You're using an outdated browser. Please upgrade to a modern browser for the best experience.
Submitted Successfully!
Thank you for your contribution! You can also upload a video entry or images related to this topic. For video creation, please contact our Academic Video Service.
Version Summary Created by Modification Content Size Created at Operation
1
Rose Parisi
 -- 1840 2023-02-21 20:52:25 |
2 layout
Camila Xu
 Meta information modification 1840 2023-02-22 01:42:07 |

Video Upload Options

We provide professional Academic Video Service to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Parisi, R.; Shah, H.; Shear, N.H.; Ziv, M.; Markova, A.; Dodiuk-Gad, R.P. Cutaneous Bullous Dermatologic Adverse Events. Encyclopedia. Available online: https://encyclopedia.pub/entry/41498 (accessed on 07 July 2025).
Parisi R, Shah H, Shear NH, Ziv M, Markova A, Dodiuk-Gad RP. Cutaneous Bullous Dermatologic Adverse Events. Encyclopedia. Available at: https://encyclopedia.pub/entry/41498. Accessed July 07, 2025.
Parisi, Rose, Hemali Shah, Neil H. Shear, Michael Ziv, Alina Markova, Roni P. Dodiuk-Gad. "Cutaneous Bullous Dermatologic Adverse Events" Encyclopedia, https://encyclopedia.pub/entry/41498 (accessed July 07, 2025).
Parisi, R., Shah, H., Shear, N.H., Ziv, M., Markova, A., & Dodiuk-Gad, R.P. (2023, February 21). Cutaneous Bullous Dermatologic Adverse Events. In Encyclopedia. https://encyclopedia.pub/entry/41498
Parisi, Rose, et al. "Cutaneous Bullous Dermatologic Adverse Events." Encyclopedia. Web. 21 February, 2023.
Cutaneous Bullous Dermatologic Adverse Events
Edit
This entry is adapted from the peer-reviewed paper 10.3390/biomedicines11020323

Anti-cancer therapy improves outcomes for cancer patients; however, many classes of anti-cancer therapy have been implicated in the induction of bullous dermatologic adverse events (DAE), leading to reduced patient quality of life and in some cases discontinuation of life-prolonging or palliative therapy. Timely and effective management of adverse events is critical for reducing treatment interruptions and preserving an anti-tumor effect. Bullous DAE may be limited to the skin or have systemic involvement with greater risk of morbidity and mortality.

bullous dermatologic adverse events cutaneous adverse events

1. Introduction

The rapid evolution of anti-cancer therapy (including chemotherapy, targeted therapy, and immunotherapy) in recent years has led to a more favorable efficacy and safety profile for a growing cancer population and improved overall survival and reduced morbidity for many cancers. Enhanced anti-cancer therapy tolerance allows more patients to stay on treatment for longer durations leading to higher anti-cancer therapy utilization and an increased incidence and prevalence of associated adverse events (AEs) [1]. Timely and effective management of AEs is critical for reducing treatment interruptions and preserving an anti-tumor effect. Dermatologic AEs (DAEs) make up to 30–50% of treatment-associated AEs, with 1–5% being bullous DAEs [2][3]. Bullous DAEs consist of vesiculobullous eczema, hand–foot skin reaction, toxic erythema of chemotherapy, bullous pemphigoid, bullous lichenoid drug eruption, lichen planus pemphigoides, pemphigus vulgaris, bullous erythema multiforme, linear IgA bullous dermatosis, bullous lupus erythematosus, Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis and SJS-like eruptions, and non-specific bullous drug eruption [4][5][6][7][8][9].
Chemotherapy is defined as the use of cytotoxic chemicals to destroy rapidly growing and differentiating cells. Chemotherapeutic drugs can be distinguished into a number of classes, including anti-metabolites, anthracyclines, alkylating agents, anti-microtubular agents, methylation inhibitors, topoisomerase inhibitors, and vinca alkaloids. These are the oldest and most established form of anti-cancer therapy available; they have many uses including both curative and symptom-reducing functions [10]. Anti-cancer therapy has advanced in the past years with the developments of targeted therapies and immunotherapies, which can be used as monotherapy or adjunctively with chemotherapy [11]. Toxic erythema of chemotherapy, linear IgA bullous dermatosis, hand–foot skin reaction, bullous lichenoid drug eruption, and Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) and SJS-like eruptions are bullous DAEs that have been associated with chemotherapy.
Targeted therapies, such as kinase inhibitors, monoclonal antibodies, and antibody-drug conjugates, aim to inhibit molecular pathways involved in tumor growth and maintenance [12][13]. Targeted therapies are typically used in tumors with known pathogenesis or survival mechanisms, for example, tumors with targetable driver mutations or specific proteins known to be involved in tumorigenesis [14]. One benefit of targeted therapies is the specific nature of their effects, which often serves to minimize adverse events as compared to cytotoxic chemotherapy [15]. Targeted therapies have been shown to induce rapid tumor regression. However, resistance can be induced by pathway bypass or mutations in target molecules at high rates. For example, up to 46% of patients receiving epidermal growth factor receptor inhibitors have developed resistance; favorable responses may be short lived [16]. Hand–foot skin reaction, toxic erythema of chemotherapy, SJS/TEN and SJS/TEN-like eruptions, and non-specific bullous drug eruption are bullous DAEs that have been associated with targeted therapy [17][18].
Immunotherapy aims to stimulate a host immune response to cause tumor destruction. Types of immunotherapy that will be discussed include immune-checkpoint inhibitors (ICI) targeting programmed cell death 1 (anti-PD1), programmed cell death ligand 1 (anti-PD-L1), cytotoxic T lymphocyte antigen 4 (anti-CTLA-4), and other ligand (anti-CD274 and anti-CD137) axes, as well as toll-like receptor (TLR) 8 agonists [19][20]. Tumor cells may become resistant to innate cytotoxic T cell induced-apoptosis; ICI serve to disinhibit T cells to restore host immune ability to destroy tumor cells [21]. TLR agonists, such as TLR7 and TLR8, activate transcription factors to induce cytokine production to subsequently induce a response against cancer cells [22]. Immunotherapy harnesses the host immune system and has the potential to treat a broad range of cancers with a durable effect on outcomes [20].

