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March 2020     Volume 4 Issue 2 
 

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Copyright 2020 The National Society for Cutaneous Medicine 

SHORT COMMUNICATIONS 
 

TNF- α Antagonist Induced Bullous Pemphigoid: A Case Report 
Aderonke Obayomi MD MPH1, Garrett Vick MD1, Tamela Charbonnet MD2 
 
1Tulane University School of Medicine Department of Dermatology, New Orleans, LA 
2Family Dermatology Specialisits, Metairie, LA 
 

 
 
 

This is a case of a 73-year-old Caucasian 
female with diabetes mellitus type 2, Graves’ 
disease, and a 4-month long history of severe 
plaque psoriasis with approximately 40 
percent body surface area involvement. For 
psoriasis, the patient was started on a 
biologic medication, with adalimumab (40 mg  
 
Figure 1. Multiple bullae overlying urticarial plaques 
on the patient’s abdomen.  

 
 

every 2 weeks) chosen due to the presence 
of mildly compromised renal function 
(creatinine of 1.1 mg/dL). The patient 
tolerated this treatment well. Shortly after the 
patient’s third injection, widespread and 
morphologically distinct skin lesions erupted. 
Physical examination revealed diffuse  
 
Figure 2. Urticarial plaque with overlying bullae on 
the patient’s right leg.  

 
 
 
 



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March 2020     Volume 4 Issue 2 
 

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Copyright 2020 The National Society for Cutaneous Medicine 

erythematous urticarial plaques with 
overlying bullae (Figures 1,2). Laboratory 
findings were remarkable for eosinophilia, 
mild leukocytosis, and skin biopsy histology 
as well as direct immunofluorescence 
demonstrating features consistent with 
bullous pemphigoid. Adalimumab was 
discontinued, and the patient was initiated on 
a prednisone taper along with adjunctive use 
of doxycycline 100mg twice daily and 
methotrexate 10mg weekly. Although the 
patient was noted to have mild renal 
dysfunction, she had few affordable 
treatment options covered by her insurance 
that would address both psoriasis and 
bullous pemphigoid other than methotrexate. 
Of note, creatinine remained stable while on 
methotrexate and did not elevate further than 
baseline level. Improvement was noted with 
reductions in number and size of bullous and 
urticarial lesions in response to this treatment 
with no new bulla after 4 months and fully 
healed erosions off both doxycycline and 
prednisone which were tapered over a total 
of 6 months of use. Despite reduction in the 
activity of bullous lesions, her psoriasis was 
noted to flare with an increase in affected 
body surface area to 25 percent. Thus, 
secukinumab (150 mg every 2 weeks) was 
started in addition to methotrexate (max dose 
of 12.5mg weekly) as treatment for patient’s 
psoriasis which cleared after 2 months. 
 
Bullous pemphigoid (BP) is an uncommon 
skin condition in which erythematous, 
urticarial papules and plaques progress to 
form tense bullae. Typically noted in elderly 
patients, bullous pemphigoid is also the most 
common autoimmune bullous disease and is 
often associated with psoriasis.1 TNF-α is a 
cytokine that is involved in systemic 
inflammation and a large number of 
autoimmune diseases, including BP. The 
serum levels of TNF-α in BP are reported to 
be correlated with the severity and number of 
lesions in a given patient and anti TNF-α 

agents have been effectively used in the 
treatment of BP. Paradoxically, there have 
also been reported cases of BP during 
treatment with anti-TNF-α therapy, as seen in 
our patient.2 However, in contrast to our 
patient, drug‐induced bullous pemphigoid is 
typically characterized by a younger age of 
onset.3 
 
With many drug-induced dermatoses, there 
is usually uncertainty in the exact culprit 
agent. In this case, the temporal relationship 
with the onset and cessation of adalimumab 
is striking. For all patients presenting with BP, 
a thorough drug history should be taken. 
Recognition of drug‐induced cases and 
prompt cessation of the offending agent may 
produce rapid improvement. As more cases 
of drug-induced BP are reported, we 
emphasize the need for further investigation 
into the incompletely understood effects of 
TNF-α antagonism on the immune system. 
 
Conflict of Interest Disclosures: None 
 
Funding: None 
 
Corresponding Author: 
Aderonke Obayomi, MD MPH  
Tulane University School of Medicine    
Department of Dermatology    
1430 Tulane Avenue 
New Orleans, LA 70130  
Phone: 504-988-5114 
Fax: 504-988-7382 
Email: aobayomi@tulane.edu 

 

References: 
1. Schiavo A.L., Ruocco E., Brancaccio G. Bullous 

pemphigoid: etiology, pathogenesis, and inducing 
factors: facts and controversies. Clin 
Dermatol. 2013;4:391–399. 

2. Altindag O., Aydeniz A., Gursoy S. A Case with 
anti TNF- α induced bullous pemphigoid. Turk J 
Rheumatol. 2010;25:214–216.  

3. Stavropoulos P.G., Soura E., Antoniou C. Drug-
induced pemphigoid: a review of the literature. J 
Eur Acad Dermatol Venereol. 2014;9:1133–
1140.   

mailto:aobayomi@tulane.edu