Pityriasis Versicolor A Review of Pharmacological Treatment Options

Expert Opinion on Pharmacotherapy
ISSN: 1465-6566 (Print) 1744-7666 (Online) Journal homepage: http://www.tandfonline.com/loi/ieop20
Pityriasis versicolor: a review of pharmacological

treatment options
Aditya K Gupta, Nataly Kogan & Roma Batra
To cite this article: Aditya K Gupta, Nataly Kogan & Roma Batra (2005) Pityriasis versicolor:
a review of pharmacological treatment options, Expert Opinion on Pharmacotherapy, 6:2,
165-178, DOI: 10.1517/14656566.6.2.165
To link to this article: http://dx.doi.org/10.1517/14656566.6.2.165
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Date: 23 February 2016, At: 22:32
Review
Monthly Focus: Anti-infectives
1. Introduction
2. Aetiology
3. Diagnosis and clinical
appearance of pityriasis
versicolor
4. Histopathology
Downloaded by [Colorado State University] at 22:32 23 February 2016
5. Goal of therapy
6. Treatment of pityriasis
versicolor
7. Conclusion
8. Expert opinion
Pityriasis versicolor: a review of

pharmacological treatment
options
Aditya K Gupta, Nataly Kogan & Roma Batra
645
Windermere Road, London, Ontario, N5X 2P1, Canada
Pityriasis versicolor is a common disorder of the skin, which is characterised by

scaly hypo- or hyperpigmented lesions on the body. The lipophilic yeast,
Malassezia, is considered to be the aetiological agent of this disease. A
number of treatment options, both topical and systemic, have been shown to
be effective. A critical evaluation of treatment options is presented.
Keywords: antifungal, Malassezia, pityriasis versicolor
Expert Opin. Pharmacother. (2005) 6(2):165178
1. Introduction
Pityriasis versicolor (PV) is a benign cutaneous disorder, usually asymptomatic,

characterised by slightly scaly patches of variable colour (pink, brown or white) and
mainly located on the upper trunk, neck and upper arms. PV generally colonises
anatomical sites abundant with sebaceous glands [1]. The symptoms may be accompanied by mild pruritis in the lesional areas.
PV is distributed worldwide; however, it is encountered more frequently in tropical climates, where the prevalence rate may be 30% [2,3]. It primarily affects young
adults of both sexes, although in tropical zones, it is also common in infancy and
even in neonates [1]. In a recent analysis, Mellen et al. [4], showed that in the US,
between 1990 and 1999, PV was diagnosed in 2.9 million office visits (110 cases per
100,000 population per year). A higher visit frequency was identified in AfricanAmericans and American Indians/Eskimos as compared with Caucasians.
Without treatment, PV is a chronic disease, and even after treatment, recurrence
may occur, affecting up to 60% of subjects 1 year following treatment and up to
80% after 2 years [5,6]. Because Malassezia yeasts are a part of the normal microflora
of the body, it is not clear why some individuals are more susceptible to this disease
than others.
2. Aetiology
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PV is the only dermatological disorder conclusively caused by Malassezia spp. Historically, it has been suggested that the rounded form of Malassezia spp., the mycelial form, previously referred to as Pityrosporum orbiculare, was the aetiological agent
[7]. The Malassezia organism may change from the saphrophytic form to the aetiological mycelial form in response to predisposing factors such as high temperature
and humidity, profuse sweating, hereditary factors, steroid medication and malignant lymphomas [3,8,9]. Altered cell-mediated immunity has been implicated as one
of the predisposing factors. Such a response has been demonstrated by lymphocyte
transformation tests in healthy individuals [10]. Lymphocyte transformation in
patients with PV, however, has been reported with diverse results [11-15]. Although
antibodies to Malassezia yeasts have been shown in normal controls as well as
10.1517/14656566.6.2.165 2005 Ashley Publications Ltd ISSN 1465-6566
165
Pityriasis versicolor: a review of pharmacological treatment options
patients with PV [16], some have shown antibody titres to be

elevated in the latter [15,17]. McGinley et al. [18] showed that
the number of yeasts and hyphae in PV lesions is much higher
than in the unaffected skin of the same patients; therefore,
overgrowth of Malassezia yeasts may cause the lesions of PV. A
positive family history of 17% has been reported [19]; thus,
hereditary factors seem to play a role in the disease. Furthermore, activation of complement via direct and alternative
pathways may play a role in the production of inflammation
which is seen in some cases of PV [20]. In addition, it has also
been suggested that skin surface amino acids are critical in the
pathogenesis of the disease [21].
Based on recent studies, it appears that the species most
frequently associated with PV are M. globosa and M. sympodialis [22]. In Canada, M. globosa was isolated from 55% of
lesional skin specimens [22]. In Tehran, Iran, the specie was
isolated in 53.3% of specimens [23]. In Spain, Crespo-Erchiga
et al. [24] also observed that the predominant specie in PV
lesions is M. globosa, as it was isolated in culture in 87% of
the cases. Aspiroz et al. [25], confirmed this finding by isolating M. globosa in 90% of PV lesions in Spanish patients.
M. furfur is also aetiological in some lesions [23,26]. The
involvement of Malassezia yeasts in the aetiology and pathogenesis of this disease is confirmed by successful attempts at
treating PV patients with antifungal therapy.
3. Diagnosis
and clinical appearance of

