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Table of Contents
CORRESPONDENCE
Year : 2020  |  Volume : 38  |  Issue : 2  |  Page : 115-116

Melanocytic nevus with amyloid deposit – Report of three cases


1 Department of Dermatology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan
2 Department of National Cheng Kung University Hospital, College of Medicine; Department of International Center for Wound Repair and Regeneration; Department of Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan
3 Department of Institute of Clinical Medicine; Department of Pathology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan

Date of Submission01-May-2019
Date of Decision04-Sep-2019
Date of Acceptance20-Sep-2019
Date of Web Publication29-May-2020

Correspondence Address:
Dr. Julia Yu-Yun Lee
Department of Dermatology, National Cheng Kung University Hospital, No. 138 Sheng-Li Road, Tainan 704
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ds.ds_36_19

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How to cite this article:
Yang HS, Hsu CK, Wu CL, Lee JY. Melanocytic nevus with amyloid deposit – Report of three cases. Dermatol Sin 2020;38:115-6

How to cite this URL:
Yang HS, Hsu CK, Wu CL, Lee JY. Melanocytic nevus with amyloid deposit – Report of three cases. Dermatol Sin [serial online] 2020 [cited 2020 Jul 3];38:115-6. Available from: http://www.dermsinica.org/text.asp?2020/38/2/115/285353



Dear Editor,

Cutaneous deposit of amyloid can derive from epithelial cells in the skin or secondary to primary systemic amyloidosis. The former is cytokeratin (CK) positive, while the latter is kappa or lambda light chain positive. Amyloid deposit is not uncommon in basal cell carcinoma,[1] seborrheic keratosis,[1] Bowen's disease, and solar keratosis, but rare in melanocytic nevi.[2] We are aware of four reported cases.[2],[3] Herein, we describe three new cases.

Case 1: A 67-year-old female presented with a 13 mm × 4 mm oval brownish plaque with irregular border and central hyperpigmentation on the left flank for 10 years. Case 2: A 68-year-old male presented with a 20-year history of a 5 mm × 4 mm hyperpigmented papule with irregular border on the back. Case 3: A 72-year-old male presented with a 6 mm × 7 mm round dark-brown papule on the nose tip for about 10 years. The lesion was excised in each case and revealed features of junctional dysplastic melanocytic nevus (Case 1) and intradermal melanocytic nevus (Cases 2 and 3). Congo red-positive amyloid deposits were present in the papillary dermis [Figure 1]. Immunohistochemical staining (ICH) for CK using AE1/AE3 (titer 1:200, Dako, Santa Clara, CA, USA), CK5/6 (titer 1:25, Dako, Santa Clara, CA, USA) and Melan A/MART1 (titer 1:25, Dako, Santa Clara, CA, USA), kappa light chain (titer 1:200, Biocare, Concord, CA, USA), and lambda light chain (titer 1:5000, Leica, Newcastle, UK) was performed. In all cases, the amyloid was positive for CK5/6-positive [Figure 1], but negative for AE1/AE3, Melan A, and kappa and lambda light chains.
Figure 1: Case 1 (a) presenting with a 13 mm × 4 mm oval brownish plaque with irregular border and central hyperpigmentation on the left flank, and (b) pathological examination showing features of junctional dysplastic nevus with abundant amyloid deposits in the papillary dermis, (c) confirmed by Congo red stain, and (d) the amyloid is positive for CK5/6. Case 2 (e) presenting with a 5 mm × 4 mm hyperpigmented papule with irregular border on the back, (f) pathological examination showing an intradermal nevus with abundant amyloid deposit in the papillary dermis, (g) confirmed by Congo red stain, and (h) the amyloid is positive for CK5/6. Case 3 (i) presenting with a 6 mm × 7 mm round dark-brown papule on the nose tip, (j) pathological examination showing intradermal melanocytic nevus with amyloid deposits in the papillary dermis, (k) confirmed by Congo red stain, and (l) the amyloid is positive for CK5/6 (H & E, original magnification: b, f × 200, j × 100; Congo red, original magnification × 200: c, g, k; IHC for CK5/6, original magnification × 200: d, h, l)

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With our three cases included, there are seven cases of melanocytic nevi (four intradermal, two compound, and one junctional) with amyloid deposition. The amyloid was observed in subepidermal area or intermingled with nevus cells. Epidermal origin or degenerating nevus cells had been suggested as the source of amyloid.[3] IHC study was performed in one reported case of intradermal nevus, where the amyloid was S100, HMB-45, and MART-1 negative.[3] In a study of CK expression in paraffin-embedded tissue of lichen and macular amyloidosis, the amyloid was AE3 (CK 1–8) positive in 50% of the cases.[4] The IHC findings in the study indicate that the amyloid was not derived from melanocytes or immunoglobulin light chains. The positive expression of CK5/6 supported the epidermal origin of the amyloid deposit in these melanocytic nevi. This finding is consistent with the report by Chang et al., in which the amyloid in the primary and secondary cutaneous amyloidosis was CK5 positive.[5] Based on their study, the authors concluded that CK5 is the major CK in the amyloid deposits of primary and secondary amyloidosis, and that “amyloid-K” is mainly originated from the basal keratinocytes. Of note, the amyloid in our cases and those studied by Change et al. was AE1/AE3 negative, thus AE1/AE3 should not be used as a marker in ICH for such purpose. In our cases, there was no prior treatment, so the amyloid deposit could not be attributed to a local insult as suggested by Hanami and Yamamoto.[3]

In conclusion, the amyloid in the three melanocytic nevi in the present study was found to be CK5/6 positive. Amyloid deposition is a very rare occurrence in melanocytic nevi. This is the first report to provide evidence of the keratinocytic origin of the amyloid in melanocytic nevi.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published, and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Olsen KE, Westermark P. Amyloid in basal cell carcinoma and seborrheic keratosis. Acta Derm Venereol 1994;74:273-5.  Back to cited text no. 1
    
2.
MacDonald DM, Black MM. Secondary localized cutaneous amyloidosis in melanocytic naevi. Br J Dermatol 1980;103:553-6.  Back to cited text no. 2
    
3.
Hanami Y, Yamamoto T. Secondary amyloid deposition in a melanocytic nevus. Int J Dermatol 2013;52:1031-2.  Back to cited text no. 3
    
4.
Apaydin R, Gürbüz Y, Bayramgürler D, Müezzinoglu B, Bilen N. Cytokeratin expression in lichen amyloidosus and macular amyloidosis. J Eur Acad Dermatol Venereol 2004;18:305-9.  Back to cited text no. 4
    
5.
Chang YT, Liu HN, Wang WJ, Lee DD, Tsai SF. A study of cytokeratin profiles in localized cutaneous amyloids. Arch Dermatol Res 2004;296:83-8.  Back to cited text no. 5
    


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