eMedicine Specialties > Pulmonology > Idiopathic Lung Disorders

Milroy Disease

Raphael J Kiel, MD, Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Infectious Diseases Division, William Beaumont Hospital

Updated: Oct 16, 2008

Introduction

Background

Lymphedema is characterized by swelling of the soft tissue secondary to obstruction of lymphatic drainage. Lymphatic obstruction causes an increase in the protein content of the extravascular tissue with subsequent retention of water. The increase in the extravascular protein stimulates proliferation of fibroblasts, organization of the fluid, and development of a "woody feeling" nonpitting swelling of the affected extremity. Fibrosis also obstructs the lymphatic channels and leads to increased protein concentration in the tissues, continuing this cycle. Lymphedema opens channels in the integument and allows bacteria to enter the subcuticular space, which overwhelms host defenses and leads to cellulitis of the extremity.

Lymphedema is classified into primary and secondary forms. Secondary lymphedema occurs as a result of obstruction of lymphatic flow by known mechanisms, ie, filariasis, silica, obstruction by a proximal mass, postsurgical mechanisms (eg, mastectomy), and fibrosis secondary to chronic infections.

Primary lymphedema is divided into 3 groups based on age of onset.¹ Congenital lymphedema that is present at birth and associated with an autosomal dominant familial history is called Milroy disease.² Lymphedema praecox (Meige disease) occurs after birth but before 35 years; the age of onset is generally in adolescence.³ Lymphedema tarda occurs in individuals older than 35 years. Of patients with primary lymphedema, 10% have Milroy disease, 80% have lymphedema praecox, and 10% have lymphedema tarda (manifesting in persons older than 35 y).

A related article posted on Medscape is " Diagnosis and Management of Lymphatic Vascular Disease."

Pathophysiology

Hypoplasia, dilation, and tortuosity of lymphatic structures characterize primary lymphedema. Failure of adequate clearance of lymphatic fluid leads to accumulation of protein in the extracellular fluid. Fibroblasts are stimulated, and the swelling becomes organized and nonpitting. Obstruction of normal lymph flow predisposes patients to recurrent infection with streptococci or staphylococci. These infections cause more lymphatic destruction and predispose patients to prolonged episodes of lymphedema and recurrent bacterial infection.⁴

A tyrosine kinase receptor specific for lymphatic vessels has been reported to be abnormally phosphorylated in patients with Milroy disease. The gene for this disease, vascular endothelial growth factor receptor 3, VEGFR3 (FLT4),^5,6 has been mapped to the telomeric part of chromosome arm 5q in the region 5q34-q35.⁷ VEGFR3 is expressed in the adult lymphatic endothelial cells. Studies in transgenic mice with overexpression of VEGFR3 ligands demonstrate the formation of new hyperplastic lymphatics. Induction of this gene may provide a potential target for future interventions in this patient population.

Frequency

United States

The primary lymphedemas occur in 1 of 10,000 individuals. Milroy disease is inherited as an autosomal dominant condition associated with variable penetrance. It is not observed as commonly as lymphedema praecox (Meige disease), which constitutes 80% of cases of primary lymphedema. Actual incidence of Milroy disease is unknown because most patients have been reported in small case-based studies. Approximately 200 cases have been described in the literature.

Mortality/Morbidity

• Primary lymphedema usually does not progress. The condition stabilizes after several years of activity.
• Patients may have recurrent streptococcal cellulitis and lymphangitis, with subsequent hospitalizations for antibiotic therapy.
• A rare complication is the appearance of lymphangiosarcoma or angiosarcoma in patients with persistent lymphedema.⁸ Some patients may develop protein-losing enteropathy and visceral involvement. Chylous ascites and chylothorax rarely occur.

Race

Milroy disease has no known racial predilection.

Sex

Milroy disease affects both sexes; however, 70-80% of cases occur in females.

Age

By definition, Milroy disease occurs in infants and is present at birth. Lymphedema praecox occurs in individuals younger than 35 years, usually in adolescents.

Clinical

History

• Edema occurs at birth and is firm to the touch, although pitting may occur with pressure. The temperature of the overlying skin is increased.
• The right lower extremity is preferentially involved. Generally, the edema involves the dorsum of the foot and does not extend beyond the level of the knee.
• Patients may also present with recurrent cellulitis, papillomatosis, large caliber leg veins, and upsloping "ski-jump" toenails.⁹
• Hydrocele was the second most common presentation after edema in males.
• Usually, several other family members have a history of congenital lymphedema.

