eMedicine Specialties > Pediatrics: Genetics and Metabolic Disease > Genetics

Neurofibromatosis: Differential Diagnoses & Workup

Author: Beth A Pletcher, MD, Associate Professor, Co-Director of The Neurofibromatosis Center of New Jersey, Department of Pediatrics, University of Medicine and Dentistry of New Jersey
Contributor Information and Disclosures

Updated: Nov 11, 2009

Differential Diagnoses

Café Au Lait Spots
Leguis syndrome
McCune-Albright Syndrome

Other Problems to Be Considered

Neurofibromatosis type 2

Workup

Laboratory Studies

  • Genetic testing 
    • Sequencing of the neurofibromin gene has a high detection rate and is the preferred molecular diagnostic study for individuals suspected to have neurofibromatosis type 1 (NF1).
    • Detection rates using current sequencing methodologies is greater than 95% in clinically affected individuals.
    • Molecular testing is sometimes also useful in confirming the diagnosis in patients with a single clinical finding (eg, multiple café-au-lait spots) in the absence of a family history. 
  • Prenatal diagnosis 
    • In a family with multiple affected members and no recognizable mutation, linkage analysis can be used to track the NF1 gene through the generations to determine which chromosome 17 region the fetus received.
    • For a parent with neurofibromatosis type 1 who is the only affected family member, sequencing can often identify a specific gene mutation. Once a mutation is identified in an affected parent, prenatal diagnosis using amniocytes or chorionic villi may be feasible.
    • When a parent has an identified gene mutation, preimplantation genetic diagnosis may also be possible, if the couple is willing and able to undergo in vitro fertilization followed by transfer of unaffected embryos.
  • Detection of a pheochromocytoma
    • Urinary free catecholamines (ie, norepinephrine and epinephrine), as well as their metabolites (ie, normetanephrine, metanephrine, and vanillylmandelic acid), measured on a 24-hour urine collection specimen are very good biochemical screening tests for suspected pheochromocytoma.12
    • Plasma catecholamines may also be measured using liquid chromatography. Measurement of free plasma metanephrine is more sensitive in the detection of a pheochromocytoma than plasma catecholamines.13

Imaging Studies

  • Radiography
    • Plain-film radiography may detect various subtle and not-so-subtle bony abnormalities associated with neurofibromatosis type 1. Dural ectasias are often seen incidentally on vertebral radiographs in individuals with neurofibromatosis type 1 or Marfan syndrome and may be harbingers of progressive scoliosis yet to come.
    • Perform radiography when the following or similar clinical findings are identified:
      • Possible modeling defects of the long bones or ribs
      • Concerns about bony erosion secondary to an adjacent plexiform neurofibroma
      • Signs of scoliosis
      • Bone pain
  • MRI and CT scans
    • In the past, head MRI and CT scanning was routinely performed in patients with neurofibromatosis type 1. Recently, many clinicians have deviated from standard screening and have opted to use head imaging only for specific indications.
    • Some clinicians perform baseline CT scanning or MRI of the head in children at the time of diagnosis and then do not recommend further scanning unless neurologic problems arise. Other clinicians believe baseline studies have limited value because even detection of an asymptomatic optic nerve glioma does not necessarily prompt medical intervention. Some groups in Europe still advocate for annual brain MRIs in children with neurofibromatosis type 1.
    • MRI has become the preferred diagnostic head imaging study in neurofibromatosis type 1. Experience over the past decade has shown MRI often reveals unidentified bright objects (UBOs) in the brain parenchyma of patients with neurofibromatosis type 1. These bright spots, seen on T2-weighted images, generally do not enhance, cause no mass effect, and often resolve as the individual ages. UBOs are believed to represent benign hamartomas in neurofibromatosis type 1 and are seen more often in children with neurofibromatosis type 1–related learning disabilities and fine motor difficulties.
    • MRI may also reveal focal brainstem lesions that may or may not enhance. Much like the optic nerve lesions, these brainstem lesions tend to be quite indolent and rarely require treatment.14
    • Consider CT scanning or MRI to evaluate ventricular size when increasing head circumferences are noted in an infant. Hydrocephalus rarely occurs in children with neurofibromatosis type 1.
    • MRI is a valuable tool to evaluate the optic nerves or optic chiasm. MRI is indicated for patients with optic nerve pallor, visual changes, proptosis, or precocious puberty. Clinicians should communicate their concerns about optic nerve pathology when ordering this test so that special orbital views are obtained.
    • Consider MRI of the head for patients with headaches that increase in frequency or intensity over time. Although brain tumors are less common in patients with neurofibromatosis type 1 than in those with neurofibromatosis type 2 (NF2), they do occur.
    • MRI has also proven useful in evaluating internal lesions (eg, mediastinal masses, spinal cord tumors, deep plexiform neurofibromas, abdominopelvic lesions, neurofibromas of the brachial or sacral plexus). Serial MRIs of plexiform lesions with volumetric measurements may prove valuable in monitoring growth over time.15
    • MRI using short T1-inversion recovery may be helpful in providing accurate volumetric measurements of plexiform neurofibromas at initial diagnosis and serially over time.
    • Although MRI is not always helpful in differentiating benign peripheral nerve sheath lesions from malignant lesions, central hypointense areas within a lesions noted on T2-weighted images (the so-called target sign) is more suggestive of a benign lesion.16 On the other hand, MRI evidence of intratumoral lobulation or T1 high-signal intensity are much more suggestive of malignant transformation.
    • CT scanning and MRI are first-line imaging studies when pheochromocytoma is suspected based on abnormal serum or urine screening tests.12
  • Positron emission tomography: F-18 fluorodeoxyglucose positron emission tomography (FDG-PET) may be used to stage and follow malignant peripheral nerve sheath tumors (MPNSTs).17
  • Scintigraphy
    • If a CT scanning and MRI are unable to identify a suspected pheochromocytoma, then metaiodobenzylguanidine (MIBG) scintigraphy is indicated.18
    • Gallium-67 scintigraphy may be used as a screening tool, especially those patients with a large plexiform neurofibroma when one or more areas within the lesion may have undergone malignant transformation.19