pityriasis versicolor
PV presents as numerous macules or slightly raised papules
with subtle scale. The lesions may coalesce or manifest as a
single patch with an irregular border. The lesions also vary in
size, from several centimetres in diameter to a size large
enough to cover most of the trunk. In larger lesions, the flaking may be apparent only at the border of the maculae. The
lesions may be hypo- or hyperpigmented, but occasionally, a
patient presents with both types. The colour of lesions varies
according to the normal pigmentation of the patient, exposure of the afflicted area to sunlight, and chronicity of the
infection [8,9].
Hyperpigmented lesions can be red, fawn, yellow-brown,
or dark brown in colour. Several theories have been proposed
to explain the depigmentation in PV. Histological differences
between hyper- and hypopigmented lesions have been
reported. Hyperpigmented lesions seem to have more spores
and hyphae than either normal or hypopigmented skin [27,28].
The brown hyperpigmented lesions of PV show increased
stratum corneum turnover and larger, singly distributed
melanosomes [29,30]. Some authors suggest that the hyperpigmentation is secondary to changes in the size or the distribution of melanosomes caused by the fungus [29]. The lighter
hyperpigmented maculae may be the result of a mild inflammatory reaction, resulting in stimulation of melanocytes and
the production of increased pigment [31,32] or increased thickness of the keratin layer [33].
166
In the case of hypopigmentation, the mechanism is not

very clear. It has been suggested that Malassezia yeasts behave
as potent ultraviolet filters [29,33,34]. Tryptophan, the main
nitrogen source in M. furfur, induces the formation of fluorochromes and pigments, which makes the yeast less sensitive
towards UV light [34,35]. However, observation of depigmentation of anatomical areas that are not exposed to UV light,
such as the genital area [33,36], makes this hypothesis questionable. Another hypothesis for development of achromia is that
the carboxylic acid metabolites of Malassezia spp., such as
azelaic acid, can block the conversion of tyrosine to melanin
via tyrosinase inhibition, leading to hypopigmented patches
[27,33,37,38]. Furthermore, Malassezia yeasts have lipooxygenase
activity that catalyses the oxygenation of unsaturated free fatty
acids, resulting in the presence of a high level of lipoperoxides
and their breakdown products, such as peroxy-radicals. Peroxidation of skin lipids may play a role in the pathogenesis of
skin alterations in PV, including damage to melanocytes with
subsequent achromia [39]. Other theories that attempt to
explain PV-induced hypopigmentation include failure in melanin granule transfer caused by increased keratinisation [33].
Although various theories have been proposed to clarify this
phenomenon, none have been validated.
Hypopigmentation is twice as common as hyperpigmentation and is usually the main reason for the patient seeking
treatment [24]. In the majority of patients, it persists following
treatment but with reduced severity [40,41]. Some dermatologists do not consider hypopigmentation to be a clinical sign
for efficacy evaluation [42].
The diagnosis of PV involves microscopy and culture. It is
preferred that skin scrapings be taken from the border of a
lesion, as this region has the highest number of yeasts. In
some cases, it is difficult to obtain adequate material by scraping, and the transparent tape method can be used [43]. The
skin scales may be digested by potassium hydroxide (KOH)
20%. The appearance of Malassezia yeasts can be enhanced if
Parkers blue/black ink is incorporated in the KOH to digest
the keratin [44]. The spaghetti and meatball appearance (mixture of globose blastoconidia and pseudomycelium) is characteristic of Malassezia yeasts in a PV lesion.
Woods light may also prove to be a useful diagnostic tool
in some cases of PV. The diagnosis is based primarily on the
typical clinical picture in combination with bright yellow
fluorescence under Woods light.
4. Histopathology
The stratum corneum in PV patients is replete with hyphae

and round budding cellular fungal elements, which are most
visible with a periodic acid-Schiff stain or methenamine silver
stain [28]. Ultrastructural studies have shown severe melanocyte damage, varying from altered melanosomes and mitochondria to actual degeneration and an overall reaction to the
fungus [45]. The damage to melanocytes could explain why
repigmentation may take several months or years to occur [45].
Expert Opin. Pharmacother. (2005) 6(2)
Gupta, Kogan & Batra
Table 1. Studies comparing topical agents in the treatment of pityriasis versicolor.

Ref.
Treatment regimen
Study MC (%)
design
[58]
Bifonazole 2% lotion versus

fenticonazole 2% lotion oncedaily for 21 days maximum
23 versus
23
DB, R
21 days:
23 (100) versus 23 (100) versus
23 (100) versus 22 (96)
22 (96)
22 (96)
[40]
Bifonazole solution once-daily

20 versus
for 2 weeks versus selenium
18
sulfide shampoo once-daily for
1 week followed by once-weekly
for 6 weeks
Op, R
1 week :
17 (85) versus
19 (95)
[113]
Bifonazole 1% solution versus

flutrimazole 1% solution
once-daily for 1 week
DB, R
[114]
Flutrimazole 1% cream versus

