The International Journal of
Lower Extremity Wounds
The Use of Corticosteroids to
Treat Keloids: A Review
Claude Roques, MD, and Luc Téot, MD
Mechanisms for keloid formation include drastic
changes in growth factor actions, collagen turnover,
mechanical forces applied over the skin, and genetic
and immunologic contributions. The use of corticos-
teroids to manage keloids increases basic fibroblast
growth factor production while decreasing transform-
ing growth factor-β1 production by human dermal
fibroblasts, endogenous vascular endothelial growth
factor, and insulin-like growth factor-1. The use of cor-
C
orticoids have been used in the treatment of
keloids and hypertrophic scars (HTS) since
1960. Though few randomized studies exist,
there is broad consensus on their use—first-line
therapy in the treatment of keloids and second-line
therapy in the treatment of HTS. Many corticoids
are used in the treatment of keloids and HTS,
including hydrocortisone acetate, methylprednisolone,
and dexamethasone, but the most commonly used
corticoid is triamcinolone acetate. The mechanisms
of development of HTS and keloid scars are largely
unknown though some studies allow better under-
standing of the modes of action of the corticos-
teroids. Corticosteroids affect fibroblast proliferation
and production capabilities, and they also inhibit the
growth of fibroblasts and are responsible for the
degeneration of fibroblasts. It has been demon-
strated that there is an increase in the production of
basic fibroblast growth factor (bFGF) and a decrease
in the production of transforming growth factor-β1
From the Pediatric Rehabilitation Centre, CSRE Lamalou le
Haut, Lamalou les Bains (CR); Burn and Plastic Surgery Unit,
Hôpital Lapeyronie, Montpellier (LT), France.
Conflict of interest: none.
Address correspondence to: Claude Roques, MD, Pediatric
Rehabilitation Centre, CSRE Lamalou le Haut, 34240 Lamalou
les Bains, France; e-mail: clauderoques@aol.com.
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Volume 7 Number 3
September 2008 137-145
© 2008 SAGE Publications
10.1177/1534734608320786
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http://online.sagepub.com
ticosteroid injections is, to date, the core treatment
available for the management of excessive tissue pro-
duction in scars. Currently, the most effective and safe
regimen for keloid management appears to be the use
of corticotherapy—injection of intradermal steroids
after a surgical excision.
Keywords: corticosteroids; keloid; hypertrophic scars;
triamcinolone acetonide
(TGF-β1) by human dermal fibroblasts, endogenous
vascular endothelial growth factor (VEGF), and
insulin-like growth factor-1 (IL-1) when induced by
corticosteroids. The response is variable, with 50%
to 100% regression and a recurrence rate of 9% to
50%.1 Their efficiency is dose dependent. Injections
may a single treatment, but combination with other
treatments has also been proposed, with better
results and less side effects. The injection has to be
in the scar and is thus often painful. The concentra-
tion of triamcinolone acetonide (TA) depends on the
amount of scar formation, the area of the body, and
the individual patient.
The Effects of Corticosteroids
on Keloid and Hypertrophic Scars
A recent study by Köse and Waseem2 compared clin-
ical, histopathological, biochemical, and molecular
differences between keloids and HTS. The process
of wound healing is regulated by different signaling
mechanisms, but it is not yet possible to determine
if a skin lesion will heal normally or develop an HTS
or keloid. Extracellular matrix components, growth
factors, fibroblastic activity, cytokines, and matrix
metalloproteinases have been associated with the
molecular basis of HTS and keloids. In spite of hav-
ing the same basic components, keloids and HTS
137
138 The International Journal of Lower Extremity Wounds / Vol. 7, No. 3, September 2008
have different molecular and biologic properties.
Fibroblasts have different behaviors in response to
stimulation from keloids or HTS. There is a greater
capacity to proliferate and produce higher levels of
collagen in keloids. On the other hand, HTS fibrob-
lasts demonstrate a modest increase in collagen pro-
duction. An abnormal balance was also observed
between proliferative and apoptotic cell death from
keloids and HTS. HTS and keloids are different
expressions of the same wound-healing process, but
their behavior and clinical appearance are quite dif-
ferent. Initially, the process of scarring is the same,
but after the stimulation of fibroblasts, there is a dif-
ferent pattern of formation in keloids and HTS. An
excessive response to the metabolic process modu-
lates growth factors and cytokines, and differences in
the apoptotic pathway induce different patterns. It is
becoming increasingly important to recognize the dif-
ferences between keloids and HTS and to treat
keloids as a separate entity different from HTS.