Physical

• Brawny edema of a lower extremity is present at birth but usually does not extend above the knee. As the edema becomes chronic, a woody feel to the tissue may develop, signaling progressive tissue fibrosis.
• Hemorrhagic verruciform xanthoma is described on the dorsum of the toes.¹⁰
• The overlying skin often exhibits a rosy hue.
• Patients may have involvement of the external genitalia as a result of associated lymphatic abnormalities, and some may have a cystic hygroma of the neck.

Causes

• The cause of Milroy disease is the failure of lymphatic vessels to develop in utero.
• On a cellular level, Milroy disease has been related to defective VEGFR3 signaling mapped to a part of chromosome arm 5q. This region codes for a tyrosine kinase receptor specific for the function of the lymphatic vessels.

Differential Diagnoses

Arteriovenous Malformations
Cellulitis
Lymphedema
Meigs Syndrome

Other Problems to Be Considered

Neurofibromatosis
Sclerema neonatorum

Workup

Laboratory Studies

• None

Imaging Studies

• Ultrasound of the leg can exclude vascular abnormalities such as arteriovenous fistula.
• Plain radiographs can exclude abnormalities of the bone.
• After a subcutaneous injection of dye, lymphangiography of patients with Milroy disease shows lymphatic vessels that cannot be cannulated.
• Lymphoscintigraphy using the subcutaneous injection of technetium-labeled colloid demonstrates an absence of lymphatic vessels.
• Fluorescence microlymphography using a light fluorescence microscope following subepidermal infection of FITC-dextran 150,000 demonstrates a lack of microlymphatics.¹¹
• MRI can also be used; however, it is more useful to show lymph trunk anatomy and causes of obstructive secondary lymphedema.

Procedures

• Biopsy of the skin is performed using standard techniques. A 25-gauge needle is used to infiltrate the skin with local anesthesia. The skin is stretched perpendicular to the desired line of the scar. A punch biopsy tool is rotated into the skin to obtain a small circle of tissue, which is sent to pathology for histologic staining. Bleeding is controlled by the application of pressure to the area or by the use of a single suture. Topical antibiotics applied twice daily speed wound healing.

Histologic Findings

Early in the disease, lymphatic vessels are conspicuously absent upon biopsy. Late in the disease, histology shows lymphangiectasia and fibrosis involving the subcutaneous skin.

Treatment

Medical Care

Treatment of patients with hereditary lymphedema is primarily directed against the prevention of infection and the control of local complications of limb swelling. Studies in mice, however, suggest that induced overexpression of VEGFR3 ligands stimulate the growth of functional lymphatic vessels.¹² An increase in lymphatics would benefit patients with primary and secondary lymphedema.

• Exercise and elevation of the extremity promote movement of fluid away from the lower extremity.
• Elastic stockings and bandages are applied in a gradient fashion, with the highest compression distally and no constriction points.
• Gentle massage or pneumatic compression can be used.
• Proper skin hygiene and use of skin moisturizers prevents drying and fissuring of skin and subsequent bacterial skin infections.
• Use an antistreptococcal antibiotic to treat recurrent cellulitis. Prophylactic antibiotic therapy, such as benzathine penicillin in low doses, may be used to prevent intermittent cellulitis. Antibiotics directed at prophylaxis should have good activity against Streptococcus pyogenes.
• No medication treats or prevents Milroy disease. Complications of this disease, including cellulitis, bacteremia, and chylothorax, are treated as required. Benzopyrones, such as coumarin or diosmin, may stimulate proteolysis of tissue proteins.

Surgical Care

• Several surgical methods have been attempted to benefit patients with Milroy disease, but none has achieved lasting success.
• Excision of the fibrotic subcutaneous tissues with coverage by split-thickness skin grafts has been described.
• Pedicular transfer of skin with healthy lymphatics to the affected limb and anastomosis to existing lymphatic channels has been tried without much success.

Consultations

• Consultation with an infectious disease specialist is indicated for the treatment of recurrent cellulitis.
• In the future, consultation with a geneticist will provide insights into familial inheritance patterns.

