with congenital hypogonadism or adults with benign prostate hypertrophy; prostate examination and serial determinations of serum prostate-specific antigen (PSA), serum testosterone, hematocrit, and serum lipids are indicated; contact dermatitis commonly occurs at application site in transdermal use; regular rotation of application sites is recommended

Steroid hormones

Estrogen replacement therapy in females with Kallmann syndrome or idiopathic hypogonadotropic hypogonadism promotes the development of secondary sex characteristics, including breast development and menstrual function, and it may prevent osteoporosis. Oral contraceptives may be used as replacement therapy in young women. A thorough discussion of estrogen replacement therapy in older (postmenopausal women) is beyond the scope of this review.


Conjugated estrogens (Premarin)

Induces the synthesis of DNA, RNA, and various proteins in target tissues. Promotes development of secondary sex characteristics.

Adult

0.625-1.25 mg/d PO for 21 d/mo or continuously

Pediatric

<12 years: Not established
>12 years: 0.3 mg PO qod for as long as 6 mo, slowly (at 6-mo intervals) increasing to adult dose

May reduce hypoprothrombinemic effect of anticoagulants; coadministration of barbiturates, rifampin, and other agents that induce hepatic microsomal enzymes may reduce estrogen levels; pharmacologic and toxicologic effects of corticosteroids may occur as a result of estrogen-induced inactivation of hepatic P450 enzyme; loss of seizure control has been noted when administered concurrently with hydantoins

Documented hypersensitivity; known or suspected pregnancy; breast cancer; undiagnosed abnormal genital bleeding; active thrombophlebitis or thromboembolic disorders; history of thrombophlebitis, thrombosis, or thromboembolic disorders

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Endometrial hyperplasia and increased risk of endometrial cancer can be prevented by adding a progestin (starting after occurrence of breakthrough bleeding or as long as 6 mo of estrogen therapy in adolescents); annual mammography is recommended in older women; endometrial biopsy is indicated for persistent, unanticipated vaginal bleeding


Ethinyl estradiol (Estinyl)

Induces the synthesis of DNA, RNA, and various proteins in target tissues. Promotes development of secondary sex characteristics.

Adult

10-20 mcg/d PO for 21 d/mo or continuously

Pediatric

Initial dose typically started at >12 years: 5-10 mcg/d PO for as long as 6 mo, slowly (in 6-mo intervals) increasing toward adult dose

Ethinyl estradiol may reduce hypoprothrombinemic effects of anticoagulants; estrogen levels may be reduced with coadministration of barbiturates, rifampin, and other agents that induce hepatic microsomal enzymes; increase in corticosteroid levels may occur when administered concurrently with ethinyl estradiol; use of ethinyl estradiol with hydantoins may reduce seizure control

Documented hypersensitivity; breast cancer; endometrial cancer; undiagnosed genital bleeding; pregnancy; active liver disease; venous thromboembolic disease

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Endometrial hyperplasia and increased risk of endometrial cancer can be prevented by adding a progestin (after occurrence of breakthrough bleeding or as long as 6 mo of estrogen therapy in adolescents); annual mammography is recommended in older women; endometrial biopsy is indicated for persistent, unanticipated vaginal bleeding


Estradiol (Estrace)

Increases synthesis of DNA, RNA, and many proteins in target tissues.

Adult

1-2 mg/d PO for 21 d/mo or continuously

Pediatric

Not established

May reduce hypoprothrombinemic effects of anticoagulants; estrogen levels may be reduced with coadministration of barbiturates, rifampin, and other agents that induce hepatic microsomal enzymes; increase in corticosteroid levels may occur when administered concurrently with ethinyl estradiol; use of ethinyl estradiol with hydantoins may reduce seizure control

Documented hypersensitivity; breast cancer; endometrial cancer; undiagnosed genital bleeding; pregnancy; active liver disease; venous thromboembolic disease

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Endometrial hyperplasia and increased risk of endometrial cancer can be prevented by adding a progestin; annual mammography recommended in older women; endometrial biopsy indicated for persistent, unanticipated vaginal bleeding; caution in hepatic impairment, migraine, seizure disorders, cerebrovascular disorders, breast cancer, or thromboembolic disease


Transdermal estradiol (Climara, Estraderm, FemPatch, Noven, Vivelle, Vivelle-Dot)

Increases synthesis of DNA, RNA, and many proteins in target tissues.

