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REVIEW ARTICLE

Pityriasis Rosea: An Update on Etiopathogenesis and Management of

Difficult Aspects
Khushbu Mahajan, Vineet Relhan1, Aditi Kochhar Relhan2, Vijay Kumar Garg1

Abstract From the Department of

Pityriasis rosea (PR) is a benign papulosquamous disorder seen commonly in clinical practice. Dermatology, North Delhi Municipal
Despite its prevalence and benign nature, there are still times when this common disorder Corporation Medical College,
Hindu Rao Hospital, 1Maulana
presents in an uncommon way or course posing diagnostic or management problems for the
Azad Medical College, 2South Delhi
treating physician. The etiopathogenesis of PR has always been a dilemma, and extensive MCD Hospital, New Delhi, India
research is going on to elicit the exact cause. This review focuses mainly on the difficult
aspects of this benign common disorder such as etiopathogenesis, atypical manifestations,
recurrent cases, differential diagnosis, therapy and pregnancy considerations. Although we Address for correspondence:
could not find a black and white solution to all these problems, we have tried to compile the Dr. Vineet Relhan,
related literature to draw out some conclusions. Maulana Azad Medical
College, New Delhi, India.
Key Words: Acyclovir, human herpesvirus‑6, 7, pityriasis rosea E‑mail: vineetrelhan@gmail.com

What was known?

• Pityriasis rosea (PR) probably has an infective etiology
• Drugs such as erythromycin and acyclovir have been tried although symptomatic management remains the best for most patients
• Secondary syphilis and dermatophytosis form an important differential diagnoses in cases of PR.

Introduction cases, the eruption improves in 2–8 weeks/time. Familial

Pityriasis rosea (PR) is a papulosquamous disorder first
described by  Robert Willan in 1798 but under another
terminology.[1] Subsequently, various names have been
given to this disorder such as pityriasis circinata, roseola
annulata, and herpes tonsurans maculosus.[2]
It typically starts with the development of a large
erythematous scaly plaque also called the herald patch
or mother patch on trunk or neck, which is followed by
an eruption of multiple secondary small erythematous
scaly lesions located predominantly on the trunk and
following the lines of cleavage on the back (Christmas
tree or inverted fir tree appearance). Collarette scaling
is seen typically. The eruption is usually preceded by
a prodrome of sore throat, gastrointestinal disturbance,
fever, and arthralgia. However, since the prodrome may
be mild and the eruption may occur sometime after the
prodrome, the patient may not give a proper history
unless elicited. The approximate incidence of PR is
0.5–2% and affects people of both sexes in 15–30 years
age group although also seen commonly in elderly and
children.[2] The disease is self‑limiting and in most
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clustering has been reported, and the disease is more
frequent in winters.
PR is a common condition easily diagnosed and managed
by most dermatologists; however, there are certain
difficult aspects or less common aspects which are faced
in everyday practice. This review has tried to focus
mainly on these aspects and also tried to compile the
relevant literature to the best possible extent. Instead of
going into detail about the known facts of the disease,
we will just focus on these aspects under various
headings.
Etiopathogenesis of Pityriasis Rosea
Numerous hypotheses have been postulated about the
exact cause of PR, incriminating both infective agents
such as viruses, bacteria, spirochetes, and noninfective
etiologies such as atopy and autoimmunity.
There are various factors which have pointed toward an
infectious etiology for this condition such as seasonal
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others to remix, tweak, and build upon the work non‑commercially, as long as the
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Website: www.e‑ijd.org For reprints contact: reprints@medknow.com

How to cite this article: Mahajan K, Relhan V, Relhan AK, Garg VK.
Pityriasis rosea: An update on etiopathogenesis and management of
DOI: 10.4103/0019-5154.185699 difficult aspects. Indian J Dermatol 2016;61:375-84.
Received: March, 2015. Accepted: January, 2016.

