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Table 1. 
Case Series: Patient Profile and Medical History*
Case Series: Patient Profile and Medical History*
Table 2. 
Thalidomide Therapy
Thalidomide Therapy
Table 3. 
Patients With Complete or Partial Response to Thalidomide Therapy per Subset of Lupus*
Patients With Complete or Partial Response to Thalidomide Therapy per Subset of Lupus*
1.
Jorizzo  JL Connective tissue disorders. Rakel  REed.Conn's Current Therapy Philadelphia, Pa WB Saunders1989;702- 707
2.
Sontheimer  RDProvost  TT Lupus erythematosus cutaneous. Sontheimer  RDProvost  TTeds.Cutaneous Manifestations of Rheumatic Diseases Baltimore, Md Williams & Wilkins1996;1- 71
3.
Furner  BB Treatment of subacute cutaneous lupus erythematosus. Int J Dermatol. 1990;29542- 547Article
4.
McCormack  LSElgart  MLTurner  ML Annular subacute cutaneous lupus erythematosus responsive to dapsone. J Am Acad Dermatol. 1984;11397- 401Article
5.
Newton  RCJorizzo  JLSolomon  AR  Jr  et al.  Mechanism-oriented assessment of isotretinoin in chronic or subacute cutaneous lupus erythematosus. Arch Dermatol. 1986;122170- 176Article
6.
Crovato  FLevi  L Clofazimine in the treatment of annular lupus erythematosus. Arch Dermatol. 1981;117249- 250Article
7.
de Berker  DDissaneyeka  MBurge  S The sequelae of chronic cutaneous lupus erythematosus. Lupus. 1992;1181- 186Article
8.
Barba-Rubio  JFranco-Gonzalez  F Lupus eritematoso discoide y talidomida. Dermatol Rev Mex. 1975;19131- 139
9.
Kyriakis  KPKontochristopoulos  GJPanteleos  DN Experience with low-dose thalidomide therapy in chronic discoid lupus erythematosus. Int J Dermatol. 2000;39218- 222Article
10.
Knop  JBonsmann  GHapple  R  et al.  Thalidomide in the treatment of sixty cases of chronic discoid lupus erythematosus. Br J Dermatol. 1983;108461- 466Article
11.
Walchner  MMeurer  MPlewig  GMesser  G Clinical and immunologic parameters during thalidomide treatment of lupus erythematosus. Int J Dermatol. 2000;39383- 388Article
12.
Calabrese  LFleischer  AB Thalidomide: current and potential clinical applications. Am J Med. 2000;108487- 495Article
13.
Stevens  RJAndujar  CEdwards  CJ  et al.  Thalidomide in the treatment of the cutaneous manifestations of lupus erythematosus: experience in sixteen consecutive patients. Br J Rheumatol. 1997;36353- 359Article
14.
Sato  EIAssis  LSLourenzi  VPAndrade  LE Long-term thalidomide use in refractory cutaneous lesions of systemic lupus erythematosus. Rev Assoc Med Bras. 1998;44289- 293Article
15.
Ordi-Ros  JCortes  FCucurull  EMauri  MBujan  SVilardell  M Thalidomide in the treatment of cutaneous lupus refractory to conventional therapy. J Rheumatol. 2000;271429- 1433
16.
Ochonisky  SVerroust  JBastuji-Garin  SGherardi  RRevuz  J Thalidomide neuropathy incidence and clinico-electrophysiologic findings in 42 patients. Arch Dermatol. 1994;13066- 69Article
17.
Aronson  IKYu  RWest  DPVan den Broek  HAntel  J Thalidomide-induced peripheral neuropathy: effect of serum factor on nerve cultures. Arch Dermatol. 1984;1201466- 1470Article
18.
Ordi  JCortes  FMartinez  NMauri  MDe Torres  IVilardell  M Thalidomide induces amenorrhea in patients with lupus disease. Arthritis Rheum. 1998;412273- 2275Article
19.
Gompel  AFrances  CPiette  JCBlanc  ASCordoliani  FPiette  AM Ovarian failure with thalidomide treatment in complex aphthosis: comment on the concise communication by Ordi et al. Arthritis Rheum. 1999;422259- 2260Article
20.
Tan  EMCohen  ASFries  JF  et al.  The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum. 1982;251271- 1277Article
21.
Sontheimer  RDMaddison  PJReichlin  MJordon  REStastny  PGilliam  JN Serologic and HLA associations in subacute cutaneous lupus erythematosus, a clinical subset of lupus erythematosus. Ann Intern Med. 1982;97664- 671Article
22.
Maddison  PJProvost  TTReichlin  M Serological findings in patients with "ANA-negative" systemic lupus erythematosus. Medicine (Baltimore). 1981;6087- 94Article
23.
Not Available, Thalidomide STEPS [booklet].  Warren, NJ Celgene Corporation1999;
24.
Rao  DGKane  NMOware  A Thalidomide neuropathy: role of F-wave monitoring. Muscle Nerve. 2000;231301- 1302Article
25.
Not Available, STEPS: Prevention and Protection. Celgene Pharmaceuticals Web site. Available at:http://www.celgene.com/steps/index.htm
26.
Wysenbeek  AJBlock  DAFries  JF Prevalence and expression of photosensitivity in systemic lupus erythematosus. Ann Rheum Dis. 1989;48461- 463Article
27.
Drosos  AADimou  GSSiamopoulou-Mavridou  AHatzis  JMoutsopoulos  HM Subacute cutaneous lupus erythematosus in Greece: a clinical, serological and genetic study. Ann Med Intern. 1990;141421- 424
28.
Sontheimer  RD Subacute cutaneous lupus erythematosus: a decade's perspective. Med Clin North Am. 1989;731073- 1090
29.
Nagy  EMeszaros  CDebreczeni  M Subacute lupus erythematosus of the skin—clinical aspects and laboratory findings. Z Hautkr. 1990;651039- 1041
30.
David-Bajar  KMBennion  SDDeSpain  JDGolitz  LELee  LA Clinical, histologic, and immunofluorescent distinctions between subacute cutaneous lupus erythematosus and discoid lupus erythematosus. J Invest Dermatol. 1992;99251- 257Article
31.
Mond  CBPeterson  MGRothfield  NF Correlation of anti-Ro antibody with photosensitivity rash in systemic lupus erythematosus patients. Arthritis Rheum. 1989;32202- 204Article
Study
January 2003

