Manuscript category: Letters to the Editor
Title: New-onset bullous pemphigoid after SARS-CoV-2 infection
Keywords: COVID-19, Bullous pemphigoid, SARS-CoV-2
Word count: 451 words
Figure count: 2
Table count: 0
Sijie Zhou1, Xue Wang1, Lizhi
Ma1, Jiaming Fan1, Xinyun
Tang1, Peimei Zhou1*
1 Department of Dermatovenereology, Chengdu Second
People’s Hospital, Qingyun Street, Chengdu, 610041, China.
Correspondence to: Peimei Zhou, M.D., Ph.D.
Department of Dermatovenereology, Chengdu Second People’s Hospital,
Qingyun Street, Chengdu, 610041, China.
Tel: +86 18908176315; E-mail: 46551704@qq.com
Funding sources: None
Conflict of interest disclosures: All authors declare no
conflicts of interest.
Data availability statement: Data sharing does not apply to
this article as no new data were created or analysed in this study.
Ethics statement: The patient consented to publish this
information.
A 78-year-old male patient with a history of diabetes, hypertension, and
renal insufficiency was diagnosed with bullous pemphigoid (BP) after
contracting coronavirus disease 2019 (COVID-19). The patient had a
positive nasopharyngeal swab for severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2) in late December 2022 and was hospitalised
for two to three weeks. After discharge, the patient developed erythema
and blisters on both hands with itching that gradually involved the
whole body. The patient presented to our dermatology department on 3
March 2023.
At presentation to the dermatology department, the patient had tense
blisters covering the entire body, some of which were breaking down,
leaving a small patchy vesicular surface with a yellowish exudate (Fig.
1). Routine blood, procalcitonin, and C-reactive protein tests suggested
infection, and a chest computed tomography exam indicated viral
pneumonia, consistent with SARS-CoV-2 infection. In addition, the
patient’s BP180 antibody levels were >150 U/mL (range:
positive >20 U/mL), and rickle cell desmosome antibodies
were negative. Furthermore, direct immunofluorescence showed linear
basal deposition of immunoglobin G and C3 (uncertain). Finally,
histological analyses of an incisional cutaneous biopsy obtained from
the patient’s left lower extremity showed the formation of subepidermal
blisters containing a few eosinophils, lymphocytes and fibrin, and some
epidermal basal cells next to the blisters were edematous, liquefied and
deformed.(Fig. 2). These findings were consistent with a BP diagnosis.
The patient’s condition did not resolve after conventional treatment
with glycyrrhizin, a Chinese herbal extract compound, and other
anti-inflammatory treatments; therefore, dupilumab (600 mg initially,
then 300 mg every two weeks after) was subcutaneously administered. The
symptoms were relieved after two weeks.
An increasing number of studies are reporting cutaneous manifestations
after COVID-19. For instance, nonspecific skin symptoms, including
urticarial lesions, chilblain-like lesions, vesicular eruptions,
maculopapular rashes, and livedo, have been
reported1,2. We identified no other reports of
COVID-19-induced BP but did find a description of BP after SARS-CoV-2
vaccination3. The vaccine mimics antigens to induce
specific immune responses in the body, similar to those produced by
humans infected with novel coronaviruses, which can cause autoimmune
symptoms4. Therefore, our case was likely associated
with a novel coronavirus infection.
BP is an autoimmune, subepidermal blistering disease occurring in
elderly individuals. The exact pathogenesis of BP is unknown, but
several factors, such as drugs, thermal or electrical burns, surgical
procedures, trauma, ultraviolet irradiation, radiotherapy, chemical
preparations, transplants, and infections, may induce or exacerbate
BP5. Yet, viral infection-induced BP has rarely been
considered. This may be because viruses, as pathogens, can induce
cross-reactive autoantibodies sharing epitopes with host cells.
Additionally, the virus can directly infect keratinocytes, induce the
expression of hidden epitopes, modify existing epitopes, or insert
envelope fragments into cells to produce new antigens, which could be
responsible for BP development6,7.