Clinicians try to find artificial and natural antagonists
to factors that regulate the phenotype of connective
tissue cells during repair. Modulation of the apoptotic
pathway using pathway inhibitors or inhibitors of col-
lagen (IL-1, tumor necrosis factor-α, interferon-α
[IFN-α], and IFN-γ, which suppress the synthesis of
collagen) and extracellular matrix synthesis would
prevent the proliferation of fibroblasts. Investigations
into novel TGF-β3 antagonists may produce new
therapeutic tools with enhanced efficacy.
Effects of Corticoids
Steroid injections have been shown to cause HTS
and keloid regression in vivo,3 mainly by decreasing
collagen and glycosaminoglycan synthesis, by reduc-
ing the inflammatory process in the wound, by
decreasing fibroblast proliferation, and by increasing
hypoxia. Furthermore, steroids may reduce plasma
protease inhibitors, thus allowing collagenase to
degrade collagen. The resistance to therapy as seen
in keloids can be caused by the fact that hydrocorti-
sone decreases the rate of collagen synthesis and the
amounts of types 1, 3, and 5 collagen mRNA in nor-
mal skin and normal scar fibroblasts, but not in
keloid cells. It reduces elastin synthesis and elastin
mRNA in normal but not in keloid fibroblasts.
Corticosteroids affect fibroblast proliferation and pro-
duction capabilities, and they also inhibit the growth
of fibroblasts and are responsible for fibroblasts
degeneration. Furthermore, corticosteroids can
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affect growth factor involvement during wound heal-
ing as shown by significantly decreased transforming
growth factor-β (TGF-β) and insulin-like growth
factor-1 (IL-1) levels as well as hydroxyproline content
in scar tissue treated with methylprednisolone. Caroll
et al4 studied in vitro human dermal fibroblasts obtained
from normal skin and from keloid scar. First, the der-
mal fibroblasts were placed into score collagen tissue
culture flasks and then into a serum free media. After
cell seeding, they obtained 24-well plates and added
0, 5, 10, or 20 μm of TA for 0, 24, 72, or 96 hours.
The results showed that 20 μm of TA caused statisti-
cally significant increases in the peak levels of bFGF
for normal and keloid fibroblast cell lines (P < .05). It
also caused statistically significant decreases in the
level of TGF-β1 for normal and keloid fibroblast cell
lines. For keloid fibroblasts, 10 μm of TA also caused
a statistically significant decrease in the level of TGF-
β1. They concluded that TA increases the production
of bFGF and decreases the production of TGF-β1 in
human dermal fibroblasts.
Prior studies of keloids have shown the presence
of inflammatory macrophage-like cells surrounded
by a disorganized collagenous deposition. The der-
mal cells of the keloid express the macrophage
marker CD68 and the oncogenic transcription fac-
tor GLI-1.5,6 Increased levels of TGF-β and other
growth factors, including IL-13 and connective tis-
sue growth factor, have been observed in keloids and
other fibrotic processes.7 Although found to be
inhibitory to cellular proliferation in vitro, in vivo
expression of TGF-β is associated with increased
angiogenesis.4 Clinically, keloids seem to be angio-
genic lesions. Gira et al8 attempted to determine
whether keloids are angiogenic lesions and whether
keloids express VEGF and showed a higher level of
expression of VEGF in the overlying epidermis com-
pared with normal epidermis.
Recently, Wu et al9 investigated whether dexam-
ethasone downregulates VEGF expression and hin-
ders keloid fibroblast proliferation in keloid
regression. They treated primary keloid fibroblasts
with different concentrations of dexamethasone, glu-
cocorticoid receptor, antagonist, VEGF-A antibody,
VEGF receptor-2, and VEGF protein. Dexamethasone
retarded keloid fibroblasts proliferation, but the sup-
pression of fibroblast proliferation by dexamethasone
pretreatment slowed down keloid fibroblast prolifera-
tion. Suppression of fibroblast proliferation by dexam-
ethasone pretreatment was reduced by adding
exogenous VEGF protein. Dexamethasone suppressed

endogenous VEGF mRNA induction and angiogene-
sis activity. Thus, dexamethasone induces keloid
regression via interaction with glucocorticoid recep-
tors and suppresses endogenous VEGF expression
and fibroblast proliferation.