Low-Dose Thalidomide Therapy for Refractory Cutaneous Lesions of Lupus Erythematosus

Author Affiliations

From the Departments of Dermatology (Drs Housman, Jorizzo, and Fleischer and Mss McCarty and Grummer) and Internal Medicine–Section on Rheumatology (Dr Sutej), Wake Forest University School of Medicine, Winston-Salem, NC. The authors have no proprietary interests in thalidomide or any competing product.

Arch Dermatol. 2003;139(1):50-54. doi:10.1001/archderm.139.1.50
Abstract

Background  Thalidomide is an anti-inflammatory agent and an immunomodulator that inhibits the production of tumor necrosis factor α. It has shown promise as a treatment option for the cutaneous manifestations of lupus erythematosus (LE).

Objective  To assess the degree of clinical response per subtype of cutaneous lupus, the duration of therapy before documented clinical improvement, and the incidence of adverse effects, including peripheral neuropathy, with low-dose thalidomide therapy at 100 mg daily in the treatment of refractory cutaneous lesions of LE.

Methods  This retrospective medical record review of patients with refractory cutaneous manifestations of LE is one of the largest modern series in the literature. There were 29 patients seen at the Department of Dermatology, Wake Forest University School of Medicine (Winston-Salem, NC), who were unresponsive to conventional agents including antimalarial agents, and who started treatment between 1998 and 2000. Twenty-three patients who took the drug for 1 month or more were included in the analysis. Clinical responses were assessed by the investigators based on statements of improvement listed in the clinic notes and were categorized as "no response," "partial response," and "complete response." Partial response was classified as either 75% or greater or less than 75% improvement. The incidence of adverse effects including peripheral neuropathy was determined.