Activity

Encourage patients to exercise after a graded support is applied to the involved extremity.

Medication

No medication treats or prevents Milroy disease. Complications of this disease, including cellulitis, bacteremia, and chylothorax, are treated as required. Antistreptococcal antibiotics (eg, cefazolin, clindamycin) can be used to treat cellulitis. Monthly penicillin G benzathine injections may be required to prevent recurrent cellulitis.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of this clinical setting.

Cefazolin (Ancef)

First-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth. Primarily active against skin flora, including Staphylococcus aureus. Typically used alone for skin and skin-structure coverage. IV and IM dosing regimens are similar.

Dosing

Adult

250 mg to 2 g IV/IM q6-12h, depending on severity of infection; not to exceed 12 g/d

Pediatric

25-100 mg/kg/d IV/IM divided q6-8h, depending on severity of infection; not to exceed 6 g/d

Interactions

Probenecid prolongs effect; coadministration with aminoglycosides may increase renal toxicity; may yield false-positive urine-dip test results for glucose

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in renal impairment; superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy

Clindamycin (Cleocin)

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (but not enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

150-450 mg/dose PO q6-8h; not to exceed 1.8 g/d; 600-1200 mg/d IV/IM divided q6-8h, depending on degree of infection

Pediatric

8-20 mg/kg/d PO as hydrochloride and 8-25 mg/kg/d PO as palmitate divided tid/qid; 20-40 mg/kg/d IV/IM divided tid/qid

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption

Contraindications

Documented hypersensitivity; regional enteritis, ulcerative colitis, hepatic impairment, antibiotic-associated colitis

Precautions

Pregnancy

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

Precautions

Adjust dose in patients with severe hepatic dysfunction; no adjustment necessary in patients with renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile

Penicillin G benzathine (Bicillin)

Interferes with synthesis of cell wall mucopeptides during active multiplication, which results in bactericidal activity. Used to treat syphilis and for prophylaxis of recurrent streptococcal infections.

Dosing

Adult

1.2 million U IM qmo

Pediatric

25,000-50,000 U/kg IM qmo; not to exceed 1.2 million U/dose

Interactions

Probenecid can increase effectiveness by decreasing clearance; coadministration with tetracyclines can decrease effectiveness

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Caution in patients with impaired renal function

Anticoagulants

May stimulate proteolysis of tissue proteins.

Warfarin (Coumadin)

Interferes with hepatic synthesis of vitamin K–dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor dose to maintain INR of 2-3.

Dosing

Adult

5-15 mg/d PO for 2-5 d; adjust dose according to desired INR

Pediatric

0.05-0.34 mg/kg/d PO; adjust dose according to desired INR

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate; medications that may increase anticoagulant effects include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Documented hypersensitivity; severe liver or kidney disease; open wounds or GI ulcers

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not switch brands after achieving therapeutic response; caution in patients with active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Follow-up

Further Outpatient Care

• See patients monthly to teach the parents proper noninvasive methods of controlling swelling of the extremity.
• Instruct parents to bring the child in for evaluation if fever associated with redness and further swelling of the extremity occurs.

Transfer

• Generally, treatment of the patient can occur in a general hospital setting. If difficulty with proper intravenous access occurs, consider transfer to a pediatric hospital.

Deterrence/Prevention

• Milroy disease is a genetically transferred illness. Watch for the development of complications of the disease (eg, cellulitis, lymphangiosarcoma).
• Prenatal screening for the presence of an abnormal gene sequence may provide parents with additional information on the possibility of their child developing Milroy disease.

Complications

• Recurrent cellulitis
• Bacteremia
• Lymphangiosarcoma
• Sarcoma
• Protein-losing enteropathy
• Chylothorax
• Chylous ascites

Prognosis

• Long-term prognosis is excellent.

Patient Education

• Milroy disease is a genetically transmitted swelling of an extremity that is present at birth and is usually not progressive. Patients develop lymphedema and can experience recurrent cellulitis, but the disease does not decrease their lifespans.

Miscellaneous

Medicolegal Pitfalls

• Physicians should be aware of Milroy disease and recognize the condition's associated familial pattern. Extensive searching for a secondary cause of this condition could result in undue morbidity for the patient.
• Physicians should be aware of the possibility of recurrent cellulitis associated with this disease, and they should establish a treatment plan with the parents that protects the child from potential complications.