© 2016 Indian Journal of Dermatology | Published by Wolters Kluwer - Medknow 375

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Mahajan, et al.: Pityriasis rosea update
variations, presence of a prodrome, familial clustering
in some cases and presence of herald patch (which may
be correlated with the inoculation point of organism)
followed by the secondary eruption and infrequent
recurrences. However, despite repeated efforts, there is
no definite evidence for a single infectious agent for
this disorder. Search for this agent led to evaluation
of a number of organisms in this disorder such as
cytomegalovirus (CMV), Epstein–Barr virus, parvovirus
B19, picornavirus, influenza and parainfluenza viruses,
Legionella spp., Mycoplasma spp., and Chlamydia spp.
infections; however, evidence exists that PR is not
associated with them.[3]
There are few reports evaluating the role of streptococcus
in PR based on premise that PR is usually preceded
by an upper respiratory tract infection. Sharma et  al.
found raised ASLO titers in 37.7% of their patients
and a positive therapeutic effect of erythromycin in
the treatment of PR, thus suggesting the involvement
of streptococcus in PR.[4] However, Parija and Thappa in
a study of 20 cases and controls found that C‑reactive
protein was negative in all patients, ASLO titers were
raised in only two patients, streptococcus hemolyticus
could be isolated on throat swab in only two patients,
and the results were not statistically significant
when compared to controls, thus refuting the role of
streptococcus in PR.[5]
Recently, there is an increasing evidence to suggest the
role of human herpes virus (HHV) in PR. In 1997, Drago
et al. first suggested the role of HHV 7 in etiology of PR
by detecting HHV 7 in peripheral blood mononuclear cells
and plasma of patients with PR and not in controls, thus
suggesting a probable causal relationship.[6] Subsequent
studies however could not find any association between
HHV 7 and PR.[7,8] Yasukawa et  al. showed a causal link
of HHV 6 and PR.[9] Watanabe et  al. performed nested
polymerase chain reaction (PCR) to detect HHV 6,
HHV 7, and CMV DNA in 14 PR patients and found that
HHV 7 DNA was present in lesional skin (93%),
nonlesional skin (86%), saliva (100%), peripheral blood
mononuclear cells (83%), and serum (100%) samples,
whereas HHV 6 DNA was detected in lesional skin (86%),
nonlesional skin (79%), saliva (80%), peripheral blood
mononuclear cells (83%), and serum (88%) samples. By
contrast, CMV DNA was not detected in these tissues.
Control samples from 12 healthy volunteers and 10
psoriasis patients demonstrated rare positivity for either
HHV 7 or HHV 6 DNA in the skin or serum. The results
indicated that HHV 6 and 7 are both responsible for
systemic active infection in a case of PR, and CMV has
no role. Authors also postulated that since the virus
was detected in saliva, patients were experiencing a
reactivation rather than a primary infection since salivary
glands act as a reservoir only in previously infected
individuals. Furthermore, the low levels of these viruses in
Indian Journal of Dermatology 2016; 61(4)
lesional skin led to the hypothesis that these viruses do
not infect skin cells directly, and PR is actually a result of
a reactive response to systemic viral replication. Authors
also postulated that the previous negative studies may
be because they did not use nested PCR and/or extracted
DNA from formalin‑fixed paraffin‑embedded tissue.[10]
Another study by Drago et  al. found herpes virus‑like
particles in PR lesional skin, thus further supporting
the role of HHV 6 and 7 in the pathogenesis of PR.[11]
Broccolo et  al. further provided additional evidence
by developing a calibrated quantitative real‑time PCR
and detecting cell‑free HHV 6 and 7 in 16 and 39% of
patients, with negative results in healthy controls and
patients with other inflammatory diseases.[12] They also
suggested like previous studies that the disease is a
result of reactivation rather than primary infection.
These studies also pointed toward the fact that HHV 7
