K Rapid Recurrence of Keloid after Pulse Dye Laser Treatment P -Y

Rapid Recurrence of Keloid after Pulse Dye Laser Treatment
PO-YU SHIH, MD, HUA-HSIN CHEN, MD, CHIEN-HSUN CHEN MD,y
HONG-SHANG HONG, MD PHD,y AND CHIH-HSUN YANG, MDy
The authors have indicated no significant interest with commercial supporters.
K
eloids and hypertrophic scarring are frequently
encountered in the clinical setting and can be
quite difficult to treat. Keloids, in particular, are
prone to overgrowth, and as disease activity can remain active for or be reactivated after years of dormancy, great deformity can arise. Differing
hypotheses regarding the formation of keloids have
led to a myriad of treatments as the pathogenesis
behind keloidal growth has not yet been fully elucidated. Pulse dye laser (PDL) has been suggested as
an effective therapeutic modality for hypertrophic
scars and keloids. We report a case of rapid recurrence of keloid within 1 week of PDL treatment for
telangiectasia.
suggested for treatment of residual erythema and
telangiectasia. One course of PDL (Candela ScleroPLUS, Candela Corp., Wayland, MA) was used the
week after the last IL steroid injection at 585-nm
wavelength delivering a fluence of 8.0 J/cm2 with
pulse duration of 1,500 ms and 5-mm spot size
with concomitant cryogenic cooling (30/20 ms;
Figure 1).
At postoperative follow-up 1 week later, the previously flattened keloid had enlarged substantially,
with accompanying erythema, pruritus, and pain
(Figure 2). On review, the patient reported no new
medication, topical agent, or lifestyle changes within
that week. Subsequently, IL steroid injections were
given biweekly for over 4 months with modest
Case Report
A 21-year-old healthy woman with Fitzpatrick Skin
Phototype IV presented for treatment of large keloids over the V-region of her chest. Her medical history was unremarkable except for facial acne
vulgaris treated with a short course of oral doxycycline and topical agents including adapalene. Her
keloids were treated with intralesional (IL) injections
of triamcinolone acetonide (diluted to 20 mg/mL
weekly for six visits, 10 mg/mL biweekly for eight
visits, 5 mg/mL biweekly for five visits, and 5 mg/mL
monthly for five visits). The protrusion of the keloids
gradually decreased, and marked improvement of
pruritus was noted. Although the size of the keloid
had also stabilized, she was still very dissatisfied with
the resulting telangiectasia and redness. PDL was
Figure 1. Baseline photograph of flattened keloid after repeated IL corticosteroid injections, just before PDL therapy
for telangiectasia.
Department of Dermatology, Chang Gung Memorial Hospital, Linkou, Taiwan; yChang Gung University College of
Medicine, Linkou, Taiwan
& 2008 by the American Society for Dermatologic Surgery, Inc. Published by Blackwell Publishing ISSN: 1076-0512 Dermatol Surg 2008;34:1124–1127 DOI: 10.1111/j.1524-4725.2008.34225.x
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SHIH ET AL
Figure 2. Appearance at follow-up 1 week later. Substantial
enlargement of the keloid combined with increased erythema, pruritus, and pain were noted.
response in terms of keloidal size and pruritus.
However, as more corticosteroids were used, local
telangiectasia, erythema, and atrophy became much
more prominent and thereby even less satisfactory
for the patient.
Discussion
Keloids are frequently encountered in the clinical
setting and can be quite difficult to treat. Differing
hypotheses regarding the formation of keloids have
led to a myriad of treatments as the pathogenesis
behind keloidal growth has not yet been fully elucidated. The complex interplay of growth factors,
cytokines, extracellular matrix components, and
collagen equilibrium is still the subject of intensive
research. Of note, transforming growth factor-b
(TGF-b), especially isotypes 1 and 2, has been shown
to be expressed in greater levels in keloidal fibroblasts compared with those derived from normal
skin and may be major contributing factors to the
process of proliferative scars.1–4 TGF-b1, in particular, has been shown to play a role in regulation of
collagen and matrix metalloproteinase (MMP) production in cultured keloidal fibroblasts. Increased
production of MMPs, in turn, had a role in the high
migratory activity of cultured keloid fibroblasts.5
In recent years, the 585-nm PDL alone or in combination with other therapies such as topical 5-fluorouracil and IL steroids has become a popular
technique in keloid treatment.6–9 The effect of PDL
has been thought to be mediated by selective damage
of the microvasculature causing decreased cellular
function, laser-induced heating of collagen fiber
disulfide bonds or collagenolysis after cytokine
stimulation.7,10 The end result is a decrease in vessel
size with significantly finer and loosely interwoven
collagen parallel to the epidermis.11 However, PDL
has also been effective in treatment of facial wrinkles12 and for photorejuvenation,13 the basis of
which was believed to be due to dermal thermal injury resulting in collagen denaturation, fibroblast
stimulation, and subsequent neocollagen formation.14 In particular, in vitro studies of keloidal fibroblasts irradiated with low-fluence PDL (3 J/cm2)
have shown increase of TGF-b1 levels, as has upregulation of other factors leading to increased collagen synthesis. This effect was not seen at a slightly
higher fluence.15 Another study using high-fluence
PDL (10–1814 J/cm2, average 14 J/cm2) showed
suppression of TGF-b1 expression.16 Whether there
is a dose-related effect with regard to TGF-b1 expression requires further exploration.
