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(c) 2022 THE AUTHORS. Published by the National Society for Cutaneous Medicine. 719 

BRIEF ARTICLE 
 

 

Linear Depigmented Macules and Patches in Elderly Man 
 

Maansi Kulkarni, BA1, Clayton Conner, MD2, Sean Igelman, MD2, Julian Trevino, MD2 

 
1 Boonshoft School of Medicine, Wright State University, Dayton, OH 
2 Department of Dermatology, Boonshoft School of Medicine, Wright State University, Dayton, OH 
 

 

 
 

 
 
PD-1 inhibitors have been associated with 
several dermatologic conditions including 
various dermatitides and vitiligo, as well as 
more serious conditions such as drug 
hypersensitivity syndrome, Stevens-Johnson 
Syndrome, and toxic epidermal necrolysis.1,2 

 
Vitiligo is not an uncommon adverse 
dermatologic condition in the setting of 
immune checkpoint inhibitor use. One study 
showed that ipilimumab-induced vitiligo was 
seen in 11% of metastatic melanoma 
patients.3 In fact, vitiligo has the highest level 
of evidence for association with all 
checkpoint inhibitor therapy. Segmental 
vitiligo, that is depigmentation in a blaschkoid 
distribution that detail embryonic cell 
migration, has yet to be reported with PD-1 
checkpoint inhibitors. 
 

 
 
An 82-year-old African American male with a 
history of small cell lung cancer presented 
with new onset spreading depigmented 
macules and patches. At the time of 
presentation, the patient had received six 
months of a chemotherapy regimen 
consisting of taxol, carboplatin, and 
durvalumab. The patient stated that he first 
noticed pink pruritic macules on the right 
dorsal forearm within weeks of starting 
chemotherapy. Within the next several 
months, these macules evolved into 
depigmented macules and patches. A similar 
small group of macules later appeared on the 
contralateral posterior neck. The patient was 
extremely bothered by the appearance of his 
condition and attempted to treat it with over-
the-counter hydrocortisone cream without 
success. The patient denied use of other 
medications as well as personal or family 
history of any autoimmune conditions. 

ABSTRACT 

The development of immune checkpoint inhibitors such as programmed cell-death receptor 1 
(PD-1) antagonists has rapidly advanced chemotherapy within the last several decades. PD-1 
targeted immunotherapy drugs like pembrolizumab, ipilimumab, nivolumab, and durvalumab 
have known associations with several immune-mediated dermatological reactions. We report 
a case in which an elderly male experienced segmental vitiligo after use of durvalumab 
therapy for small cell lung cancer. Distinct from non-segmental vitiligo, segmental vitiligo 
presents in a unilateral blaschkoid distribution and typically does not cross the midline. To our 
knowledge, checkpoint inhibitor-induced segmental vitiligo has yet to be documented. 

INTRODUCTION CASE REPORT 



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March 2023     Volume 7 Issue 2 
 

(c) 2022 THE AUTHORS. Published by the National Society for Cutaneous Medicine. 720 

Physical examination revealed a linear 
distribution of depigmented macules 
coalescing into patches on the proximal 
posterior right upper arm with distal extension 
curving anteriorly towards the right dorsal 
forearm (Figure 1). An additional linear 
grouping of four small, depigmented macules 
was present on the left posterior neck 
immediately adjacent to midline (Figure 2). 
All depigmented macules demonstrated 
accentuation with Wood’s lamp examination. 
 

 
Figure 1. Blaschkoid distribution of 
depigmentation is observed on the proximal 
posterior right upper arm with distal extension 
curving anteriorly towards the right forearm. 