References

1. Levinson KL, Feingold E, Ferrell RE, Glover TW, Traboulsi EI, Finegold DN. Age of onset in hereditary lymphedema. J Pediatr. Jun 2003;142(6):704-8. [Medline].

2. Dahlberg PJ, Borer WZ, Newcomer KL, Yutuc WR. Autosomal or X-linked recessive syndrome of congenital lymphedema, hypoparathyroidism, nephropathy, prolapsing mitral valve, and brachytelephalangy. Am J Med Genet. Sep 1983;16(1):99-104. [Medline].

3. Wheeler ES, Chan V, Wassman R, Rimoin DL, Lesavoy MA. Familial lymphedema praecox: Meige's disease. Plast Reconstr Surg. Mar 1981;67(3):362-4. [Medline].

4. Namnyak S, Adhami Z, Toms G, Jenks P. Pasteurella multocida septicaemia in Milroy's disease. J Infect. Sep 1995;31(2):175-6. [Medline].

5. Irrthum A, Karkkainen MJ, Devriendt K, Alitalo K, Vikkula M. Congenital hereditary lymphedema caused by a mutation that inactivates VEGFR3 tyrosine kinase. Am J Hum Genet. Aug 2000;67(2):295-301. [Medline].

6. Butler MG, Dagenais SL, Rockson SG, Glover TW. A novel VEGFR3 mutation causes Milroy disease. Am J Med Genet A. Jun 1 2007;143A(11):1212-7. [Medline].

7. Evans AL, Brice G, Sotirova V, Mortimer P, Beninson J, Burnand K, et al. Mapping of primary congenital lymphedema to the 5q35.3 region. Am J Hum Genet. Feb 1999;64(2):547-55. [Medline].

8. Offori TW, Platt CC, Stephens M, Hopkinson GB. Angiosarcoma in congenital hereditary lymphoedema (Milroy's disease)--diagnostic beacons and a review of the literature. Clin Exp Dermatol. Mar 1993;18(2):174-7. [Medline].

9. Ghalamkarpour A, Morlot S, Raas-Rothschild A, Utkus A, Mulliken JB, Boon LM, et al. Hereditary lymphedema type I associated with VEGFR3 mutation: the first de novo case and atypical presentations. Clin Genet. Oct 2006;70(4):330-5. [Medline].

10. Wu JJ, Wagner AM. Verruciform xanthoma in association with milroy disease and leaky capillary syndrome. Pediatr Dermatol. Jan-Feb 2003;20(1):44-7. [Medline].

11. Bollinger A, Amann-Vesti BR. Fluorescence microlymphography: diagnostic potential in lymphedema and basis for the measurement of lymphatic pressure and flow velocity. Lymphology. Jun 2007;40(2):52-62. [Medline].

12. Karkkainen MJ, Saaristo A, Jussila L, Karila KA, Lawrence EC, Pajusola K, et al. A model for gene therapy of human hereditary lymphedema. Proc Natl Acad Sci U S A. Oct 23 2001;98(22):12677-82. [Medline].

13. Albornoz MA, Myers AR. Recurrent septic arthritis and Milroy's disease. J Rheumatol. Nov 1988;15(11):1726-8. [Medline].

14. American Medical Association. William Forsyth Milroy (1855-1942): hereditary edema of the lower legs. JAMA. Apr 8 1968;204(2):166. [Medline].

15. Baginski D, Telang GH, Koblenzer PJ. Answers to Self-Assessment Examination of the American Academy of Dermatology. J Am Acad Dermatol. 1997;37:146-7.

16. Bollinger A. Microlymphatics of human skin. Int J Microcirc Clin Exp. Feb 1993;12(1):1-15. [Medline].

17. Bollinger A, Isenring G, Franzeck UK, Brunner U. Aplasia of superficial lymphatic capillaries in hereditary and connatal lymphedema (Milroy's disease). Lymphology. Mar 1983;16(1):27-30. [Medline].

18. Broström LA, Nilsonne U, Kronberg M, Söderberg G. Lymphangiosarcoma in chronic hereditary oedema (Milroy's disease). Ann Chir Gynaecol. 1989;78(4):320-3. [Medline].