2. Cutaneous Bullous Dermatologic Adverse Events

2.1. Vesiculobullous Eczema

Anti-cancer therapy-induced eczema is not uncommon, with an estimated incidence of 17% following ICI therapy, specifically nivolumab. Acute, severe forms of eczema have manifested with bullous features in a few reports [8][23][24][25][26]. Vesiculobullous eczema is graded as CTCAE eczema grades 1–3.
There has been one case of vesiculobullous eczema reported 3 months after nivolumab initiation. The patient clinically presented with prodromal erythematous plaques on the dorsum of the hands followed by a diffuse, scaly, bullous eruption involving the upper and lower extremities [8]. Pathogenesis related to anti-cancer-therapy-induced vesiculobullous eczema has not yet been postulated. However, idiopathic bullous eczema is hypothesized to result from over-expression of aquaporin 3 and aquaporin 10 in keratinocytes throughout the mid and upper epidermis, resulting in epidermal fissuring and subsequent vesicle formation secondary to cutaneous water and glycerol outflow [27].
Histopathology may reveal spongiotic dermatitis along with lymphocytic dermal infiltrates; Civatte bodies and parakeratosis may also be present. DIF can be utilized to exclude bullous pemphigoid (BP) [8].
Vesiculobullous eczema may be treated with topical and oral corticosteroids; PD-1 inhibitor therapy may be held for high grade eruptions. Vesiculobullous eczema has reportedly resolved following nivolumab cessation; however, mild eczema has been noted to persist for months [8].

