eMedicine Specialties > Dermatology > Connective Tissue Diseases

CREST Syndrome: Treatment & Medication

Author: Kyle L Horner, MD, MS, Staff Physician, Department of Dermatology, Penn State Milton S Hershey Medical Center
Coauthor(s): Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle
Contributor Information and Disclosures

Updated: Sep 22, 2009

Treatment

Medical Care

  • Globally
    • The diagnosis of CREST syndrome carries with it both physical and psychological consequences, so a holistic approach to patient care should be taken. An evaluation of organ involvement, patient education regarding the clinical course, patient and family support, and treatment based on disease severity and organ involvement are necessary.54,55
    • A pilot study of multidisciplinary patient education for persons with systemic sclerosis showed that patients may benefit from meeting others with the disease, may learn more about the disease, and may actually experience some pain relief.56
    • Depression affects approximately 45% of patients with systemic sclerosis and 64% also develop anxiety; thus, early assessment and treatment of these psychological issues is recommended.57,58
    • European investigators have been conducting phase I and II studies on the use of hematopoietic stem cell transplantation for severe systemic sclerosis, and randomized trials are proceeding. Only further research and time will tell if this is a useful therapy for severe scleroderma in the future.59
    • Tamoxifen has been studied for use in patients with scleroderma and CREST syndrome, but it was not shown to be efficacious.60
  • Calcinosis
    • No large, prospective, placebo-controlled trials have been performed to study the treatment of calcinosis. The literature predominantly consists of reports and series. Therefore, keep in mind that calcinosis has resolved spontaneously in as many as 55% of patients in some series, as noted by Fink and Cook in 1986.61
    • Treatment with oral corticosteroids is not usually considered effective, but, according to Hazen et al,62 intralesional corticosteroid therapy has been associated with improvement of calcinosis.
    • Several case reports have demonstrated the efficacy of probenecid.
    • Early case reports suggested that diltiazem was associated with regression of calcific deposits and improvement of symptoms. A 1998 case series of 12 patients by Vayssairat et al63 did not confirm these findings.
    • A 1987 small randomized placebo-controlled trial by Berger et al64 using low-dose warfarin reduced urinary levels of Gla protein and reduced extraskeletal uptake on bone scans in 2 of 3 patients after 18 months of follow-up care. No changes in plain radiographs or clinical assessment were noted in these patients. Cukierman et al65 used low-dose dose warfarin on 3 patients with systemic sclerosis, and 2 of the patients, who had newly diagnosed, diffuse, and relatively small calcinotic lesions, responded to warfarin treatment, with complete resolution of the calcinosis. As reported in 1998, Lassoued et al66 used warfarin in patients with extensive calcinosis and saw no benefit. Low-dose warfarin may be helpful in selected patients with early or mild disease.
    • Several case reports have shown that aluminum hydroxide may be useful for calcinosis.67
    • Bisphosphonate treatment has had only limited success. Etidronate appeared to help calcinosis in one patient with scleroderma; however, another study reported failure. Alendronate was used successfully in one patient with calcinosis associated with juvenile dermatomyositis. The other bisphosphonates, pamidronate, risedronate, zoledronate, and ibandronate, have not been studied for calcinosis.67,68,69,70
    • In one case series, 8 of 9 patients with limited systemic sclerosis had a good response to low-dose minocycline.71
    • Suppression of intermittent local inflammatory reactions can be achieved by low-dose colchicine.72
    • Kalajian et al found intravenous immunoglobulin therapy to be unreliable.73
    • In summary, no consistently reliable pharmacological treatment seems to be available to prevent or eliminate calcinosis. One or a combination of the above treatments may be tried on a case-by-case basis; however, larger randomized trials are needed to prove efficacy.
  • Raynaud phenomenon
    • Advise all patients with Raynaud phenomenon to use good hand and body warming techniques. Goodfield et al74 have shown that according to laser Doppler flowmetry, secondary Raynaud phenomenon patients respond appropriately to simple warming techniques compared with controls. Reinforce the wearing of gloves, a hat, and a coat outdoors and, if necessary, indoors. The importance of keeping the core body and hand temperature elevated cannot be overemphasized.
