eMedicine Specialties > Rheumatology > Soft Tissue and Regional Rheumatic Disease
Reflex Sympathetic Dystrophy
Updated: Aug 5, 2009
Introduction
Background
Reflex sympathetic dystrophy (RSD) is a clinical syndrome of variable course and unknown cause characterized by pain, swelling, and vasomotor dysfunction of an extremity. This condition is often the result of trauma or surgery. In 1864, Mitchell referred to this malady as causalgia, a Greek word meaning burning pain. Newer taxonomy refers to RSD as a type of complex regional pain syndrome (CRPS), which may develop after an initiating event such as trauma or surgery or may occur spontaneously.1 Under this classification, causalgia is a type of CRPS that develops after nerve injury. In patients with either of these conditions, sympathetic mediation of the pain (ie, improvement with sympathetic blockade) may or may not be evident.
Pathophysiology
The pathogenesis of RSD is unknown. Three conditions are deemed important in the development of RSD, including a persistent painful lesion, a predisposition or susceptibility to developing RSD, and an abnormal sympathetic reflex. Susceptibility factors are unknown and may include genetic predisposition (HLA typing)2 and, in some patients, a tendency toward increased sympathetic activity. This includes cold hands, hyperhidrosis, or a history of fainting.
Healthy individuals undergo a sympathetic response to injury, with vasoconstriction designed to prevent blood loss and swelling. This initial response soon subsides and gives way to vasodilatation and increased capillary permeability, allowing tissue repair.
In patients with RSD, this sympathetic response continues unabated. The reasons for the perpetuation of the response are unknown but may be related to central dysregulation of nociceptive impulses. This dysregulation may be mediated by wide dynamic range neurons in the spinal cord. Prolonged ischemia caused by the vasoconstriction produces more pain, establishing a reflex arc that promotes further sympathetic discharge and vasospasm. This is compounded by the local response to trauma, with liberation of substantial amounts of proinflammatory mediators, such as histamine, serotonin, and bradykinin. The result is a swollen, painful, stiff, nonfunctioning extremity. At least partial sympathetic mediation of this phenomenon is likely because of the ability of sympathetic nerve blockade to relieve pain and other features of RSD in some patients.
Frequency
United States
An estimated 5% of patients who experience trauma to the upper extremity develop RSD, although this figure is not known with certainty because of confusion over the diagnosis. Extremity immobilization can trigger RSD. Without prophylactic measures (active physical therapy), RSD can develop in 12-20% of people who experience a hemiplegic stroke.
Mortality/Morbidity
RSD causes essentially no mortality.
Race
No racial predilection exists.
Sex
Sexual distribution is equal.
Age
- The age of onset in most patients with RSD is 30-60 years, and the mean age is 49 years.
- RSD affects children and carries a much better prognosis than in adults.3
Clinical
History
The 3 clinical stages of reflex sympathetic dystrophy (RSD) are acute, subacute, and chronic. The acute form lasts approximately 3 months. Pain, often burning in nature, is one of the first symptoms that initially limits function. Swelling, redness with vasomotor instability that worsens with dependency, hyperhidrosis, and coolness to the touch are common physical findings. Demineralization of the underlying bony skeleton begins because of disuse.
If the process is not arrested or reversed in the acute phase, the condition may progress to the subacute stage, which can last for up to 9 months. The patient develops persistent severe pain in the extremity and fixed edema that would have been reversible with elevation during the acute phase. The redness of the acute stage gives way to cyanosis or pallor and hyperhidrosis to dry skin. Loss of function progresses, both because of increased pain and fibrosis of the joints caused by chronic inflammation. In the hand, this leads to flexion deformity of the fingers. The skin and subcutaneous tissues begin to atrophy. Demineralization of the underlying bony skeleton becomes pronounced.
If the process continues, the chronic phase may develop approximately 1 year after disease onset. This stage may last for many years or can be permanent. Pain is more variable during this period. It may continue undiminished or abate. Edema tends to subside over time, leaving fibrosis around the involved joints. The skin is dry, pale, cool, and shiny. Flexion and extension creases are absent. Loss of function and stiffness are marked, and osteoporosis is extreme. In the upper extremity, this can manifest as a frozen shoulder and claw hand.
