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 Table of Contents  
LETTER TO EDITOR
Year : 2021  |  Volume : 7  |  Issue : 2  |  Page : 101-103

Successful treatment of actinic reticuloid with nonsteroidal immunosuppressive drugs


Department of Dermatology, Venereology and Leprology, Bharati Vidyapeeth Deemed to be University, Medical College, Pune, Maharashtra, India

Date of Submission09-Mar-2021
Date of Decision08-Sep-2021
Date of Acceptance08-Nov-2021
Date of Web Publication13-Dec-2021

Correspondence Address:
Bhavna Haresh Chandwani
707, Sindh Society, Aundh, Pune 411007, Maharashtra.
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijdd.ijdd_8_21

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How to cite this article:
Chandwani BH, Lunge SB, Sardesai VR. Successful treatment of actinic reticuloid with nonsteroidal immunosuppressive drugs. Indian J Drugs Dermatol 2021;7:101-3

How to cite this URL:
Chandwani BH, Lunge SB, Sardesai VR. Successful treatment of actinic reticuloid with nonsteroidal immunosuppressive drugs. Indian J Drugs Dermatol [serial online] 2021 [cited 2022 Jan 28];7:101-3. Available from: https://www.ijdd.in/text.asp?2021/7/2/101/332428



Dear Editor,

Actinic reticuloid is a rare, chronic, persistent photosensitive dermatosis first described by Ive in 1969.[1] It is included under a spectrum disorder- chronic actinic dermatitis. Light spectrum involved in pathogenesis of actinic reticuloid (AR) is ultraviolet A (UVA), ultraviolet B (UVB), and visible light as well. It usually affects elderly men and lesions have a typical distribution in photoexposed areas.[2]

A 61-year-old woman, resident of Pune, a retired police officer, presented to our institute with itchy, dark lesions on face, and outer aspect of both forearms since 9–10 years. The lesions appeared insidiously on the forehead with gradual involvement of both cheeks, temples, nose, and forearms. On inquiry, the patient gave the history of regular, prolonged photo-exposure. The patient consulted many doctors for the above complaints and was prescribed multiple topical medications; however, there was no relief. She did not give the history of lesions elsewhere on the body, no preexisting dermatosis, and no history of any drug intake prior to the appearance of lesions. She is not a known case of hypertension, diabetes mellitus, or any other comorbidity.

On examination, the skin type of the patient was Fitzpatrick type V. There was presence of multiple, thick hyperpigmented lichenified indurated plaques with scaling on photoexposed areas such as forehead, temples, cheeks, nose, extensor aspect of both forearms, and dorsum of hands. There were no lesions elsewhere.

The differential diagnosis considered here were photodermatitis, subacute cutaneous lupus erythematosus, Jessner’s lymphocytic Infiltration of skin, and lymphoma cutis.

The findings of the routine laboratory investigations such as complete blood count with differentials and comprehensive metabolic panel were within normal limits. Photopatch test and patch test could not be performed due to the patient’s financial constraints.

A punch biopsy of the skin was performed from the lesions; the histopathological examination revealed hyperkeratosis, parakeratosis with prominent granular cell layer, and irregular acanthosis with elongation of rete ridges. Superficial dermis showed perivascular inflammatory infiltrate composed of lymphocytes and few polymorphs. The subcutis showed congested blood vessels and sparse mononuclear inflammatory cells [Figure 1].
Figure 1: H&E stained sections with magnification of 4× (A) on light microscope showing hyperkeratosis, parakeratosis with prominent granular cell layer, and irregular acanthosis with elongation of rete ridges. Superficial dermis showed perivascular inflammatory infiltrate composed of lymphocytes and few polymorphs. The subcutis showed congested blood vessels and sparse mononuclear inflammatory cells. H&E stained section with magnification of 10× (B) on light microscope showing hyperkeratosis, parakeratosis with prominent granular cell layer, and irregular acanthosis with elongation of rete ridges. Superficial dermis showed perivascular inflammatory infiltrate composed of lymphocytes and few polymorphs. The subcutis showed congested blood vessels and sparse mononuclear inflammatory cells

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On the basis of the clinical features and histopathology report, the diagnosis of AR was made.

The patient was counseled about the disease and measures of strict photoprotection. The patient was started on oral azathioprine 100 mg/day and hydroxychloroquine 300 mg/day in tapering doses. The topical treatment was in the form of a broad-spectrum sunscreen during the day and potent topical corticosteroid––clobetasol propionate 0.1% cream diluted with an emollient applied at bedtime for 2 weeks.

With regular follow-up up to 6 months, our patient showed an excellent response to the treatment with a marked reduction in thickness of plaques and no new lesions [Figure 2].
Figure 2: (A) Pre-treatment photograph showing hyperpigmented, thick, and lichenified plaques with scaling on forehead and nose. (B) Pre-treatment photograph showing hyperpigmented, thick, and lichenifed plaques with scaling on forehead, temples, and nose. (C) Post-treatment photograph showing post-inflammatory hyperpigmentation on forehead and nose. (D) Post-treatment photograph showing post-inflammatory hyperpigmentation on forehead, temples, and nose

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AR has been reported in Caucasians, Latin Americans, Japanese, and Indians.[3],[4] Not many cases have been reported in the Indian scenario. The mainstay of treatment is photoprotection. The occupation of the patient must be taken into account while counseling the patient regarding photoprotection. Oral corticosteroids are used for the initial control of disease and in cases of acute flares. As the disease process requires a long-term therapy, the need for steroid-sparing immunosuppressive drugs arises. These include azathioprine,[5],[6] cyclosporine hydroxychloroquine,[7],[8] and mycophenolate mofetil. Other drugs such as thioguanine, danazol, thalidomide, etretinate, infliximab, and IFN-α have been reported to be effective in small case series.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/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.



 
  References Top

1.
Ive FA, Magnus IA, Warin RP, Jones EW. “Actinic reticuloid”: A chronic dermatosis associated with severe photosensitivity and the histological resemblance to lymphoma. Br J Dermatol1969;81:469-85.  Back to cited text no. 1
    
2.
Somani VK. Chronic actinic dermatitis: A study of clinical features. Indian J Dermatol Venereol Leprol 2005;71:409-13.  Back to cited text no. 2
[PUBMED]  [Full text]  
3.
Roelandts R. Chronic actinic dermatitis. J Am Acad Dermatol 1993;28:240-9.  Back to cited text no. 3
    
4.
Hawk JL. Chronic actinic dermatitis. Photodermatol Photoimmunol Photomed 2004;20:312-4.  Back to cited text no. 4
    
5.
Murphy GM, Maurice PD, Norris PG, Morris RW, Hawk JL. Azathioprine treatment in chronic actinic dermatitis: A double-blind controlled trial with monitoring of exposure to ultraviolet radiation. Br J Dermatol 1989;121:639-46.  Back to cited text no. 5
    
6.
Srinivas CR, Balachandran C, Shenoi SD, Acharya S. Azathioprine in the treatment of Parthenium dermatitis. Br J Dermatol 1991;124:394-5.  Back to cited text no. 6
    
7.
Lim HW, Morison WL, Kamide R, Buchness MR, Harris R, Soter NA. Chronic actinic dermatitis: An analysis of 51 patients evaluated in the United States and Japan. Arch Dermatol 1994;130:1284-9.  Back to cited text no. 7
    
8.
Haynes HA, Bernhard JD, Gange RW. Actinic reticuloid: Response to combination treatment with azathioprine, hydroxychloroquine, and prednisone. J Am Acad Dermatol 1984;10:947-52.  Back to cited text no. 8
    


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