reactivation might cause reactivation of HHV 6 however
vice versa is not true. The role of HHV 8 has also been
studied with both positive[13] and negative results.[14]
In light of the above studies, HHV 6 and 7 are the most
likely etiologic agents for PR and further studies should
be targeted toward establishing their definite role.
Atypical Variants of Pityriasis Rosea
Atypical manifestations of PR are commonly seen in
dermatological practice, and it should be remembered
that most of these variants are atypical in morphology
and not in prognosis, and thus a high sense of clinical
suspicion is needed to avoid overtreating a patient.
However, it is also important not to ascribe any unusual
or atypical skin eruption to atypical PR unless other
dermatoses have been excluded. The incidence of atypical
PR is 20%.[15] The atypicality may be in morphology, size,
distribution, course, or symptoms.[2] Some authors believe
that children are more predisposed to atypical variants
than adults with atopy playing a facultative role.[16]
The various atypical morphologies described in literature
are discussed below:
• Vesicular: It presents as a generalized eruption of
2–6 mm vesicles or as a rosette of vesicles. It may be
severely pruritic, is most commonly seen in children
and young people, and may affect the head, palms,
and soles. It needs to be differentiated from varicella
and dyshidrosis[17]
• Purpuric (hemorrhagic) PR presents as macular purpura
on skin and sometimes over the oral mucosa[18]
• Urticarial PR  (PR urticata) presents with lesions
similar to urticarial wheals often accompanied by
intense pruritus[19]
• Generalized papular PR is a rare form of the disorder
that is more common in young children, pregnant
women, and Afro‑Caribbeans. It presents as multiple
small 1–2 mm papules which may occur along with
classic patches and plaques[20]
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Mahajan, et al.: Pityriasis rosea update
• Lichenoid lesions can be observed in the course of
atypical PR but is more commonly caused by drugs
such as gold, captopril, barbiturates, D‑penicillamine,
and clonidine[21]
• Erythema multiforme (EM)‑like PR: They present with
targetoid lesions along with the classical lesions of
PR. An associated herpetic or dermatophytic infection
should be ruled out in such cases. Histopathologically,
EM and PR may show similar features except satellite
cell necrosis which is a distinguishing feature seen
only in EM where lymphocytes are seen attached to
scattered necrotic keratinocytes[21]
• Follicular: The secondary lesions here are typically
follicular and present in groups or isolated fashion;
however, associated classical lesions may also be present
in the same patient.[16] Differential diagnoses such as
follicular lichen planus, keratosis pilaris and atopic
dermatitis with a follicular element should be excluded
• Giant: Gigantic PR is rarely reported in the literature
and was named after Darier. It consists of plaques
and circles of very large size ranging from 5 cm to
7 cm wherein the individual lesions may reach the
size of the palm of the patient[22]
• Exfoliative dermatitis
• Atypical herald patch: Herald patch may be absent in
20% of patients or present with secondary eruptions
or may occur at unusual sites such as face, scalp,
genitalia, or other sites
• Sometimes, the two atypical variants may coexist
in the same patient as reported by Sinha et  al.,
where a 16‑year‑old girl presented with two atypical
morphological variants‑generalized papular and
EM‑like.[23]
The lesions may present in atypical site or distribution
as described:
• Inverse: Here, the lesions are predominantly present
in acral and flexural areas involving axilla, groin, and
face[24]
• Acral: Polat reported a 14‑year‑old male patient
who had a palmar herald patch with truncal lesions
of PR.[25] Zawar described an infant with the acral
distribution of both primary and secondary lesions
where classical annular scaly lesions were located on
wrists, palms, lower legs, feet, and sole with sparing
