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Dry skin linked to multikinase inhibitor treatment

Definition: Dry skin is also referred to as xerosis or xerosis cutis, and typically manifests with flaky, dull, scaly, and itchy skin.1-3 Pruritus (itching) is a symptom of dry skin.1

Incidence: Dry skin is commonly (≥1/100 to <1/10) or very commonly (>1/10) seen in patients treated with some multikinase inhibitors including, cabozantinib, imatinib, regorafenib, sorafenib, sunitinib, dasatinib, pazopanib, midostaurin or vandetanib.4-13 In addition, eczema is reported to be very common (>1/10) in patients treated with imatinib or common (≥1/100 to <1/10) in patients treated with sunitinib or dasatinib.7, 8, 11

Grading and lesion characteristics: According to the CTCAEv5.0,14 dry skin is, “A disorder characterised by flaky and dull skin; the pores are generally fine, the texture is a papery thin texture”. The CTCAEv5.0 uses the term dry skin, whereas the MESTT15 classification uses the term cutaneous xerosis.

Table 6: Grading of Dry Skin According to the CTCAEv5.0

Grade

Description

1

Covering <10% BSA and no associated erythema or pruritus

2

Covering 10-30% BSA and associated with erythema or pruritus; limiting instrumental ADL

3

Covering >30% BSA and associated with pruritus; limiting self-care ADL

ADL: Activities of Daily Living, BSA: Body Surface Area

Table 7: Grading of Xerosis according to MESTT

Grade

Description

1

Scaling/flaking covering < 10% BSA, NO erythema/pruritus/effect on emotions or functioning

2

2A Scaling/flaking covering 10-30% BSA, + pruritus OR effect on emotions/functioning

2B As 2A AND effect on emotions/functioning + erythema

3

3A Scaling/flaking covering >30% BSA AND pruritus AND erythema AND effect on emotions/functioning AND + fissuring/ cracking

3B As 3A + signs of super infection

BSA: Body Surface Area

Onset: Dry skin with multikinase inhibitors tends to appear 2–3 months after the initiation of therapy and is persistent, often lasting for several months.16-18 Onset of pruritus occurs alongside the onset of xerosis. 

Resolution: Dry skin associated with multikinase inhibitor therapy is reported to not be cumulative, is typically reversible, and generally does not require treatment discontinuation.16-17 It is important to be aware that dry skin may become complicated through secondary infection by Staphylococcus aureus or Herpes simplex virus. Also see Prophylaxis and treatment - reactive management - skin changes – Pruritus.  

Related Links

References

  1. Lacouture ME, et al. Support Care Cancer. 2011;19:1079–1095.
  2. Robert C, et al. Lancet Oncol. 2005;6:491-500.
  3. Chanprapaph, K, et al. Dermatology Research and Practice. 2014;2014:1-8.
  4. European Medicines Agency. Stivarga (regorafenib) Summary of Product Characteristics 2018.
  5. European Medicines Agency. Nexavar (sorafenib) Summary of Product Characteristics 2018.
  6. European Medicines Agency. Caprelsa (vandetanib) Summary of Product Characteristics 2019.
  7. European Medicines Agency. Sutent (sunitinib) Summary of Product Characteristics 2019.
  8. European Medicines Agency. Glivec (imatinib) Summary of Product Characteristics 2019.
  9. European Medicines Agency. Cabometyx (cabozantinib) Summary of Product Characteristics 2019.

  10. European Medicines Agency. Cometriq (cabozantinib) Summary of Product Characteristics 2019.
  11. European Medicines Agency. Sprycel (dasatinib) Summary of Product Characteristics 2019.
  12. European Medicines Agency. Votrient (pazopanib) Summary of Product Characteristics 2018.
  13. European Medicines Agency. Rydapt (midostaurin) Summary of Product Characteristics 2018.
  14. National Cancer Institute Cancer Therapy Evaluation Program. Common Terminology Criteria for Adverse Events and Common Toxicity Criteria [v5.0]. 27 November 2017. (Accessed 15 April 2019).
  15. MASCC EGFR Inhibitor Skin Toxicity Tool (MESTT). (Accessed 15 April 2019).
  16. Belum VR, Fischer A, Choi JN, Lacouture ME. Curr Oncol Rep. 2013;15:249–259.
  17. Manousaridis I, et al. J Eur Acad Dermatol Venereol. 2013;27:11–18.
  18. Robert C, et al. Semin Oncol. 2012;39:227–240.

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