The mechanisms involved are complex and
remain unclear. Corticosteroids suppress healing by
3 different mechanisms. First, inflammation is sup-
pressed by inhibition of leukocyte and monocyte
migration and phagocytosis. Second, corticosteroids
are potent vasoconstrictors that reduce the delivery
of oxygen and nutrients to the wound bed. Third, the
antimitotic effect inhibits keratinocytes and fibrob-
lasts, slowing reepithelialization and new collagen
formation. The inhibition of fibroblast proliferation
by corticosteroids may be dose dependent and may
not be seen at lower concentrations, as evidenced by
tissue culture studies. The corticosteroid injections
seem to decrease collagen and glycosaminoglycan
synthesis by reducing the inflammatory process in
the wound, by decreasing fibroblast proliferation,
and by increasing hypoxia. They lead to a decrease
of the production of endogenous VEGF, TGF-β, and
IL-1 and an increase in the production of bFGF.
The Corticotherapy as Monotherapy
Intralesional steroid injections are the frequently
used treatment modality for keloids scars and HTS.
They are often used as an initial therapy, either alone
or in conjunction with other treatment options.
When used as monotherapy,1 steroid injections
have a highly variable response rate of 50% to 100%
and a recurrence rate of 9% to 50%. This treatment is
most effective in younger proliferative scars. Although
less effective in softening and flattening older prolif-
erative scars, especially keloids, it often provides
symptomatic relief for itching and pain. There are
several different steroid preparations, including
hydrocortisone acetate, methylprednisolone acetate,
dexamethasone, and TA. TA is the most commonly
used, although no particular advantage has been
clearly demonstrated for any particular corticosteroid.
The individual clinical response is highly variable and
no standard protocol has been developed. There is
considerable variation among practitioners in the
dose, frequency, and duration of treatment. Rahban
and Garner10 proposed performing 2 to 3 injections of
Kenalog (Bristol-Myers Squibb, Princeton, NJ), at a
dose of 10 mg/mL, approximately 4 to 8 weeks apart.
Despite its benefits, intralesional steroid injections
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Use of Corticosteroids to Treat Keloids / Roques, Téot 139
have several possible adverse side effects, including
hypopigmentation, skin and subcutaneous fat atrophy,
telangiectasias, necrosis, ulcerations, and cushingoid
habitus. The risk of complication is greater when inad-
vertent injection of surrounding normal tissue occurs.
Darzi et al11 evaluated different methods of
treating keloidal scars, including the use of intrale-
sional TA. The dosage administered was dependent
on the keloidal scar surface area: patients with a
keloidal scar surface area of 1 to 2 cm2 received a
total dose of 20 to 40 mg of TA 0.1%, those with 2
to 6 cm2 received 60 to 80 mg, and those with 6 to
12 cm2 received 80 to 120 mg. Seventeen of the scars
were keloidal scars. At 10-year follow-up, 71% of the
treated keloidal scars evidenced full flattening and
29% had partial flattening. Symptom relief was seen
in 71% of the treated keloidal scars, although this
outcome measure was not defined. Four injections
were given until the total dose was reached. Robles
et al12 recommended that triamcinolone acetonide
(Kenalog) be typically used at a concentration rang-
ing from 10 to 40 mg/mL, depending on the size and
location of the lesion. For lesions on the trunk or
extremities, therapy is usually initiated at 40 mg/mL
and then titrated accordingly at subsequent visits.
Multiple injections at regular monthly intervals are
generally required for larger keloids. In a recent
review of literature, Atiyeh13 reviewed evidence-based
therapies, standard practices, and emerging meth-
ods. Injections produce objective reductions in scar
volume for significant numbers of patients, with
improvement of scar pliability, height, and symptoms
such as itching. Insoluble TA (10-40 mg/mL), the
most common corticosteroid used for the treatment
of scars, may be administered alone or in combina-
tion with lidocaine to reduce the pain associated with
the injection. Usually, several treatments at once or
twice a month are required to achieve the desired
results. Despite relatively few randomized, prospec-
tive studies, there is a broad consensus that injected
triamcinolone is efficacious. It is the first-line ther-
apy for the treatment of keloids and the second-line
therapy for the treatment of HTS if other easier treat-
ments have not been efficacious. Local or systemic
complications with this combination therapy may be
insignificant. Because of promising results, further
use and evaluation of this combination method of
treatment are recommended. Topical steroid creams
have been used with varying success, but it must be
noted that absorption through an intact epithe-
lium into the deep dermis is limited. A prospective,
140 The International Journal of Lower Extremity Wounds / Vol. 7, No. 3, September 2008
randomized study showed that topical steroids do not
reduce scar formation in postburn deformities. It
also has been demonstrated recently that limited use
of corticosteroids topically fails to reduce scar for-
mation. Muneuchi et al14 studied the long-term out-
come of injection of TA into keloid scars in Asian
patients. Between 1985 and 2003, they treated 109
keloid scars in 94 patients by injecting 1 to 10 mg of
TA depending on the size of the lesion at 4-week
intervals. There was little morbidity reported, and 31
patients gave up treatment within 10 injections
because of pain and lack of immediate improvement.