2.2. Hand–Foot Skin Reaction (HFSR), Bullous Type

Hand–foot skin reaction (HFSR) is a painful eruption of sharply demarcated hyperkeratotic erythematous papules and plaques on pressure points of palmar-plantar surfaces and distal phalanges; when moderate to severe (grade ≥ 2), the manifestations are often bullous. Blisters are often tender and heal into hyperkeratotic inflamed calluses [7][28]. HFSR has been reported in about 30% of patients on targeted therapies, most commonly vascular endothelial growth factor (VEGF) inhibitors, including kinase inhibitors such as sorafenib, sunitinib, axitinib, pazopanib, and regorafenib, or anti-angiogenetic drugs, such as vemurafenib and dabrafenib [28][29][30][31][32][33][34].
Anti-cancer induced HFSR incidence and severity is typically dose-dependent [7][28]. HFSR usually causes a localized erythematous reaction [7]. HFSR is typically graded as CTCAE bullous dermatitis grade 2–3.
Pathogenesis of HFSR is still not known. Various theories have been proposed. HFSR is postulated to be the result of direct blockade of VEGFR, PDGFR, and EGFR in healthy tissue. [35][36][37][38]. PDGFR, in particular, is highly expressed in the eccrine gland ductal epithelium. Eccrine excretion of the inciting drug is postulated to cause direct dermal toxicity and/or inhibit receptors, such as PDGFR, leading to impaired wound healing especially in frictional areas [38]. High friction and pressure areas, such as on the palmar-plantar surfaces as well as on the elbows and knees, are constantly exposed to recurrent microtrauma; thus, at these locations the lesions are often higher grade due to their limited vascular supply [7][38]. Further, some researchers have suggested that HFSR may be equivalent to a Koebner phenomenon, which is the development of new skin lesions secondary to trauma [39].
Although this is typically a clinical diagnosis and does not require skin biopsy, bullous HFSR histopathology usually demonstrates characteristic keratinocyte damage in the form of vacuolar degeneration, keratinocyte apoptosis or necrosis, and intracytoplasmic eosinophilic bodies; these features often cause intraepidermal cleavage. There may be intraepidermal blisters in the stratum malpighii. Additional features that may be present include dyskeratotic cells, papillomatosis, epidermal acanthosis, or parakeratosis [7].
HFSR treatment ideally begins with prophylactic techniques prior to initiating anti-cancer therapy, such as a hand and foot skin exam to identify predisposing hyperkeratotic skin. Patients with hyperkeratotic skin on anti-cancer therapies implicated in the development of HFSR may benefit from wearing thick gloves and socks to prevent friction or trauma to palmar-plantar surfaces [28].
If bullous HFSR develops, treatments should be based on grade of severity. Treatment starts with emollients and lifestyle changes to reduce palmar-plantar friction and can escalate to topical corticosteroids, topical keratolytic agents, and if needed, systemic pain medications. Lastly, patients may benefit from anti-cancer dose modifications or discontinuation [28].

2.3. Toxic Erythema of Chemotherapy (TEC)

Toxic erythema of chemotherapy (TEC) is a common diagnosis encompassing a spectrum of cutaneous eruptions secondary to the use of anti-cancer therapy, including palmar-plantar erythrodysesthesia (PPE) and severe bullous flexural dermatitis (SBFD) [40][41][42]. TEC is also known as malignant intertrigo when involving the intertriginous skin. Diagnosis is of exclusion and based on clinical presentation, histologic findings, and known associations [5]. TEC is graded as CTCAE palmar-plantar erythrodysesthesia syndrome grades 1–3.
