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 Table of Contents  
Year : 2022  |  Volume : 9  |  Issue : 2  |  Page : 139-140

Sunitinib-induced localized depigmentation over melasma in an elderly woman

Department of Dermatology, Venereology, and Leprosy, Vijayanagar Institute of Medical Sciences, Ballari, Karnataka, India

Date of Submission17-Feb-2022
Date of Decision13-May-2022
Date of Acceptance30-May-2022
Date of Web Publication12-Aug-2022

Correspondence Address:
MD Sambasiviah Chidambara Murthy
Department of Dermatology, Venereology, and Leprosy, Vijayanagar Institute of Medical Sciences, Ballari 583104
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pigmentinternational.pigmentinternational_

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How to cite this article:
Murthy SC, Shankar M, Nagaraj N, Srikantaiah M. Sunitinib-induced localized depigmentation over melasma in an elderly woman. Pigment Int 2022;9:139-40

How to cite this URL:
Murthy SC, Shankar M, Nagaraj N, Srikantaiah M. Sunitinib-induced localized depigmentation over melasma in an elderly woman. Pigment Int [serial online] 2022 [cited 2022 Sep 26];9:139-40. Available from: https://www.pigmentinternational.com/text.asp?2022/9/2/139/353666

Melasma is a common acquired pigmentary condition, occurring on the face. Sunitinib is a chemotherapeutic agent effective against solid tumors including renal cell cancer, gastrointestinal stromal tumors, and clear cell ovarian cancer.[1],[2] We report a case of sunitinib-induced localized depigmentation over melasma.

A 62-year-old woman presented with pus filled lesions over both legs for 3 days. She had been diagnosed with metastatic ovarian cancer over the last 6 months and was on sunitinib 50 mg once daily for 4 weeks in repeated 6-week cycles. Incidentally, localized depigmentation was noted over preexisting melasma (>12 years) on both the sides of face, 1 month after starting sunitinib. There was no other drug intake, photosensitivity, joint pain, or other systemic complaints. Family history was unremarkable. Cutaneous examination showed pyoderma over both the legs. Melasma involving centrofacial and malar areas (light brown, epidermal) with depigmentation was seen over bilateral zygomatic area and partially over nose [Figure 1]a and ba and b]. Other cutaneous, hair, and nail examinations showed age-related changes. Mucosae were normal.
Figure 1 (a) Depigmentation over melasma on malar areas. (b) Depigmentation over left malar area and nose.

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Her routine hematological examination showed mild pancytopenia, whereas, biochemical and urine examinations were normal. As she was least concerned about the lesions over face, she neither consented for biopsy nor interested in further management. Only pyoderma was treated with topical and systemic antibiotics. However, a telephonic interview with her relatives after 3 months revealed her death secondary to malignancy.

Melasma is more prevalent in females and darker skin types, predominantly attributed to ultraviolet (UV) exposure and hormonal influences. Melasma is generally a clinical diagnosis consisting of symmetric reticulated hypermelanosis in three predominant facial patterns, that is, centrofacial, malar, and mandibular.[3] The etiology of melasma is multifactorial among which UV light plays an important role in triggering and exacerbating the disorder. UV light is thought to induce reactive oxygen species by activating inducible nitric oxide and promoting melanogenesis. Recently, visible light is also known to play a role in inducing pigmentation.[3]

Histologically, there is an increased epidermal and/or dermal pigmentation, enlarged melanocytes, increased melanosomes, solar elastosis, dermal blood vessels, and perivascular lymphohistiocytic infiltrates. Various modalities of treatment include topical, oral, and procedural which have shown varying efficacies. Topical therapies include hydroquinone, tretinoin, corticosteroids, and triple combination creams. Oral therapies for melasma include tranexamic acid, Polypodium leucotomos extract, and glutathione. Procedures including chemical peels, microneedling, radiofrequency, and lasers, are also used as primary or adjunctive treatments for melasma.[3]

Sunitinib (SU11248; Sutent; Pfizer, New York, NY, USA) is a multitargeted tyrosine kinase inhibitor which has antitumor and antiangiogenic activities. It is an orally bioavailable molecule that inhibits vascular endothelial growth factor receptor-2, platelet-derived growth factor receptor-beta, and c-Kit receptor. The US Food and Drug Administration approved sunitinib for the treatment of metastatic renal cell cancer in January 2006.

Sunitinib is associated with many cutaneous side effects, including acral erythema, bullous dermatosis, edema, skin discoloration, stomatitis, subungual splinter hemorrhages, hand-foot syndrome, and leukotrichia.[4] Systemic side effects include fatigue, hypertension, abdominal pain, pancytopenia, acute kidney injury, stroke, and allergic reaction.[1] Sunitinib-induced depigmentation has been reported previously in a patient with renal cell carcinoma.[4] In our patient, there was preexisting melasma for several years which was resistant to several therapies, but showed clinical depigmentation after the initiation of oral sunitinib. Wood lamp could not be done in our patient; however, it shows accentuation of depigmented patches and may detect additional lesions not visible with ambient lighting.[4]

Drug-induced depigmentation usually starts in a few days to months (1–42 months), after the initiation of therapy. It is localized to photo-exposed areas like face, neck, hand, and arms, excluding traumatic pathogenesis, in contrast to classical vitiligo in which genitalia, wrist, and perioral regions are involved, possibly due to Koebner phenomenon. Drug-induced depigmentation begins as speckled hypopigmented macules, becoming confluent into patches with shaded and jagged edges, in contrast to homogenous patches with sharp edges in vitiligo. Positive family history may be present in vitiligo.[5],[6]

Melasma is still a challenging condition to treat, with significant psychological effects. Difficulty in treating melasma is noted by the available as well as increasing number of therapeutic modalities available. Therapeutic efficacy may vary due to several factors including variability in clinical presentation and response to treatment amongst different genders, skin phototypes, and ethnicities. Topical sunitinib, could be a newer addition to the dermatologist’s armamentarium for melasma in future.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Chan JK, Brady W, Monk BJ et al. A phase II evaluation of sunitinib in the treatment of persistent or recurrent clear cell ovarian carcinoma: an NRG Oncology/Gynecologic Oncology Group Study (GOG-254). Gynecol Oncol 2018;150:247-52.  Back to cited text no. 1
Anglesio MS, George J, Kulbe H et al. IL-6-STAT3-HIF signaling and therapeutic response to the angiogenesis inhibitor sunitinib in ovarian clear cell cancer. Clin Cancer Res 2011;17:2538-48.  Back to cited text no. 2
Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther (Heidelb) 2017;7:305-18.  Back to cited text no. 3
Al Enazi MM, Kadry R, Mitwali H. Skin depigmentation induced by Sunitinib treatment of renal cell carcinoma. J Am Acad Dermatol 2009;61:905-6.  Back to cited text no. 4
Jalalat SZ, Cohen PR. Gefitinib-associated vitiligo: report in a man with parotid squamous cell carcinoma and review of drug-induced hypopigmentation. Dermatol Online J 2013;19:20020.  Back to cited text no. 5
Ramondetta A, Ribero S, Conti L et al. Clinical and pathological relevance of drug-induced vitiligo in patients treated for metastatic melanoma with anti-PD1 or BRAF/MEK inhibitors. Acta Derm Venereol 2020;100:adv0000.  Back to cited text no. 6


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