Morphea‐like discoid lupus erythematosus in a patient with a history of polyacrylamide gel injection: A case report

Discoid lupus erythematosus (DLE) is an autoimmune disease with multifactor etiology which develops in genetically susceptible patients. Rarely, DLE lesions can mimic other connective tissue disorders such as morphea. The growing application of soft tissue fillers is associated with increasing complications. Some substances used for soft tissue augmentation such as silicon implants may trigger lupus erythematosus diseases.

In this report, we present the case of a 60-year-old woman, who had been injected with PAAG many years ago and has been removing it since then.

| C A S E REP ORT
A 60-year-old woman presented to our dermatology clinic complaining of violaceous patches and plaques on her left thigh, groin, and flank, both axillaries and sub-mammary (Figure 1).The lesions appeared 3 weeks ago with no pruritus, pain, or scaling, with sharp borders without induration.The patient had no arthralgia, fever, myalgia, or any other systemic symptoms or signs.She mentioned a similar lesion on the back of her neck about 6 years ago, which disappeared after 2 years without any medical interventions.
The past medical history was significant for the injection of PAAG gel to her face about 18 years ago.Several aspiration and drainage sessions were performed to address abscess and nodule formation, as well as to remove residual filler from the face.The last session of drainage was about 3 months prior to the current presentation.Additionally, she reported a diagnosis of Hashimoto thyroiditis 3 years ago and is currently undergoing treatment with levothyroxine.
In her laboratory data, ANA and ANCA were positive.CRP, ESR, RF, complement C3 and C4, SS-A/Ro antibodies, SS-B/La antibodies, anti-CCP, antiphospholipid antibodies, and autoantibodies against ds-DNA were in the normal range.Her hematologic and urinary analyses were normal.
Atypical pityriasis rosea, morphea, and parapsoriasis were considered as primary differential diagnoses.A punch biopsy was taken.Lichenoid interface reaction with superficial-deep dermal perivascular-perieccrine lymphocyte inflammation, mild epidermal atrophy, and mild basement membrane thickening most in favor of collagen vascular disease including lupus erythematosus was reported in microscopic examination (Figure 2).PAS staining showed mild basement membrane thickening.In Alcian blue staining, no dermal mucin deposition was detected.Discoid lupus erythematosus was the final diagnosis.
She was treated with hydroxychloroquine 200 mg twice daily for 3 months (Figure 3).Plasmacytoid dendritic cells (pDCs) endocytose immune complexes such as autoantibodies and RNA/DNA, which consequently activate toll-like receptor 7 (TLR7) and TLR9 within the endosome.This activation triggers the production of Type I interferon which, in turn, results in an increased inflammatory response and further activation of the adaptive immune system. 8 the year 2015, R. Haber et al presented a case involving a patient who suffered from systemic lupus erythematosus.What makes this case particularly intriguing is that the patient had a prior medical history of receiving a polyalkylimide dermal filler injection in the nasolabial folds 5 years ago.This report states that the fillers may initiate inflammation by either activating macrophages and T cells or acting as immune adjuvants. 9rvaert et al proposed that fillers could potentially trigger autoimmune disorders.They reported 32 individuals who had undergone breast implant surgery using silicon fillers and presented symptoms aligning with autoimmune/ inflammatory syndrome induced by adjuvants (ASIA).Recently it has been suggested that filler injections, used for aesthetic purposes such as polyacrylamide, polyalkylimide, and hyaluronic acid, might also function as adjuvants and potentially develop ASIA in susceptible patients. 11 we mentioned earlier, fillers are not entirely safe-free and some adverse reactions are reported subsequent to the injection.Some of the adverse reactions linked to the injection of polyalkylimide filler reported include delayed granulomatous reactions, nodules, skin induration, and pseudo-abscesses.It is uncommon but possible for patients to develop systemic signs and symptoms resulting from delayed immune-mediated adverse effects. 12Further investigation is necessary to evaluate the long-term adverse reactions of these substances.

| DISCUSS ION
It is undeniable that fillers have played a significant role in cosmetics, increasing self-confidence, and subsequently improving the quality of human social relationships as Pamatmat et al conducted a case series using polyl-lactic acid filler for the treatment of facial cutaneous atrophy in three patients suffering from scleroderma, CREST syndrome, and systemic lupus erythematosus in this regards.As there is a concern about flare-ups of these diseases following cosmetic procedures, the patients in the study were followed up for approximately 2 years and did not experience any adverse effects or disease reactivation.However, it is crucial for dermatologists to be caution because of the potential link between filler injection and autoimmune diseases, along with their potential long-term adverse effects. 13 our case report, it is important to note that we do not have enough evidence to establish a direct relationship between the use of PAAG filler or the drainage process and the development of DLE.This limitation should be taken into consideration when interpreting the findings.Therefore, it cannot be conclusively stated that these dermal fillers are associated with immune-related conditions but due to the fact that the injection of dermal fillers is increasing around the world, it is important for physicians to consider these potential adverse effects.
DLE is the most frequent cutaneous lupus erythematosus (CLE).DLE most commonly presents with erythematous and scaly papules, dyspigmentation, and atrophic scarring, with a preference for sunexposed areas.In few cases, DLE lesions appear in Blaschko lines mimicking morphea.Our patient presented with skin lesions similar to morphea; however, histopathologic findings favored DLE.Further laboratory evaluation revealed positive C-ANCA and FANA. 7Innate and adaptive immune systems are involved in the pathophysiology of CLE.Certain genetic factors, along with specific environmental triggers like exposure to ultraviolet light, activate the innate immune system.This activation subsequently leads to the initiation of adaptive immune responses and the development of skin lesions associated with CLE.These skin lesions are characterized by interface dermatitis which creates a self-amplifying cycle.

F I G U R E 1
At the first session, the patient had violaceous patches and plaques with sharp borders without induration or scaling on her left thigh, groin, and flank, both axillaries and sub-mammary.(A) The lesion on the left flank where the biopsy was taken.(B) The lesions on the left axillary and submammary.ASIA was described by Shoenfeld et al in 2011.Adjuvants, such as silica, aluminum hydroxide, medical injectable implants, and infectious compounds have the ability to stimulate the immune system, leading to increased production of antibodies against a pathogen.

F
I G U R E 2 A punch biopsy was taken from a lesion on the left flank.(A) Low-power image shows skin tissue with epidermal atrophy and superficial and deep perivascular inflammation.Note that there is no sclerosis and the peri adnexal adipose tissue is preserved (hematoxylin and eosin (H&E) stain, magnification 40×).(B)The epidermis is atrophic and shows lichenoid tissue reaction with basal layer vacuolar degeneration and presence of few Civatte bodies.Mild thickening of the basement membrane is noted.The infiltrate is composed of small lymphocytes (H&E stain, magnification 400×).F I G U R E 3 After 3 months of treatment, her lesions showed improvement.(A) The lesion in the left flank.(B) The lesion on the left axillary and sub-mammary.