Other Tests

  • EEG is indicated for patients who exhibit symptoms that suggest a seizure disorder. Seizures are reported more often in children and adults with neurofibromatosis type 1.
  • Myelography is occasionally needed to clarify the extent of a spinal cord tumor. MRI alone generally suffices for making medical or surgical decisions.
  • Visual evoked potentials (VEPS) may prove helpful in detecting optic nerve gliomas or assessing tumor progression in patients with previously diagnosed optic pathway tumors.

Procedures

  • Slit-lamp examination
    • Slit-lamp examination by an experienced ophthalmologist provides essential diagnostic information in older children and adults who present with only one clinical criterion (eg, multiple café au lait spots).
    • Lisch nodule occurrence appears to depend on age; more than 95% of individuals with neurofibromatosis type 1 older than 10 years exhibit this finding.
    • Slit-lamp examination is also valuable in determining whether the parents of an affected child carry the NF1 mutation, even when the parent has no other signs of the condition.
  • Laser treatment
    • Laser removal of neurofibromas (whether medically or cosmetically indicated) is a common procedure for individuals with neurofibromatosis type 1.
    • Recent advances in laser technology allow nonsurgical removal of small cutaneous neurofibromas; however, careful surgical resection of small or large neurofibromas may leave a smaller, less prominent scar.
    • Although laser treatment has been used to remove various cutaneous hyperpigmented lesions (eg, port wine stains, tattoos), it has not proven effective in permanent removal of café au lait spots.

Histologic Findings

  • Neurofibromas are typically well-differentiated tumors containing elongated spindle-shaped cells and pleomorphic fibroblastlike cells. Inflammatory cells rarely occur in these otherwise benign-appearing lesions. Optic gliomas are also quite indolent and generally are low-grade lesions; optic nerve lesions associated with neurofibromatosis type 1 are less aggressive than optic nerve tumors in the general population and respond better to current therapies.
  • Neurofibromas, typically of the large or deep plexiform variety, sometimes undergo malignant transformation to neurofibrosarcomas. Unlike benign neurofibromas, neurofibrosarcomas are characteristically hypercellular with giant cells, an increased number of mitoses, and vascular proliferation. Because rests of malignant cells may embed between larger masses of benign cells in a plexiform neurofibroma, careful examination of a plexiform tumor is important; take samples from multiple regions to confirm the lesion is benign.