A thorough general history is strongly suggested. Maintaining a high index of suspicion is important because proper treatment requires rapid diagnosis and prompt therapy.
- RSD commonly involves only one extremity. It is bilateral in approximately 25% of cases but is usually more prominent on one side.
- Pain
- Usually constant and disproportionate to the precipitant injury
- May be exacerbated by ambient factors such as loud noises and emotional factors (eg, stress, light touch, active motion, passive motion)
- May be described as burning, cutting, searing, pressure, or tearing
- Usually begins locally but may progress to involve the entire extremity
- Possible evidence of prior increased sympathetic activity
- Hyperhidrosis
- Cold hands
- Fainting
- Prior trauma, which may be trivial or significant (eg, Colles fracture), with or without diagnosable nerve injury
- Prior surgery
- Recent limb immobilization due to hemiplegic stroke, myocardial infarction
- Systemic disease such as diabetes
Physical
Perform a thorough physical examination followed by a focused examination of the involved extremity. Patients with RSD may present with suggestive physical findings that point to a presumptive diagnosis.
- Edema
- Edema is the most consistent physical finding and is always disproportionate to the severity of the precipitant injury or event.
- Pain, swelling, and color change may be more prominent with dependency in the early stages.
- Edema worsens rather than improves and extends beyond the region of initial concern.
- It evolves into a brawny, nonpitting edema that may progress to an intense fibrosis in all the joints of the extremity.
- Stiffness is more severe than expected and may be very distressing to the patient.
- Discoloration
- Varies depending on the stage of disease
- May be dusky, cyanotic, pale, or red and may eventually lead to skin hypopigmentation
- Begins as redness over the metacarpophalangeal (MCP) or proximal interphalangeal (PIP) joint flexion creases early in the disease and progresses as a streak across the palm
- Abnormal skin moisture
- Hyperhidrosis (early)
- Dry skin (late)
- Tenderness is initially localized but may progress to generalized tenderness. Exquisite tenderness, both periarticular and interarticular, is often present. Patients may exhibit allodynia (ie, pain with nonnoxious stimuli) and hyperpathia (ie, persistent pain after light pressure).
- Atrophy of the skin and subcutaneous fat pads
- Fibrosis of the palmar fascia
- Absence of extensor and flexor creases over joints
- Frozen shoulder, flexion deformities of the fingers, claw hand
Causes
RSD is usually posttraumatic or postsurgical; however, it can occur in a previously healthy extremity with no known trigger.
- Trauma
- Penetrating wounds
- Lacerations
- Abrasions
- Venipuncture
- Intramuscular injection of medication or illicit drugs
- Gunshot wounds
- Crush injuries and blunt trauma
- Neck or shoulder injuries
- Acute traumatic carpal tunnel syndrome
- Chest trauma
- Sprain, fracture, or dislocation
- Penetrating wounds
- Postsurgery
- Carpal tunnel release
- Dental extractions
- Cervical rib resection
- Fracture repair (Colles fracture)
- Postarthroscopy
- Local disease
- Nerve compression syndromes
- Arthritis
- Tissue ischemia
- Stenosing tenosynovitis
- Systemic disease
- Myocardial infarction
- Stroke
- Pancoast tumor
- Pancreatic cancer
- Herpes zoster
Differential Diagnoses
Acute Nerve Injury
Cellulitis
Septic Arthritis
Upper Extremity Occlusive Disease
Workup
Laboratory Studies
- Levels of acute-phase reactants (ie, erythrocyte sedimentation rate [ESR], C-reactive protein) are generally within the reference range.
Imaging Studies
- Plain radiography
- Plain radiographs usually demonstrate pronounced demineralization in the underlying bony skeleton of the involved extremity (ie, Sudeck atrophy) that may become more severe with disease progression. No joint erosions are present.
- Demineralization begins at the ends of the bones and progresses to become homogeneous.