A number of anti-cancer drugs have been reported in association with TEC. The most commonly reported drugs include cytotoxic chemotherapies with an overall incidence of 3–64%, most commonly doxorubicin and cyclophosphamide; others include, paclitaxel, gemcitabine, decitabine, cytarabine, daunorubicin, methotrexate, cyclosporine, FOLFIRI (leucovorin calcium, 5-fluorouracil, and irinotecan), and vinorelbine [25][43][44][45]. Antibody drug conjugates such as brentuximab vedotin and enfortumab vedotin have also been reported to cause TEC [5][23][40][46][47][48]. It is important to note that bullous TEC secondary to enfortumab vedotin can present with widespread blistering and appear similar to TEN [47]. Few cases have been reported with no to minimal mucosal involvement; as such, it is included as a cutaneous DAE [47][49][50][51]. DAE onset typically ranges from days to months after anti-cancer therapy initiation [23][43][52].
TEC typically presents as red-purple patches and plaques, with bullae and erosions in severe cases, favoring the hands, feet, and intertriginous skin [40][47]. TEC typically spares the mucous membranes and lacks confluent erythroderma, which helps to differentiate it from SJS/TEN in otherwise ambiguous cases [40]. TEC may initially present with tingling and burning paresthesia as well as erythema in palms, fingers, and soles. Symptoms classically progress to involve edema, blisters, and ulcerations [44].
Pathogenesis of cytotoxic chemotherapy therapy-induced TEC is likely related to drug accumulation in eccrine sweat glands and subsequent local toxicity [43]. The pathogenesis of TEC secondary to enfortumab vedotin therapy is postulated to be the same mechanism as cytotoxic chemotherapy but more specifically inducing toxicity by depositing the cytotoxic monomethyl auristatin E (MMAE) in tissues expressing nectin-4, such as the skin. Enfortumab vedotin induces apoptosis of keratinocytes expressing nectin-4, causing dysfunctional cell-cell adherence and bullae formation [23][46].
Laboratory studies in TEC are typically within normal limits, and apparent lab abnormalities are typically attributed to the chemotherapy itself [23]. Though diagnosis can be made clinically and biopsy is rarely indicated, on histopathology, TEC presents with thickened epidermis with dyskeratosis and suprabasalar acantholysis as well as eccrine duct atypia. Interface dermatitis with necrotic keratinocytes and focal eccrine gland/duct necrosis may also be seen [5]. Increased mitotic figures without evidence of epidermal regeneration, squamatization of the basal layer, and syringosquamous metaplasia and the presence of only scattered necrotic keratinocytes suggest TEC over TEN histologically [40]. Histopathologic features of TEC include parakeratosis, epidermal acanthosis, papillomatosis, and vacuolar degeneration. The granular layer may be absent. Vasodilation and perivascular mononuclear cell infiltrates may also be present in the dermis [7]. Histopathology of bullous TEC lesions induced by enfortumab vedotin, specifically, may uniquely reveal disrupted cytoskeletons, as evidenced by abnormal and arrested mitoses as well as apoptotic cells with minimal dermal lymphocytic infiltration and epidermal dysmaturation [24]. DIF may demonstrate IgG and C3 cell surface deposits in the epidermis corresponding with the location of nectin-4, as well as intermittent linear deposition of IgM at the dermo-epidermal junction (DEJ) [46].
TEC does not typically require anti-cancer therapy discontinuation [53]. Rather, it is a toxicity and requires symptomatic treatment including treatment with topical corticosteroids, topical lidocaine, cold compresses, or oral corticosteroids; IVIg can be used in severe cases [5][23][40][43]. Some patients may require oral pain medications [43]. Dexamethasone administered in conjunction with cytotoxic chemotherapy has been shown to reduce the risk of developing TEC [54].