    • Behavior therapy, including temperature biofeedback and autogenic training, has been evaluated in the treatment of scleroderma-associated Raynaud phenomenon. In 1989, Freedman75 demonstrated an improvement of finger blood flow and elevation of finger temperature with biofeedback training. A large, randomized, controlled trial, however, showed no clinical benefit with temperature biofeedback; however, this has been criticized because the patients may not have been adequately trained in the technique.76 These researchers76 claim that thermal biofeedback is efficacious if proper hand warming technique is used.
    • Calcium channel blockers are the mainstay of medical therapy for Raynaud phenomenon. Short-acting calcium channel blockers have been effective, yet they are frequently associated with adverse effects (eg, headache, flushing, dizziness, edema). In a recent study by the Raynaud's Treatment Study Investigators, sustained-release nifedipine reduced attack frequency by approximately 60% and was well tolerated. Some literature has suggested that calcium channel blockers are less effective in scleroderma-associated Raynaud phenomenon than in primary Raynaud disease, but Meyrick Thomas et al77 demonstrated the effectiveness of nifedipine in this group in a longer-duration trial. A 2005 meta-analysis of calcium channel blocker therapy for Raynaud phenomenon by Thompson et al78 showed a small benefit in reducing the severity and frequency of ischemic attacks (an average of 2.8-5 fewer attacks/wk and a 33% reduction in severity).
    • Topical nitroglycerin and topical glyceryl trinitrate have been used in patients with Raynaud phenomenon. Several studies have shown that they both increase blood flow at the application site and they may help with symptomatic management of vasospasms.79,80,81
    • Prostaglandin E1, prostacyclin I2, and iloprost (a prostacyclin-I2 analogue) have been evaluated for treatment of Raynaud phenomenon. Prostaglandins may be beneficial because of their vasodilatory and antiplatelet effects. None of these treatments is approved by the US Food and Drug Administration for the treatment of Raynaud phenomenon. Use of these agents should be reserved for patients whose Raynaud phenomenon has resulted in severe ischemia or nonhealing ulcers.
      • Intravenous infusions of prostacyclin I2 (epoprostenol) in patients with severe Raynaud phenomenon demonstrated substantial clinical improvement. The frequency and duration of attacks were reduced, and significant healing of digital ulcers occurred.
      • Intravenous prostaglandin E1 (alprostadil) has been beneficial in some small studies, particularly in patients with sepsis or necrosis.
      • Oral iloprost therapy showed a trend toward improvement of the severity and duration of attacks in patients with scleroderma. Intravenous iloprost reduced the severity, frequency, and duration of Raynaud attacks; helped with ulcer healing82 ; and showed an increase in quality of life.83
    • Antiplatelet therapy has had mixed results. Ticlopidine showed benefit in one case and was ineffective in another study.84 Clopidogrel has not been studied in Raynaud phenomenon. Cilostazol has shown some benefit in open-label trials, and a recent double-blinded randomized trial showed that it significantly increased the mean brachial artery diameter; however, the patient's subjective symptoms did not appear to improve.85,86 Recombinant tissue plasminogen activator produces only transient improvement in blood flow in patients with digital ischemia and is not recommended for Raynaud phenomenon.87
    • A 2000 pilot study by Denton et al88 suggests that low molecular heparin may be beneficial for severe Raynaud phenomenon; however, further evaluation is necessary.
    • Some evidence has shown that plasma exchange may help with the symptoms of Raynaud phenomenon; however, it is unlikely to affect the disease course.89,90,91
    • Losartan, an ACE inhibitor, has been shown in 2 trials to reduce the frequency and severity of vasospastic episodes.92,93 A review of the literature94 concluded that ACE inhibitors and angiotensin II receptor blockers may provide minor relief for Raynaud phenomenon; however, the benefit is not proven to be any better than the current treatment of choice, which is calcium channel blockers.
    • Case reports95,96 have suggested that the phosphodiesterase V inhibitors, sildenafil and tadalafil, may also be effective. An open-label pilot trial of vardenafil97 also showed promise.