Improvement in subjective symptoms was seen in 52
of the remaining 63 patients (82%). In objective
symptoms, fair or better results were seen in 40 of 63
(63%) and good or better results in 25 of 63 (39%).
The treatment method required 20 to 30 injections
over 3 to 5 years. Although they did not achieve as
good results as in other studies, certainly it was safer
because they used a smaller dose of a steroid.
The complications of intralesional steroid use
include skin atrophy, hypopigmentation or hyperpig-
mentation, and the development of telangiectasias.
Because patients typically require multiple needle
sticks, especially for larger lesions, some clinicians
advocate pretreatment with topical lidocaine or the
addition of lidocaine in the syringe to help alleviate
injection-associated pain. Intralesional steroid injec-
tions may be impractical for very large or multiple
keloids, because the pain associated with the injec-
tion may be considerable and there is the additional
concern due to large doses of corticosteroids.
Although the use of corticosteroids to suppress
abnormal scar formation has been relatively effective
for the most part, it also has been a troublesome
therapy. Intralesional corticosteroid injection is asso-
ciated with significant injection pain, even using
standard doses of triamcinolone (40 mg/mL), with up
to 63% of patients experiencing some side effects.
The most common side effects of this treatment ther-
apy are hypopigmentation, skin and subcutaneous fat
atrophy, telangiectasias, rebound effects, and inef-
fectiveness. After intralesional injection, linear
hypopigmentation also may develop secondary to
lymphogenous uptake of the corticosteroid crystals.
Complications are few, usually being local skin color
changes, prominent vascular markings, or subcuta-
neous atrophy. Cushing’s syndrome following intrale-
sional administration of triamcinolone acetate has
been described in adult patients. Retota and Lo15
reported on 2 pediatric cases of Cushing’s syndrome
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following treatment of hypertrophic burn scars with
intralesional TA. The conclusion was that intrale-
sional TA should be used with an increased degree of
caution in the pediatric population.
The concentration of TA may be 10 to 40 mg/mL,
depending on the amount of scar formation, the size
and location of the lesion, and the individual patient.
About 2 to 3 injections are usually sufficient, although
occasionally injections continue for 6 months or more,
depending on the type of the scar.1 Intralesional corti-
costeroid administration shows a highly variable
response rate of 50% to 100% with a recurrence rate of
9% to 50%. Side effects of corticosteroids are skin atro-
phy, hypopigmentation or depigmentation, telangiec-
tasias, necrosis, ulceration, and Cushingoid features.
Therapeutic Associations With
Corticosteroids
Numerous authors propose a therapeutic associa-
tion in the corticotherapy to improve results. Results
may be improved when corticosteroids are combined
with other therapies, such as surgery, pulsed-dye
laser (PDL) irradiation, 5-fluorouracil (5-FU), and
cryotherapy.13 Surgical excision with intraoperative
local injection of TA followed by repeat injection at
weekly intervals for 2 to 5 weeks, depending on the
symptomatic relief, and then monthly injections for
4 to 6 months may yield good results. Complete
symptomatic relief can be achieved with this combi-
nation for all patients within 5 weeks of surgery. An
objective response in terms of no recurrence can be
noted in 91.9% of patients with keloids and in
95.24% of patients with HTS. Kauth et al16 wanted
to determine the efficacy of TA in reducing the pro-
α1(I) collagen mRNA in the dermis when TA is
injected into the wound bed immediately after sur-
gical excision of the keloid. Six patients with previ-
ously untreated keloids were studied. Three were
treated with 10 mg/mL of TA immediately after exci-
sion of the keloid (experimental group); the other 3
patients were not treated with TA until 2 weeks after
excision (control). Punch biopsy specimens were
obtained from the TA-treated sites 2 weeks after the
removal of the keloid and from the wounds of the
control group of patients before they were treated with
TA. Sections were prepared for in situ hybridization
analysis of the pro-α1(I) collagen mRNA, as well as for
histochemical analysis of collagen fibers. All keloids
showed greatly elevated levels of pro-α1(I) collagen
mRNA in the dermis. Postsurgical wounds injected

with TA after removal of the keloid expressed
decreased pro-α1(I) collagen transcripts when com-
pared with skin not treated with TA. The collagen
bundles were also thinner and less dense in the TA-
treated skin. Downregulation of the type I collagen
gene expression is elicited by immediate TA injec-
tion after keloid excision. This suggests that preven-
tion of recurrent keloid growth is possible if surgical
excision is accompanied by immediate TA injection
into the wound bed and that healing of the wound is
not apparently compromised by inhibition of type I
collagen gene expression. Combination therapy10
with surgery also shows variable recurrence rates of
0% to 100%, but with a mean of less than 50%.