More on Neurofibromatosis

Overview: Neurofibromatosis
Differential Diagnoses & Workup: Neurofibromatosis
Treatment & Medication: Neurofibromatosis
Follow-up: Neurofibromatosis
Multimedia: Neurofibromatosis
References
[ CLOSE WINDOW ]

References

  1. Dugoff L, Sujansky E. Neurofibromatosis type 1 and pregnancy. Am J Med Genet. Dec 2 1996;66(1):7-10. [Medline].

  2. Darrigo LG Jr, Geller M, Bonalumi Filho A, et al. Prevalence of plexiform neurofibroma in children and adolescents with type I neurofibromatosis. J Pediatr (Rio J). Nov-Dec 2007;83(6):571-3. [Medline].

  3. Porter DE, Prasad V, Foster L, et al. Survival in Malignant Peripheral Nerve Sheath Tumours: A Comparison between Sporadic and Neurofibromatosis Type 1-Associated Tumours. Sarcoma. 2009;2009:756395. [Medline].

  4. Rodriguez FJ, Perry A, Gutmann DH, et al. Gliomas in neurofibromatosis type 1: a clinicopathologic study of 100 patients. J Neuropathol Exp Neurol. Mar 2008;67(3):240-9. [Medline].

  5. Krab LC, Aarsen FK, de Goede-Bolder A, et al. Impact of neurofibromatosis type 1 on school performance. J Child Neurol. Sep 2008;23(9):1002-10. [Medline].

  6. Brunetti-Pierri N, Doty SB, Hicks J, et al. Generalized metabolic bone disease in Neurofibromatosis type I. Mol Genet Metab. May 2008;94(1):105-11. [Medline].

  7. Stevenson DA, Schwarz EL, Viskochil DH, et al. Evidence of increased bone resorption in neurofibromatosis type 1 using urinary pyridinium crosslink analysis. Pediatr Res. Jun 2008;63(6):697-701. [Medline].

  8. Seitz S, Schnabel C, Busse B, Schmidt HU, Beil FT, Friedrich RE. High bone turnover and accumulation of osteoid in patients with neurofibromatosis 1. Osteoporos Int. May 5 2009;[Medline].

  9. Rea D, Brandsema JF, Armstrong D, Parkin PC, Deveber G, Macgregor D. Cerebral Arteriopathy in Children With Neurofibromatosis Type 1. Pediatrics. Aug 24 2009;[Medline].

  10. Ardagil A, Yaylali S, Erbil H, et al. The prevalence of anisometropia aniso-astigmatism and amblyopia in neurofibromatosis type 1. Eur J Ophthalmol. May-Jun 2009;19(3):470-4. [Medline].

  11. Spurlock G, Bennett E, Chuzhanova N, et al. SPRED1 mutations (Legius syndrome): another clinically useful genotype for dissecting the neurofibromatosis type 1 phenotype. J Med Genet. Jul 2009;46(7):431-7. [Medline].

  12. Karagiannis A, Mikhailidis DP, Athyros VG, et al. Pheochromocytoma: an update on genetics and management. Endocr Relat Cancer. Dec 2007;14(4):935-56. [Medline].

  13. Lenders JW, Pacak K, Walther MM, et al. Biochemical diagnosis of pheochromocytoma: which test is best?. JAMA. Mar 20 2002;287(11):1427-34. [Medline].

  14. Ullrich NJ, Raja AI, Irons MB, et al. Brainstem lesions in neurofibromatosis type 1. Neurosurgery. Oct 2007;61(4):762-6; discussion 766-7. [Medline].

  15. Tucker T, Friedman JM, Friedrich RE, et al. Longitudinal study of neurofibromatosis 1 associated plexiform neurofibromas. J Med Genet. Feb 2009;46(2):81-5. [Medline].

  16. Iannicelli E, Rossi G, Almberger M, et al. Integrated imaging in peripheral nerve lesions in type 1 neurofibromatosis. Radiol Med (Torino). Apr 2002;103(4):332-43. [Medline].

  17. Benz MR, Tchekmedyian N, Eilber FC, et al. Utilization of positron emission tomography in the management of patients with sarcoma. Curr Opin Oncol. Jul 2009;21(4):345-51. [Medline].