Results  Of the 23 patients, 17 (74%) demonstrated complete resolution of the cutaneous manifestations of LE, whereas 3 patients (13%) demonstrated 75% or greater partial improvement; 3 patients (13%) had less than 75% partial clinical improvement; and 21 patients (91%) who demonstrated a complete or partial response did so within 8 weeks of initiating thalidomide therapy.

Conclusions  Based on the results of this case series, we believe that thalidomide should be given prime consideration as a treatment for antimalarial drug–resistant interface lesions of LE. The design of prospective, randomized, double-blind, placebo-controlled trials for this indication is warranted.

CUTANEOUS manifestations of lupus erythematosus (LE) are chronic, disfiguring lesions that may be associated with systemic disease. These cutaneous lesions can be simply classified into 3 categories of lesions: (1) vascular lesions seen in systemic lupus erythematosus (SLE); (2) interface lesions seen in chronic cutaneous lupus erythematosus (CCLE), subacute cutaneous lupus erythematosus (SCLE), or SLE; or (3) special lesions as seen in LE profundus or in vesiculobullous lesions.1 There is potential for overlap between CCLE and SCLE, between CCLE and LE profundus, and between CCLE/SCLE and SLE.2

First-line therapy for cutaneous manifestations of LE has traditionally been antimalarial agents (hydroxychloroquine sulfate and/or quinacrine hydrochloride) along with sun protection.2,3 Other systemic treatments include dapsone, retinoids, clofazimine, and/or intralesional triamcinolone.2,46 However, owing to the chronicity of this disease, patients may be unresponsive or become refractory to conventional treatment and/or may have lesional recurrences.2 Moreover, many patients with discoid lesions go on to develop destructive or deforming scarring and/or pigmentary disturbances.2,7 This need for effective treatment led to the use of thalidomide as an alternate therapeutic modality for cutaneous LE.

Early reports of thalidomide use for the treatment of cutaneous manifestations of LE were by Barba-Rubio and Franco-Gonzalez8 in 1975.810 In 1983, Knop et al10 reported complete or marked benefit in 54 of 60 patients treated with a high thalidomide dosage (400 mg/d), which was then reduced to a minimum of 50 to 100 mg/d. Its anti-inflammatory and immunomodulatory properties that inhibit the production of tumor necrosis factor α are thought to contribute to its efficacy in cutaneous LE.11,12 In addition to treating SLE and cutaneous LE, thalidomide has been successfully used to treat chronic inflammatory diseases including prurigo nodularis, erythema nodosum leprosum, graft-vs-host disease, rheumatoid arthritis, aphthous stomatitis, and Behçet syndrome.11,12

Recent reports also confirm the efficacy of thalidomide for cutaneous LE in dosages ranging from 50 to 200 mg/d, with a complete response reported in 44% to 72% of patients and partial response reported in 28% to 37% of patients.9,13,14 Using 100-mg daily dose of thalidomide, a recent trial reported 12 (63%) of 19 patients with cutaneous lupus had complete improvement, 4 (21%) had partial improvement, and 3 (16%) had no response.15 The duration of thalidomide therapy needed for maximum benefit has been reported as anywhere from 12 to 16 weeks.13,15 In one series, thalidomide-induced sensory peripheral neuropathy, documented with a nerve conduction study, was reported in 21% of patients.16,17 Besides this and the significant risk of teratogenicity, other best documented adverse effects include paresthesias without associated clinical or electrophysiologic findings, drowsiness/fatigue, dizziness, weight gain, amenorrhea, constipation, headache, and nausea.9,10,1315,18,19