Certain clinicians regularly inject preoperatively
with steroids until no further regression of the scar
is noted followed by excision. The scar edges are
injected at the time of surgery and postoperatively
for varying lengths of time. Donkor17 described a
technique used by the author for the management of
head and neck keloids. He reviewed patients pre-
senting with new and recurrent keloid of the head
and neck. The surgical technique involved the
intralesional excision of the bulk of the keloid.
Primary closure of the ensuring defect was achieved
at operation. At the time of suture removal, between
10 and 14 days postoperative, 40 mg TA was injected
into the residual lesion. The injection was repeated on
2 more occasions at monthly intervals. All patients
were followed-up for at least 2 years. Eighteen patients
were successfully treated with no sign of recurrence in
any of them. The main complication was hypopig-
mentation at the site of the original lesion. He con-
cluded that the technique was found to be effective for
the treatment of moderately sized new and recurrent
keloid scars of the head and neck and is therefore rec-
ommended. Davison et al18 compared the effect of
INF-α2b as postexcisional adjuvant therapy and tri-
amcinolone in 39 keloids. The wound bed was
injected twice with either INF-α2b (treatment group;
n = 13 keloids) or triamcinolone (control group; n = 26
keloids) at surgery and 1 week later. Among the 13
keloids that were treated with postoperative intrale-
sional INF-α2b, 7 recurred (54% recurrence rate). In
contrast, in the 26 keloids that received triamcinolone
(control group), only 4 recurred (15% recurrence
rate). Recurrence in either group did not correlate
with location of the keloid or race.
Cryotherapy has also been combined with
intralesional corticosteroid injections with varying
results.18 Some authors reported that initial treat-
ment of the scar with cryotherapy induces edema
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Use of Corticosteroids to Treat Keloids / Roques, Téot 141
and cellular breakdown, resulting in decreased den-
sity of the fibrous tissue, making injection easier and
effective. In addition, cryotherapy may provide anes-
thesia prior to infiltration. Cryotherapy has been
used in conjunction with corticosteroid injections.19
Hirshowitz et al20 injected triamcinolone after 2
cycles of freezing. They used 2 different cryogens,
nitrous oxide and liquid nitrogen. The mean number
of treatments needed was between 2 and 8, depend-
ing on the location of the keloidal scar. Complete
regression was seen in 41 of 58 patients (70%).
However, there was no description of adverse
effects. Cryosurgery and intralesional TA produced
flattening and hypopigmentation. Ceilley and
Babin21 reported their experience with freezing
keloidal scars and then, after they thawed, injecting
them with TA (10-20 mg/mL). Several injections
were usually necessary, with benefits beginning at 8
weeks. The authors conclude that there could be a
synergistic effect between the 2 treatments and pro-
posed the need for controlled studies to confirm
their opinion. Farahnaz et al22 compared the results
of treatment of these skin conditions with bleomycin
tattoo with cryotherapy and triamcinolone injection.
This study involved 45 patients with HTS or keloid.
Patients were divided into 2 groups: patients group
A (23 patients) were treated with bleomycin tattoo,
and patients in group B were treated with cryother-
apy and triamcinolone injection. There were 4 ther-
apeutic sessions 1 month apart. All patients were
followed-up for 3 month after the end of treatment.
The therapeutic response was determined as reduc-
tion of lesion size or flattening relative to initial size.