    • Alpha-adrenergic antagonists have received some interest recently as a new treatment for Raynaud phenomenon. An experimental selective alpha(2C)-adrenergic receptor blocker was well tolerated and improved digital skin perfusion during recovery from cooling in patients with Raynaud phenomenon associated with scleroderma.98 One case report describes a patient who paradoxically experienced worsening of Raynaud phenomenon while using the alpha-2 adrenergic antagonist yohimbine.99 Further research is needed before the efficacy and safety of this class of drugs can be established for use in this disease.
    • Bosentan, an orally active competitive endothelin-1 antagonist that blocks the endothelin receptors, is being used for systemic sclerosis-associated pulmonary arterial hypertension, and this agent may also help alleviate vasospasm and prevent digital ulceration; however, clinical trials need to be performed first.100
    • A pilot study with fluoxetine and a case report on paroxetine suggest that the selective serotonin reuptake inhibitors might be effective as novel treatments for Raynaud phenomenon.101,102
    • The following therapeutic ladder is suggested for the treatment of patients with Raynaud phenomenon:
      • Reduce and remove risk factors and triggers. Stop smoking, avoid beta-blockers, and avoid any remediable underlying cause (eg, use of vibratory equipment).103
      • Teach hand and body warming activities.
      • Administer long-acting formulations of calcium channel blockers.
      • Add topical nitroglycerin paste to this regimen if required.
  • Esophageal dysmotility
    • The treatment of esophageal dysmotility and gastroesophageal reflux in scleroderma patients is the same as in patients without scleroderma. Systemic immunosuppressants are not helpful.
    • Emphasize behavior changes (eg, weight loss; elevating head of bed; reduction of caffeine, tobacco, alcohol, chocolate intake and avoidance prior to recumbency; eating small meals; waiting 3-4 h after eating before lying down).
    • Administration of H2 blockers (eg, ranitidine, famotidine, nizatidine) may help symptoms, but use of a proton-pump inhibitor should be instituted if erosive esophagitis is present. Motility-promoting agents may help with symptoms. Cisapride has been shown to increase lower esophageal pressure and the amplitude of esophageal contractions in healthy patients and to stimulate esophageal motility with resultant symptomatic improvement in one patient with progressive systemic sclerosis.104
    • Esophageal dilatation can help when significant dysphagia or regurgitation occur in the presence of an esophageal stricture.
  • Sclerodactyly
    • Various treatment regimens including corticosteroids, nonsteroidal anti-inflammatory drugs, D-penicillamine, IFN-gamma, cyclosporine, and cytostatic drugs have been used with limited success in scleroderma.
      • An open-label study of calcitriol had promising results; however, a recent double-blinded, placebo-controlled trial was too small to draw any conclusions.105
      • After retrospective data showed the benefits of D-penicillamine for scleroderma skin changes, Clements et al106 performed the first randomized controlled trial of D-penicillamine in scleroderma. This trial compared high-dose D-penicillamine (750-1000 mg/d) to low-dose D-penicillamine (125 mg qod) in patients with early diffuse cutaneous scleroderma. The mean skin thickness score improved over 2 years of treatment in both groups, and no advantage was seen to using the higher dose of D-penicillamine.106 This study had no placebo group and the authors concluded later that they were not able to tell whether either dose was effective or ineffective.
      • D-penicillamine cannot, therefore, be recommended until placebo-controlled trials are conducted to show effectiveness.
    • The natural course of diffuse dermal sclerosis involves skin softening after 4-5 years; therefore, placebo-controlled trials are essential for determining an effective therapy. Skin involvement in limited scleroderma typically is not severe; therefore, attempts are not usually made to treat skin involvement.
  • Telangiectasia: Pulsed-dye laser treatment has been shown to be effective for the treatment of facial telangiectasia, but this has not been specifically studied in CREST patients.107 Many treatment modalities have been used with success to treat symptomatic GI telangiectasia (eg, medical treatment with estrogen-progesterone or desmopressin, laser ablation, sclerotherapy).