  18. Pacak K, Eisenhofer G, Ahlman H, et al. Pheochromocytoma: recommendations for clinical practice from the First International Symposium. October 2005. Nat Clin Pract Endocrinol Metab. Feb 2007;3(2):92-102. [Medline].

  19. Levine E, Huntrakoon M, Wetzel LH. Malignant nerve-sheath neoplasms in neurofibromatosis: distinction from benign tumors by using imaging techniques. AJR Am J Roentgenol. Nov 1987;149(5):1059-64. [Medline].

  20. Lee AG. Neuroophthalmological management of optic pathway gliomas. Neurosurg Focus. 2007;23(5):E1. [Medline].

  21. Binning MJ, Liu JK, Kestle JR, et al. Optic pathway gliomas: a review. Neurosurg Focus. 2007;23(5):E2. [Medline].

  22. Laigle-Donadey F, Doz F, Delattre JY. Brainstem gliomas in children and adults. Curr Opin Oncol. Nov 2008;20(6):662-7. [Medline].

  23. Packer RJ, Jakacki R, Horn M, et al. Objective response of multiply recurrent low-grade gliomas to bevacizumab and irinotecan. Pediatr Blood Cancer. Jul 2009;52(7):791-5. [Medline].

  24. Wojtkowiak JW, Fouad F, LaLonde DT, et al. Induction of apoptosis in neurofibromatosis type 1 malignant peripheral nerve sheath tumor cell lines by a combination of novel farnesyl transferase inhibitors and lovastatin. J Pharmacol Exp Ther. Jul 2008;326(1):1-11. [Medline].

  25. Ambrosini G, Cheema HS, Seelman S, et al. Sorafenib inhibits growth and mitogen-activated protein kinase signaling in malignant peripheral nerve sheath cells. Mol Cancer Ther. Apr 2008;7(4):890-6. [Medline].

  26. Johansson G, Mahller YY, Collins MH, et al. Effective in vivo targeting of the mammalian target of rapamycin pathway in malignant peripheral nerve sheath tumors. Mol Cancer Ther. May 2008;7(5):1237-45. [Medline].

  27. Cui Y, Costa RM, Murphy GG, et al. Neurofibromin regulation of ERK signaling modulates GABA release and learning. Cell. Oct 31 2008;135(3):549-60. [Medline].

  28. Gerszten PC, Burton SA, Ozhasoglu C, et al. Radiosurgery for benign intradural spinal tumors. Neurosurgery. Apr 2008;62(4):887-95; discussion 895-6. [Medline].

  29. Bravo EL, Tagle R. Pheochromocytoma: state-of-the-art and future prospects. Endocr Rev. Aug 2003;24(4):539-53. [Medline].

  30. Wolkenstein P, Rodriguez D, Ferkal S, et al. Impact of neurofibromatosis 1 upon quality of life in childhood: a cross-sectional study of 79 cases. Br J Dermatol. Apr 2009;160(4):844-8. [Medline].

  31. [Guideline] Radtke HB, Sebold CD, Allison C, Haidle JL, Schneider G. Neurofibromatosis type 1 in genetic counseling practice: recommendations of the National Society of Genetic Counselors. J Genet Couns. Aug 2007;16(4):387-407. [Medline].

  32. Baralle D, Mattocks C, Kalidas K, et al. Different mutations in the NF1 gene are associated with Neurofibromatosis-Noonan syndrome (NFNS). Am J Med Genet A. May 15 2003;119A(1):1-8. [Medline].

  33. Barton B, North K. Social skills of children with neurofibromatosis type 1. Dev Med Child Neurol. Aug 2004;46(8):553-63. [Medline].

  34. Chander S, Westphal SM, Zak IT, et al. Retroperitoneal malignant peripheral nerve sheath tumor: evaluation with serial FDG-PET. Clin Nucl Med. Jul 2004;29(7):415-8. [Medline].

  35. DeClue JE, Cohen BD, Lowy DR. Identification and characterization of the neurofibromatosis type 1 protein product. Proc Natl Acad Sci U S A. Nov 15 1991;88(22):9914-8. [Medline].

  36. Deliganis AV, Geyer JR, Berger MS. Prognostic significance of type 1 neurofibromatosis (von Recklinghausen Disease) in childhood optic glioma. Neurosurgery. Jun 1996;38(6):1114-8; discussion 1118-9. [Medline].