228 versus
bifonazole 1% cream once-daily 221
for 4 weeks
DB, R
[63]
Tioconazole 1% lotion versus

clotrimazole 1% solution
twice-daily for 4 weeks
16 versus
16
Op
16 (100) versus 16 (100) versus 16 (100) versus CC at 8 weeks:

16 (100)
16 (100)
16 (100)
16 (100) versus
15 (94)
[115]
Tioconazole base 1% versus

miconazole nitrate 2% cream
6 versus 4
SB
6 (100) versus
4 (100)
[53]
Clotrimazole 1% cream versus

Whitfields ointment twice-daily
for 4 weeks
17 versus
14
DB, R
4 weeks:
14 (80) versus
11 (79)
[48]
Econazole nitrate 1% cream

65 versus
once-daily for 21 days versus
65
selenium sulfide 2.5% shampoo
on days 1, 2, and 3; placebo on
days 4 6
SB, R
[64]
Oxiconazole 1% cream versus

20 versus
econazole 1% cream twice-daily 19
for 3 6 weeks
DB, R
19 (95) versus
17 (89)
[73]
Terbinafine 1% cream versus

20 versus
bifonazole 1% cream for mean 20
duration of 3.1 versus 3.7 weeks
(p < 0.005)
SB, R
4 weeks:
20 (100) versus
20 (100) versus 19 (95)
19 (95)
[111]
Ciclopirox olamine 1% cream

versus clotrimazole 1% cream
DB, R
20 versus
20
60 versus
53
CC (%)
Complete
cure (%)
Follow-up
MC at 4 weeks:
19 (95) versus
15/19 (22)
8 (40) versus
2 (10)
4 (20) versus
8 (40)
3 & 9 weeks: all

remained CC and
MC
166 (73) versus

144 (65)
6 (100) versus
4 (100)
6 (100) versus
4 (100)
6 weeks: all
remained cured
60 (92) versus
58 (89)
19 (95) versus
17 (89)
46 (77) versus
24 (45)
2 weeks: 44/50
(88) versus 32/44
(73) remained
cured
CC: Clinical cure; DB: Double-blind; MC: Mycological cure; N: Sample number; Op: Open; R: Randomised; SB: Single-blind.
5. Goal
of therapy
The main challenge with the treatment of PV is the recurrence of the disease. The goal of therapy should therefore be
to customise a safe and efficacious treatment, so that improvement occurs with low recurrence rates. An appropriate prophylactic treatment to prevent recurrence of PV is also an
important consideration. Furthermore, in todays healthcare
climate, the cost of treatment is a significant factor. The cost
of PV treatment modalities vary widely. The newer oral antifungals are effective following short-term regimens, thus
reducing the cost compared with a traditional long-term

course of therapy. Similarly, short-term topical treatments
may be a consideration in many patients.
6. Treatment
of pityriasis versicolor
6.1 Topical
treatments
There are numerous topical treatments of PV, and the consequent decrease in the number of Malassezia yeasts often parallels the clinical improvement (Table 1). Many topical
treatments have proved to be effective in the control of PV.
167
Table 2. Efficacy of nonspecific topical antifungal agents in the treatment of pityriasis versicolor.
Ref.
Treatment regimen
Study
design
[41]
Zinc pyrithione 1% shampoo once-daily

for 2 weeks
20
Op
[55]
Zinc pyrithione 1% shampoo versus

vehicle once-daily for 2 weeks
20 versus
20
[52]
Propylene glycol 50% twice-daily for

2 weeks
20
[102]
A. Selenium sulfide 2.5% lotion

48
B. Selenium sulfide 2.5% lotion + 0.2%
38
colorants once-daily for 1 week
C. Vehicle + 0.2% colorants once-daily for 46
1 week
[46]
MC (%)
CC (%)
Complete
cure (%)
Follow-up
20 (100)
2 weeks: 18/18
(100) remained
cured
20 (100)
versus 0
2 weeks: 20 (100)
versus 0
20 (100)
DB, R
39 (81)
27 (71)
7 (15)
2.5% selenium disulfide suspension

30 versus Op
applied once versus once + prophylactic
29
treatment once every 3 months for 1 year
30 (100)
versus 29
(100)
30 (100)
versus 29
(100)
24 months: 14
(47) versus 25 (86)
remained cured
CC: Clinical cure; DB: Double-blind; MC: Mycological cure; N: Sample number; Op: Open; R: Randomised.
Table 3. Efficacy of topical bifonazole in the treatment of pityriasis versicolor.

Ref.
Treatment regimen
Study
design
MC (%)
CC (%)
[60]
1% cream versus vehicle

once-daily for 2 weeks
14 versus
15
DB, R
11 (79) versus
5 (33)
10 (71) versus
9 (60)
[103]
1% cream once-daily for

2 weeks versus 1 week
32 versus
29
DB
32 (100) versus 30 (94) versus

28 (96)
24 (83)
[104]
1% gel once-daily for 2 weeks 121
Op,
113 (93)
98 (81)
98 (81)
[62]
A) 1% solution applied once