Surgical Care

  • Calcinosis: Surgical excision of localized painful large deposits can relieve symptoms; recurrence is rare. Saddic et al report a case of painful fingertip calcinosis treated with surgical debridement.108 If calcinosis is diffuse, recurrence is more common. Overzealous debridement to remove all calcinosis is apt to compromise digital viability and should be avoided.109 Successful palliation and significant remission of calcinosis using a carbon dioxide laser has been shown in 2 case reports with a total of 7 patients.110,111
  • Raynaud phenomenon: Cervical sympathectomy is less beneficial for scleroderma patients than for patients with Raynaud phenomenon secondary to peripheral vascular disease. Newer surgical approaches include digital sympathectomy, with or without revision of surgically correctable vascular disease. In the event of nonhealing digital ulcers, amputation, unfortunately, sometimes is unavoidable.
  • Esophageal dysmotility: Surgical therapy may help gastroesophageal reflux in general. Common techniques use complete or partial surgical wraps around the gastroesophageal junction to increase LES pressure and reduce reflux. The degree of tightness of the wrap inversely correlates with the reduction of reflux; however, the scleroderma cohort of patients may not tolerate a tight wrap. They are more likely to experience abdominal discomfort and dysphagia as a result. Therefore, avoid surgery for reflux in scleroderma patients except in the most severe refractory cases.
  • Sclerodactyly: If sclerodactyly is causing extensive contractures, a carefully planned and precisely performed operative treatment has been shown to have good success with a high level of patient satisfaction.109
  • Telangiectasia: Bowel resection for uncontrollable GI bleeding from telangiectasia is rarely necessary.

Consultations

  • Rheumatologists often primarily follow CREST syndrome patients. Referral to a rheumatologist is advised.
  • Dermatologists are often involved early and aid in the diagnosis of CREST syndrome.
  • Gastroenterologists may be asked to perform endoscopy for evaluation of esophageal disease. A gastroenterologist also should be consulted for an evaluation of GI bleeding resulting from telangiectasia and for the treatment of the condition.
  • Psychiatrists may be consulted to evaluate and treat depression and anxiety.
  • Occupational or physical therapy may be helpful if a patient has digit and hand strength deficits due to sclerodactyly.

Diet

No special recommendations are needed.

Activity

No special recommendations are needed.

Medication

The goal of pharmacotherapy is to reduce morbidity and to prevent complications.

Calcium channel blockers

These agents are used as part of therapy for Raynaud phenomenon.


Nicardipine (Cardene)

Used for vasodilatation and possible antiplatelet effects. Start with lowest dose available. Extended-dose preparations and agents with fewer negative inotropic effects are preferred.

Adult

20 mg PO tid

Pediatric

Not recommended

Fentanyl and alcohol may increase hypotensive effects; calcium channel blocker may increase cyclosporine levels; H2 blockers (cimetidine), erythromycin, nafcillin, and azole antifungals may increase toxicity (avoid combination or monitor closely); carbamazepine may reduce bioavailability (avoid this combination); rifampin may decrease levels (monitor and adjust dose of calcium channel blocker)

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

Adjust dose in renal/hepatic impairment; may cause lower extremity edema; allergic hepatitis has occurred but is rare


Nifedipine (Procardia)

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery; adverse reactions occur predominantly with short-acting formulations and include peripheral edema, headache, dizziness, and tachycardia; calcium channel blockers may worsen gastroesophageal reflux; SR formulations are associated with fewer adverse effects.