METHODS

Patients treated with thalidomide between 1998 and 2000 at the Department of Dermatology at the Wake Forest University School of Medicine (Winston-Salem, NC) were identified. The medical records of all 29 patients with a clinicopathologic diagnosis of CCLE, SCLE, SLE, or LE profundus were retrospectively reviewed. Although overlap can exist between these diagnoses,2 the clinical criteria for confirmation of each diagnosis included the following: for SLE, patients met 4 of the 11 American Rheumatism Association criteria20; for CCLE, patients had discoid lesions and a negative finding on evaluation for SLE (pertinent laboratory findings may include a low positive antinuclear antibody titer, a positive anti-Ro/SSA antibody, and/or a negative anti–double-stranded DNA/anti-La/SSB antibody); for SCLE, patients had erythematous macules and papules that evolved into scaly, papulosquamous and/or annular, polycyclic plaques, especially in a photo distribution, with a positive anti-Ro/SSA or anti-La/SSB antibody2,21,22; for LE profundus, patients had deep, firm nodules and a negative workup for SLE (pertinent laboratory findings may include a positive antinuclear antibody titer and a negative anti–double-stranded DNA antibody).2 All clinical diagnoses were confirmed by histopathologic review of cutaneous lesional biopsy specimens.

Most (28 of 29) patients had failed standard therapy with antimalarial agents (hydroxychloroquine sulfate and/or quinacrine hydrochloride).2,3 Other failed systemic treatments included dapsone, retinoids, clofazimine, and/or intralesional triamcinolone.2,46 In addition, some patients were treated by their rheumatologist for systemic manifestations of lupus and received more aggressive therapy, including oral prednisone, methotrexate, cyclosporine, and/or azathioprine (Table 1). In treating all 29 patients, we adhered to the System for Thalidomide Education and Prescribing Safety (STEPS) protocol,23 and patients were initially prescribed 100 mg of thalidomide by mouth at bedtime, which was tapered to 50 mg after complete clinical improvement.22 Nerve conduction studies along with neurologic examinations were performed by a neurologist at baseline, after 6 months of thalidomide therapy, and yearly thereafter. We were unable to obtain relapse rates beyond December 2000, since the medical record review was conducted within 1 to 2 months of the inclusion date end point of December 31, 2000.

STEPS Protocol

1. Description. The Food and Drug Administration (FDA) has mandated that all patients prescribed thalidomide enroll in the STEPS program, which was developed to help ensure that fetal exposure to thalidomide does not occur. All prescribers and pharmacists must register with the pharmaceutical company to prescribe and dispense thalidomide.

2 Patient Requirements. All patients must be counseled regarding the benefits, the risk of birth defects, and other adverse effects and precautions associated with thalidomide therapy via booklets and/or videotapes. In addition to serial pregnancy tests, a woman of childbearing potential must use 2 kinds of birth control during treatment and for 4 weeks before and after therapy. A man must use a latex condom every time he has intercourse with a woman and for 4 weeks after concluding treatment. After patient and prescriber sign the consent form, 1 copy stays with the prescriber, 1 copy goes to the STEPS program coordinating center (Boston University School of Public Health), 1 copy is for the patient, and 1 copy is delivered to the pharmacy along with the prescription. Each patient must participate in a mandatory and confidential survey.

3. Drug Dosing. Thalidomide is prescribed at 100 mg by mouth each night, and prescriptions are written for 28 days only. At initiation of therapy, the dosage may be decreased to 50 mg for a few nights to decrease unwanted drowsiness. Those who do not respond within 1 month of therapy may be prescribed 150 mg at bedtime. A patient who responds with clearing and is stable at the prescribed dosage may have the prescription adjusted to the lowest effective dose.

4. Monitoring. All female patients must be followed up every 28 days with a pregnancy test, whereas all male patients must be seen every 3 months or less. All patients must have baseline nerve conduction tests, with repeat testing at 6 months, 1 year, and then yearly thereafter.24 Baseline laboratory testing includes a complete blood cell count, with a differential and platelet count to check for possible neutropenia, which is especially recommended for patients positive for human immunodeficiency virus, and may be obtained at baseline and at each visit. All patients are followed up regarding adverse effects and progression of disease.

In addition to demographic data, information collected from the dermatology clinic medical records included all cutaneous manifestations of lupus, results from histopathologic examination, diagnostic laboratory results, previous and/or failed therapies, laboratory results while receiving thalidomide therapy, and thalidomide dosing and response. Clinical response was assessed by the investigators based on statements of improvement listed in the clinic notes and was categorized as "no response," "partial response" (including percentage of improvement), and "complete response" and was temporally related to the initiation of thalidomide. The incidence of adverse effects, including peripheral neuropathy, was determined. The reason(s) for not initiating or discontinuing thalidomide treatment was also noted.