- Radionuclide imaging: Findings on 3-phase bone scan are positive in 50-90% of patients, and this study is most useful in early disease. Findings on the delayed image (ie, third phase) are generally abnormal, with increased uptake in the articular and periarticular structures of the involved extremity. Of course, this finding is not specific for reflex sympathetic dystrophy (RSD) but is supportive of that diagnosis in the appropriate clinical situation. In third-stage RSD, the bone scan findings may be normal, but the plain radiographs generally reveal profound demineralization of the affected extremity.
Treatment
Medical Care
The natural history of reflex sympathetic dystrophy (RSD) is variable and unpredictable, the pathogenesis is unknown, and few controlled treatment trials exist. Thus, evidence-based treatment guidelines do not exist, and the approach depends largely on the specialty of the treating physician. Even if a disturbance in sympathetic nervous system function is important in the development of the clinical syndrome, not all patients respond to sympatholytic medications or to chemical or surgical sympathectomy.
Clinical experience teaches that early recognition and treatment are necessary to avoid permanent disability and that the effectiveness of treatment is limited once the patient has reached the chronic fibrotic stage. Certainly, the incidence and severity of RSD can be greatly reduced by initiating prophylactic measures in situations that are known to be triggers (eg, hemiplegic stroke, Colles fracture). These measures include immediate and aggressive mobilization of the involved extremity with passive and then active range-of-motion exercises. Similarly, in patients with established RSD, physical and occupational therapy are key components of any therapeutic regimen.
Two major approaches to the medical treatment of early RSD exist: sympathetic blockade and anti-inflammatory therapy. Although these are not mutually exclusive, the order of usage is generally specialty-dependent, with anesthesiologists/surgeons starting with the former and internists/rheumatologists starting with the latter.
- Sympathetic block (upper extremity, stellate; lower extremity, lumbar)
- Ensure that this is performed by a trained individual.
- Inject a local anesthetic into the stellate and upper dorsal sympathetic ganglia to block the efferent sympathetic impulses from the involved extremity. Lidocaine or bupivacaine, with or without epinephrine, is usually used.
- This procedure warms the skin, inhibits sweating, and causes flushing.
- A successful blockade is indicated by the development of ipsilateral Horner syndrome, ie, ptosis, miosis, and enophthalmos.
- Symptoms usually abate within 30 minutes, confirming the diagnosis. Once the patient is adequately blocked, ensure their participation in hand therapy. Although the interruption lasts only a few hours, the benefits may persist for several days.
- Use 1-2 blocks per week. An average of 4-5 blocks is required to permanently relieve symptoms. For symptoms that are not adequately relieved after 4-5 blocks, institute a continuous stellate blockade via a subcutaneously placed catheter or conduct an operative sympathectomy.
- Sympatholytic drugs
- Sympatholytic drugs may be efficacious when used alone in early disease.
- Sympatholytic drugs may be beneficial in combination with sympathetic block or sympathectomy in later stages of the disorder.
- Regional intravenous sympathetic blockade with sympatholytic drugs, such as phenoxybenzamine, using a Bier block–like procedure may be helpful, but results have varied. This is most useful in early disease.
- A randomized study performed in 2000 suggested that intrathecal baclofen, a GABA-receptor agonist, relieved the dystonia and, in some cases, the hand pain in patients with RSD.4 This suggests that GABA-ergic inhibitory pathways may also be important in the pathogenesis of RSD.
- Anti-inflammatory medications (corticosteroids, calcitonin)
- Although nonsteroidal anti-inflammatory drugs (NSAIDs) may provide some symptomatic pain relief in patients with RSD, they are not effective in altering the skin changes or natural history of the process and thus play only a supportive role. On the other hand, a course of high-dose corticosteroids, eg, prednisone 30-40 mg/d tapering over 2-4 weeks, can dramatically reduce pain, swelling, and stiffness. This enables the institution of an aggressive physical-therapy program. In general, corticosteroids are of most value in early RSD (acute and subacute) when the bone scan shows increased uptake in the involved extremity.
- Calcitonin is not an anti-inflammatory medication per se but has been reported to reverse the inflammatory changes and reduce pain in early RSD, especially in patients with hyperdynamic blood flow. Subcutaneous injections of 100-160 units are administered daily for 4-8 weeks, then every other day for 3-6 weeks. A few reports suggest that intranasal calcitonin5 and oral bisphosphonates may also be effective in treating RSD.