While numerous studies have shown the effectiveness of PDL in treatment of vascular lesions, keloidal
and hypertrophic scars, and photorejuvenation and
wrinkle improvement, the adverse effects associated
to PDL alone have been rare. Of note, one review of
adverse effects in 500 patients treated with the PDL
found only atrophic scarring (0.8%), hyperpigmentation (1%), hypopigmentation (2.6%), and dermatitis (2%) but no hypertrophic scarring was noted.17
Subsequently, however, limited cases with delayedonset hypertrophic scarring have been reported18,19
as have mild scarring and texture changes at higher
fluences (12 J/cm2).20 More common side effects associated with higher fluences were primarily purpura
and pigmentary changes.21 With these in mind,
selection of appropriate laser parameters was challenging for this patient. As her primary complaint
was that of residual telangiectasia, parameters for
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treatment of facial telangiectasia were used as preliminary guidelines. However, this selection would
entail a therapy with moderate-high fluence of
9.0 J/cm2 (range 8.5–10.0 J/cm2),22 energy levels
even higher than which she was given. Another
consideration would be the treatment site; a reduction of at least 10% to 20% in fluence for areas
prone to scarring such as the anterior chest or neck
or areas where tissue is delicate such as the periorbital regions has been advised.23 Thus given the
location of her telangiectasia (the chest), the nature
of the lesion (new-onset telangiectasia after treatment of keloid with IL corticosteroids), and her
Fitzpatrick phototype (Type IV), a lower fluence
(8.0 J/cm2) was used. Nevertheless, rapid recurrence
of keloid was still noted within 1 week’s time.
It is possible that this scarring phenomenon and
other side effects of PDL may be more pronounced
in darker-skinned individuals since more melanin is
present in the skin. As more energy is absorbed
by the melanin and surrounding soft tissue causing
tissue injury, lesser fluence would be transduced
and available for absorption by hemosiderin, the
target chromophore in keloidal blood vessels, thus
decreasing overall treatment efficacy. Skin redness
has been shown to have a similar effect as
pigmentation.21
Several cases of hypertrophic scarring in laser use,
including PDL, in conjunction with isotretinoin use
have been reported.24 These have led to the clinical
avoidance of laser treatment in patients under isotretinoin therapy. Although our patient had previously used a retinoid derivative, adapalene, the
topical agent had been discontinued many months
previously and had only been used over the face.
Moreover, there have been no reports of adapalenerelated keloid development. Thus, it is unlikely to
have been significant in this keloidal recurrence.
Therefore, while it remains statistically uncommon
for keloid formation or recurrence to develop after
PDL therapy, clinicians should be aware that lasers
with photorejuvenative effects, such as PDL, may be
responsible for activation of keloid development.
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References
1. Burd A, Huang L. Hypertrophic response and keloid diathesis:
two very different forms of scar. Plast Reconstr Surg
2005;116:150e–7e.
2. Smith P, Mosiello G, Deluca L, et al. TGF-beta2 activates proliferative scar fibroblasts. J Surg Res 1999;82:319–23.
3. Mukhopadhyay A, Tan EK, Khoo YT, et al. Conditioned medium
from keloid keratinocyte/keloid fibroblast coculture induces contraction of fibroblast-populated collagen lattices. Br J Dermatol
2005;152:639–45.
4. Polo M, Smith PD, Kim YJ, et al. Effect of TGF-beta2 on proliferative scar fibroblast cell kinetics. Ann Plast Surg
1999;43:185–90.