RESULTS

Of the total 29 patients, there were 6 men and 23 women. The mean ± SD age of men at the onset of thalidomide therapy was 48 ± 10.8 years, and of women, 41 ± 12.1 years. There were 7 African Americans (6 women and 1 man) and 22 whites (17 women and 5 men; Table 1). Patient 1 was lost to follow-up after the initiation of treatment. Five of 29 patients (patients 9, 10, 21, 23, and 26) discontinued thalidomide treatment within 1 month of initiating therapy, citing fear of using the drug or concerns about possible adverse effects as the reason; therefore, their clinical response was unknown (Table 2). These 6 patients were excluded from data analysis; thus, all results reported are per an evaluable patient analysis. The causes of death for patients 12 and 29 were confirmed with a review of inpatient records and death certificates. Therefore, there were 6 patients who took thalidomide for less than 1 month and whose clinical response was unknown (Table 2), and 23 patients took the drug for more than 1 month and were assessed (including patients 11 and 22; Table 3).

Of the 23 patients treated for longer than 1 month, 17 (74%) demonstrated complete resolution of the cutaneous manifestations of lupus, whereas 3 (13%) demonstrated 75% or greater partial improvement, and 3 (13%) had less than 75% partial clinical improvement. All 23 patients had some level of improvement with either a partial or complete response after initiation of thalidomide therapy, 15 (65%) exhibited a complete response, and 6 (26%) demonstrated a partial response in the first 2 months of starting thalidomide therapy (Table 3). The most common diagnosis of those with a complete response to thalidomide was SLE (9 patients [39%];Table 3).

Of the 23 patients who were followed up for longer than 1 month, 5 (22%) had documented sensory, axonal neuropathy via a nerve conduction study while receiving thalidomide treatment (all baseline nerve conduction study results were normal). The duration of thalidomide treatment before obtaining a positive nerve conduction study result ranged from 8 to 16 months, with a mean of 11.6 months (Table 2). The incidence rate of reported paresthesias, even those unrelated to thalidomide therapy, was 26% (6 of 23 patients), but only 2 of the 5 patients with a positive nerve conduction study result complained of paresthesias (Table 2). The incidence rate of drowsiness/fatigue was 17% (4 patients); of dizziness, 13% (3 patients); of nausea or headache, 9% (2 patients); and of weight gain or constipation, 4% (1 patient). There were no reports of amenorrhea or pregnancies during thalidomide therapy (Table 2).

COMMENT

This case series further confirms thalidomide's efficacy in treating refractory cutaneous interface manifestations of LE. However, it is reserved as a secondary line of therapy because of its cost to the patient (approximately $567 for a 28-day course at 100 mg/d); the degree of monitoring by the STEPS protocol; its teratogenicity and adverse effects including peripheral neuropathy; and the availability of antimalarial therapy.2,23 System to Manage Accutane-Related Teratogenicity (SMART) program monitoring requirements for isotretinoin have prepared dermatology office staff for STEPS, and new biologic tumor necrosis factor α inhibitors that are being promoted for use in psoriasis cost 3 times what thalidomide costs. It is our observation that dermatologists are currently more likely to refer patients who are candidates for thalidomide therapy. The STEPS protocol has been enhanced as of July 30, 2001.25

Lupus erythematosus is an autoimmune disorder in which the etiology may be a combination of environmental, hormonal, and genetic factors that lead to polyclonal B-cell activation.2 One major environmental factor is UV light, which can precipitate cutaneous lesions in patients with CCLE, SLE, and SCLE,2,2630 especially in patients producing anti-Ro/SSA autoantibodies.2,31 Therefore, for patients with interface lesions with a high potential for scarring or disfigurement, thalidomide may be a good choice for spring and summer seasonal therapy. Moreover, patients are more likely to tolerate the monitoring of thalidomide if they are treated for a finite period of time, thus decreasing the inconvenience and the risk of adverse effects.