B) 1% solution applied
once-daily on days 1 and 3
C) 1% solution applied
once-daily on days 1, 3 and 6
30
30
Op, R
18 (60)
19 (63)
22 (73)
21 (70)
18 (60)
19 (63)
25 (83)
27 (90)
25 (83)
A) 2.5% cream: once on

day 1
28
4 weeks:
15 (54)
16 (57)
B) once-daily on days 1, 2, 3
C) once-daily on days 1, 3, 5
36
35
36 (100)
34 (97)
35 (97)
34 (97)
[105]
[106]
30
Complete Follow-up
cure (%)
2 weeks: 11 (79)
versus 4 (27) cured
2 weeks: all patients
remained MC and all
but one CC (Group 2)
3 months: 23/29 (79)
cured
22/29 (73) cured
27/29 (90) cured
A) 1% spray applied on day 1 30

of 4 consecutive months
B) Applied on first 3 days of
30
month 1 and once-monthly on
day 1 of following 3 months
Op, R
Op, R
4 months:
23 (77)
25 (83)
1 year: all reported

remission within
3 months
Lost to follow-up
Lost to follow-up
23 (77)
25 (83)
Nonspecific topical antifungal agents

These agents are the oldest treatments available for PV and are
so-called because they do not possess direct antifungal activity
(Table 2). Generally, they act by physically and/or chemically
removing infected dead tissue and by preventing the invasion
of newly formed or forming keratinised tissues.
6.1.1
168
Selenium sulfide is available as a 2.5% lotion, cream or shampoo. It has long been known to be effective in the treatment of
PV [46,47], but a high rate of relapse is generally expected [46].
Selenium sulfide is as effective as some of the more recent specific antifungal agents used in the topical treatment of PV [40,48];
however, the course of treatment is often longer [40].
Table 4. Efficacy of topical terbinafine in the treatment of pityriasis versicolor.

Ref.
Treatment regimen
Study MC (%)
design
CC (%)
Complete
cure (%)
[42]
Terbinafine 1% solution
versus placebo twice-daily
for 1 week
76 versus
34
DB, R
8 weeks:
62 (81) versus
14 (41)
55 (72) versus
9 (26)
(47) versus (29)
[107]
Terbinafine 1% solution
96 versus
versus vehicle twice-daily for 46
7 days
DB, R
1 week: 57
(59) versus 26
(56)
45 (47) versus
14 (30)
[108]
A) Terbinafine 1% solution
versus vehicle twice-daily for
1 week
B) Terbinafine 1% solution
versus vehicle once-daily for
1 week
[74]
192 versus DB, R

96
8 weeks: CC: 69/85

(81) versus 13/43 (31);
MC: 70/85 (82) versus
14/43 (32)
2 weeks:
108 (56) versus
34 (35)
MC at 8 weeks: 123
(64) versus 32 (33)
MC at 8 weeks: 25 (50)
versus 14 (28)
50 versus
50
Terbinafine 1% emulsion gel 31 versus

versus placebo gel once-daily 30
for 1 week
DB, R
Follow-up
1 week : 11/29 8 weeks: 21/28 (75)

(39) versus
versus 4/89 (14)
7/29 (24)
remained cured
CC: Clinical cure; DB: Double-blind; MC: Mycological cure; N: Sample number; R: Randomised.
Benzoyl peroxide was successfully used to treat PV as early

as 1977 [49]. A clearing of 100% was obtained with either 5 or
10% benzoyl peroxide gel after 3 weeks of treatment [49,50].
The vehicle for benzoyl peroxide, however, is propylene glycol, which has been reported to be effective in the treatment
of PV when used alone [51,52]. It is not certain whether the
beneficial effect of the benzoyl peroxide gel is in response to
the vehicle or the active agent.
Whitfields ointment consists of 3% salicylic acid and
6% benzoic acid in an emulsifying ointment [53]. It is a keratolytic agent and is effective against PV [53].
The combination of sulfur and salicylic acid has shown efficacy in PV management [54].
Zinc pyrithione 1% shampoo applied for 2 weeks is effective
in the treatment of PV [41,55]. Fredriksson et al. [55] showed that
zinc pyrithione shampoo base, which contains only regular surfactants without any known antifungal properties, does not
contribute to the curative effect of zinc pyrithione.
6.1.2
Specific topical antifungal agents
6.1.2.1 Azoles
The azole drugs have become an important class of treatment

for PV. This group of antifungal agents possesses a fungistatic,
rather than a fungicidal effect, and works by inhibiting the
biosynthesis of ergosterol, thus preventing the formation of
fungal cell membrane.
Ketoconazole was the first oral antifungal agent used to
successfully treat PV. Short-term (1- or 3-day) use of ketoconazole 2% shampoo has been demonstrated to be highly
effective in relieving the signs and symptoms of PV [56].
Ketoconazole 2% cream is effective when applied once-daily
for 2 weeks [57].
Bifonazole (Table 3) produces irreversible changes in
Malassezia yeasts as seen through the electron microscopy.
Bifonazole 1% cream, spray, solution, gel and powder are