Adult

1 skin patch (delivering 0.05-0.10 mg/d) is applied once (Climara, FemPatch) or twice (Estraderm, Noven, Vivelle, Vivelle-Dot) per wk

Pediatric

Not established

May reduce hypoprothrombinemic effects of anticoagulants; estrogen levels may be reduced with coadministration of barbiturates, rifampin, and other agents that induce hepatic microsomal enzymes; increase in corticosteroid levels may occur when administered concurrently with estradiol; use of estradiol with hydantoins may reduce seizure control

Documented hypersensitivity; breast cancer; endometrial cancer; undiagnosed genital bleeding; pregnancy; active liver disease; venous thromboembolic disease

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Endometrial hyperplasia and increased risk of endometrial cancer can be prevented by adding a progestin; annual mammography is recommended in older women; endometrial biopsy is indicated for persistent, unanticipated vaginal bleeding

Progestins

Medroxyprogesterone is usually administered to female patients on estrogen replacement therapy for 12-14 d/mo. Induces secretory changes in endometrium and leads to withdrawal bleeding, which is essential for prevention of estrogen-induced endometrial hyperplasia. Patients on combination oral contraceptives already receive a progestin and do not need additional medroxyprogesterone therapy.


Medroxyprogesterone (Provera)

Stops endometrial cell proliferation, allowing organized sloughing of cells after withdrawal. Typically does not stop acute bleeding episode but produces a normal bleeding episode following withdrawal.

Adult

5-10 mg/d PO for 12-14 d/mo

Pediatric

2.5-5 mg/d PO for 12-14 d/mo (starting after occurrence of breakthrough bleeding on estrogen therapy)

May decrease effects of aminoglutethimide

Documented hypersensitivity; cerebral apoplexy; undiagnosed vaginal bleeding; thrombophlebitis; liver dysfunction

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Edema, bloating, nausea, cholestatic jaundice, mood swings, depression, and exacerbation of glucose intolerance may occur

Hypothalamic releasing hormones

Pulsatile administration of gonadorelin (GnRH) by subcutaneous (SC) or preferably intravenous (IV) infusion restores pituitary-gonadal axis function and fertility in the majority of people with Kallmann syndrome and idiopathic hypogonadotropic hypogonadism. Some patients with GnRH receptor mutations may respond to high-dose GnRH therapy. Gonadorelin is no longer commercially available in the US.


Gonadorelin (GnRH, Factrel, Lutrepulse)

Stimulates pituitary release of LH.

Adult

Males: 25-600 ng/kg (bolus) IV/SC q2h, generally needs to be continued for about 2 y
Females: 25-250 ng/kg (bolus) IV/SC q60-90min, up to q360min depending on phase of menstrual cycle
Titrated to effect in males and females

Pediatric

Not established

Decreases effects of oral contraceptives, digoxin, phenothiazines, and dopamine antagonists; increases effects of androgens, glucocorticoids, spironolactone, and levodopa

Documented hypersensitivity; ovarian cysts

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution if pregnancy is suspected; skin reactions (local and generalized), headache, nausea, and rare anaphylactic reactions may occur

Gonadotropins

These successfully restore fertility in most patients with Kallmann syndrome or idiopathic hypogonadotropic hypogonadism. Patients with idiopathic hypogonadotropic hypogonadism and AHC may have an intrinsic defect in spermatogenesis and may not respond to gonadotropin therapy. In men, hCG should be used alone for as long as 1 year and may be effective alone in patients with partial gonadotropin deficiency. Having verified that androgen levels are normal on hCG therapy, FSH should be added to the regimen after that period. In addition, induction of puberty with FSH and LH after a period of FSH priming has been proposed in boys.22 In females, ovulation induction protocols are complex and vary. A detailed discussion of these protocols is beyond the scope of this review.