Surgical Care
- Upper thoracic or lumbar sympathectomy
- Consider this procedure if the relief achieved with sympathetic blockade and anti-inflammatory therapy has not permanently resolved the RSD and relapse has occurred despite continuing treatment. These procedures are reserved for patients who have had an initial response to sympathetic blockade and are thus likely have a sympathetically mediated process.
- Indications include disease duration of longer than 6 months and failure of permanent resolution after 5 percutaneous sympathetic blocks are performed.
- The most significant improvement following surgical sympathectomy is pain relief, although circulation, range of motion, strength, and function are usually somewhat improved.
- Choose sympathectomy early in the course of disease because, once joint fibrosis develops, minimal functional improvement occurs. Pain relief, however, is still significant in late disease.
- If surgery of the involved extremity is required, perform it after the sympathectomy.
- Ensure that a surgical sympathectomy is performed by an adequately trained individual.
- Chemical sympathectomy
- Inject phenol or alcohol to ablate the sympathetic chain.
- Perform this only if the patient is at a very high surgical risk for hoarseness from a recurrent laryngeal nerve injury, lung injury, or permanent Horner syndrome.
- Spinal cord stimulation: In 2000, a controlled trial demonstrated the efficacy of epidural implantation of a spinal cord stimulator in pain relief and functional improvement in RSD (hand or foot) compared with physical therapy alone.6,7
Consultations
- Multiple consultants are often needed in challenging RSD cases, including an anesthesiologist who specializes in pain management and who is capable of performing sympathetic blocks, an internist/rheumatologist capable of supervising anti-inflammatory regimens, and a surgeon who is capable of performing surgical sympathectomy.
- Consultation with a physical therapist and occupational therapist (hand therapist) is important to institute aggressive exercise programs.
Activity
- Physical and occupational therapy
- As discussed above, an aggressive range-of-motion exercise program is an essential part of RSD management. However, especially after sympathetic block or sympathectomy, this may have to be a graduated regimen, with patient-directed passive range of motion to tolerance and, later, active range of motion. When appropriate (eg, in patients with hemiplegia), the entire extremity requires attention.
- Following the stellate block or sympathectomy, hand therapy may proceed without causing further pain. Ensure that the therapist does not cause pain, usually by avoiding application of passive motion. Patients can safely apply passive motion because they know when motion becomes painful.
- Massage of the involved extremity is an important component of therapy.
- The patient requires close follow-up, education, and encouragement to maintain an exercise routine.
- Heat therapy relaxes muscle spasms, improves motion, and relieves pain.
- Judicious use of splinting with Thermoplast and Velcro straps in the balanced hand position may help to prevent shortening of the collateral ligaments of involved joints and may provide intermittent pain relief. The splint must be comfortably fit. Remove it frequently throughout the day for exercise and massage.
- Record routine measurements of the patient's strength and range of motion. This provides encouragement to the patient and facilitates communication between the therapist and the treating physician.
Medication
Several drugs, either alone or in combination with sympathetic blockade, may be efficacious in prolonging the duration of symptomatic relief. Some of these drugs reduce the activity of the sympathetic nervous system, whereas others are primarily anti-inflammatory.
Sympatholytics
These medications reduce the activity of the sympathetic nervous system.
Clonidine (Catapres)
Stimulates alpha2-adrenoreceptors in brain stem, activating an inhibitory neuron, which in turn results in reduced sympathetic outflow. These effects result in a decrease in vasomotor tone and heart rate.
Dosing
Adult
Initial: 0.1 mg PO bid
Maintenance: 0.2-0.6 mg/d PO divided bid/tid; not to exceed 2.4 mg/d PO
Pediatric
Not established
Interactions
Tricyclic antidepressants inhibit hypotensive effects of clonidine; coadministration of clonidine with beta-blockers may potentiate bradycardia; tricyclic antidepressants may enhance hypertensive response associated with abrupt clonidine withdrawal; hypotensive effects of clonidine are enhanced by narcotic analgesics
Contraindications
Documented hypersensitivity
Precautions
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
Caution in cerebrovascular disease, coronary insufficiency, sinus node dysfunction, and renal impairment
Guanethidine (Ismelin)
Prevents release of norepinephrine from adrenergic nerve endings in response to sympathetic stimulation. Decreases sympathetically mediated vasoconstriction.