effective in PV management [58-61]. In some patients a single
application may be sufficient for successful treatment [59,62].
Clotrimazole is a broad spectrum tritylimidazole derivative
that is effective against PV [63-65]. 1% clotrimazole cream
and 1% solution are effective and safe for the treatment of PV
[66].
Miconazole and econazole are two closely related synthetic
phenythyl imidazole derivatives. Miconazole nitrate is available in a 2% cream formulation. Econazole nitrate is available
as a 1% foaming solution, cream or shampoo. All of these formulations are effective against PV when used once-daily
[67,68].
Sertaconazole is a broad-spectrum antifungal agent. 1 or
2% sertaconazole cream applied twice-daily for 4 weeks is
effective against PV [69].
Fenticonazole is an imidazole derivative, with a wide spectrum of antimycotic and antibacterial activities. Fenticonazole
2% lotion has shown efficacy in the treatment of PV [58].
Tioconazole is a 1-substituted imidazole. Both the 1%
lotion and cream are effective treatments of PV [63,70].
Fluconazole, applied topically, is effective in PV management. 2% fluconazole shampoo was confirmed to be effective
when applied for 5 consecutive days [71].
6.1.2.2 Terbinafine
Terbinafine (Table 4) is a member of the fungicidal class of

allylamines. These drugs, as with the thiocarbamates, work by
inhibiting squalene epoxidation during sterol synthesis, thus
disrupting membrane synthesis in fungi [72]. Topical terbinafine is effective against PV [42,73,74]. It is available in 1% solution, emulsion, or cream formulations.
6.1.2.3 Ciclopiroxolamine
169
Table 5. Efficacy of other topical antifungal agents in the treatment of pityriasis versicolor.
Ref.
Treatment regimen
[69]
Study
design
MC (%)
1% versus 2% sertaconazole 11 versus

cream twice-daily for
10
4 weeks
DB, R
11 (100) versus 11 (100) versus 11 (100) versus 8 weeks: 100%

10 (100)
10 (100)
10 (100)
complete cure in
both groups
[109]
Econazole 1% foaming
solution, once-daily for
3 versus 6 days
Op
4 weeks:
39 (91) versus
46 (96)
[68]
Econazole nitrate 1% cream 67 versus

versus placebo once-daily for 59
2 3 weeks
DB, R
3 weeks:
53 (79) versus
37 (63)
[70]
Tioconazole 1% cream
65
Op
[64]
Clotrimazole 1% solution
22
Op
3 weeks:
22 (100)
22 (100)
[66]
A) Clotrimazole 1% solution
2 weeks
B) Clotrimazole 1% cream
2 weeks
116
versus
107
10 versus
8
DB, R
96 (83) versus
68 (64)
96 (83) versus
68 (64)
8 (80) versus
3 (38)
8 (80) versus
3 (38)
[110]
Clotrimazole 1% solution
versus vehicle twice-daily for
2 weeks
35 versus
33
DB
[71]
Fluconazole 2% shampoo
versus vehicle applied for
5 consecutive days
16 versus
16
DB, R
6 days: 12
(75%) versus 0
[57]
Ketoconazole 2% cream
51 versus
versus placebo once-daily for 50
11 22 days (mean 14 days)
DB, R
43 (84) versus
11 (22)
34 (67) versus
11 (22)
[56]
A) Ketoconazole 2%
103
shampoo once on day 1 plus
placebo once-daily for next
2 days
B) Ketoconazole 2%
106
shampoo once-daily for
3 days
C) Placebo once-daily for
103
3 days
DB, R
31 days:
79 (78)
31 days:
71 (69)
89 (84)
77 (73)
11 (11)
5 (5)
[111]
Ciclopirox 1% cream versus

vehicle twice-daily for
2 weeks
73 versus
72
[76]
Ciclopiroxolamine 0.1%
solution for 4 8 weeks
[112]
Isoconazole 1% cream
twice-daily for 3 8 weeks
43 versus
48
CC (%)
4 weeks:
41 (95) versus
46 (96)
Complete
cure (%)
Follow-up
4 weeks:
39 (91) versus
46 (96)
53 (81.5)
1 year: 3/9 (33)
relapsed
2 weeks: 30 (86)
versus 17 (52)
2 weeks: 13 (81%)
versus 0 cured
43 (84) versus
5 (10)
Ketoconazole group
cure rates: 1 year:
42/51 (82)
2 years: 16/51 (33)
DB, R
36 (49) versus
17 (24)
2 weeks: 37/61 (61)

versus 17/62 (27)
remained cured
90
Op
4 weeks:
67 (74);
8 weeks:
77 (86)
24
Op
23 (96)
6 weeks:
3 (12) relapsed
This hydroxy-pyridone interferes with the uptake and accumulation of products required for cell membrane synthesis.
The effectiveness of ciclopirox olamine has been supported in
a number of studies (Table 5) [75,76].
170
6.2 Oral
treatments
Most recently, oral treatments have been developed. The advantages of oral medications include increased patient compliance,
due to the fact that these treatments are more convenient than
Table 6. Studies comparing systemic antifungal agents in the treatment of pityriasis versicolor.
Ref. Treatment regimen
Study design MC (%)
CC (%)
Follow-up
[89]
Fluconazole 300 mg/week single dose

for 2 weeks versus ketoconazole
400 mg/week single dose for 2 weeks
50 versus DB, R
50
2 weeks: 30 (60)
versus 28 (56);
8 weeks: 45 (90)
versus 44 (88)
[86]
A) Ketoconazole 400 mg single dose
45
24 (53)
30 (67)
B) Ketoconazole 200 mg/day for