Follicle-stimulating hormone (Fertinex, Follistim)

Stimulates gonadal steroid production. Either recombinant or human purified hormone may be used.

Adult

Males: 75-150 U IM q3-5d
Females: Ovulation induction protocols are complex and vary

Pediatric

Not established

Documented hypersensitivity; pregnancy; ovarian cysts; tumors of the breast, ovary, or endometrium

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Risk of ovarian hyperstimulation syndrome necessitates close monitoring by experienced reproductive endocrinologists; serious respiratory distress, thromboembolic events, and atelectasis may occur


Human chorionic gonadotropin (Chorex, Pregnyl, Profasi, Novarel)

Stimulates production of gonadal steroid hormones.

Adult

Males: 1000-2000 U IM 3 times/wk
Females: Ovulation induction protocols are complex and vary

Pediatric

Not established

Documented hypersensitivity; prostate cancer

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Gynecomastia, edema, headache, irritability, depression, and pain at injection sites may occur

Ovulation stimulators

Clomiphene acts as an antiestrogen to decrease negative estrogen feedback on hypothalamus. In addition, clomiphene may have effects on the pituitary gland and ovaries and can induce ovulation in women with hypothalamic amenorrhea. Clomiphene is not likely to be effective in patients with Kallmann syndrome or idiopathic hypogonadotropic hypogonadism.


Clomiphene citrate (Clomid, Milophene, Serophene)

Stimulates release of pituitary gonadotropins.

Adult

Females: 50-100 mg/d (as much as 250 mg/d as an off-label therapy) PO for 5 d, starting on the fifth day after withdrawal bleeding

Pediatric

Not established

Documented hypersensitivity; liver disease; undiagnosed uterine bleeding; ovarian cysts; pregnancy

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Vasomotor flushing, headache, breast discomfort, nausea, vomiting, abdominal bloating, and ovarian hyperstimulation syndrome may occur; variety of visual symptoms reported; prolonged use of clomiphene may increase risk for ovarian cancer

More on Kallmann Syndrome and Idiopathic Hypogonadotropic Hypogonadism

Overview: Kallmann Syndrome and Idiopathic Hypogonadotropic Hypogonadism
Differential Diagnoses & Workup: Kallmann Syndrome and Idiopathic Hypogonadotropic Hypogonadism
Treatment & Medication: Kallmann Syndrome and Idiopathic Hypogonadotropic Hypogonadism
Follow-up: Kallmann Syndrome and Idiopathic Hypogonadotropic Hypogonadism
Multimedia: Kallmann Syndrome and Idiopathic Hypogonadotropic Hypogonadism
References
Further Reading
[ CLOSE WINDOW ]

References

  1. Dode C, Levilliers J, Dupont JM, et al. Loss-of-function mutations in FGFR1 cause autosomal dominant Kallmann syndrome. Nat Genet. Apr 2003;33(4):463-5. [Medline].

  2. Pitteloud N, Quinton R, Pearce S, et al. Digenic mutations account for variable phenotypes in idiopathic hypogonadotropic hypogonadism. J Clin Invest. Feb 2007;117(2):457-63. [Medline]. [Full Text].

  3. Monnier C, Dode C, Fabre L, et al. PROKR2 missense mutations associated with Kallmann syndrome impair receptor signalling-activity. Hum Mol Genet. Sep 29 2008;[Medline].

  4. Abreu AP, Trarbach EB, de Castro M, et al. LOSS-OF-FUNCTION MUTATIONS IN THE GENES ENCODING PROKINETICIN-2 OR PROKINETICIN RECEPTOR-2 CAUSE AUTOSOMAL RECESSIVE KALLMANN SYNDROME. J Clin Endocrinol Metab. Aug 5 2008;[Medline].

  5. Pitteloud N, Zhang C, Pignatelli D, et al. Loss-of-function mutation in the prokineticin 2 gene causes Kallmann syndrome and normosmic idiopathic hypogonadotropic hypogonadism. Proc Natl Acad Sci U S A. Oct 30 2007;104(44):17447-52. [Medline]. [Full Text].