5. Fujiwara M, Muragaki Y, Ooshima A. Keloid-derived fibroblasts
show increased secretion of factors involved in collagen turnover
and depend on matrix metalloproteinase for migration. Br J
Dermatol 2005;153:295–300.
6. Asilian A, Darougheh A, Shariati F. New combination of
triamcinolone, 5-fluorouracil, and pulsed-dye laser for treatment of keloid and hypertrophic scars. Dermatol Surg
2006;32:907–15.
7. Alster TS, Tanzi EL. Hypertrophic scars and keloids: etiology and
management. Am J Clin Dermatol 2003;4:235–43.
8. Tanzi EL, Alster TS. Laser treatment of scars. Skin Ther Lett
2004;9:4–7, http://www.skintherapyletter.com/2004/9.1/2.html
Accessed March 4, 2007.
9. Alster TS. Laser scars revision. In: Alster TS, Apfelberg DB, editors. Cosmetic laser surgery. 2nd ed. Wiley-Liss: New York; 1999.
p. 227–35.
10. Reiken SR, Wolfort SF, Berthiaume F, et al. Control of hypertrophic scar growth using selective photothermolysis. Lasers Surg
Med 1997;21:7–12.
11. Manuskiatti W, Fitzpatrick RE. Treatment response of keloidal
and hypertrophic sternotomy scars. Arch Dermatol 2002;138:
1149–55.
12. Bjerring P, Egevist H, Clement M, et al. Selective non-ablative
wrinkle reduction by laser. J Cutan Laser Ther 2000;2:9–15.
13. Michel JL. ED2000s: 585 nm collagen remodeling pulsed dye
laser. J Cosmet Laser Ther 2003;5:201–3.
14. Kelly KM, Majaron B, Nelson S. Nonablative laser and light rejuvenation. Arch Facial Plast Surg 2001;3:230–5.
15. Yu HY, Chen DF, Wang Q, et al. Effects of lower fluence pulsed
dye laser irradiation on production of collagen and the mRNA
expression of collagen relative gene in cultured fibroblasts in vitro.
Chin Med J 2006;119:1543–7.
16. Kuo YR, Wu WS, Jeng SF, et al. Suppressed TGF-b1 expression is
correlated with up-regulation of matrix metalloproteinase-13 in
keloid regression after flashlamp pulsed-dye laser treatment.
Lasers Surg Med 2005;36:38–42.
17. Levine VJ, Geronemus RG. Adverse effects associated with the
577 and 585 nanometer pulsed dye laser in the treatment of cutaneous vascular lesions: a study of 500 patients. J Am Acad
Dermatol 1995;32:613–7.
SHIH ET AL
18. Swinehart JM. Hypertrophic scarring resulting from flashlamppumped pulsed-dye surgery. J Am Acad Dermatol 1991;25:
845–6.
19. Wlotzke U, Hohenleutner U, Adb-El-Raheem TA, et al. Sideeffects and complications of flashlamp-pumped pulse dye laser
therapy of port-wine stains: a prospective study. Br J Dermatol
1996;134:475–80.
20. Swinehart JM. Textural change following treatment of facial telangiectasia with the tunable pulsed-dye laser. Arch Dermatol
1999;135:472–3.
21. Haedersdal M, Gniadecka M, Efsen J, et al. Side effects from
the pulsed dye laser: the importance of skin pigmentation and
skin redness. Acta Dermatol Venereol (Stockholm) 1998;78:
445–50.
22. Alam M, Dover JS, Arndt KA. Treatment of facial telangiectasia
with variable-pulse high fluence pulsed-dye laser: comparison of
efficacy with fluences immediately above and below the purpura
threshold. Dermatol Surg 2003;29:681–5.
23. Rothfleisch JE, Kosann MK, Levine VJ, et al. Laser treatment
of congenital and acquired vascular lesions. Dermatol Clin
2002;1:1–18.
24. Bernestein LJ, Geronemus RG. Keloid formation with the 585-nm
pulsed dye laser during isotretinoin treatment. Arch Dermatol
1997;133:111–2.
Address correspondence and reprint requests to: Hua-Hsin
Chen, MD, Department of Dermatology, Division of
Dermatologic Surgery, Chang Gung Memorial Hospital,
199 Tun-Hwa North Road, Taipei 105, Taiwan, or
e-mail: [email protected]
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