Adult

IR: 10 mg PO tid initially; increase to 10-30 mg PO tid/qid
SR: 30-60 mg PO qd initially; increase prn to 30-90 mg PO qd; may be administered bid

Pediatric

IR: 0.6-0.9 mg/kg/24h divided tid/qid

Caution with coadministration of any agent that can lower BP, including beta-blockers and opioids (H2 blockers may increase toxicity)

Documented hypersensitivity; symptomatic hypotension; persistent dermatologic reactions

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

May cause lower extremity edema; allergic hepatitis has occurred rarely

Prostaglandins

Agents included as part of therapy for Raynaud phenomenon.


Alprostadil (Prostaglandin E1)

Strong vasodilator of all vascular beds.

Adult

6-10 ng/kg/min IV for up to 72 h

Pediatric

Not established

Coadministration with anticoagulants may increase bleeding risk because of shared effects on platelet aggregation

Pregnancy

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

Precautions

Initiation of alprostadil requires experienced personnel and physiologic monitoring; bradycardia, hypotension, and/or postural hypotension, fever, headache, and flushing can occur

Antidepressants

For treatment of Raynaud phenomenon.


Fluoxetine (Prozac)

Selectively inhibits presynaptic serotonin reuptake with minimal or no effect in reuptake of norepinephrine or dopamine.
May cause more adverse GI effects than other SSRIs now currently available, which is the reason it is not recommended as a first choice. May be given as a liquid and a cap.
May give as 1 dose or divided doses. Presence of food does not appreciably alter levels. Because of long half-life (72 h), may take up to 4-6 wk to achieve steady state levels.
Long half-life is an advantage and a drawback. If it works well, an occasional missed dose is not a problem; if problems occur, eliminating all active metabolites takes a long time. The choice depends on adverse effects and drug interactions. Adverse effects of SSRIs seem to be quite idiosyncratic; thus, relatively few reasons exist to prefer one to another at this point if dosing is started at a conservative level and advanced as tolerated.

Adult

20 mg/d PO

Pediatric

Not established

Inhibits CYP450 isoenzymes 2C9, 2C19, 2D6, and 3A4; increases toxicity of diazepam and trazodone by decreasing clearance; also increases toxicity of MAOIs and highly protein-bound drugs; serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death) occurs with simultaneous use of other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan), so discontinue other serotonergic agents at least 2 wk prior to beginning SSRIs

Documented hypersensitivity; concurrently taking MAOIs or took them in the last 2 wk; coadministration with thioridazine

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

Known or suspected history of mania or hypomania; caution in hepatic impairment and history of seizures; MAOIs should be discontinued at least 14 d before initiating therapy

Phosphodiesterase enzyme inhibitors

For Raynaud phenomenon.


Cilostazol (Pletal)

Affects vascular beds and cardiovascular function. May improve blood flow by altering rheology of red blood cells. Produces nonhomogenous dilation of vascular beds, with more dilation in femoral beds than in vertebral, carotid, or superior mesenteric arteries.
Cilostazol and its metabolites are inhibitors of phosphodiesterase III and, as a result, cyclic AMP is increased, which leads to inhibition of platelet aggregation and vasodilation.

Adult

100 mg PO bid

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Diltiazem, erythromycin, grapefruit juice, itraconazole, ketoconazole, macrolide antibiotics, and omeprazole may increase levels

Documented hypersensitivity; CHF; coadministration with grapefruit juice

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 impairment; do not prescribe or administer without thoroughly reading complete prescribing information

Histamine H2 antagonists

For symptomatic relief of reflux resulting from esophageal dysmotility.