  6. Dode C, Teixeira L, Levilliers J, et al. Kallmann syndrome: mutations in the genes encoding prokineticin-2 and prokineticin receptor-2. PLoS Genet. Oct 20 2006;2(10):e175. [Medline]. [Full Text].

  7. Canto P, Munguía P, Söderlund D, et al. Genetic analysis in patients with Kallmann syndrome: coexistance of mutations in prokineticin receptor 2 and KAL1. J Androl. Aug 21 2008;[Medline].

  8. Merke DP, Tajima T, Baron J, et al. Hypogonadotropic hypogonadism in a female caused by an X-linked recessive mutation in the DAX1 gene. N Engl J Med. 1999;340(16):1248-52. [Medline].

  9. Clement K, Vaisse C, Lahlou N, et al. A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Nature. Mar 26 1998;392(6674):398-401. [Medline].

  10. Pralong FP, Gomez F, Castillo E, et al. Complete hypogonadotropic hypogonadism associated with a novel inactivating mutation of the gonadotropin-releasing hormone receptor. J Clin Endocrinol Metab. Oct 1999;84(10):3811-6. [Medline].

  11. Seminara SB, Messager S, Chatzidaki EE, et al. The GPR54 gene as a regulator of puberty. N Engl J Med. Oct 23 2003;349(17):1614-27. [Medline]. [Full Text].

  12. Dhillo WS, Chaudhri OB, Patterson M, et al. Kisspeptin-54 stimulates the hypothalamic-pituitary gonadal axis in human males. J Clin Endocrinol Metab. Dec 2005;90(12):6609-15. [Medline].

  13. Gottsch ML, Cunningham MJ, Smith JT, et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology. Sep 2004;145(9):4073-7. [Medline]. [Full Text].

  14. Miura K, Acierno JS, Seminara SB. Characterization of the human nasal embryonic LHRH factor gene, NELF, and a mutation screening among 65 patients with idiopathic hypogonadotropic hypogonadism (IHH). J Hum Genet. 2004;49(5):265-8. [Medline].

  15. Fromantin M, Gineste J, Didier A, et al. [Impuberism and hypogonadism at induction into military service. Statistical study]. Probl Actuels Endocrinol Nutr. May 3 1973;16:179-99. [Medline].

  16. Filippi G. Klinefelter's syndrome in Sardinia. Clinical report of 265 hypogonadic males detected at the time of military check-up. Clin Genet. Oct 1986;30(4):276-84. [Medline].

  17. Seminara SB, Hayes FJ, Crowley WF Jr. Gonadotropin-releasing hormone deficiency in the human (idiopathic hypogonadotropic hypogonadism and Kallmann''s syndrome): pathophysiological and genetic considerations. Endocr Rev. Oct 1998;19(5):521-39. [Medline]. [Full Text].

  18. Trarbach EB, Silveira LG, Latronico AC. Genetic insights into human isolated gonadotropin deficiency. Pituitary. 2007;10(4):381-91. [Medline].

  19. Seminara SB, Achermann JC, Genel M, et al. X-linked adrenal hypoplasia congenita: a mutation in DAX1 expands the phenotypic spectrum in males and females. J Clin Endocrinol Metab. Dec 1999;84(12):4501-9. [Medline].

  20. Beranova M, Oliveira LM, Bedecarrats GY, et al. Prevalence, phenotypic spectrum, and modes of inheritance of gonadotropin-releasing hormone receptor mutations in idiopathic hypogonadotropic hypogonadism. J Clin Endocrinol Metab. Apr 2001;86(4):1580-8. [Medline].

  21. Quinton R, Duke VM, de Zoysa PA, et al. The neuroradiology of Kallmann's syndrome: a genotypic and phenotypic analysis. J Clin Endocrinol Metab. Aug 1996;81(8):3010-7. [Medline]. [Full Text].

  22. Raivio T, Wikstrom AM, Dunkel L. Treatment of gonadotropin-deficient boys with recombinant human FSH: long-term observation and outcome. Eur J Endocrinol. Jan 2007;156(1):105-11. [Medline].

