[Skip to Content]
Sign In
Individual Sign In
Create an Account
Institutional Sign In
OpenAthens Shibboleth
[Skip to Content Landing]
Views 654
Citations 0
March 4, 2020

Complete Remission of Hypertrophic Discoid Cutaneous Lupus Erythematosus After Treatment of Chronic Hepatitis C With Direct-Acting Antivirals

Author Affiliations
  • 1Department of Dermatology, Hospital Clínic de Barcelona, Institut d’Investigació Biomèdica August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain
  • 2Liver Unit, Hospital Clínic de Barcelona, Institut d’Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Centro de Investigación Biomédica en Red en Enfermedades Hepáticas y Digestivas (CIBERehd), University of Barcelona, Barcelona, Spain
JAMA Dermatol. Published online March 4, 2020. doi:10.1001/jamadermatol.2020.0013

The pathophysiologic features of lupus erythematosus (LE) are complex, and multiple factors have been suggested, such as genetics, drugs, and infections. Although an association of hepatitis C virus (HCV) infection with LE has not been clearly established, a higher proportion of HCV infection among patients with LE has been reported.1,2 In this observation, we report a case of refractory hypertrophic discoid cutaneous LE with complete remission after the treatment of HCV with direct-acting antivirals (DAAs).

Report of a Case

A 42-year-old woman with chronic HCV genotype 1B infection since childhood (viral load of 764 000 IU/mL) was diagnosed as having systemic LE in 2010 when she was admitted to the hospital with toxic epidermal necrolysis–like subacute cutaneous LE. She fulfilled 7 of 11 of the American College of Rheumatologists criteria for systemic LE (malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, antinuclear antibody positivity [>1/640], and anti–double-stranded DNA antibody positivity [16 IU/mL]). At a follow-up examination 6 years later, the patient presented with alopecic patches on the scalp; erythematous, scaly plaques on the face; oral lesions; and verrucous, hyperkeratotic plaques on both hands (Figure, A).

Figure.  Hypertrophic Discoid Cutaneous Lupus Erythematosus
Hypertrophic Discoid Cutaneous Lupus Erythematosus

A, Roundish, verrucous, hyperkeratotic plaques on both hands. B, Complete clinical response after treatment of hepatitis C virus infection with direct-acting antivirals (sofosbuvir/velpatasvir combination therapy).

A biopsy specimen from the hand showed hyperkeratosis, interface dermatitis, a dense perivascular and periadnexal lymphohistiocytic infiltrate, and dermal mucin deposits. Clusters of CD123-positive cells were observed. A periodic acid–Schiff stain demonstrated thickening of the basement membrane. On the basis of clinical and histologic findings, a diagnosis of hypertrophic discoid cutaneous LE was made. Mycophenolic acid and prednisone were prescribed because the patient had previously experienced a cutaneous adverse reaction to hydroxychloroquine, and acitretin was not well tolerated. She had been treated with mycophenolic acid (720 mg twice a day), prednisone (2.5-20.0 mg/d), and 0.1% tacrolimus ointment for more than 2 years with only a partial response. The patient was evaluated at the hepatology department for chronic HCV infection. Laboratory tests revealed a viral load of 776 000 IU/mL; transaminase levels were normal, and results of ultrasonography and transient elastography ruled out hepatic cirrhosis.

The patient received DAA therapy with sofosbuvir/velpatasvir (400 mg/100 mg once daily) combination therapy. Four weeks later, a marked improvement in mucocutaneous lesions was noticed, and the prednisone and mycophenolic acid were tapered and then discontinued. The patient completed 12 weeks of sofosbuvir/velpatasvir treatment, which led to a complete remission of the oral, facial, and acral lesions (Figure, B) and of arthralgia. At this point, the viral load was undetectable. The patient has remained asymptomatic without treatment and has maintained an undetectable viral load after 18 months of follow-up.