  37. Evans DG, Baser ME, McGaughran J, et al. Malignant peripheral nerve sheath tumours in neurofibromatosis 1. J Med Genet. May 2002;39(5):311-4. [Medline].

  38. Feldmann R, Denecke J, Grenzebach M, et al. Neurofibromatosis type 1: motor and cognitive function and T2-weighted MRI hyperintensities. Neurology. Dec 23 2003;61(12):1725-8. [Medline].

  39. Gutmann DH, Collins FS. The neurofibromatosis type 1 gene and its protein product, neurofibromin. Neuron. Mar 1993;10(3):335-43. [Medline].

  40. Habiby R, Silverman B, Listernick R, et al. Precocious puberty in children with neurofibromatosis type 1. J Pediatr. Mar 1995;126(3):364-7. [Medline].

  41. Health supervision for children with neurofibromatosis. American Academy of Pediatrics Committee on Genetics. Pediatrics. Aug 1995;96(2 Pt 1):368-72. [Medline].

  42. Heuschkel R, Kim S, Korf B, et al. Abdominal migraine in children with neurofibromatosis type 1: a case series and review of gastrointestinal involvement in NF1. J Pediatr Gastroenterol Nutr. Aug 2001;33(2):149-54. [Medline].

  43. Hughes RJ, Scoble JE, Reidy JF. Renal angioplasty in non-atheromatous renal artery stenosis: technical results and clinical outcome in 43 patients. Cardiovasc Intervent Radiol. Sep-Oct 2004;27(5):435-40. [Medline].

  44. Karadimas P, Hatzispasou E, Bouzas EA. Retinal vascular abnormalities in neurofibromatosis type 1. J Neuroophthalmol. Dec 2003;23(4):274-5. [Medline].

  45. Korf BR. Malignancy in neurofibromatosis type 1. Oncologist. 2000;5(6):477-85. [Medline].

  46. Listernick R, Ferner RE, Piersall L, et al. Late-onset optic pathway tumors in children with neurofibromatosis 1. Neurology. Nov 23 2004;63(10):1944-6. [Medline].

  47. Mahoney DH Jr, Cohen ME, Friedman HS, et al. Carboplatin is effective therapy for young children with progressive optic pathway tumors: a Pediatric Oncology Group phase II study. Neuro Oncol. Oct 2000;2(4):213-20. [Medline].

  48. Matsumine A, Kusuzaki K, Nakamura T, et al. Differentiation between neurofibromas and malignant peripheral nerve sheath tumors in neurofibromatosis 1 evaluated by MRI. J Cancer Res Clin Oncol. Jul 2009;135(7):891-900. [Medline].

  49. Mautner VF, Kluwe L, Thakker SD, et al. Treatment of ADHD in neurofibromatosis type 1. Dev Med Child Neurol. Mar 2002;44(3):164-70. [Medline].

  50. Mentzel HJ, Seidel J, Fitzek C, et al. Pediatric brain MRI in neurofibromatosis type I. Eur Radiol. Apr 2005;15(4):814-22. [Medline].

  51. Mohrenschlager M, Engst R, Muller-Weihrich S, et al. Association of urticaria pigmentosa with café-au-lait spots, neurofibromas and neurofibroma-like neoplasms: a mere coincidence?. Dermatology. 2003;206(4):297-302. [Medline].

  52. Nakakura S, Shiraki K, Yasunari T, et al. Quantification and anatomic distribution of choroidal abnormalities in patients with type I neurofibromatosis. Graefes Arch Clin Exp Ophthalmol. Oct 2005;243(10):980-4. [Medline].

  53. Neurofibromatosis. Conference statement. National Institutes of Health Consensus Development Conference. Arch Neurol. May 1988;45(5):575-8. [Medline].

  54. Ng YT, North KN. Visual-evoked potentials in the assessment of optic gliomas. Pediatr Neurol. Jan 2001;24(1):44-8. [Medline].

  55. North KN, Riccardi V, Samango-Sprouse C, et al. Cognitive function and academic performance in neurofibromatosis. 1: consensus statement from the NF1 Cognitive Disorders Task Force. Neurology. Apr 1997;48(4):1121-7. [Medline].