References

  1. Apalla, Z.; Lallas, A.; Delli, F.; Lazaridou, E.; Papalampou, S.; Apostolidou, S.; Gerochristou, M.; Rigopoulos, D.; Stratigos, A.; Nikolaou, V. Management of immune checkpoint inhibitor-induced bullous pemphigoid. J. Am. Acad. Dermatol. 2021, 84, 540–543.
  2. Deutsch, A.; Leboeuf, N.R.; Lacouture, M.E.; McLellan, B.N. Dermatologic Adverse Events of Systemic Anticancer Therapies: Cytotoxic Chemotherapy, Targeted Therapy, and Immunotherapy. Am. Soc. Clin. Oncol. Educ. Book 2020, 40, 485–500.
  3. Apalla, Z.; Rapoport, B.; Sibaud, V. Dermatologic immune-related adverse events: The toxicity spectrum and recommendations for management. Int. J. Womens Dermatol. 2021, 7, 625–635.
  4. Kuo, A.M.; Markova, A. High Grade Dermatologic Adverse Events Associated with Immune Checkpoint Blockade for Cancer. Front. Med. 2022, 9, 898790.
  5. Jennings, E.; Huang, S.; Lee, J.B.; Cha, J.; Hsu, S. Toxic erythema of chemotherapy secondary to gemcitabine and paclitaxel. Dermatol. Online J. 2020, 26, 1–3.
  6. Wouters, A.; Durieux, V.; Kolivras, A.; Meert, A.P.; Sculier, J.P. Bullous Lupus under Nivolumab Treatment for Lung Cancer: A Case Report with Systematic Literature Review. Anticancer Res. 2019, 39, 3003–3008.
  7. Yang, C.H.; Lin, W.C.; Chuang, C.K.; Chang, Y.C.; Pang, S.T.; Lin, Y.C.; Kuo, T.T.; Hsieh, J.J.; Chang, J.W. Hand-foot skin reaction in patients treated with sorafenib: A clinicopathological study of cutaneous manifestations due to multitargeted kinase inhibitor therapy. Br. J. Dermatol. 2008, 158, 592–596.
  8. Zhao, C.Y.; Hwang, S.J.E.; Consuegra, G.; Chou, S.; Fernandez-Peñas, P. Anti-programmed cell death-1 therapy-associated bullous disorders: A systematic review of the literature. Melanoma Res. 2018, 28, 491–501.
  9. Boyle, M.M.; Ashi, S.; Puiu, T.; Reimer, D.; Sokumbi, O.; Soltani, K.; Onajin, O. Lichen Planus Pemphigoides Associated with PD-1 and PD-L1 Inhibitors: A Case Series and Review of the Literature. Am. J. Dermatopathol. 2022, 44, 360–367.
  10. Amjad, M.T.; Chidharla, A.; Kasi, A. Cancer Chemotherapy. In StatPearls; StatPearls Publishing: Treasure Island, FL, USA, 2022.
  11. Falzone, L.; Salomone, S.; Libra, M. Evolution of Cancer Pharmacological Treatments at the Turn of the Third Millennium. Front. Pharmacol. 2018, 9, 1300.
  12. Padma, V.V. An overview of targeted cancer therapy. Biomedicine 2015, 5, 19.
  13. Pettinato, M.C. Introduction to Antibody-Drug Conjugates. Antibodies 2021, 10, 42.
  14. Baudino, T.A. Targeted Cancer Therapy: The Next Generation of Cancer Treatment. Curr. Drug Discov. Technol. 2015, 12, 3–20.
  15. Baldo, B.A.; Pham, N.H. Adverse reactions to targeted and non-targeted chemotherapeutic drugs with emphasis on hypersensitivity responses and the invasive metastatic switch. Cancer Metastasis Rev. 2013, 32, 723–761.
  16. Aldea, M.; Andre, F.; Marabelle, A.; Dogan, S.; Barlesi, F.; Soria, J.C. Overcoming Resistance to Tumor-Targeted and Immune-Targeted Therapies. Cancer Discov. 2021, 11, 874–899.
  17. Postow, M.A.; Sidlow, R.; Hellmann, M.D. Immune-Related Adverse Events Associated with Immune Checkpoint Blockade. N. Eng. J. Med. 2018, 378, 158–168.
  18. Martins, F.; Sofiya, L.; Sykiotis, G.P.; Lamine, F.; Maillard, M.; Fraga, M.; Shabafrouz, K.; Ribi, C.; Cairoli, A.; Guex-Crosier, Y.; et al. Adverse effects of immune-checkpoint inhibitors: Epidemiology, management and surveillance. Nat. Rev. Clin. Oncol. 2019, 16, 563–580.
  19. Farooq, M.; Batool, M.; Kim, M.S.; Choi, S. Toll-Like Receptors as a Therapeutic Target in the Era of Immunotherapies. Front. Cell Dev. Biol. 2021, 9, 756315.
  20. Kennedy, L.B.; Salama, A.K.S. A review of cancer immunotherapy toxicity. CA Cancer J. Clin. 2020, 70, 86–104.
  21. Granier, C.; De Guillebon, E.; Blanc, C.; Roussel, H.; Badoual, C.; Colin, E.; Saldmann, A.; Gey, A.; Oudard, S.; Tartour, E. Mechanisms of action and rationale for the use of checkpoint inhibitors in cancer. ESMO Open 2017, 2, e000213.