of trunk and proximal parts of limbs.[26] In such
patients, EM, syphilis, necrolytic acral erythema, and
drug eruptions should be excluded
• Unilateral: This is an extremely rare variant reported
in both children and adult where the lesions were
located on one side of body and patient had herald
patch with classical secondary lesions[27,28]
• Blaschkoid pattern: Here, the lesions follow the
Blaschko’s line[29]
• Limb‑girdle: Also known as PR of Vidal; here, the
eruption is limited to shoulders or pelvic girdle, thus
377
involving axilla and groins. Lesions are usually larger
and more annular[2]
• Oral mucosa: It may be involved in 16% of patients,
and the lesions may be punctuate, erosive, bullous,
or hemorrhagic but are usually asymptomatic in
nature[2]
• Localized: Here, the eruptions are localized to
one part of the body. Ahmed and Charles‑Holmes
reported a 44‑year‑old woman with an acute onset
of a localized eruption on her left breast whose
morphology was similar to PR.[30] Zawar reported a
case of a child who presented with the onset of PR
in scalp, clinically mimicking pityriasis amiantacea.[31]
Atypical symptoms
Pruritus may or may not be present in a patient. PR
irritate is a variant in which patient presents with
extreme itching, especially on contact with sweat and
thus has multiple excoriations over the body.[15]
Pityriasis rosea in dark‑skinned
Dark‑skinned individuals have been shown to have
certain atypical features such as face may be involved
frequently, papular lesions are more common, eruption
tends to be more itchy, and subsequent postinflammatory
hyperpigmentation is frequent.[32]
In most of the atypical presentations above, there were
some clinical pointers to the disease such as presence
of prodrome, occurrence of a primary lesion followed by
secondary lesion and in most cases, coexistent classical
lesions were also present. Thus, a clinician should always
look for these signs to make a diagnosis of PR in atypical
cases. In most cases, histopathology is usually needed to
rule out other simulating disorders.
These atypical variants may not fulfill the diagnostic
criteria (discussed below) completely, but it should be
understood that since most patients do not need specific
treatment modalities, a good clinical acumen to rule out
the differentials, and identify a case of atypical PR is
more important than to put a case of atypical PR to the
test of a diagnostic criterion.
Pityriasis Rosea and Vaccination
PR like eruptions has been reported after vaccinations
such as Bacillus Calmette–Guerin, influenza, H1N1,
diphtheria, smallpox, hepatitis B and pneumococcus.[2,33,34]
Papakostas et al. postulated that vaccine‑induced PR may
be a result of reactivation of HHV virus secondary to
immune stimulation by the vaccine or due to molecular
mimicry with a viral epitope triggering a T‑cell mediated
response.[34]
Recurrent Pityriasis Rosea
Recurrences of PR are believed to be rare and studies
have reported the second episode in 1–3% of
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patients.[35,36] Multiple recurrences (>2) are considered a
very rare presentation of this very common condition.
However, there are case reports of patients with more
than two episodes, with a maximum of five episodes
reported so far in the literature.[19,35‑41] The exact etiology
is not known but it is postulated that like other HHV
viruses (varicella zoster virus and Epstein-Barr virus)
which are associated with reactivation; reactivation of
HHV6 and 7 (postulated in etiopathogenesis of PR) may
be responsible for recurrent episodes.[40]
On literature review of these recurrent cases, it can
be concluded that recurrences present in a varied
fashion, i.e., the eruption may or may not be similar
in morphology, severity, and distribution to the first
episode; herald patch may be absent or present at a
different site; there is no seasonal predominance, no
particular age group or sex that gets affected, and the
time interval between the episodes is variable.
Thus, the incidence of recurrent PR may just be an