19. Cohen SR, Payne DK, Tunkel RS. Lymphedema: strategies for management. Cancer. Aug 15 2001;92(4 Suppl):980-7. [Medline].

20. Edwards EA. Cutaneous Changes in Peripheral Vascular Disease. In: Fitzpatrick T, Eisen A, Wolff K, Freedberg I, Austen KF, eds. Dermatology in General Medicine. 2^nd ed. New York, NY: McGraw-Hill; 1979:1392-5.

21. Ersek RA, Danese CA, Howard JM. Hereditary congenital lymphedema (Milroy's disease). Surgery. Nov 1966;60(5):1098-103. [Medline].

22. Farhud DD, Farhud I, Walizadeh GR, Djaber-Ansari M. Congenital hereditary lymphedema (Nonne/Milroy). Padiatr Padol. 1989;24(4):305-7. [Medline].

23. Ferrell RE, Levinson KL, Esman JH, Kimak MA, Lawrence EC, Barmada MM, et al. Hereditary lymphedema: evidence for linkage and genetic heterogeneity. Hum Mol Genet. Dec 1998;7(13):2073-8. [Medline].

24. From L. Vascular Neoplasms, Pseudoneooplasms and Hyperplasias. In: Fitzpatrick T, Eisen A, Wolff K, Freedberg I, Austen KF, eds. Dermatology in General Medicine. 2^nd ed. New York, NY: McGraw-Hill; 1979:736-7.

25. Gregl A, von Heyden D, Jentsch F, Yu D. [Primary lymphedema]. Z Lymphol. Jul 1983;7(1):21-8. [Medline].

26. Margileth A. Dermatologic Conditions Neonatology. In: Avert GB, ed. Pathophysiology and Management of the Newborn. 3^rd ed. Philadelphia, Pa: JB Lippincott; 1987:1253-4.

27. Mehta SD, Robinson RJ, Bern SA. Pedal manifestations of Milroy's disease. J Am Podiatr Med Assoc. Aug 1996;86(8):400-2. [Medline].

28. Offret H, Labrune B. [Primary conjunctival-palpebral lymphedema and Milroy disease]. J Fr Ophtalmol. 1994;17(11):679-82. [Medline].

29. Pap Z, Biró T, Szabó L, Papp Z. Syndrome of lymphoedema and distichiasis. Hum Genet. 1980;53(3):309-10. [Medline].

30. Partsch H, Urbanek A, Wenzel-Hora B. The dermal lymphatics in lymphoedema visualized by indirect lymphography. Br J Dermatol. Apr 1984;110(4):431-8. [Medline].

31. Rock A, Camitta BM. The Lymphatic System. In: Behrman RE, Kliegman RM, Jensen HB, eds. Nelson Textbook of Pediatrics. 16^th ed. Philadelphia, Pa: WB Saunders; 2000:1528.

32. Ryan TJ, Champion RH. Disorders of Lymphatic Vessels. In: Champion RH, Ebling FJG, Burton JL, eds. Textbook of Dermatology. 5^th ed. Oxford, England: Oxford Blackwell Scientific; 1992:2018-23.

33. Sigstad H, Aagenaes O, Bjorn-Hansen RW, Rootwelt K. Primary lymphoedema combined with hereditary recurrent intrahepatic cholestasis. Acta Med Scand. Sep 1970;188(3):213-9. [Medline].

34. St Louis JD, McCann RL. Lymphatic System. In: Townsend CM Jr, ed. Sabiston Textbook of Surgery. 16^th ed. Philadelphia, Pa: WB Saunders; 2001:1446-51.

35. Tiwari A, Cheng KS, Button M, Myint F, Hamilton G. Differential diagnosis, investigation, and current treatment of lower limb lymphedema. Arch Surg. Feb 2003;138(2):152-61. [Medline].

Keywords

Milroy disease, congenital lymphedema, lymphedema congenita, noninfectious hereditary elephantiasis, autosomal dominant lymphedema, lymphatic obstruction, fibrosis, cellulitis, Meige disease, lymphedema tarda, lymphedema praecox

Contributor Information and Disclosures

Author

Raphael J Kiel, MD, Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Infectious Diseases Division, William Beaumont Hospital
Raphael J Kiel, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Geriatrics Society
Disclosure: Nothing to disclose.

Medical Editor

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St. Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)