10 days
C) Fluconazole 400 mg single dose
D) Fluconazole 150 mg/week for
4 weeks
45
33 (73)
33 (73)
12 months: 6/24 (2)

relapsed
1/33 (3.5) relapsed
45
45
37 (82)
29 (64)
36 (80)
27 (60)
0 relapsed
2/29 (6.9) relapsed
[87]
A) Fluconazole 450 mg single dose

B) Fluconazole 300 mg/week for
2 weeks
C) Itraconazole 200 mg/day for 7 days
30
30
30
1 month: 21
(70)
29 (97)
24 (80)
18 (60)
23 (77)
22 (73)
2 months: 6 (21) relapsed

5 (17) relapsed
2 (7) relapsed
[88]
Fluconazole 400 mg versus

Itraconazole 400 mg
20 versus Op, R
20
[131]
Fluconazole 600 mg/day versus

Itraconazole 400 mg/day for 15 days
27 versus Op
25
Op, R
Op, R
12 weeks: 41 (82) versus

39 (78) remained MC;
no significant difference
between treatment groups
8 weeks: 13 (65) 4 (20) versus

versus 4 (20)
1 (5)
7 (35) versus 12 (60)

relapsed
22 (80) versus 12 weeks: 4 (14) versus

19 (74)
5 (20) relapsed
Table 7. Efficacy of systemic ketoconazole in the treatment of pityriasis versicolor.

Ref.
Treatment regimen
Study MC (%)
design
[77]
200 mg/day versus

placebo for 14 days
10 versus DB, R
10
[79]
A. 400 mg single dose

107
B. 400 mg/day for 2 days 164
C. 400 mg/day for 2 days 281
followed by 400 mg every
2 weeks for 3 months
CC (%)
Complete
cure (%)
Follow-up
9 (100) versus
2 (20)
Op
57 (70)
134 (82)
273 (97)
[116] 200 mg/day versus

placebo for 28 days
34 versus DB, R
32
[117] 200 mg/day for 28 days
90
Op
84 (93), 6
cleared after
extra 14 day
treatment
3 months: 8 (9) relapsed
[118] 400 mg single dose to

200-400 mg/day for 28
days
82
Op
78 (95)
6 (7) relapsed
DB, R
10 (83)
9 (75)
8 (67)
Cure rates at 10 weeks: 7/9 (78)

8/10 (80)
9/10 (90)
[78]
A. 200 mg/day for 5 days 12

C. 200 mg/day for 25 days 12
[93]
34 (100)
33 (97) versus
versus 3 (9) 0
6 months: 51/107 (48) relapsed

6 months: 49/164 (30) relapsed
6 months: 16/273 (5.7) relapsed
60
Op
3 months: 55
(92)
3 months:
57 (95)
A. 200 mg/day for 21 days 32

Op
3 weeks: 26
(81)
5 weeks: 32
(100)
26 (81)
32 (100)
1 year: 12/33 (36) versus 24/32

relapsed
2 years: 24 (40) remained CC,

20 (33) remained MC and
36 (60) relapsed
[120] 400 mg single dose versus 60 versus Op, R

200 mg/day for 10 days
60
25 (42) versus
31 (51)
1 month: no significant
difference between two groups
6 (30)
4 weeks: MC: 17 (85)
20
Op
171
Table 8. Efficacy of systemic itraconazole in the treatment of pityriasis versicolor.

Ref.
Treatment regimen
Study MC (%)
design
[122]

versus 100 mg/day for
10 days
15 versus Op, R
15
0 versus 2
13 (87) versus
12 (80)
3 months: all patients

remained clear of PV
[96]

versus 7 days
13 versus Op, R
15
10 (77) versus
13 (87)
3 (23) versus 2 (13) 10 (77)

versus
13 (87)
3 months: 1 patient in
second group remained
cured
[83]
20
Op
20 (100)
20 (100)
20 (100)
40 weeks: 19 (95)
completely cured
[123]
A) 50 mg/day for 14 days

B) 100 mg/day for 5 days
C) 100 mg/day for 10 days
D) 100 mg/day for 15 days
E) 200 mg/day for 5 days
17
12
12
12
20
Op
8 (47)
7 (58)
7 (58)
12 (100)
14 (70)
2 months: 2/18 patients

available for follow-up
relapsed. Both patients
were from group A
[124]

versus 100 mg/day,
twice-daily for 5 days
15 versus Op
15
100% in both
groups
100% in both
groups
100% in
both groups
2 weeks:
hyperpigmentation
disappeared. No relapse
[125]
200 mg/day versus

22 versus Op, R
20
21 (95) versus
15 (75)
22 (100) versus
18 (90)
[126]
100 mg twice-daily versus