The present study again confirms the efficacy of low-dose thalidomide at 100 mg by mouth each night for the cutaneous manifestations of LE. Previous studies suggested that 12 to 16 weeks of thalidomide therapy were needed for maximum benefit13,15; however, our data illustrate that 21 (91%) of 23 patients who demonstrated a complete or partial response did so within 8 weeks of initiating thalidomide therapy. Physicians may be more likely to use thalidomide knowing that if the patient responds, he or she will usually do so within 2 months of initiating therapy, thus controlling cost and saving time spent on monitoring and education. Of note, patients may demonstrate a response within 2 weeks of initiating thalidomide therapy, but since our follow-up visits are 1 month after baseline per STEPS, the first opportunity to assess improvement is not usually less than 4 weeks.

The incidence of both treatment-related and unrelated paresthesias (26%) in this case series is consistent with that reported in previous studies.10 However, one series reported 35 to 37 months of therapy prior to developing a documented sensory, axonal neuropathy, whereas we note a range of 8 to 16 months.16 Although drowsiness/fatigue or dizziness were the 2 most frequently reported adverse effects, only 2 of 6 patients discontinued therapy as a result.

The STEPS protocol has limited the use of this efficacious drug and may have made physicians less motivated to prescribe thalidomide. New developments in dermatology including the introduction of the SMART Program monitoring requirements for isotretinoin and the acceptance of newer, most costly biologic tumor necrosis factor α inhibitors into dermatologic practice should obviate those limitations to thalidomide use. Using thalidomide in a seasonal fashion (from spring to fall) increases the likelihood of compliance and usage by both physicians and patients. Based on this case series, we believe that low-dose thalidomide should be given prime consideration in the treatment of antimalarial drug–resistant interface lesions of LE and has earned a niche on the therapeutic ladder in the management of these lesions.

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Article Information

Corresponding author: Joseph L. Jorizzo, MD, Department of Dermatology, Wake Forest University School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157-1071 (e-mail: jjorizzo@wfubmc.edu).

Accepted for publication January 4, 2002.

Dr Jorizzo has spoken previously regarding the use of thalidomide in dermatology practice and has received honoraria for this on several occasions. There were no outside sources of support for this study.