Dosing
Adult
Initial: 10 mg/d PO; may increase q5-7d by 10-12.5 mg/d
Maintenance: 25-50 mg/d PO
Pediatric
0.2 mg/kg/d PO; increase q7-10d by 0.2 mg/kg prn
Interactions
Tricyclic antidepressants, methylphenidate, thioxanthenes, phenothiazines, sympathomimetics, anorexiants, and haloperidol may reduce effects of guanethidine; minoxidil, epinephrine, and norepinephrine may increase the toxicity of guanethidine
Contraindications
Documented hypersensitivity; congestive heart failure; pheochromocytoma; current MAOI use or use within the last 14 d
Precautions
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
Caution in congestive heart failure, asthma, peptic ulcer disease, and regional vascular disease
Phenoxybenzamine (Dibenzyline)
Produces a long-lasting blockade of alpha-adrenergic receptors in smooth muscle and exocrine glands. Blocks epinephrine-induced and norepinephrine-induced vasoconstriction.
Dosing
Adult
Initial: 10 mg PO qd; increase by 10 mg/d PO at 2-d intervals
Maintenance: 20-40 mg/d PO divided bid/tid
Pediatric
0.2 mg/kg PO qd; not to exceed 10 mg
Interactions
When used concurrently, alpha-adrenergic agonists decrease effects of medication; beta-blockers increase toxicity
Contraindications
Documented hypersensitivity; those to whom a fall in blood pressure would be undesirable
Precautions
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
Caution in cerebral or coronary arteriosclerosis and renal impairment; can worsen symptoms of respiratory tract infections
Prazosin (Minipress)
Dilates both arteries and veins by blocking postsynaptic alpha1-adrenergic receptors.
Dosing
Adult
1 mg PO bid/tid initially; increase gradually to 6-15 mg/d PO divided bid/tid maintenance; not to exceed 20-40 mg/d PO
Pediatric
Not established
Interactions
Acute postural hypotensive reaction from beta-blockers may worsen; indomethacin may decrease antihypertensive activity of prazosin; verapamil may increase serum prazosin levels and may increase patient's sensitivity to prazosin-induced postural hypotension; prazosin may decrease antihypertensive effects of clonidine
Contraindications
Documented hypersensitivity
Precautions
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
Caution in renal insufficiency
Anti-inflammatory agents
Although little evidence exists for systemic inflammation in reflex sympathetic dystrophy (RSD), prominent local inflammation with pain, tenderness, swelling, redness, and loss of function is present.
Prednisone (Deltasone, Meticorten, Orasone)
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Dosing
Adult
30-40 mg/d PO divided bid; taper over 2-4 wk as symptoms resolve
Pediatric
4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2-4 wk as symptoms resolve
Interactions
Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Contraindications
Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
Endocrine agents
These agents may inhibit osteoclastic bone resorption.
Calcitonin (Miacalcin, Osteocalcin)
Lowers elevated serum calcium levels in patients with multiple myeloma, carcinoma, or primary hyperparathyroidism. Can expect a higher response when serum calcium levels are high. Onset of action is approximately 2 h following injection, and activity lasts for 6-8 h. May lower calcium levels for 5-8 d by about 9% if administered q12h. IM route is preferred at multiple injection sites with dose >2 mL. It can also be administered via intranasal spray.
Calcitonin is also an effective agent to treat metabolic bone disease such as osteoporosis. Through some unknown mechanism, it appears to have an analgesic effect on bone pain, such as occurs with osteoporotic vertebral collapse. The mechanism by which calcitonin relieves the symptoms of RSD is unknown.
Dosing
Adult
100-160 U/d SC for 4-8 wk, followed by 1 injection qod for 3-6 wk
Pediatric
Not established
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
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
Hypocalcemia may occur; examine urine sediment during prolonged therapy
Follow-up
Deterrence/Prevention
Knowing the triggers for reflex sympathetic dystrophy (RSD), especially extremity immobilization for any cause, and recognizing the disease process early and instituting prompt therapy are the most important aspects of prevention.
