Journal of Cutaneous and Aesthetic Surgery
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   Table of Contents     
CASE REPORT  
Year : 2015  |  Volume : 8  |  Issue : 2  |  Page : 111-113
Treatment of laser resistant granuloma faciale with intralesional triamcinolone acetonide and 5-fluorouracil combination therapy


1 Royal Melbourne Hospital, Melbourne, Australia
2 Dermatology Institute of Victoria, Melbourne, Australia

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Date of Web Publication9-Jun-2015
 

   Abstract 

This report describes a sixty year old male with biopsy proven Granuloma Faciale (GF). The patient had been unsuccessfully treated with multiple therapies. A mixture 0.8 ml 5-Fluorouracil (5FU) and 0.2 ml Kenacort-A was trialled initially to treat this patient, followed by a more varied mixture ratio. These were given at intervals ranging from two weeks to two months. The patient received a total of twenty injections over a period of more than three years. An excellent response was noted and the patient is now able to tolerate long treatment free periods of between nine and twelve months. 5FU is a simple injection material and can be considered by clinicians as an option for treatment of GF.

Keywords: Combination therapy, granuloma faciale, intralesional steroid, 5-fluorouracil

How to cite this article:
Norris DL, Apikian M, Goodman GJ. Treatment of laser resistant granuloma faciale with intralesional triamcinolone acetonide and 5-fluorouracil combination therapy. J Cutan Aesthet Surg 2015;8:111-3

How to cite this URL:
Norris DL, Apikian M, Goodman GJ. Treatment of laser resistant granuloma faciale with intralesional triamcinolone acetonide and 5-fluorouracil combination therapy. J Cutan Aesthet Surg [serial online] 2015 [cited 2019 Sep 22];8:111-3. Available from: http://www.jcasonline.com/text.asp?2015/8/2/111/158450



   Introduction Top


Granuloma faciale (GF) is an uncommon benign inflammatory condition of the skin with characteristic clinical and histological features. Pinkus originally described the name in 1952, although there had been earlier reports of eosinophilic granulomas. [1] It mostly affects the face, particularly sun-exposed areas such as the cheeks, forehead, nose, preauricular region and ears. Patients are most commonly middle-aged white males, and affected sites are often asymptomatic. The clinical differential diagnosis includes lupus vulgaris, discoid lupus erythematosus, fungal infection, sarcoidosis, mycobacteriosis, lymphocytoma cutis, Jessner's lymphocytic infiltrate and cutaneous lymphoma. [2] Histopathology results show a dense granulomatous infiltrate of the upper two-thirds of the dermis, often with associated eosinophils. [3] The epidermis is spared, with a Grenz zone and leucocytoclastic vasculitis in the upper dermis.


   Case Report Top


A man in his sixties was referred for evaluation of biopsy proven GF [Figure 1]. He had a known history of epilepsy. The lesion was first noted 15 years prior when a persistent, erythematous, indurated plaque appeared with associated telangiectasia over the right side of his forehead. Histopathologic findings were consistent with granuloma faciale showing a dense mixed infiltrate within the dermis, comprising of plasma cells, eosinophils, neutrophils and macrophages. Findings were consistent with a vasculitis, without fibrinoid necrosis. No defined Grenz zone was noted [Figure 2] and [Figure 3].
Figure 1: Patient prior to treatment

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Figure 2: Histopathology of biopsy; mention magnification power

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Figure 3: Histopathology of biopsy; high power mention magnification

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GF is notoriously difficult to treat. Multiple modalities have been used in the past with variable success including single therapy or combinations of colchicine, dapsone, antimalarials, gold injections, isoniazid, clofazimine, topical psoralen with UVA, corticosteroids, cryosurgery and various laser therapies. [2],[4] This patient had been treated with a number of these topical therapies prior to referral to our centre, each with poor results.

The patient was initially commenced on topical calcineurin antagonist (compounded tacrolimus 0.1%), before undergoing four treatments of vascular beam laser therapy at 595 nm and long pulsed 532 settings. This induced purpura, but again failed to produce a significant effect. Following this, a small improvement was noted with seven treatments of intralesional corticosteroid administration consisting of 5-10 mg of triamcinolone acetonide 10 mg/ml Kenacort-A 10 (KA10, Aspen Pharmaceuticals, St Leonards, Australia). Central atrophy was noted, but little change was seen at the edge of the lesion which remained thick and prominent [Figure 4]. The response was considered inadequate by both the patient and clinician. Systemic therapies were briefly considered but avoided in this patient, due to his comorbidities and long-term use of carbamazepine for epilepsy control.
Figure 4: Lesion following IL corticosteroid treatment only, prior to introduction of 5FU

