Halting the Progression of Cicatricial Alopecia with Injectable Platelet-Rich Fibrin

Abstract

Discoid lupus erythematosus (DLE) is a chronic variant of cutaneous lupus erythematosus characterized by well-defined erythematous plaques with adherent scales and follicular plugging. The affected scalp shows erythema, edema, atrophy, alopecia, and telangiectasia. Trichoscopy of DLE shows branching capillaries, white patches, keratin plugs, reduced follicular ostia, and white dots and blue-gray dots arranged in speckles pattern. Prompt diagnosis and aggressive, early multimodal therapy helps in preventing disfiguring hair loss and psychosocial sequelae. Hereby, we present a case of reversal of hair loss in DLE with newer modalities of treatment such as injectable platelet-rich fibrin.

INTRODUCTION

Discoid lupus erythematosus (DLE) is a chronic variant of cutaneous lupus erythematosus characterized by well-defined erythematous plaques with scale, often predominantly featured on the face, ears, anterior neck, and scalp.[1] Dermoscopy plays important role in the diagnosis of this condition.[2]

Managing cicatricial alopecia is a matter of contention for all trichologists given the disfiguring, recalcitrant, and irreversible nature of the disease and the psychosocial conflict associated with the scarring alopecia.

A common consensus among many practicing trichologists is to manage cicatricial alopecia with a multitude of therapies to inhibit the progression of underlying pathology and salvage the uninjured hair follicles and try to promote hair regrowth with either endogenous or exogenous growth factors.[3] Newer modalities such as injectable platelet-rich fibrin (i-PRF) are the advanced version of platelet-rich fibrin (PRF) i-PRF in liquid form which has stem cells with high regenerative potential.[4] PRF is a new platelet concentrate concept which accumulates platelets and releases cytokines in fibrin clots.[5]

CASE REPORT

A 32-year-female hailing from a metropolitan city, a daily wage worker presented to our hospital with a complaint of increasing patchy hair loss from the vertex of the scalp of long-standing duration.

The patient reported that she had developed a small patch of hair loss over her vertex of the scalp for the past 10 years. The patch was neither painful nor pruritic. She did not seek any prior consultation for her patchy hair loss. However, after an episode of accidental trauma to the scalp at her workplace 3 months ago, the patch started to increase in size which was associated with pain, pruritus, and hyperpigmentation.

She reported applying topical creams and lotions which were prescribed by a general physician with no relief in her complaints and hair regrowth.

While she did gave a history of photosensitivity, however, she denied a history of fever, joint pain, weight loss, and oral ulcers. Her obstetric, medical, and surgical histories were nonsignificant.

Cutaneous examination revealed multiple alopecic plaques coalescing to form a single 10 cm × 12 cm well-defined plaque with depigmentation, atrophy, and telangiectasia at the center. Multiple plaques with central depigmentation and peripheral hyperpigmentation with thick adherent scales over the vertex of scalp [Figure 1].

Figure 1.

Multiple plaques with depigmentation, hyperpigmentation and thick adherent scales (red circle) at the periphery of the lesion at the vertex of the scalp

Hair pull test was negative, and carpet tack sign was positive.

Dermoscopy showed dilated vessels, areas of scarring, and dyspigmentation [Figure 2].

Figure 2.

Dermoscopy showed dilated vessels, areas of scaring and dyspigmentation

Her complete blood count, liver function test, renal function tests, blood glucose, serum electrolytes, and urine analysis were found to be within normal limits.

Screening for antinuclear antibodies was found to be negative. A baseline ophthalmological evaluation was performed before starting Hydroxychloroquine.

A 4-mm punch biopsy including subcutaneous fat was taken from the scalp and submitted for histopathological analysis which revealed epidermal atrophy, basement membrane thickening, melanin incontinence, and periadnexal and perivascular lymphocytic infiltrate suggestive of DLE [Figure 3].

Figure 3.

H and E stain showing epidermal atrophy, basement membrane thickening, melanin incontinence and periadnexal and perivascular lymphocytic infiltrate

She was prescribed oral hydroxychloroquine sulfate (6.5 mg/kg/day) 200 mg twice a day and topical tacrolimus lotion (0.1%) at night application, The left side of the lesion was treated with intralesional triamcinolone acetonide 5 mg/ml and the right side was given a trial of i-PRF every 3 weeks. The patient underwent four sessions of i-PRF and intralesional corticosteroid injection. i-PRF was prepared as per the method described by Choukroun et al.[5]

Figure 4 Our patient responded to our treatment with 60% response to therapy after 3 months of treatment period. Figure 5 There was an appreciable reduction in erythema, telangiectasia, and disease activity.

Figure 4.