Complications
Disease progression may lead to an unusable stiff extremity that is constantly painful. This leads some patients to commit suicide.
Prognosis
Prognosis is better in younger patients and with institution of early treatment.
Patient Education
- Ensure that the patient understands this confusing disease entity.
- Encouragement and family support are important for maintaining the physical therapy program and treatment regimen.
Miscellaneous
Medicolegal Pitfalls
- Potential medicolegal pitfalls include misdiagnosis, delayed diagnosis, incorrect treatment, and failure to refer to appropriate specialists.
Special Concerns
- Some uncontrolled studies have reported encouraging results with transcutaneous nerve stimulation and acupuncture for pain reduction.
References
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Kemler MA, van de Vusse AC, van den Berg-Loonen EM, et al. HLA-DQ1 associated with reflex sympathetic dystrophy. Neurology. Oct 12 1999;53(6):1350-1. [Medline].
Cimaz R, Matucci-Cerinic M, Zulian F, Falcini F. Reflex sympathetic dystrophy in children. J Child Neurol. Jun 1999;14(6):363-7. [Medline].
van Hilten BJ, van de Beek WJ, Hoff JI, et al. Intrathecal baclofen for the treatment of dystonia in patients with reflex sympathetic dystrophy. N Engl J Med. Aug 31 2000;343(9):625-30. [Medline].
Gobelet C, Waldburger M, Meier JL. The effect of adding calcitonin to physical treatment on reflex sympathetic dystrophy. Pain. Feb 1992;48(2):171-5. [Medline].
Kemler MA, Barendse GA, Van Kleef M, et al. Electrical spinal cord stimulation in reflex sympathetic dystrophy: retrospective analysis of 23 patients. J Neurosurg. Jan 1999;90(1 Suppl):79-83. [Medline].
Kemler MA, Barendse GA, van Kleef M, et al. Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. N Engl J Med. Aug 31 2000;343(9):618-24. [Medline].
Driessens M, Dijs H, Verheyen G, Blockx P. What is reflex sympathetic dystrophy?. Acta Orthop Belg. Jun 1999;65(2):202-17. [Medline].
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Keywords
reflex sympathetic dystrophy, RSD, causalgia, Sudeck's atrophy, Sudeck-Leriche syndrome, minor traumatic dystrophy, major traumatic dystrophy, shoulder-hand syndrome, neurovascular dystrophy, post-traumatic vasomotor disorder, sympathetic neurovascular dystrophy, post-traumatic vasospasm, postinfarct sclerodactyly, traumatic angiospasm, transient regional osteoporosis, algodystrophy, complex regional pain syndrome, CRPS
Contributor Information and Disclosures
Author
Don R Revis Jr, MD, Consulting Staff, Department of Surgery, Division of Plastic and Reconstructive Surgery, University of Florida College of Medicine
Don R Revis Jr, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Society for Aesthetic Plastic Surgery, and American Society of Plastic Surgeons
Disclosure: Nothing to disclose.
Coauthor(s)
Elliot Goldberg, MD, Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine
Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology
Disclosure: Nothing to disclose.
Medical Editor
Robert E Wolf, MD, PhD, Professor Emeritus, Department of Medicine, Louisiana State University Health Sciences Center at Shreveport; Chief, Rheumatology Section, Medical Service, Overton Brooks Veterans Administration Medical Center of Shreveport
Robert E Wolf, MD, PhD is a member of the following medical societies: American College of Rheumatology, Arthritis Foundation, and Society for Leukocyte Biology
Disclosure: Nothing to disclose.
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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Managing Editor
Lawrence H Brent, MD, Associate Professor of Medicine, Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center
Lawrence H Brent, MD is a member of the following medical societies: American Association of Immunologists, American College of Physicians, and American College of Rheumatology
Disclosure: Genentech Honoraria Speaking and teaching; Genentech Grant/research funds Other; Amgen Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Immunology Honoraria Speaking and teaching
CME Editor
Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Chief Editor
Herbert S Diamond, MD, Professor of Medicine, Temple University School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital
Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa
Disclosure: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; West Penn Allegheny Health System None Board membership