100 mg/day
24 versus Op
23
4 weeks: 23 (96) 10 (42) versus

versus 23 (100) 14 (61)
[127]
50 mg/day versus
100 mg/day for maximum
of 4 weeks
14 versus Op, R
13
5 (36) versus 8
(62)
11 (79) versus
13 (100)
[128]
100 mg/day for 2 weeks

versus placebo
17 versus DB
16
11/15 (73)
versus 0
10/15 (67) versus

1/14
[97]

versus placebo
18 versus DB, R
17
[129]

versus placebo
8 versus
5
[85]
400 mg (single dose)

versus 200 mg/day for
7 days
24 versus Op, R
26
DB
CC (%)
Complete
cure (%)
Follow-up
4 weeks: none regained

original colour
All patients that were

not cured after 2 weeks
received additional 2
weeks treatment; 100%
were cured
5 weeks:
12 (67)
versus 2 (12)
7 (88) versus 0
20 (83) versus
23 (88)
18 (75) versus
21 (81)
6 weeks: (see MC and

CC). Two regimens are
equally effective
topical therapies. Not only are they less time-consuming for the
patient, but the length of the treatment is often much shorter
compared to topical medications (Table 6).
Terbinafine, administered orally, has been shown to be ineffective in treating PV as fungicidal levels are not attained in
the stratum corneum [42].
Ketoconazole 200 mg/day for 5, 10 and 28 days is effective
in the treatment of PV (Table 7) [57,77,78]. Another option is
the use of a single dose of 400 or 200 mg administered on
three occasions 12 h apart [79]. As ketoconazole is excreted in
eccrine sweat, it is recommended that the patient work up a
sweat following ingestion of ketoconazole. This aids in the
172
delivery of the drug to the skin. Ketoconazole is generally

well-tolerated with minimal side effects.
Itraconazole (Table 8), a triazole derivative with strong
keratophilic and lipophilic properties [80], has been shown to
be highly active in vitro against a wide range of fungi including Malassezia spp. [81,82]. In vitro studies with Candida spp.
suggest that itraconazole inhibits the morphogenetic transformation from yeast cells into mycelium, resulting in
abnormalities of the yeast cell wall with an increase in cell volume and defective cell division. This action is due in part to
the accumulation of C-14 methylated sterols which disturb
membrane properties and cell growth [83].
Cauwenbergh et al. [84] reported that the minimal total

dose of itraconazole required for mycological response in PV
is 1000 mg, and that treatment for < 5 days is not adequate.
The authors further observed that the time of assessment was
critical in determining the outcome of treatment. If the assess-
ment of desquamation or scaling was made at the end of a

short course of therapy, the outcome was rather poor; however, 3 4 weeks after therapy, the clinical picture was much
better. The results of mycological assessment were similar at
all assessment times [84]. Kose et al. [85] showed that a single
Table 9. Efficacy of systemic fluconazole in the treatment of pityriasis versicolor.

Ref.
Treatment regimen
Study design
MC (%)
CC (%)
Follow-up
[130]
Single dose 400 mg
23
Op
3 weeks: 14 (61)
17 (74)
6 weeks: 5 (22) remained

mycologically cured
[90]
A) 150 mg/week for 4 weeks

207
B) 300 mg/week for 4 weeks
190
C) 300 mg/2 weeks for 4 weeks 206
Op, R
161 (78)
177 (93)
179 (87)
CC: Clinical cure; MC: Mycological cure; N: Sample number; Op: Open; R: Randomised.
Table 10. Studies comparing oral and topical antifungal agents in the treatment of pityriasis versicolor.
Ref
Treatment regimen
Study design
MC (%)
CC (%)
[132]
Itraconazole 200 mg/day for 5 days versus

selenium sulfide 2.5% shampoo once-daily
for 7 days
20 versus 20
Op, R
3 weeks: 13 (65)
versus 20 (100)
17 (85) versus 16
(80)
CC: Clinical cure; MC: Mycological cure; N: Sample number; Op: Open; R: Randomised.
dose of itraconazole 400 mg/day was as effective as itraconazole 200 mg/day for 7 days in the treatment of PV. These
data, however, need to be confirmed by further investigation.
Fluconazole (Table 9) taken orally is effective in PV management. The drug is effective at various doses: single dose
fluconazole 400 mg/week [86-88]; 300 mg/week for 2 [87,89] or
4 [90] weeks; 300 mg every 2 weeks for 4 weeks [90]; or
150 mg/week for 4 weeks [86].
6.3 Prophylactic
treatment of pityriasis versicolor

PV has a tendency to recur following treatment. The recurrence rate is variable, ranging from 60 to 90% within
2 years [91]. An appropriate prophylactic treatment to prevent
recurrence of PV that is safe and effective is an important consideration. Faergemann et al. [92] conducted a trial in which
following open treatment with itraconazole 200 mg/day for
7 days, patients entered a double-blind, placebo-controlled,
6-month prophylactic phase. In the itraconazole treated group
(400 mg/month) the mycological cure was 88% (90 of 102)
compared with 57% (56 of 99) of patients in the placebo
group (p < 0.001) [92]. The authors suggested that prophylactic treatment should be administered to patients who present
with frequent recurrences.
Ketoconazole may also be considered in the prophylaxis
against PV. In a placebo-controlled study, Faergemann et al.
[93] treated 15 patients with ketoconazole 200 mg/day on
3 consecutive days every month. Only 1 of 15 (7%) patients
treated with ketoconazole relapsed, compared with 7 (47%)
patients receiving placebo [93]. Ketoconazole 400 mg/month
may also be an effective prophylaxis against PV [94].
7. Conclusion
PV is a chronic and recurrent disorder, and repetitive treatment courses are often necessary. Exogenous and endogenous predisposing factors are probably of major importance
for the disease and its recurrence. A wide range of antifungal
agents are effective in the treatment of PV. In a broad sense,
all these medications are at least transiently effective if used
appropriately. Some of the agents are far more effective in
producing prolonged cures. Spontaneous cure of PV is not
common, and the disease will persist for many years if left
untreated.
8. Expert
opinion
Because of the lipophilic nature of Malassezia spp., patients