Therapeutic response was 88.3 ± 14% in group A
and 67.4 ± 22.5% in group B (P < .001). In group A,
69% of the patients were asymptomatic after the end
of treatment, but in group B, only 49% of the
patients were asymptomatic. In group A, there was
no relation between therapeutic response and lesion
size (P = .58, NS), but in group B, smaller lesions
(<100 mm2) had better therapeutic response than
larger ones (P = .007). It was concluded that
bleomycin tattoo is more effective in the treatment
of HTS and keloids when compared with the tradi-
tional treatment, cryotherapy plus triamcinolone
injection, especially in larger scars. Very often it is
difficult to force the injection into the hard mass of
a keloid. This problem could be overcome by soften-
ing the lesion either with cryotherapy or PDL, by
addition of hyaluronidase, or by topical application
of an immunomodulator such as Imiquimod.23 A
recent study by Boutli-Kasapidou et al24 evaluated the
142 The International Journal of Lower Extremity Wounds / Vol. 7, No. 3, September 2008
efficiency of polytherapy. Twenty patients with hyper-
trophic and keloidal scars received two 15-second
cycles (30 seconds in total) of cryotherapy treatment
monthly at every session for 12 months with intrale-
sional injections of AT 0.1% (10-40 mg/mL), and once
monthly for 3 months. Topical application of silicone
gel was added 3 times daily (for 12 months). The con-
trol group included 10 patients who received treat-
ment with silicone sheeting. After 1 year, there was
improvement in all the parameters studied, especially
in terms of symptoms, cosmetic appearance, and
associated signs (P < .0001), compared with baseline
and the control group. Their study suggests that poly-
therapy may be an effective tool in the therapy of
hypertrophic and keloidal scars.
The association of PDL and intralesional corti-
costeroid injections was also proposed. Manuskiatti
et al25 compared the clinical response of keloidal and
hypertrophic scars on median sternotomy scars after
treatment with intralesional corticosteroid alone or
combined with 5- 5-FU, 5-FU alone, and the 585-
nm flashlamp-pumped PDL. The study was a
prospective, randomized controlled trial. Ten patients
with previously untreated keloidal or hypertrophic
scars at least 6 months after surgery that were con-
sidered problematic by the patients were included.
Five segments were randomly treated with 4 different
regimens: (1) laser radiation with a 585-nm PDL (5
J/cm2), (2) intralesional TA (20 mg/mL), (3) intrale-
sional 5-FU (50 mg/mL), and (4) intralesional TA (1
mg/mL) mixed with 5-FU (45 mg/mL). One segment
of each scar received no treatment and served as a
control. Scar height, erythema, and pliability were
evaluated before and every 8 weeks after treatment.
Patients’ subjective evaluations were tabulated.
Histological sections of segments were examined in 1
biopsy sample per segment at week 32. There was a
statistically significant clinical improvement in all
the treated segments. No significant difference in
treatment outcome versus method of treatment was
noted. However, intralesional formulas resulted in
faster resolution than the PDL: scar induration
responded better to intralesional formulas, scar tex-
ture responded better to the PDL, and scar erythema
responded in the same way as the control with all
treatments. Adverse sequelae, including hypopig-
mentation, telangiectasias, and skin atrophy, were
observed in 50% (5/10) of the segments that received
corticosteroid intralesionally alone. No long-term
adverse sequelae were demonstrated in the segments
treated with other modalities.
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Alster26 compared scars treated with PDL with
and without intralesional corticosteroids. A total of
22 females with bilateral, symmetric hypertrophic
breast reduction (inframammary) scars were
included in the study. Scars had been present for 4
to 72 months (mean duration of 18.5 months).
Scars were randomly assigned to receive PDL
injected immediately after laser irradiation. Each
patient had 1 inframammary scar treated with the
PDL alone and the contralateral scar treated with a
combination of PDL and corticosteroids. All laser
treatments and steroid injections were performed by
the investigator at 6-week intervals. Two treatments
were delivered to each scar using either PDL alone
or PDL followed immediately by 10- to 20-mg
intralesional triamcinolone. Photographic documen-
tation and clinical evaluations were made before
each treatment and 6 weeks after the second (final)
treatment by 2 independent assessors blinded to the
study protocol using a standard quartile grading
scale improvement. Pliability scores and symptom
scores were also recorded. Scar biopsies were
obtained before and after treatment in 4 patients.
Histological evaluations were made by a board-certi-
fied dermatopathologist who was also blinded to the
study protocol. Treatment of hypertrophic infra-
mammary scars with PDL irradiation effected sig-
nificant clinical and histological improvement in all
study patients. The adjunctive use of intralesional
corticosteroids did not significantly enhance clinical
outcome in the study, except in terms of decreasing
pruritus within particularly symptomatic scars. The
relatively low dose of injected corticosteroid (10-20
mg as opposed to 20-40 mg) may have accounted for
the limited improvement observed in the combina-
tion protocol. Higher corticosteroid concentrations
could have potentially yielded better results but
would have also increased the risk of unwanted side
effects such as skin atrophy and telangiectasias in
this delicate body location.