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The mild response of the lesion to intralesional steroids led to the idea of using intralesional 5-fluorouracil (5FU) as a steroid-sparing or replacement agent, in a similar way to the use of 5FU in hypertrophic and keloid scarring. [5],[6] 5FU acts in a similar way to a steroid agent in keloid and hypertrophic scars, without the unwanted atrophic effects. [7] As first described by Fitzpatrick in the treatment of scars in 1999, an 80:20 mix of 80% 5FU (DBL Fluorouracil, 500 mg/10 ml, Hospira Australia Pty Ltd, Melbourne, Australia) and 20% KA10 was used to initiate treatment. [8] This yielded a mixture in a 1 ml syringe of 0.8 ml 5FU and 0.2 ml KA10. When initially reported, the small amount of steroid was added to the 5FU to limit the pain of injection. [8] The patient received intralesional KA10 and 5FU combination injections initially to the outer rim, and subsequently over the entire lesion. Various mixture quantities were used, ranging from 0.1 to 0.3 ml of KA10 given in combination with 0.7-0.95 ml of 5FU. These were given at intervals ranging from 2 weeks to 2 months according to patient availability and convenience.

The patient has now received a total of twenty injections over a period of more than 3 years. An excellent response has been noted and the patient is now able to tolerate long treatment-free periods between 9 and 12 months [Figure 5]. The small volume of KA10 relative to 5FU in the mixture suggests the response can primarily be attributed to the inclusion of 5FU, as the patient had not adequately responded to a pure steroid injection at higher concentration received initially.
Figure 5: Patient post treatment with combination KA10/5FU therapy

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   Discussion Top


It is largely unknown why 5FU has been useful in this case. As a pyrimidine analogue, 5FU is transformed inside the cell to form cytotoxic metabolites that are incorporated into DNA and RNA, inducing cell cycle arrest and apoptosis. It is possible that 5FU had an apoptic effect on the inflammatory cells making up the infiltrate. 5FU is a simple and safe injection material and should be considered by clinicians as an option for treatment of GF. The response rate in patients with GF is not rapid (although similar to the rate seen with use in keloid scarring), and many injections are necessary to achieve success. The utility is in its' ability to induce long periods of remission in the form of a disease-free interval, without the atrophy and rebound effects that are present with intralesional corticosteroids and other therapies.

Prior to commencing this treatment it is recommended that clinicians perform a blood screening tests including a full blood panel, renal and liver function tests. This should be repeated every 2-3 months following the first treatment. This treatment is unsuitable for pregnant or lactating women.

At the first session, a clinician should begin by using an 80:20 mix of 0.8 ml 5FU and 0.2 ml KA10. Total volume administered at subsequent sessions is at the clinician discretion and should be based on the size of the lesion and its response to the initial treatment. It is not recommended to use greater than 2 ml of an 80:20 mix per treatment.

This case demonstrates the success of intralesional 5FU in a subject with laser treatment resistant GF.

 
   References Top

1.
Pinkus H. Granuloma faciale. Dermatologica 1952;105:85-99.  Back to cited text no. 1
[PUBMED]    
2.
Ludwig E, Allam JP, Bieber T, Novak N. New treatment modalities for granuloma faciale. Br J Dermatol 2003;149:634-7.  Back to cited text no. 2
    
3.
Mehregan A, Hashimoto K, Mehegran D. Pinkus' Guide to Dermatohistopathology. 6 th ed. East Norwalk, Conn: Appleton and Lange; 1995.  Back to cited text no. 3
    
4.
Dowlati B, Firooz A, Dowlati Y. Granuloma faciale: Successful treatment of nine cases with a combination of cryotherapy and intralesional corticosteroid injection. Int J Dermatol 1997;36:548-51.  Back to cited text no. 4
    
5.
Sadeghinia A, Sadeghinia S. Comparison of the efficacy of intralesional triamcinolone acetonide and 5-fluorouracil tattooing for the treatment of keloids. Dermatol Surg 2012;38:104-9.  Back to cited text no. 5
    
6.
Huang L, Cai YJ, Lung I, Leung BC, Burd A. A study of the combination of triamcinolone and 5-fluorouracil in modulating keloid fibroblasts in vitro. J Plast Reconstr Aesthet Surg 2013;66:e251-9.  Back to cited text no. 6
    
7.
Gupta S, Kalra A. Efficacy and safety of intralesional 5-fluorouracil in the treatment of keloids. Dermatology 2002;204:130-2.  Back to cited text no. 7
    
8.
Fitzpatrick RE. Treatment of inflamed hypertrophic scars using intralesional 5-FU. Dermatol Surg 1999;25:224-32.  Back to cited text no. 8
    

Top
Correspondence Address:
Dr. Diana L Norris
C/O RMH, Grattan St, Parkville, Victoria - 3204
Australia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-2077.158450

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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