Pre and posttreatment - Left side of the lesion was treated with intralesional triamcinolone acetonide 5 mg/ml and right side was given a trial of i-PRF. i-PRF: Injectable platelet-rich fibrin

Figure 5.

Pre and posttreatment after 2 months

Hair regrowth was found to be more significant on the right side which was treated with i-PRF as compared to the left side treated with intralesional steroid. We noticed that the side treated with i-PRF had predominant pigmented hairs regrowth in contrast to regrowth of white hairs on the side treated with intralesional steroid [Figure 6]. This observation has not been previously reported till date.

Figure 6.

Right side treated with i-PRF had predominant pigmented hairs regrowth in contrast to regrowth of white hairs on the left side treated with intralesional steroid. i-PRF: Injectable platelet-rich fibrin

DISCUSSION

DLE is a chronic variant of cutaneous lupus erythematosus characterized by well-defined erythematous plaques with scale, often predominantly featured on the face, ears, anterior neck, and scalp. More than half of patients with DLE first present with scalp involvement and one of the most common causes of cicatricial alopecia.[1]

The goal of the management of cicatricial alopecia is the prompt diagnosis and treatment to arrest the disease activity and prevent irreversible hair loss.

Conventionally, DLE is treated with topical and intralesional steroids as first line for a span of 8–10 weeks.[6] In case of nonresponse to therapy, antimalarials (hydroxychloroquine sulfate, 6.5 mg/kg in the dose of 200–400 mg/day) prove effective in early progressive disease.

Oral corticosteroids (prednisolone equivalent 1 mg/kg, for initial actively progressing disease, tapered over 8 weeks) and oral retinoids (acitretin and isotretinoin, 10–40 mg/day) can be considered.

Failure of second-line medication might warrant the use of thalidomide, topical immunomodulators (0.1% tacrolimus and 1% pimecrolimus), oral Vitamin E, oral gold, dapsone, mycophenolate mofetil, methotrexate, azathioprine, clofazimine, systemic or intralesional interferon alpha-2, monoclonal anti-cluster of differentiation 4 antibodies, topical 5-FU, topical tazarotene, and imiquimod.

In our case, standard management protocol was not followed. Due to the psychological stress and physical discomfort to the patient, we decided to start her on a multitude of therapies considering the irreversible nature of the disease and the need for rapid remission.

She was treated with oral hydroxychloroquine sulfate (6.5 mg/kg/day) 200 mg twice a day and topical tacrolimus lotion (0.1%) at night application.[7]

The left side of the lesion was treated with intralesional triamcinolone acetonide 5 mg/ml and the right side was given a trial of i-PRF every 3 weeks. i-PRF was prepared as per the method described by Choukroun et al.[5] 10 ml of blood collected in a plain bulb (without an anticoagulant) was centrifuged at 700 rpm for 4 mins. The i-PRF liquid (supernatant) is collected using 31G insulin syringes and only blood clot is discarded. i-PRF fluid does not need a preactivation before using and can be directly injected.

i-PRF is an advanced version of PRF in liquid form which can be injected and contains stem cells with high regenerative potential.[5] PRF is actually a new platelet concentrate concept which accumulates platelets and the released cytokines in a fibrin clot.

Low speed of centrifugation gives a higher number of leukocytes, platelets, and growth factors enhancing the regeneration process. i-PRF is centrifuged at 700 rpm for 4 min. PRF is a fully autologous product and thus alleviates the need for the use of an external anticoagulant.[8]

PRF was developed with the idea of keeping methodology convenient and applicable for clinical use.[5,9] Its three-dimensional fibrin network mimics the extracellular matrix in terms of its structure,[10] which creates an environment for cells to function optimally.

i-PRF induces differentiation of stem cells, prolongs survival of dermal papillary cells, prolongs the anagen phase of the hair cycle, and increases perifollicular vascular plexus by multiple mechanisms through various growth factors. These act on stem cells in the bulge area of the follicles, stimulating the development of new follicles.

Further, it is proposed to cause follicular hyperpigmentation by helping in the rejuvenation process and is responsible for melanocytes migration from the remnants of hair follicles and from the surrounding normal skin. The release of various growth factors must have acted as mitogenic stimuli for the melanocytes.

i-PRF induces differentiation of stem cells by prolonging the survival of dermal papillary cells, and the release of various growth factors increases perifollicular vascular plexus by multiple mechanisms. It acts on stem cells in the bulge area of the follicles, stimulating the development of new follicles, and promoting neovascularization.[4]

CONCLUSION

Early and multimodal aggressive therapy in rapidly progressive DLE might reverse early alopecic patches and save hair follicles from the destructive process.

The use of i-PRF can be considered an adjuvant modality of treatment in active cases of DLE.

However, better-designed, larger, and long-term trials with placebo control are needed to confirm its effectiveness.

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.