  22. Schön, M.P.; Schön, M. TLR7 and TLR8 as targets in cancer therapy. Oncogene 2008, 27, 190–199.
  23. Krause, T.; Bonnekoh, H.; Dilling, A.; Nast, A.; Metz, M. A distinctive bullous skin reaction associated with enfortumab vedotin-ejfv treatment for metastatic urothelial cancer: A case report. J. Dtsch. Dermatol. Ges. 2021, 19, 1781–1783.
  24. Guerrois, F.; Thibault, C.; Lheure, C.; Sohier, P.; Bensaid, B.; Ingen-Housz-Oro, S.; Dupin, N. Life-threatening skin reaction with Enfortumab Vedotin: Six cases. Eur. J. Cancer 2022, 167, 168–171.
  25. Lacouture, M.E.; Patel, A.B.; Rosenberg, J.E.; O’Donnell, P.H. Management of Dermatologic Events Associated with the Nectin-4-directed Antibody-Drug Conjugate Enfortumab Vedotin. Oncologist 2022, 27, e223–e232.
  26. Dobry, A.S.; Virgen, C.A.; Hosking, A.M.; Mar, N.; Doan, L.; Lee, B.; Smith, J. Cutaneous reactions with enfortumab vedotin: A case series and review of the literature. JAAD Case Rep. 2021, 14, 7–9.
  27. Soler, D.C.; Bai, X.; Ortega, L.; Pethukova, T.; Nedorost, S.T.; Popkin, D.L.; Cooper, K.D.; McCormick, T.S. The key role of aquaporin 3 and aquaporin 10 in the pathogenesis of pompholyx. Med. Hypotheses 2015, 84, 498–503.
  28. Gomez, P.; Lacouture, M.E. Clinical presentation and management of hand-foot skin reaction associated with sorafenib in combination with cytotoxic chemotherapy: Experience in breast cancer. Oncologist 2011, 16, 1508–1519.
  29. McLellan, B.; Ciardiello, F.; Lacouture, M.E.; Segaert, S.; Van Cutsem, E. Regorafenib-associated hand-foot skin reaction: Practical advice on diagnosis, prevention, and management. Ann. Oncol. 2015, 26, 2017–2026.
  30. Abdel-Rahman, O.; Fouad, M. Risk of mucocutaneous toxicities in patients with solid tumors treated with sunitinib: A critical review and meta analysis. Expert Rev. Anticancer Ther. 2015, 15, 129–141.
  31. Anwaier, A.; Chen, J.; Zhou, H.; Zhao, X.; Zheng, S.; Li, X.; Qu, Y.; Shi, G.; Zhang, H.; Wu, J.; et al. Real-world data on the efficacy and safety of pazopanib in IMDC favorable- and intermediate-risk metastatic renal cell carcinoma: A multicenter retrospective cohort study of Chinese patients. Transl. Androl. Urol. 2022, 11, 694–709.
  32. Baize, N.; Abakar-Mahamat, A.; Mounier, N.; Berthier, F.; Caroli-Bosc, F.X. Phase II study of paclitaxel combined with capecitabine as second-line treatment for advanced gastric carcinoma after failure of cisplatin-based regimens. Cancer Chemother. Pharmacol. 2009, 64, 549–555.
  33. Kwakman, J.J.M.; Elshot, Y.S.; Punt, C.J.A.; Koopman, M. Management of cytotoxic chemotherapy-induced hand-foot syndrome. Oncol. Rev. 2020, 14, 442.
  34. Lacouture, M.E. Dermatologic Principles and Practice in Oncology: Conditions of the Skin, Hair, and Nails in Cancer Patients; Wiley-Blackwell: Hoboken, NJ, USA, 2013.
  35. Zhu, Y.; Zhang, X.; Lou, X.; Chen, M.; Luo, P.; He, Q. Vascular endothelial growth factor (VEGF) antibody significantly increases the risk of hand-foot skin reaction to multikinase inhibitors (MKIs): A systematic literature review and meta-analysis. Clin. Exp. Pharmacol. Physiol. 2018, 45, 659–667.
  36. Luo, P.; Yan, H.; Chen, X.; Zhang, Y.; Zhao, Z.; Cao, J.; Zhu, Y.; Du, J.; Xu, Z.; Zhang, X.; et al. s-HBEGF/SIRT1 circuit-dictated crosstalk between vascular endothelial cells and keratinocytes mediates sorafenib-induced hand–foot skin reaction that can be reversed by nicotinamide. Cell Res. 2020, 30, 779–793.
  37. Eaby-Sandy, B.; Grande, C.; Viale, P.H. Dermatologic toxicities in epidermal growth factor receptor and multikinase inhibitors. J. Adv. Pract. Oncol. 2012, 3, 138–150.
  38. Belum, V.R.; Serna-Tamayo, C.; Wu, S.; Lacouture, M.E. Incidence and risk of hand-foot skin reaction with cabozantinib, a novel multikinase inhibitor: A meta-analysis. Clin. Exp. Dermatol. 2016, 41, 8–15.