  23. Raivio T, Falardeau J, Dwyer A, et al. Reversal of idiopathic hypogonadotropic hypogonadism. N Engl J Med. Aug 30 2007;357(9):863-73. [Medline]. [Full Text].

  24. Hoffman AR, Crowley WF Jr. Induction of puberty in men by long-term pulsatile administration of low-dose gonadotropin-releasing hormone. N Engl J Med. Nov 11 1982;307(20):1237-41. [Medline].

  25. Iovane A, Aumas C, de Roux N. New insights in the genetics of isolated hypogonadotropic hypogonadism. Eur J Endocrinol. Nov 2004;151 Suppl 3:U83-8. [Medline].

  26. Layman LC. The molecular basis of human hypogonadotropic hypogonadism. Mol Genet Metab. Oct 1999;68(2):191-9. [Medline].

  27. Nachtigall LB, Boepple PA, Pralong FP, et al. Adult-onset idiopathic hypogonadotropic hypogonadism--a treatable form of male infertility. N Engl J Med. Feb 6 1997;336(6):410-5. [Medline].

  28. Pawlowitzki IH, Diekstall P, Schadel A, et al. Estimating frequency of Kallmann syndrome among hypogonadic and among anosmic patients. Am J Med Genet. Feb 1987;26(2):473-9. [Medline].

  29. Pitteloud N, Acierno JS Jr, Meysing A, et al. Mutations in fibroblast growth factor receptor 1 cause both Kallmann syndrome and normosmic idiopathic hypogonadotropic hypogonadism. Proc Natl Acad Sci U S A. Apr 18 2006;103(16):6281-6. [Medline].

  30. Pitteloud N, Acierno JS Jr, Meysing AU, et al. Reversible Kallmann syndrome, delayed puberty, and isolated anosmia occurring in a single family with a mutation in the fibroblast growth factor receptor 1 gene. J Clin Endocrinol Metab. Mar 2005;90(3):1317-22. [Medline]. [Full Text].

  31. Quinton R, Cheow HK, Tymms DJ, et al. Kallmann's syndrome: is it always for life?. Clin Endocrinol (Oxf). Apr 1999;50(4):481-5. [Medline].

  32. Rugarli EI, Ballabio A. Kallmann syndrome. From genetics to neurobiology. JAMA. Dec 8 1993;270(22):2713-6. [Medline].

  33. Silveira LF, MacColl GS, Bouloux PM. Hypogonadotropic hypogonadism. Semin Reprod Med. Nov 2002;20(4):327-38. [Medline].

  34. Waldstreicher J, Seminara SB, Jameson JL, et al. The genetic and clinical heterogeneity of gonadotropin-releasing hormone deficiency in the human. J Clin Endocrinol Metab. Dec 1996;81(12):4388-95. [Medline]. [Full Text].

[ CLOSE WINDOW ]

Keywords

Kallmann syndrome, KS, idiopathic hypogonadotropic hypogonadism, IHH, gonadotropin-releasing hormone, De Morsier syndrome, olfactogenital dysplasia, acquired idiopathic hypogonadotropic hypogonadism, gonadotropin-releasing hormone deficiency, hypothalamic amenorrhea, GnRH deficiency, DAX1, fertile eunuch syndrome, classic KS, classic IHH, congenital KS, congenital IHH, adult-onset IHH, acquired IHH, X-linked KS, gonadal steroid replacement therapy, anosmia, hyposmia

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Nicholas A Tritos, MD, DSc, MMSc, FACE, FACP, Assistant Professor of Medicine, Tufts University School of Medicine; Senior Staff Physician, Department of Endocrinology, Lahey Clinic Medical Center
Nicholas A Tritos, MD, DSc, MMSc, FACE, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Medical Association, Endocrine Society, Massachusetts Medical Society, and Pituitary Society
Disclosure: Nothing to disclose.

Medical Editor

Ghassem Pourmotabbed, MD†, Former Associate Professor, Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Tennessee School of Medicine and Health Science Center
Ghassem Pourmotabbed, MD† is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, and Endocrine Society
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 and 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.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.