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Table of Contents
Year : 2021  |  Volume : 39  |  Issue : 2  |  Page : 109-110

Multiple porokeratosis developed in association with the worsening of diabetes mellitus

1 Department of Dermatology, Fukushima Medical University, Fukushima, Japan
2 Department of Dermatology, Ohta Nishinouchi General Hospital, Fukushima, Japan

Date of Submission14-Jan-2021
Date of Decision09-Feb-2021
Date of Acceptance22-Feb-2021
Date of Web Publication23-Jun-2021

Correspondence Address:
Dr. Toshiyuki Yamamoto
Department of Dermatology, Fukushima Medical University, Hikarigaoka 1, Fukushima 960-1295
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ds.ds_10_21

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How to cite this article:
Yamamoto T, Orikasa R. Multiple porokeratosis developed in association with the worsening of diabetes mellitus. Dermatol Sin 2021;39:109-10

How to cite this URL:
Yamamoto T, Orikasa R. Multiple porokeratosis developed in association with the worsening of diabetes mellitus. Dermatol Sin [serial online] 2021 [cited 2022 Dec 3];39:109-10. Available from: https://www.dermsinica.org/text.asp?2021/39/2/109/319143

Dear Editor,

Various skin manifestations are observed in patients with diabetes mellitus (DM); however, porokeratosis in association with DM is rarely reported. We herein report an unusual case in which porokeratosis multiply developed along with rapid worsening of DM.

A 51-year-old male developed asymptomatic eruptions on the lower extremities that appeared 2 years previously. He had a marked obesity (body mass index: 40.56), and was suffering from DM for several years. He had been treated with metformin hydrochloride and alogliptin (DPP-4 inhibitor) for his diabetes, which however was not well-controlled and glucose levels rapidly increased. In parallel, the eruptions were increased in number and spread to the upper extremities. He was referred to the diabetes medicine for better control of his DM, and also visited dermatology department. Physical examination showed well-circumscribed, brownish keratotic plaques with slightly elevated borders on the left thigh and bilateral lower legs [Figure 1]a. One of the lesions showed a verrucous nodule. In addition, similar eruptions were scattered on the forearms and dorsum of the hands [Figure 1]b. Blood chemistry results showed elevated aspartate aminotransferase (75 U/L; normal: 13–33), alanine aminotransferase (98 U/L; normal: 8–42), blood sugar (247 mg/dl), and HbA1c (9.7%), although kidney function was normal. Histological examination of the keratotic lesion revealed irregular, mild acanthosis of the epidermis and a cornoid lamella in the cornified layers [Figure 1]c. A second biopsy from the edge of the erythematous plaque showed cornoid lamella in the corneal layer. Treatment with topical Vitamin D3 ointment (calcipotriol) was started, which however was not effective.
Figure 1: (a) Clinical features showing several well-circumscribed erythemas with elevated borders. One of them was verrucous (arrow). (b) Similar erythemas on the forearm and dorsum of the hand. (c) Histological features showing an irregularly elongated epidermis, a column of parakeratosis, and dyskeratotic keratinocytes.

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After glycemic control by switching DPP-4 inhibitor to sodium glucose cotransporter 2 inhibitor, the appearance of skin lesions ceased, but preexisting lesions did not disappear.

In the present case, porokeratosis appeared and increased in number along with rapid elevation of HbA1c, where its level shifted from 7.7% to 9.7%. One of the porokeratosis lesions assumed a keratotic appearance. Verrucous porokeratosis or hyperkeratotic porokeratosis frequently involves the buttocks and genitogluteal regions. Histological examination shows a digitate epidermis with numerous columns of parakeratosis overlying epidermal cells along with a diminished granular layer and dyskeratotic keratinocytes.[1] By contrast, our case did not exhibit verrucous epidermal changes on histology.

To date, several cases of porokeratosis have been reported in patients with DM;[2],[3],[4] however, there was only one similar case in which disseminated superficial porokeratosis suddenly developed in association with an exacerbation of DM.[3] Previous studies have shown that glucose altered the differentiation, proliferation, and migration of keratinocytes.[5],[6] A high glucose environment changes the proliferation/differentiation balance, which may have been relevant to the acute induction of porokeratosis in a susceptible individual like our case.

Our patient had been treated with DPP-4 inhibitor, when porokeratosis appeared. There are a few case reports of drug-induced superficial porokeratosis.[7],[8],[9],[10] It is well-known that bullous pemphigoid is induced under treatment with DPP-4 inhibitors. In addition, it has been shown that DPP-4 inhibitors influence keratinocytes;[11] however, to our knowledge, cases of porokeratosis during the use of DPP-4 inhibitors have not been reported. Since our case did not develop disseminated lesions, it may be unlikely that porokeratosis was induced by DPP-4 inhibitor, but further studies are necessary.

Declaration of patient consent

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

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Conflicts of interest

There are no conflicts of interest.

  References Top

Takiguchi RH, White KP, White CR Jr., Simpson EL. Verrucous porokeratosis of the gluteal cleft (porokeratosis ptychotropica): A rare disorder easily misdiagnosed. J Cutan Pathol 2010;37:802-7.  Back to cited text no. 1
Yalcin B, Uysal PI, Kadan E, Bozdoğan Ö. Eruptive disseminated porokeratosis in a patient with type 2 diabetes mellitus. Am J Dermatopathol 2016;38:e125-7.  Back to cited text no. 2
Nakamura M, Fukamachi S, Tokura Y. Acute onset disseminated superficial porokeratosis associated with exacerbation of diabetes mellitus due to development of anti-insulin antibodies. Dermatoendocrinol 2010;2:17-8.  Back to cited text no. 3
Chen TJ, Chou YC, Chen CH, Kuo TT, Hong HS. Genital porokeratosis: A series of 10 patients and review of the literature. Br J Dermatol 2006;155:325-9.  Back to cited text no. 4
Spravchikov N, Sizyakov G, Gartsbein M, Accili D, Tennenbaum T, Wertheimer E. Glucose effects on skin keratinocytes: Implications for diabetes skin complications. Diabetes 2001;50:1627-35.  Back to cited text no. 5
Hu SC, Lan CE. High-glucose environment disturbs the physiologic functions of keratinocytes: Focusing on diabetic wound healing. J Dermatol Sci 2016;84:121-7.  Back to cited text no. 6
O'Donnell BP, Dawson NA, Weiss RB, Myers CE, James WD. Suramin-induced skin reactions. Arch Dermatol 1992;128:75-9.  Back to cited text no. 7
Hwang SM, Choi EH, Ahn SK. Disseminated superficial actinic porokeratosis like drug eruption: A case report. J Korean Med Sci 1999;14:227-9.  Back to cited text no. 8
Goulding JM, Teoh JK, Carr RA, Humphreys F, Gee BC. Eruptive disseminated superficial porokeratosis with rapid resolution: A drug-induced phenomenon? Clin Exp Dermatol 2009;34:895-7.  Back to cited text no. 9
Mangas C, Espeli V, Blum R. A case of eruptive disseminated porokeratosis in a cancer patient after trastuzumab and exemestane treatment: Cancer related or drug induced phenomenon? Actas Dermosifiliogr 2018;109:559-60.  Back to cited text no. 10
Long M, Cai L, Li W, Zhang L, Guo S, Zhang R, et al. DPP-4 inhibitors improve diabetic wound healing via direct and indirect promotion of epithelial-mesenchymal transition and reduction of scarring. Diabetes 2018;67:518-31.  Back to cited text no. 11


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