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Cutaneous vasculitis associated with molecular tergeted therapies: systematic review of the literature

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Abstract

Cutaneo us vasculitis (CV) has a broad spectrum of etiologies, and drugs are one of the main culprits. With the increasing use of targeted therapies in medicine, especially in rheumatology and oncology, the number of CV cases reported due to these drugs has increased. Therefore, the recognition and treatment of CV associated with targeted agents have become more and more important. In the literature, anti-TNFs (n = 73, 59.5%), secukinumab (n = 7, 6%), rituximab (n = 5, 4%), tocilizumab (n = 1, 0.8%), ustekinumab (n = 8, 6.5%), abatacept (n = 3, 2.4%), Janus kinase inhibitors (n = 3, 2.4%), alemtuzumab (n = 3, 2.4%), and immune checkpoint inhibitors (n = 20, 16%) have been reported as responsible agents. However, our knowledge of the pathogenetic mechanisms is fairly limited, and the standardized management is yet to be established. Furthermore, though it is uncommon, this complication may pose a safety issue. In this manuscript, we reviewed the literature on CV with or without systemic involvement related to targeted agents. We also proposed the pathogenetic mechanisms of these adverse events. Thus, we aimed to make it easier for clinicians to manage similar cases by reviewing the diagnosis and treatment processes.

Key Points

• It should be kept in mind that targeted therapies can lead to CV with or without systemic signs, which sometimes withholds their uses.

• Since targeted therapies are often used in the treatment of autoimmune and inflammatory diseases, CV associated with targeted therapies is difficult to recognize, and it is often mistakenly attributed to the underlying disease.

• Although the pathogenesis of CV associated with targeted therapies is not fully understood, there are several proposed mechanisms.

• Corticosteroids are the mainstay of treatment after discontinuation of the offending targeted agent.

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Abbreviations

CV:

Cutaneous vasculitis

LCV:

Leukocytoclastic vasculitis

NSAID:

Non-steroid anti-inflammatory drug

LV:

Lymphocytic vasculitis

TNF:

Tumor necrosis factor

ICI:

Immune checkpoint inhibitor

IQR:

Interquartile range

DIF:

Direct immunofluorescence

CHCC:

Chapel Hill Consensus Conference

ANCA:

Anti-neutrophilic cytoplasmic antibodies

ANA:

Anti-nuclear antibody

dsDNA:

Double stranded deoxyribonucleic acid

ENA:

Extractable nuclear antibody

CBC:

Complete blood count

BUN:

Blood urea nitrogen

CT:

Computed tomography

PD1:

Programmed death 1

IBD:

Inflammatory bowel disease

RA:

Rheumatoid arthritis

PSD:

Psoriatic disease

AS:

Ankylosing spondylitis

PP:

Palpable purpura

ER:

Erythematous rash

UR:

Urticarial rash

GI:

Gastrointestinal

AZA:

Azathioprine

MTX:

Methotrexate

LEF:

Leflunomide

CYC:

Cyclophosphamide

HQ:

Hydroxychloroquine

SEC:

Secukinumab

IFN-γ:

Interferon-gamma

NSAIDs:

Nonsteroid antiinflammatory drugs

TNF-α:

Tumor necrosis factor-alpha

LTB4:

Leukotriene B4

HLA:

Human leukocyte antigen

ICAM 1:

Intercellular adhesion molecule 1

MPGN:

Membranoproliferative glomerulonephritis

LE:

Lupus erythematosus

cPAN:

Cutaneous polyarteritis nodosa

GPA:

Gronulomatous polyangiitis

anti-RNApol:

Anti-ribonucleic acid polymerase

RF:

Rheumatoid factor

CCP:

Cyclic citrullinated peptide

CIC:

Circulating immune complexes

RBC:

Red blood cells

TC:

T cell

PC:

Plasma cell

DC:

Dendritic cell

IC:

Immune complexes

PMNL:

Polymorphonuclear leukocyte

EC:

Endothelial cell

MAC:

Membrane attack complex

NET:

Neutrophil extracellular traps

TH:

T helper

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Acknowledgements

The authors would like to thank Cerrahpasa Medical Faculty Department of Pathology for their contribution with histopathological illustrations.

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Authors and Affiliations

  1. Department of Internal Medicine, Cerrahpasa Medical Faculty, Istanbul University-Cerrahpasa, Kocamustafapasa str., Number: 53, Cerrahpasa 34098 Fatih, Istanbul, Turkey

    Tumay Ak, Rana Berru Durmus & Muhammed Onel

  2. Department of Internal Medicine, Cerrahpasa Medical Faculty, Istanbul University-Cerrahpasa, Istanbul, Turkey

    Muhammed Onel

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  1. Tumay Ak
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Tumay Ak designed the search strategy and topic, and wrote the manuscript. Rana Berru Durmus and Muhammet Onel contributed to the article and case selection. Tumay Ak, Rana Berru Durmus, and Muhammet Onel provided critical review, integrity, and clarity to the manuscript. All authors discussed the conclusions and contributed to the final version of the manuscript.

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Ak, T., Durmus, R.B. & Onel, M. Cutaneous vasculitis associated with molecular tergeted therapies: systematic review of the literature. Clin Rheumatol 42, 339–357 (2023). https://doi.org/10.1007/s10067-022-06406-6

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