  56. Parsa CF, Hoyt CS, Lesser RL, et al. Spontaneous regression of optic gliomas: thirteen cases documented by serial neuroimaging. Arch Ophthalmol. Apr 2001;119(4):516-29. [Medline].

  57. Riccardi VM. Neurofibromatosis: Phenotype, Natural History and Pathogenesis. 2nd ed. Baltimore, Md: Johns Hopkins University Press; 1992..

  58. Schrimsher GW, Billingsley RL, Slopis JM, et al. Visual-spatial performance deficits in children with neurofibromatosis type-1. Am J Med Genet A. Jul 30 2003;120A(3):326-30. [Medline].

  59. Scott RM, Smith JL, Robertson RL, et al. Long-term outcome in children with moyamoya syndrome after cranial revascularization by pial synangiosis. J Neurosurg. Feb 2004;100(2 Suppl Pediatrics):142-9. [Medline].

  60. Solomon J, Warren K, Dombi E, et al. Automated detection and volume measurement of plexiform neurofibromas in neurofibromatosis 1 using magnetic resonance imaging. Comput Med Imaging Graph. Jul 2004;28(5):257-65. [Medline].

  61. Thiagalingam S, Flaherty M, Billson F, et al. Neurofibromatosis type 1 and optic pathway gliomas: follow-up of 54 patients. Ophthalmology. Mar 2004;111(3):568-77. [Medline].

  62. Tubbs RS, Rutledge SL, Kosentka A, et al. Chiari I malformation and neurofibromatosis type 1. Pediatr Neurol. Apr 2004;30(4):278-80. [Medline].

  63. Vinters HV, Kerfoot C, Catania M, et al. Tuberous sclerosis-related gene expression in normal and dysplastic brain. Epilepsy Res. Sep 1998;32(1-2):12-23. [Medline].

  64. Virdis R, Street ME, Bandello MA, et al. Growth and pubertal disorders in neurofibromatosis type 1. J Pediatr Endocrinol Metab. Mar 2003;16 Suppl 2:289-92. [Medline].

  65. Vivarelli R, Grosso S, Calabrese F, et al. Epilepsy in neurofibromatosis 1. J Child Neurol. May 2003;18(5):338-42. [Medline].

  66. Zacharia TT, Jaramillo D, Poussaint TY, et al. MR imaging of abdominopelvic involvement in neurofibromatosis type 1: a review of 43 patients. Pediatr Radiol. Mar 2005;35(3):317-22. [Medline].

  67. Zoller M, Rembeck B, Akesson HO, et al. Life expectancy, mortality and prognostic factors in neurofibromatosis type 1. A twelve-year follow-up of an epidemiological study in Goteborg, Sweden. Acta Derm Venereol. Mar 1995;75(2):136-40. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

neurofibromatosis, NF, classic neurofibromatosis, neurofibromatosis type 1, NF1, neurofibromatosis type 2, NF2, von Recklinghausen disease, hamartomas, optic nerve gliomas, spinal cord tumors, scoliosis, long-bone abnormalities, treatment, diagnosis

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Beth A Pletcher, MD, Associate Professor, Co-Director of The Neurofibromatosis Center of New Jersey, Department of Pediatrics, University of Medicine and Dentistry of New Jersey
Beth A Pletcher, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Medical Genetics, American Medical Association, and American Society of Human Genetics
Disclosure: Nothing to disclose.

Medical Editor

Ian Krantz, MD, Department of Pediatrics, Assistant Professor, University of Pennsylvania and Children's Hospital of Philadelphia
Ian Krantz, MD is a member of the following medical societies: American Society of Human Genetics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Leonard G Feld, MD, PhD, MMM, FAAP, Sara H Bissell and Howard C Bissell Endowed Chair in Pediatrics, Chief Medical Officer, Levine Children's Hospital, Carolinas Medical Center
Leonard G Feld, MD, PhD, MMM, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Physician Executives, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Juvenile Diabetes Foundation International
Disclosure: Nothing to disclose.

CME Editor

Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Bruce Buehler, MD, Professor, Department of Pediatrics, Pathology and Microbiology, Executive Director, Hattie B Munroe Center for Human Genetics, University of Nebraska Medical Center
Bruce Buehler, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Pediatrics, American Association on Mental Retardation, American College of Medical Genetics, American College of Physician Executives, American Medical Association, and Nebraska Medical Association
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.