with PV should be instructed to avoid applying oils to the
skin. Recurrence of the disease is of major concern, and prophylactic therapy may often be beneficial. Fungal remnants
may last months to years, allowing the continued spread of
infection. Fungal infection treated in one area may recur in a
different area of the body because of the ability of the organism to travel [95]. Failure to recognise a fungal aetiology early
may result in a more extensive infection that is more difficult
to treat.
An ideal topical drug should be one that is effective, easy
to apply all over the body, requires therapy of short duration,
is free from adverse effects, and is inexpensive. Topical therapies require a well-motivated and compliant patient for success. Systemic therapies could be considered an alternative
(Table 10), especially if the disease is widespread, recurrent, if
173
the patient is immunocompromised, or following failure or

non-compliance with topical therapies. The oral regimens
preferred by the authors include: itraconazole 200 mg daily
for 7 days (a total of 1400 mg) [85,96,97]; ketoconazole 200 mg
repeated 3 times 12 h apart (a total of 600 mg) [79]; or
interactions. Such interactions may

occur because different agents tend to
use common systems for their absorption, metabolism and secretion [98-101].
When problems do arise, they can
often be overcome or minimised by
varying the dosage regimens, or by
drug monitoring [101]. Treatment
selection must be based on the patients
age, medical condition, length of therapy and likelihood of compliance,
potential drug interactions, cost of
therapy, and patient and physician
preferences.
More concerted efforts to educate
patients and physicians may aid in
faster recognition and appropriate treatment of PV.
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Affiliation
Aditya K Gupta MD, PhD, FRCP1,2,3,

Nataly Kogan MSc2 & Roma Batra PhD2
Address for correspondence
1University of Toronto, and the Sunnybrook and
Womens College Health Sciences Center
(Sunnybrook site), Toronto, Ontario, Canada
2Mediprobe Research, Inc., London, Ontario,
Canada
3645 Windermere Road, London, Ontario,
N5X 2P1, Canada
Tel: +1 519 657 4222;
Fax: +1 519 657 4233;
E-mail: agupta@execulink.com

Pityriasis Versicolor A Review of Pharmacological Treatment Options

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Expert Opinion on Pharmacotherapy

ISSN: 1465-6566 (Print) 1744-7666 (Online) Journal homepage: http://www.tandfonline.com/loi/ieop20

Pityriasis versicolor: a review of pharmacological

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Pityriasis versicolor: a review of

Windermere Road, London, Ontario, N5X 2P1, Canada

Pityriasis versicolor is a common disorder of the skin, which is characterised by

Pityriasis versicolor (PV) is a benign cutaneous disorder, usually asymptomatic,

For reprint orders, please

10.1517/14656566.6.2.165 2005 Ashley Publications Ltd ISSN 1465-6566

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Pityriasis versicolor: a review of pharmacological treatment options

patients with PV [16], some have shown antibody titres to be

and clinical appearance of

In the case of hypopigmentation, the mechanism is not

The stratum corneum in PV patients is replete with hyphae

Expert Opin. Pharmacother. (2005) 6(2)

Gupta, Kogan & Batra

Downloaded by [Colorado State University] at 22:32 23 February 2016

Table 1. Studies comparing topical agents in the treatment of pityriasis versicolor.

Bifonazole 2% lotion versus

Bifonazole solution once-daily

Bifonazole 1% solution versus

Flutrimazole 1% cream versus

Tioconazole 1% lotion versus

16 (100) versus 16 (100) versus 16 (100) versus CC at 8 weeks:

Tioconazole base 1% versus

Clotrimazole 1% cream versus

Econazole nitrate 1% cream

Oxiconazole 1% cream versus

Terbinafine 1% cream versus

Ciclopirox olamine 1% cream

3 & 9 weeks: all

166 (73) versus

reducing the cost compared with a traditional long-term

Expert Opin. Pharmacother. (2005) 6(2)

Pityriasis versicolor: a review of pharmacological treatment options

Downloaded by [Colorado State University] at 22:32 23 February 2016

Zinc pyrithione 1% shampoo once-daily

Zinc pyrithione 1% shampoo versus

Propylene glycol 50% twice-daily for

A. Selenium sulfide 2.5% lotion

2.5% selenium disulfide suspension

Table 3. Efficacy of topical bifonazole in the treatment of pityriasis versicolor.

1% cream versus vehicle

1% cream once-daily for

32 (100) versus 30 (94) versus

1% gel once-daily for 2 weeks 121

A) 1% solution applied once

A) 2.5% cream: once on

A) 1% spray applied on day 1 30

1 year: all reported

Nonspecific topical antifungal agents

Expert Opin. Pharmacother. (2005) 6(2)

Gupta, Kogan & Batra

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