  39. Sibaud, V.; Delord, J.P.; Chevreau, C. Sorafenib-induced hand-foot skin reaction: A Koebner phenomenon? Target Oncol. 2009, 4, 307–310.
  40. Lu, A.; Endicott, A.; Tan, S.Y.; Klufas, D.M.; Merrill, E.; Arakaki, R.; LeBoit, P.E.; Fox, L.; Haemel, A. Toxic epidermal necrolysis-like toxic erythema of chemotherapy: 2 illustrative cases. JAAD Case Rep. 2021, 15, 56–59.
  41. Bolognia, J.L.; Cooper, D.L.; Glusac, E.J. Toxic erythema of chemotherapy: A useful clinical term. J. Am. Acad. Dermatol. 2008, 59, 524–529.
  42. Parker, T.L.; Cooper, D.L.; Seropian, S.E.; Bolognia, J.L. Toxic erythema of chemotherapy following i.v. BU plus fludarabine for allogeneic PBSC transplant. Bone Marrow Transpl. 2013, 48, 646–650.
  43. Chauhan, P.; Gupta, A.; Kumar, S.; Bishnu, A.; Nityanand, S. Palmar-plantar erythrodysesthesia associated with high-dose methotrexate: Case report. Cancer Rep. 2020, 3, e1270.
  44. Webster-Gandy, J.D.; How, C.; Harrold, K. Palmar-plantar erythrodysesthesia (PPE): A literature review with commentary on experience in a cancer centre. Eur. J. Oncol. Nurs. 2007, 11, 238–246.
  45. Imen, A.; Amal, K.; Ines, Z.; Sameh el, F.; Fethi el, M.; Habib, G. Bullous dermatosis associated with gemcitabine therapy for non-small-cell lung carcinoma. Respir. Med. 2006, 100, 1463–1465.
  46. Penny, C.L.; Quow, K.; Rundle, C.W.; Al-Rohil, R.N.; Cardones, A.R.; Kheterpal, M.K.; Fresco, A.I. Clinical and direct immunofluorescence characteristics of cutaneous toxicity associated with enfortumab vedotin. Br. J. Dermatol. 2022, 187, 126–127.
  47. Birmingham, S.W.; Moon, D.J.; Kraus, C.N.; Lee, B.A. Enfortumab Vedotin-Associated Toxic Epidermal Necrolysis-like Toxic Erythema of Chemotherapy. Am. J. Dermatopathol. 2022, 44, 933–935.
  48. Smith, S.M.; Milam, P.B.; Fabbro, S.K.; Gru, A.A.; Kaffenberger, B.H. Malignant intertrigo: A subset of toxic erythema of chemotherapy requiring recognition. JAAD Case Rep. 2016, 2, 476–481.
  49. Nguyen, M.N.; Reyes, M.; Jones, S.C. Postmarketing Cases of Enfortumab Vedotin-Associated Skin Reactions Reported as Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis. JAMA Dermatol. 2021, 157, 1237–1239.
  50. Viscuse, P.V.; Marques-Piubelli, M.L.; Heberton, M.M.; Parra, E.R.; Shah, A.Y.; Siefker-Radtke, A.; Gao, J.; Goswami, S.; Ivan, D.; Curry, J.L.; et al. Case Report: Enfortumab Vedotin for Metastatic Urothelial Carcinoma: A Case Series on the Clinical and Histopathologic Spectrum of Adverse Cutaneous Reactions From Fatal Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis to Dermal Hypersensitivity Reaction. Front. Oncol. 2021, 11, 621591.
  51. Francis, A.; Jimenez, A.; Sundaresan, S.; Kelly, B. A rare presentation of enfortumab vedotin-induced toxic epidermal necrolysis. JAAD Case Rep. 2021, 7, 57–59.
  52. Chamberlain, F.; Farag, S.; Williams-Sharkey, C.; Collingwood, C.; Chen, L.; Mansukhani, S.; Engelmann, B.; Al-Muderis, O.; Chauhan, D.; Thway, K.; et al. Toxicity management of regorafenib in patients with gastro-intestinal stromal tumour (GIST) in a tertiary cancer centre. Clin. Sarcoma Res. 2020, 10, 1.
  53. Bodea, J.; Caldwell, K.J.; Federico, S.M. Bevacizumab, with Sorafenib and Cyclophosphamide Provides Clinical Benefit for Recurrent or Refractory Osseous Sarcomas in Children and Young Adults. Front. Oncol. 2022, 12, 864790.
  54. Karol, S.E.; Yang, W.; Smith, C.; Cheng, C.; Stewart, C.F.; Baker, S.D.; Sandlund, J.T.; Rubnitz, J.E.; Bishop, M.W.; Pappo, A.S.; et al. Palmar-plantar erythrodysesthesia syndrome following treatment with high-dose methotrexate or high-dose cytarabine. Cancer 2017, 123, 3602–3608.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Others
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Rose Parisi
,
Hemali Shah
,
Neil H. Shear
,
Michael Ziv
,
Alina Markova
,
Roni P. Dodiuk-Gad
View Times: 780
Revisions: 2 times (View History)
Update Date: 22 Feb 2023
Table of Contents
    1000/1000
    Hot Most Recent
    Academic Video Service
    Feedback