References
1.
Jorizzo  JL Connective tissue disorders. Rakel  REed.Conn's Current Therapy Philadelphia, Pa WB Saunders1989;702- 707
2.
Sontheimer  RDProvost  TT Lupus erythematosus cutaneous. Sontheimer  RDProvost  TTeds.Cutaneous Manifestations of Rheumatic Diseases Baltimore, Md Williams & Wilkins1996;1- 71
3.
Furner  BB Treatment of subacute cutaneous lupus erythematosus. Int J Dermatol. 1990;29542- 547Article
4.
McCormack  LSElgart  MLTurner  ML Annular subacute cutaneous lupus erythematosus responsive to dapsone. J Am Acad Dermatol. 1984;11397- 401Article
5.
Newton  RCJorizzo  JLSolomon  AR  Jr  et al.  Mechanism-oriented assessment of isotretinoin in chronic or subacute cutaneous lupus erythematosus. Arch Dermatol. 1986;122170- 176Article
6.
Crovato  FLevi  L Clofazimine in the treatment of annular lupus erythematosus. Arch Dermatol. 1981;117249- 250Article
7.
de Berker  DDissaneyeka  MBurge  S The sequelae of chronic cutaneous lupus erythematosus. Lupus. 1992;1181- 186Article
8.
Barba-Rubio  JFranco-Gonzalez  F Lupus eritematoso discoide y talidomida. Dermatol Rev Mex. 1975;19131- 139
9.
Kyriakis  KPKontochristopoulos  GJPanteleos  DN Experience with low-dose thalidomide therapy in chronic discoid lupus erythematosus. Int J Dermatol. 2000;39218- 222Article
10.
Knop  JBonsmann  GHapple  R  et al.  Thalidomide in the treatment of sixty cases of chronic discoid lupus erythematosus. Br J Dermatol. 1983;108461- 466Article
11.
Walchner  MMeurer  MPlewig  GMesser  G Clinical and immunologic parameters during thalidomide treatment of lupus erythematosus. Int J Dermatol. 2000;39383- 388Article
12.
Calabrese  LFleischer  AB Thalidomide: current and potential clinical applications. Am J Med. 2000;108487- 495Article
13.
Stevens  RJAndujar  CEdwards  CJ  et al.  Thalidomide in the treatment of the cutaneous manifestations of lupus erythematosus: experience in sixteen consecutive patients. Br J Rheumatol. 1997;36353- 359Article
14.
Sato  EIAssis  LSLourenzi  VPAndrade  LE Long-term thalidomide use in refractory cutaneous lesions of systemic lupus erythematosus. Rev Assoc Med Bras. 1998;44289- 293Article
15.
Ordi-Ros  JCortes  FCucurull  EMauri  MBujan  SVilardell  M Thalidomide in the treatment of cutaneous lupus refractory to conventional therapy. J Rheumatol. 2000;271429- 1433
16.
Ochonisky  SVerroust  JBastuji-Garin  SGherardi  RRevuz  J Thalidomide neuropathy incidence and clinico-electrophysiologic findings in 42 patients. Arch Dermatol. 1994;13066- 69Article
17.
Aronson  IKYu  RWest  DPVan den Broek  HAntel  J Thalidomide-induced peripheral neuropathy: effect of serum factor on nerve cultures. Arch Dermatol. 1984;1201466- 1470Article
18.
Ordi  JCortes  FMartinez  NMauri  MDe Torres  IVilardell  M Thalidomide induces amenorrhea in patients with lupus disease. Arthritis Rheum. 1998;412273- 2275Article
19.
Gompel  AFrances  CPiette  JCBlanc  ASCordoliani  FPiette  AM Ovarian failure with thalidomide treatment in complex aphthosis: comment on the concise communication by Ordi et al. Arthritis Rheum. 1999;422259- 2260Article
20.
Tan  EMCohen  ASFries  JF  et al.  The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum. 1982;251271- 1277Article
21.
Sontheimer  RDMaddison  PJReichlin  MJordon  REStastny  PGilliam  JN Serologic and HLA associations in subacute cutaneous lupus erythematosus, a clinical subset of lupus erythematosus. Ann Intern Med. 1982;97664- 671Article
22.
Maddison  PJProvost  TTReichlin  M Serological findings in patients with "ANA-negative" systemic lupus erythematosus. Medicine (Baltimore). 1981;6087- 94Article
23.
Not Available, Thalidomide STEPS [booklet].  Warren, NJ Celgene Corporation1999;
24.
Rao  DGKane  NMOware  A Thalidomide neuropathy: role of F-wave monitoring. Muscle Nerve. 2000;231301- 1302Article
25.
Not Available, STEPS: Prevention and Protection. Celgene Pharmaceuticals Web site. Available at:http://www.celgene.com/steps/index.htm
26.
Wysenbeek  AJBlock  DAFries  JF Prevalence and expression of photosensitivity in systemic lupus erythematosus. Ann Rheum Dis. 1989;48461- 463Article
27.
Drosos  AADimou  GSSiamopoulou-Mavridou  AHatzis  JMoutsopoulos  HM Subacute cutaneous lupus erythematosus in Greece: a clinical, serological and genetic study. Ann Med Intern. 1990;141421- 424
28.
Sontheimer  RD Subacute cutaneous lupus erythematosus: a decade's perspective. Med Clin North Am. 1989;731073- 1090
29.
Nagy  EMeszaros  CDebreczeni  M Subacute lupus erythematosus of the skin—clinical aspects and laboratory findings. Z Hautkr. 1990;651039- 1041
30.
David-Bajar  KMBennion  SDDeSpain  JDGolitz  LELee  LA Clinical, histologic, and immunofluorescent distinctions between subacute cutaneous lupus erythematosus and discoid lupus erythematosus. J Invest Dermatol. 1992;99251- 257Article
31.
Mond  CBPeterson  MGRothfield  NF Correlation of anti-Ro antibody with photosensitivity rash in systemic lupus erythematosus patients. Arthritis Rheum. 1989;32202- 204Article
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