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E-IJD® - CORRESPONDENCE
Year : 2022  |  Volume : 67  |  Issue : 5  |  Page : 626
Pityriasis rubra pilaris significantly improved after treatment for chronic focal infection


Department of Dermatology, Fukushima Medical University, Fukushima, Japan

Date of Web Publication29-Dec-2022

Correspondence Address:
Masato Ishikawa
Department of Dermatology, Fukushima Medical University, Fukushima
Japan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijd.ijd_1016_20

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How to cite this article:
Ishikawa M, Igari S, Hiraiwa T, Hanami Y, Yamamoto T. Pityriasis rubra pilaris significantly improved after treatment for chronic focal infection. Indian J Dermatol 2022;67:626

How to cite this URL:
Ishikawa M, Igari S, Hiraiwa T, Hanami Y, Yamamoto T. Pityriasis rubra pilaris significantly improved after treatment for chronic focal infection. Indian J Dermatol [serial online] 2022 [cited 2023 Jan 30];67:626. Available from: https://www.e-ijd.org/text.asp?2022/67/5/626/366086




Sir,

A 54-year-old man was referred to our department complaining of non-itchy eruptions on his extremities and trunk that had appeared 5 months ago. He had been treated with topical corticosteroid ointment and retinoid; however, the eruptions did not completely improve. Physical examination revealed a number of brown, flattened keratotic papules surrounding the hair follicles, as well as erythematous lesions with scales on the limbs, buttocks and trunk [Figure 1]a and [Figure 1]b. In addition, there was hyperkeratosis on the palms and soles [Figure 1]c. Laboratory examination revealed a positive anti-nuclear antibody (1:320), whereas all other results were within the normal limit. An initial biopsy revealed irregular acanthosis and parakeratotic foci in the stratum corneum [Figure 1]d. An additional biopsy showed a large keratotic plug composed of several parakeratotic layers and perifollicular infiltration of inflammatory cells. We diagnosed the patient as having pityriasis rubra pilaris (PRP). Although we did not perform bacterial culture tests, radiographic images showed chronic periodontitis and maxillary sinusitis. The patient underwent treatments with teeth extraction and macrolide antibiotics, which resulted in significant improvement of eruptions after 2 months [Figure 2]. At 3 years follow-up, the patient was free from recurrence.
Figure 1: Physical examination revealed a number of brown, flattened keratotic papules surrounding the hair follicles, and erythematous lesions with scales, on the right lower limb (a), and buttocks (b). (c) There was hyperkeratosis on the soles of his feet. (d) The biopsy specimen revealed irregular acanthosis and parakeratotic foci in the stratum corneum (hematoxylin–eosin staining, original magnification × 200)

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Figure 2: Significant improvement in the eruptions after treatment with teeth extraction and macrolide antibiotics. (a) Before treatment. (b) After 2 months

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In the present case, the eruptions were significantly improved after treatment for chronic focal infection. There have been a few reports of PRP in adult patients associated with infections except human immunodeficiency virus infection.[1] However, PRP associated with bacterial infections has been mainly found in juvenile patients, reports of which have suggested that the bacterial infection contributed to the development of PRP as a superantigen.[2]

Recent studies have indicated that the interleukin (IL)-23/IL-17 pathway plays an essential role in the pathogenesis of PRP. Feldmeyer et al.[3] demonstrated upregulated levels of pro-inflammatory innate cytokines and T-helper (Th) 17 cytokines in the lesional skin of three PRP patients. They also reported a case of PRP treated with ustekinumab, showing that the Th17 cytokine levels were consistent with clinical and histopathological improvements.[3] However, Matsuda et al.[4] reported a PRP case that developed erythroderma after anti-IL-17A therapy but improved after the blockade of IL-12/23 p40, suggesting that IL-12 also contributed to the development of PRP.

Chronic focal infections have been shown to cause various inflammatory diseases involving ILs. Bacterial products enhance the production of IL-12 and IL-23, and Porphyromonas gingivalis induces IL-17A production in the bacterial microenvironment of chronic periodontitis.[5] These findings suggest that the production of IL-12, IL-17 and IL-23 can be enhanced by chronic focal infection and may contribute to the development of PRP.

In conclusion, a chronic focal infection may play an important role in the pathogenesis of PRP, and its treatment may be an effective therapeutic approach for adult PRP. Therefore, we should check for focal infection before we begin treatment in PRP patients.

Declaration of patient consent

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

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Kawara S, Miyake M, Oiso N, Kawada A. Pityriasis rubra pilaris with preceding cytomegalovirus infection. Dermatology2009;219:350-2.  Back to cited text no. 1
    
2.
Yamamoto T, Yokoyama A. Lymphocyte response to superantigen in a patient with childhood-onset pityriasis rubra pilaris. Int J Dermatol1999;38:639-40.  Back to cited text no. 2
    
3.
Feldmeyer L, Mylonas A, Demaria O, Mennella A, Yawalkar N, Laffitte E, et al. Interleukin 23-helper T cell 17 axis as a treatment target for pityriasis rubra pilaris. JAMA Dermatol20153:304-8.  Back to cited text no. 3
    
4.
Matsuda T, Yamazaki F, Ueda-Hayakawa I, Kambe N, Okamoto H. Case of pityriasis rubra pilaris progressed to generalized erythroderma following blockade of interleukin-17A, but improved after blockade of interleukin-12/23 p40. J Dermatol2019;46:70-2.  Back to cited text no. 4
    
5.
Moutsopoulos NM, Kling HM, Angelov N, Jin W, Palmer RJ, Nares S, et al. Porphyromonas gingivalis promotes Th17 inducing pathways in chronic periodontitis. J Autoimmun2012;39:294-303.  Back to cited text no. 5
    


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