Asilian et al27 examined the effectiveness of a com-
bination of intralesional steroid, 5-FU, and PDL in the
treatment of HTS and keloids. A total of 69 patients
were randomly assigned to treatment with intrale-
sional triamcinolone, intralesional triamcinolone plus
intralesional 5-FU, and triamcinolone, 5-FU and PDL
treatment. The investigators reported that after 12
weeks good to excellent improvements were reported
by a blinded observer in 15% of subjects treated with
triamcinolone alone, in 40% of subjects treated with
triamcinolone plus 5-FU, and in 70% of subjects

treated with all 3 modalities. A comparative study of
treatment on keloids with INF-α2b and TA was
recently published by Lee et al.28 They compared the
efficacy and side effects of keloid treatment using
IFN-α2b and TA, and TA only. Twenty lesions (com-
bined TA + IFN-α2b group) and 20 control lesions
(TA-only group) were studied in 19 patients (14
women and 5 men). The age range was 7 to 51 years
(mean age, 24.6 years). Both groups were treated
with TA every 2 weeks. The combined TA + IFN-α2b
group was treated with intralesional injection of
IFN-α2b, twice a week. Statistically significant
decreases in depth (81.6%, P = .005) and volume
(86.6%, P = .002) were observed in lesions of the
combined TA + IFN-α2b group. In the TA-only
group, the decreases in depth (66.0%, P = .281) and
volume (73.4%, P = .245) were not statistically sig-
nificant. The main side effects were fever and flulike
symptoms, mild pain, and inflammation at the injec-
tion site. Intralesional IFN-α2b is an effective and
safe treatment for keloids. Although the recurrence
rate is as yet unknown, more than 80% improvement
was noted in the majority of cases. Hence, adjuvant
intralesional IFN-α2b should be considered, partic-
ularly for patients who have a history of failed corti-
costeroid injections.
Berman and Flores29 proposed to determine
whether postsurgical adjunctive therapy reduces
such recurrences. They determined the rate of recur-
rence after excision alone (n = 43) and postoperative
injection with TA (n = 65) or INF-α2b (n = 16). Of
the lesions excised without postoperative injections,
51.1% (22 of 43) recurred, 58.4% of TA-treated
lesions (38 of 65) recurred, and 18.7% of IFN-α2b-
treated lesions (3 of 16) recurred (P = .025).
Postoperative TA injections do not reduce the num-
ber of keloid recurrences. However, injection of
keloid excision sites with IFN-α2b offers a thera-
peutic advantage over keloid excision. Other thera-
peutic associations have also been proposed.
Berman et al30 evaluated the tolerability and efficacy
of intralesional etanercept compared with intrale-
sional TA for the treatment of keloids. Twenty sub-
jects were randomly treated with either 25 mg
etanercept or 20 mg TA monthly injections for 2
months. All subjects had negative PPDs within 1
year of study enrollment. Subjects were evaluated at
baseline and weeks 4 and 8. Adverse events were
noted and study keloids were photographed during
each evaluation. Data were analyzed using the 2-
tailed Student’s t test and mean percentage change
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Use of Corticosteroids to Treat Keloids / Roques, Téot 143
measured at weeks 4 and 8 versus baseline. All
(10/10) subjects treated with etanercept and 8/10
subjects treated with TA completed the study (P < .15).
There were no systemic or unexpected application-
site adverse events noted in either group. Both treat-
ments were safe and well tolerated. There were no
statistically significant reductions in the parameters
studied for the patients treated with etanercept
when compared with TA. However, etanercept sig-
nificantly reduced pruritus at week 8 when com-
pared with baseline, whereas TA did not achieve a
significant reduction in pruritus at week 8 when
compared with baseline. Both etanercept and TA, at
the administered doses, were safe and well tolerated.
TA improved 11/12 parameters, confirming its main-
stay use for the treatment of keloids. Etanercept
improved 5/12 parameters and significantly reduced
pruritus, whereas TA did not significantly reduce
pruritus. Further studies are needed to determine
the effects of injecting higher etanercept concentra-
tions for more prolonged keloid treatment periods.