Viruses have been accepted as etiologic or triggering agents in the etiopathogenesis of autoimmune disorders. Hepatitis C virus has been linked to immunopathologic manifestations ranging from serologic autoantibody positivity and immune complex–mediated disorders (eg, vasculitis, cryoglobulinemia, glomerulonephritis) to overt autoimmune diseases, including thyroiditis, hepatitis, and Sjögren syndrome. The connection between systemic LE and HCV is still uncertain. Case-control studies have shown a higher proportion of HCV infection among patients with systemic LE.1,2 Some authors suggest that HCV infection may mimic systemic LE, whereas others accept it as a triggering factor for the latter disease.1,2

The introduction of DAA agents has revolutionized the management of HCV infection, with a sustained virologic response in more than 95% of cases. Current guidelines recommend that all patients with HCV infection be considered for DAA therapy.3 Improvement or total remission of some HCV-associated dermatoses, including lichen planus, porphyria cutanea tarda, and symptomatic cryoglobulinemia, has been observed after successful DAA treatment.4,5 To our knowledge, no cases of systemic or cutaneous LE with complete remission after DAA therapy have been reported to date, although a case of subacute cutaneous LE triggered by DAA treatment for HCV infection was described in 2019.6

This patient fulfilled the criteria for systemic LE together with the characteristic clinical and histologic features of hypertrophic discoid cutaneous LE. We believe that HCV infection may have acted as a trigger, disrupting immunity and aggravating cutaneous involvement. Screening for HCV infection could be considered in patients with refractory cutaneous LE, and in the case of positive findings, DAA therapy is recommended.

Back to top
Article Information

Corresponding Author: José M. Mascaró Jr, MD, Department of Dermatology, Hospital Clínic de Barcelona, IDIBAPS, Carrer de Villarroel 170, 08036 Barcelona, Spain (jmmascaro_galy@ub.edu).

Published Online: March 4, 2020. doi:10.1001/jamadermatol.2020.0013

Conflict of Interest Disclosures: Dr Forns reports receiving personal fees from Gilead Sciences and AbbVie. No other disclosures were reported.

Additional Contributions: We thank the patient for granting permission to publish this information.

Ramos-Casals  M, Font  J, García-Carrasco  M,  et al.  Hepatitis C virus infection mimicking systemic lupus erythematosus: study of hepatitis C virus infection in a series of 134 Spanish patients with systemic lupus erythematosus.  Arthritis Rheum. 2000;43(12):2801-2806. doi:10.1002/1529-0131(200012)43:12<2801::AID-ANR21>3.0.CO;2-VPubMedGoogle ScholarCrossref
Wang  S, Chen  Y, Xu  X, Hu  W, Shen  H, Chen  J.  Prevalence of hepatitis B virus and hepatitis C virus infection in patients with systemic lupus erythematosus: a systematic review and meta-analysis.  Oncotarget. 2017;8(60):102437-102445. doi:10.18632/oncotarget.22261PubMedGoogle Scholar
European Association for the Study of the Liver.  EASL recommendations on treatment of hepatitis C.  J Hepatol. 2018;69(2):461-511. doi:10.1016/j.jhep.2018.03.026PubMedGoogle ScholarCrossref
Morgado-Carrasco  D, Combalia  A, Fustà-Novell  X, Mascaró  JM  Jr, Iranzo  P.  Aggressive erosive lichen planus associated with hepatitis C responding to sofosbuvir/ledipasvir treatment.  Indian J Dermatol Venereol Leprol. 2019;85(3):326-329.PubMedGoogle Scholar
Combalia  A, To-Figueras  J, Laguno  M, Martínez-Rebollar  M, Aguilera  P.  Direct-acting antivirals for hepatitis C virus induce a rapid clinical and biochemical remission of porphyria cutanea tarda.  Br J Dermatol. 2017;177(5):e183-e184. doi:10.1111/bjd.15502PubMedGoogle ScholarCrossref
Prenner  A, Blum  R, Beltraminelli  H, Stirnimann  G, Borradori  L.  Subacute cutaneous lupus erythematosus triggered by an antiviral treatment combination for hepatitis C virus infection.  J Eur Acad Dermatol Venereol. 2019;33(3):e129-e131. doi:10.1111/jdv.15330PubMedGoogle ScholarCrossref
Limit 200 characters
Limit 25 characters
Conflicts of Interest Disclosure

Identify all potential conflicts of interest that might be relevant to your comment.

Conflicts of interest comprise financial interests, activities, and relationships within the past 3 years including but not limited to employment, affiliation, grants or funding, consultancies, honoraria or payment, speaker's bureaus, stock ownership or options, expert testimony, royalties, donation of medical equipment, or patents planned, pending, or issued.

Err on the side of full disclosure.

If you have no conflicts of interest, check "No potential conflicts of interest" in the box below. The information will be posted with your response.

Not all submitted comments are published. Please see our commenting policy for details.

Limit 140 characters
Limit 3600 characters or approximately 600 words