underestimation of the actual incidence as the cases
may be seen by different physicians at different times or
due to the benign nature of the condition, patient may
not visit the physician or may not give a proper history
of recurrence.
However, we suggest that following things should always
be kept in mind before labeling a patient as a case of
recurrent PR:
• Venereal disease research laboratory (VDRL) should be
performed to rule out secondary syphilis
• KOH should be performed to rule out dermatophytosis
• Ideally, a biopsy should be taken to rule out other
conditions that may mimic PR and present with
recurrences such as guttate psoriasis, pityriasis
lichenoides chronica (PLC), erythema annulare
centrifugum, and nummular eczema. Eslick reported
a patient who presented with a skin condition which
was initially diagnosed as PR; however, due to the
persistence and change in appearance of the lesions,
the diagnosis was later altered to guttate psoriasis[42]
• Drug‑induced PR like rashes may be an important
cause of recurrent PR, and thus, a proper history
of drug intake must be elicited as some of the
very commonly used drugs such as omeprazole and
nonsteroidal anti‑inflammatory drugs are implicated
in causing drug‑induced PR. A detailed list of
drugs causing PR is tabulated below [Table 1].[2,43]
Clinically, drug‑induced PR may not present with
herald patch or typical collarette of scale and does
not resolve completely until the drug is withdrawn.
Histologically, these show interface dermatitis with
eosinophils.
Zawar reported a patient with recurrent PR like
eruptions secondary to mustard oil application.[44] This
patient was initially diagnosed as recurrent PR, but after
Indian Journal of Dermatology 2016; 61(4)
Table 1: Drugs responsible for pityriasis
rosea‑like eruptions
Medications reported as responsible of PR‑like eruptions
ACE‑inhibitors Arsenic compounds
NSAIDs Barbiturates
Omeprazole Bismuth
Metronidazole Beta‑blockers
Isotretinoin Clonidine
Gold salts Griseofulvin
Imatinib mesylate Meprobamate
Interferon Penicillin
Vaccine
ACE: Angiotensin‑converting‑enzyme, NSAIDs: Nonsteroidal
anti‑inflammatory drugs, PR: Pityriasis rosea
patch testing and on proper history, it was realized that
instead of atypical PR, it was just a case of contact
reaction to mustard oil, thus further stressing the role of
proper history of drugs or some chemical use in a case
of recurrent PR.
Diagnosis, Differential Diagnosis, and
Relevant Investigations in a Case of
Pityriasis Rosea
A case of PR is diagnosed mainly on clinical grounds.
Chuh[45] proposed diagnostic criteria for PR [Table 2].
Zawar and Chuh studied its acceptability and validity
in Indian population and found it to be 100% specific
and sensitive thus establishing its validity in Indian
population.[46]
However, although the criteria have been verified
in Indian population, its validity in atypical cases
still needs to be established as most of the atypical
presentations described in literature may not strictly
comply with the diagnostic criteria given by Zawar et al.
Histopathology
A biopsy is needed in atypical cases, and it mainly helps
in excluding other differentials rather than diagnosing
PR as the histopathological examination in a case of
PR is relatively nonspecific and resembles a subacute
or chronic dermatitis. Epidermal changes include focal
parakeratosis, diminished granular layer, and spongiosis.
Small spongiotic vesicles, although infrequently seen,
are a characteristic feature. Papillary dermis shows
edema with mild perivascular lymphohistiocytic
infiltrate. Exocytosis of infiltrate into epidermis may
be seen. Studies have revealed that dyskeratotic cells
in the epidermis and extravasated erythrocytes in the
dermis are characteristic histopathological findings
in a case of PR and are seen in approximately 60% of
patients.[2,21,47,48] Herald patch shows less spongiosis, more
hyperplasia, and both superficial and deep perivascular
infiltration.
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Table 2: Diagnostic criteria of pityriasis rosea