Beuth et al31 investigated the safety and efficacy
of Contractubex administration to HTS in routine
outpatient practice and compared it with corticos-
teroid treatment. This was a multicenter, retrospec-
tive cohort study based on 38 randomly selected
practices. Data from 859 patients fulfilling the
inclusion criteria were assessed and analyzed. Of
these, 771 patients were eligible for the per protocol
treatment with Contractubex (n = 555) and corti-
costeroid (n = 216). The safety and efficacy of local
administration of Contractubex to HTS was com-
pared with corticosteroid treatment. At the end of
the defined treatment periods (minimum 28 days for
local therapy with 1 intralesional corticosteroid
application), normalization of the pretreatment
pathological parameters (erythema, pruritus, consis-
tency) of HTS was more frequent (42.5%) after
Contractubex per protocol treatment when com-
pared with corticosteroid per protocol treatment
(22.2%). After adjusting imbalances of baseline
characteristics between the treatment groups by the
propensity score, the odds ratio was 2.274, demon-
strating a significant superiority (P < .001) of
Contractubex treatment when compared with corti-
costeroid treatment. The time to normalization of
erythema, pruritus, and consistency was signifi-
cantly (P = .034) shorter with Contractubex treat-
ment (median 344 days) than with corticosteroids
(median 507 days). No unexpected or severe adverse
events occurred in the Contractubex-treated patients.
144 The International Journal of Lower Extremity Wounds / Vol. 7, No. 3, September 2008
Apart from moderate pruritus (10% Contractubex vs
1% corticosteroids), adverse events were signifi-
cantly (P < .001) more frequent in corticosteroid-
treated patients (telangiectasias 15% vs 7% Contractubex,
cutaneous atrophy of scars 10% vs 2% Contractubex,
cutaneous atrophy of scar surrounding skin tissue
11% vs 1% Contractubex). For assessment of nor-
malization of erythema, pruritus, and consistency of
HTS and for time to normalization, local adminis-
tration of Contractubex was significantly more
effective than corticosteroid treatment. Concerning
safety, Contractubex treatment was associated with
significantly less adverse events than topical corti-
costeroid application.
The association with surgery can be proposed
intraoperatively using local injection of TA, then
weekly during 2 to 5 weeks, with results ranging
between 0% and 100% of recurrences,13,14,16 or being
injected directly into the scar at days 10 to 14 posto-
pratively,17 the authors concluding that the technique
is effective on the recent small keloids or recurrent
keloids. Compared with the interferon18 injected into
the site, the results with TA were better after 1 week
of treatment, but the groups were not identical.
Cryotherapy has also been proposed in conjunc-
tion with injections of TA; it improves tolerance to
the injections18-23 by a local anesthetic effect due to
scar softening. The association would allow a syner-
gistic action of the 2 techniques20,21; also, the num-
bers of patients were small and the studies were not
controlled. However, bleomycin tattoo seems to
have better effects than injecting TA associated with
cryotherapy.22 Combined treatment with 5-FU, 5-
FU alone, and PDL showed no significant difference
in treatment outcome when compared with standard
methods of treatment.25
Scar hardness responded better to intralesional
injections, scar texture responded better to the PDL,
and scar erythema responded similarly to the control
whatever the proposed treatment. Poor results were
observed in 50% of the cases.
Another study compared the effectiveness of a
combination of intralesional steroid, 5-FU, and PDL
and the results showed that 70% of subjects treated
with a combination of the 3 modalities obtained unex-
pectedly good to excellent results.27 The combination
TA + IFN-α2b produced better results than TA alone.28
Conclusions
Since the publication of recommendations in 2002
few randomized studies with a large number of patients
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have been published.1 Mechanisms for keloid forma-
tion32 include alterations in growth factors, collagen
turnover, tension alignment, and genetic and immuno-
logic contributions. Corticosteroids induce increase in
the production of bFGF and a decrease in the pro-
duction of TGF-1 by human dermal fibroblasts,
endogenous VEGF, and IL-1. Intralesional injections
require a concentration of TA from 10 to 40 mg/mL,
depending on the amount of scar tissue, the size and
location of the lesion, and the personal variation of the
patient’s response. Two or 3 successive injections are
usually sufficient, although sporadic injections may be
administered for 6 months or more, depending on the
type of scar.1 Intralesional corticosteroid administra-
tion shows a highly variable response rate of 50% to
100%, with a recurrence rate of 9% to 50%.
The International Advisory Panel on Scar
Management1 has recommended the use of intrale-
sional steroid injections for the treatment of keloid
and hypertrophic scars. The authors also highlight
that apart from the technique of silicone gel sheet-
ing other treatment therapies have not been suffi-
ciently demonstrated. The use of corticosteroid
injections is, to date, the core treatment modality
available to physicians for the management of
abnormally elevated scars. The most successful
treatment of keloid scars is with combined therapy
involving steroids and surgical excision, with the
success rate exceeding 80%. The combination ther-
apy, using surgical excision followed by intradermal
steroid or other adjuvant therapy, currently appears
to be the most effective and safe current regimen for
keloid management.
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