Famotidine (Pepcid)

Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Adult

20-40 mg PO bid

Pediatric

1-2 mg/kg/24h qd or divided bid; not to exceed 40 mg qd

May decrease effects of ketoconazole and itraconazole

Pregnancy

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

Precautions

If changes in renal function occur, consider adjusting dose or discontinuing treatment


Nizatidine (Axid)

Competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Adult

150 mg PO bid

Pediatric

Not established

Pregnancy

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

Precautions

Caution in renal or liver impairment; if changes in renal function occur, consider adjusting dose or discontinuing treatment; adjust dose in renal impairment


Ranitidine (Zantac)

Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen concentrations.

Adult

300 mg PO qd or divided bid

Pediatric

4-5 mg/kg/24h divided q8-12h

May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin

Pregnancy

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

Precautions

Caution in renal or liver impairment; if changes in renal function occur, consider adjusting dose or discontinuing treatment

Proton-pump inhibitors

For treatment of reflux symptoms resulting from esophageal dysmotility.


Omeprazole (Prilosec)

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.

Adult

20 mg PO qd

Pediatric

0.3-3.3 mg/kg/24h

May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin

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

Bioavailability may increase in older patients; safety of use in breastfeeding unknown; adverse effects include headache, diarrhea, rash, nausea, and constipation


Lansoprazole (Prevacid)

Inhibits gastric acid secretion.

Adult

15 mg PO qd for GERD; 30 mg PO qd for erosive esophagitis

Pediatric

Not established

May decrease effects of ketoconazole and itraconazole; may increase theophylline clearance

Pregnancy

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

Precautions

Consider adjusting dose in liver impairment; adverse effects include nausea, diarrhea, anorexia, fatigue, and rash

Antihypertensive agents

For Raynaud phenomenon.


Losartan (Cozaar)

Nonpeptide angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors. Does not affect response to bradykinin and is less likely to be associated with cough and angioedema. For patients unable to tolerate ACE inhibitors. Less effective in patients with scleroderma than those with primary Raynaud phenomenon. May modify some serum markers of vascular damage and possibly modulate some of the underlying tissue damage in scleroderma.

Adult

50 mg PO qd initially; not to exceed 100 mg/d

Pediatric

Not recommended

May increase digoxin, lithium, and allopurinol levels; probenecid may increase levels; coadministration with diuretics increase hypotensive effects; NSAIDs may reduce hypotensive effects; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

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

Pregnancy category D in second and third trimesters; caution in patients with unilateral or bilateral renal artery stenosis


Nitroglycerin (Nitro-Bid, Nitro-Dur, Nitrogard)

Relaxes smooth muscle all over the body, including those of the LES and esophageal body.

Adult

Topical: 2% ointment, 0.5- to 1-inch rubbed on affected area q4-6h prn; include 10- to 12-h nitrate-free interval/d
Transdermal: 0.2-mg/h patch qd with patch off 10-12 h/d

Pediatric

Not established

Aspirin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of calcium channel blockers (dose adjustment of either agent may be necessary)

Documented hypersensitivity; severe anemia, shock, postural hypotension, head trauma, closed-angle glaucoma, or cerebral hemorrhage

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 coronary artery disease, and low systolic blood pressure

More on CREST Syndrome

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Differential Diagnoses & Workup: CREST Syndrome
Treatment & Medication: CREST Syndrome
Follow-up: CREST Syndrome
Multimedia: CREST Syndrome
References
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Further Reading

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Kyle L Horner, MD, MS, Staff Physician, Department of Dermatology, Penn State Milton S Hershey Medical Center
Kyle L Horner, MD, MS is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Pennsylvania Academy of Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle
Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Kathleen David-Bajar, MD, Former Consultant to the Army Surgeon General, Department of Dermatology, Brooke Army Medical Center
Kathleen David-Bajar, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, Chief, Division of Dermatology, University of Louisville School of Medicine
Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology
Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Honoraria Consulting; Centocor Honoraria Consulting; Medicis Honoraria Consulting; Celgene Honoraria Consulting

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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