A patient is diagnosed as having PR if
On at least one occasion or clinical encounter, he/she has all the essential clinical features and at least one of the optional clinical
features, and
On all occasions or clinical encounters related to rash, he/she does not have any of the exclusional clinical features
Essential clinical features Optional clinical features (at least one to be present) Exclusional clinical features
Discrete circular or oval lesions Truncal and proximal limb distribution, with <10% of Multiple small vesicles at the
Scaling on most lesions lesions distal to mid upper arm or mid‑thigh center of two or more lesions
Peripheral collarette scaling Orientation of most lesions along the direction of ribs Most lesions on palmar or
with central clearance on at A heral patch (not necessarily largest) appearing at plantar skin surfaces
least two occasions least 2 days before the generalized eruption Clinical or serological
evidence of secondary syphilis
PR: Pityriasis rosea

There are numerous conditions which need to be
excluded while diagnosing a case of PR and have been
discussed below:
• Secondary syphilis: This is important, especially
in sexually active adults. A detailed sexual history
followed by examination to look for signs of healed
chancre, lymphadenopathy, mucosal lesions, and
lesions on palms and soles should be done. Patient
should be subjected to a VDRL testing or any of the
specific or nonspecific treponemal tests available for
confirmation. Histopathology will show the presence
of plasma cells in a case of secondary syphilis
• Dermatophytosis: The herald patch may mimic tinea
corporis, and thus, a KOH examination should be
performed
• Guttate psoriasis: It presents as scaly erythematous
plaques and can be differentiated by the lack of
herald patch, typical rain drop appearance of lesions
rather than Christmas tree appearance, the presence
of Auspitz sign and finally a biopsy
• Pityriasis lichenoides chronica: The secondary lesions
of PR might be confused with PLC, however, in a
case of PLC, the herald patch is absent, and course
of diseases is prolonged and may last from months to
years. Thus, it is an important differential in a case
of PR which does not resolute
• Subacute cutaneous lupus erythematosus  (SCLE): It
can be differentiated by history of photosensitivity,
other signs of LE, photodistribution of lesions, and
histopathology, which in case of SCLE will show
epidermal atrophy and basal vacuolar change
• Nummular eczema: The lesions do not show a
predominance for trunk, are itchy, may show oozing,
and respond rapidly to topical steroids
• Cutaneous T‑cell lymphoma: Initial patch stage
shows predominance for trunk, is mildly pruritic,
and does not respond to topical steroids, thus closely
mimicking PR. Multiple serial biopsies are needed for
final diagnosis.
Other rare differentials that might need to be excluded
are lichen planus, erythema annulare centrifugum,
379
pityriasis versicolor, pigmentary purpuric dermatoses
(in case of purpuric PR), drug eruptions, vasculitis, and
pityriasis versicolor.
Treatment of Pityriasis Rosea
As PR is a self‑limiting disorder, most patients just
need to be counseled regarding the natural course of
the disease instead of putting them on an aggressive
treatment protocol. Most patients would just need
emollients, antihistaminics, and sometimes topical
steroids to control pruritus. There are a lot of concerns
with therapeutics in this disorder:
• Since the disease is self‑limiting, it is always
difficult to determine if the disease improved with
medications or followed its natural course
• Since the etiopathogenesis is not clearly known,
therapeutics aimed to a particular etiologic agent
cannot be relied upon
• Most of the treatments tried are based on few reports
and thus anecdotal in nature
• There are conflicting results for almost all the
therapies that have been tried
• Benefit‑risk ratio will always be biased toward risk in
a disease which follows a natural course of resolution
and thus, the concern of adverse effect with any
treatment used
• Use of antibiotics may increase the chances of
resistance in the individual and society as a whole
• It is usually not clear whether the treatment being
used is directed to control the symptoms or alter the
natural course of disease or to hasten resolution of
skin lesions or to improve the quality of life, because
in this disease, the symptomatology and the extent
of rash are not directly correlated.
Numerous therapies have been tried in various
studies [Table 3], but the Cochrane review did not find
adequate evidence for the efficacy of any of these.[49]
Cochrane review on interventions in PR excluded 13
out of 16 studies due to lack of proper randomization.
Thus, it was suggested that better‑randomized studies
should be performed, and since there is no well‑proven
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intervention, all studies evaluating any particular
modality should be placebo controlled. Furthermore, the
outcome measures with any treatment should not be
evaluated beyond 2 weeks as spontaneous remission is
likely at 2–12 weeks.
There are no significant studies regarding the use of
antihistamines and emollients on an extensive literature
search. The rest of the therapies used have been
discussed in detail below.
Steroids
Though topical and systemic steroids are sometimes used
in cases of PR, there is a lack of substantial evidence
supporting or refuting their use. There is not much of
published literature on the use of corticosteroids (CS) in
PR. Leonforte published an article reporting exacerbation
of PR on CS administration. They included 18 patients,
in which 13 patients were already treated with CS and
5 were given steroids to assess its efficacy. Most of the
Table 3: Treatments tried for pityriasis rosea
Topical Systemic
Emollients Antihistamines
Antihistamine creams UV light
Corticosteroids Corticosteroids
Antibiotics
Antivirals
UV: Ultraviolet
patients experienced a mild or severe exacerbation in
the form of increased pruritus, irritation, or number of
lesions, and it was more common and severe in patients
in whom CS was started in the initial stage of the
disease.[50] Hence, considering the viral etiology of the
disease, oral steroids may not be a good option, and
use of topical preparations should be limited to patients
experiencing severe pruritus. However, further studies
are needed to establish the role of CS in PR.
Macrolides
The mechanism of action of macrolides in PR is not
known; however, it is believed that they act more
through their anti‑inflammatory and immunomodulatory
actions rather than the antibiotic effect. The various
studies evaluating the role of macrolides in PR have
been tabulated below [Table 4].
As can be concluded from Table 4, although the initial
study showed a favorable response to erythromycin,
subsequent studies found macrolides to be ineffective
and comparable to placebo treatment. Thus, there is
no rationale of using these antibiotics until further
large‑scale randomized controlled studies are done since
the risk of developing resistance to these antibiotics may
outweigh the probable benefit they may offer.
Antivirals
The rationale behind the use of antivirals in PR is that
the course of the disease follows that of a viral exanthem,