 
A 4 mm punch biopsy of the right upper arm 
revealed basal vacuolization, apoptotic 
keratinocytes, and numerous pigment-laden 
macrophages. Areas of epidermis lacked 
pigmentation. A Fontana-Masson stain 
confirmed dermal melanophages as well as 
the absence of basal melanin. Furthermore, 
SOX-10 and Melan-A showed absence of 
melanocytes while colloidal iron stains with 
and without hyaluronidase demonstrated no 
increase in dermal mucin. These findings, in 
conjunction with clinical presentation and 
Wood lamp testing, were consistent with a 
diagnosis of vitiligo. In the context of the 
specific blaschkoid distribution of the 
depigmented macules and patches primarily 
on the right upper extremity, the timeline of 
the patient’s exposure to durvalumab, and 
absence of personal or family history of 
autoimmunity, we concluded that the patient 
was experiencing durvalumab-induced 
segmental vitiligo. The patient was started on 
narrow band UVB phototherapy twice weekly 
and triamcinolone 0.1% ointment twice daily, 
which immediately halted further progression 
of the depigmentation and has resulted in 
repigmentation of many areas over the past 
4 months of treatment. 
 

 
Figure 2. An additional linear arrangement of 
depigmented macules is seen on the left 
posterior neck immediately adjacent to midline. 



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Understanding the proposed mechanism of 
checkpoint inhibitor-induced vitiligo requires 
an appreciation for the physiologic function of 
the programmed cell-death receptor 
pathway. PD-1 is a receptor expressed on 
the surface of T cells while its ligand, PDL-1, 
is found on dendritic cells and macrophages. 
The interaction ultimately leads to attenuation 
of the T-cell response. This pathway, in which 
T-cell response can be weakened, has an 
important role in cancer progression. Some 
malignancies evolve to overexpress PDL-1, 
which weakens cytotoxic T cell response and 
allows malignant cells to evade immune 
response. Thus, the PD-1/PDL-1 pathway is 
an excellent chemotherapy target as it 
restores the immune system ’s ability to 
combat malignant cells.3 Utilization of this 
pathway, however, may come at a cost in 
regard to autoimmunity. Segmental vitiligo is 
defined as depigmented macules affecting 
isolated body parts in a blaschkoid 
distribution (or embryonic epidermal cell 
migration patterns) that typically does not 
cross the midline4; however, in our patient, a 
small linear grouping does appear on the 
contralateral posterior neck. The significance 
of dermatological conditions that follow a 
blaschkoid distribution, while well 
documented, remains unclear. Furthermore, 
the reason depigmentation in our patient 
follows this unique pattern is uncertain 
currently, and further investigation into this 
phenomenon is required. 
 

 
 
Depigmented macules develop in vitiligo due 
to autoimmune T cell-mediated destruction of 
melanocytes. The proposed mechanism for 
PD-1 inhibitor-induced vitiligo suggests that 
immune effector cells target a shared antigen 

among malignant cells and healthy 
melanocytes. PD-1 inhibitors furthermore 
create an environment in which such 
autoimmune destruction remains unchecked. 
We hypothesize that a similar mechanism is 
at play in our patient with the affected 
melanocytes expressing a shared or similar-
appearing antigen with the patient’s small cell 
lung cancer due to genetic mosaicism. 
Another possible explanation is that the 
affected cells are somehow less robust and 
are more prone to cellular death also due to 
genetic mosaicism. Although checkpoint 
inhibitor-induced vitiligo is well established, 
our case report remains unique, as to our 
knowledge, durvalumab-induced segmental 
vitiligo has yet to be documented. 
 
Durvalumab use has been associated with 
several dermatological conditions. FDA 
clinical trial data showed that of 1,889 
patients on durvalumab, 26% experienced 
rash or dermatitis with discontinuation of the 
drug occurring in 0.1%. Only 0.3% of patients 
reported affliction with non-segmental 
vitiligo.5 It is important to accurately 
catalogue these dermatological reactions in 
order to optimize care for patients. Vitiligo, 
both segmental and non-segmental, should 
be recognized as potential dermatological 
conditions associated with durvalumab use.  
Further study regarding the significance of 
the segmental distribution is needed, though 
it does not appear to infer any deleterious 
consequences for our patient, as he is 
responding well to treatment. 
 
Conflict of Interest Disclosures: None 
 
Funding: None 
 
Corresponding Author: 
Maansi Kulkarni, BA 
Boonshoft School of Medicine 
Wright State University 
3640 Col. Glenn Hwy 
Dayton, OH 45436  
Email: kulkarni.31@wright.edu  

DISCUSSION 

CONCLUSION 



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