Table 4: Studies evaluating the role of macrolides in pityriasis rosea

Author Journal, year Type of trial Study population and intervention Reponse Conclusion
Sharma JAAD, 2000 Nonrandomized 45 patients: Erythromycin (250 mg 73.3% cure rate in Erythromycin is
et al.[4] placebo QID, children ‑ 20-40 mg/kg in four 2 weeks in t/t group effective in PR
controlled divided doses)
45 patients: Placebo
Bigby[51] Arch Dermatol, Supported role of
2000 erythromycin in PR
Amer and Paediatrics, 2006 Randomized 49 patients: Azithromycin (12 mg/ Azithromycin not
Fisher[52] double‑blind kg/day to a max of 500 mg/day) effective
placebo
controlled
Rasi J Drugs Nonrandomized 104 patients: Erythromycin (200 mg No significant difference Erythromycin
et al.[53] Dermatol, 2008 double‑blind QID, children ‑ 20-40 mg/kg in four at week 2, 4, 6 and not effective in
controlled divided doses) 8 weeks clearance of lesions
80 patients: Placebo
Bukhari[54] J Drugs Erythromycin not
Dermatol, 2008 effective
Pandhi IJDVL, 2014 Randomized 35 patients: Azithromycin No statistical difference Azithromycin not
et al.[55] double‑blind 35 patients: Placebo in PR severity score and effective
controlled pruritus assessed by VAS
between two groups
Ahmed J Coll Physicians Randomized 30 patients: Clarithromycin No significant difference Clarithromycin not
et al.[56] Surg Pak, 2014 double‑blind 30 patients: Placebo at 2 weeks after effective
controlled presentation (P=0.598)
PR: Pityriasis rosea, VAS: Visual analog scale
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i.e., seasonal occurrence, presence of prodromal
symptoms, self‑resolution, and also probable involvement
of HHV 6 and 7 in its etiopathogenesis. Acyclovir is the
only antiviral that has been tried and various studies
assessing its efficacy have been tabulated [Table 5].
However, a note should be made of the fact that although
acyclovir has been shown to be effective against HHV 6,
it is not very effective against HHV 7 as this virus lacks
thymidine kinase gene, on which the action of acyclovir
is dependent. Thus, other antivirals such as foscarnet,
cidofovir and ganciclovir which have activity against HHV
might be effective in PR, however, in view of serious
side effects such as myelosuppression and nephrotoxicity
associated with them, there is no rationale of their use
in a benign disorder like PR and thus they have not been
tried as yet.
As can be deciphered from Table 5, acyclovir does
lead to a faster resolution of lesions as compared
to placebo, and thus may be an effective treatment
modality. Furthermore, it is important to note that
the response is significantly better even at the 7th day
when spontaneous resolution is unlikely, thus pointing
toward the therapeutic effectiveness of acyclovir. Drago
et  al. postulated that earlier the treatment is started,
better is the response with better clearance (17.2 days
vs. 19.7 days) and fewer new lesions in patients treated
in the 1st week than in those treated later.[57] Ganguly
however found no significant difference in clearance if
the treatment was started earlier.[59] Since most of the
herpes virus infections need an early institution of
antiviral agents; in light of above findings, we believe
that this aspect needs to be studied in further detail
with respect to PR, and till then, institution of acyclovir
therapy should not be withheld even if patients present
Table 5: Studies evaluating the role of acyclovir in PR
Author Journal, Year Type of trial,
study population
Drago et al.[57] JAAD 2006 Non randomized,
non blinded
87 patients
Rassai et al.[58] JEADV 2011 Randomized,
investigator‑blind
study, 64 patients
Ganguly et al.[59] Journal of Randomized,
Clinical and double‑blind,
Diagnostic placebo controlled
Research 2014 study, 73 patients
Das et al.[60] Indian Observer-blind,
Dermatology randomized (1:1)
Online trial, 24 patients
Journal 2015
later than 1 week. This is also because cases which
prompt an aggressive treatment from the caregiver are
those which do not improve on symptomatic treatment
and thus present more than a week after the onset.
Regarding dose of acyclovir, both high and low doses
have been seen to be beneficial; thus, a comparative
study needs to be done to know if one is better than
other. Despite the probable therapeutic effectiveness,
there is a single report of PR occurring in a patient on
suppressive acyclovir therapy for herpes genitalis.[61]
Comparison Between Acyclovir and
Erythromycin
There are two studies which have compared the above
two modalities, i.e., high dose acyclovir and erythromycin
and both have found acyclovir to be more effective
than erythromycin. In the study by Ehsani et  al.,
30 patients were recruited and at the end of 8 weeks,
13 versus 6 patients achieved complete cure in acyclovir
and erythromycin group, respectively with a P < 0.05.
Resolution of pruritus was also faster with acyclovir
although the results were not significant statistically.[62]
In another study by Amatya et  al., 42 patients were
enrolled, and results with acyclovir were again found to
be better at 1, 2, 4, and 6 weeks.[63]
Thus, acyclovir seems to be a promising therapy for
treatment of PR leading to faster resolution of lesions
and also helping in relieving pruritus.
Phototherapy
There are few studies evaluating the role of phototherapy
in PR. This might work by altering the immunology
in the skin and has been used on the premise of its
usefulness in various other inflammatory disorders.
Intervention Reponse
Oral acyclovir (800 mg 5 times Regression of lesions: 28% vs 4% at
daily) vs placebo for one week 7 days, 79% vs 4% at 14 days
2 weeks study period Clearance of lesions: 18.5 vs 37.9 days
Low dose acyclovir (400 mg Resolution of lesions: 78.5% vs 27%
five times a day for a week) vs at 2 weeks
follow up without treatment Statistical significant decrease in
4 weeks study period erythema, decrease in scaling not
significant statistically
Acyclovir 800 mg five times Resolution of lesions:
a day for a week vs placebo 7th day: 53.33% vs 10%
14th day: 86.66% vs 33.33%
Acyclovir 400 mg tablets Group A: fewer new lesions than
thrice daily for 7 days along Group B (P=0.046), complete response
with cetirizine and calamine in all patients vs 83% in Group B,
(group A) vs only cetirizine significant reduction in lesional score
and calamine (group B) and pruritus at 2nd week in group A
381 Indian Journal of Dermatology 2016; 61(4)
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Mahajan, et al.: Pityriasis rosea update
Merchant and Hammond did first controlled study in
1974 using quartz lamp in 66 patients and found better
results on treated site.[64] Subsequently, Arndt et al. did a
controlled study on 20 patients using ultraviolet B (UVB)
therapy (0.8  Minimal erythema dose (MED) dose on day
1 with 17% increase daily for 5 days) on the right side
with shielding of the left side. The extent of disease and
pruritus control was better on treated side (50% and
47% respectively).[65] Leenutaphong and Jiamton did a
bilateral comparison study by giving UVB (80% of MED
followed by 10–20% increase if no erythema in 10 daily
doses) on the right side and 1 J of UVA radiation on
the left side as placebo. Ten daily erythemogenic doses
of UVB exposure significantly decreased the disease
severity score with significant difference seen after the
third sitting. However, in the follow‑up period at 2 and
4 weeks, there was no difference in severity score or
pruritus; thus, the authors concluded that UVB decreased
the severity scores during treatment but did not alter the
course of disease or pruritus.[66] Castanedo‑Cazares et al.[67]
reported worsening of a patient after phototherapy with
UVB thus raising doubts of its therapeutic effectiveness
in PR. Recently, Lim et  al.[68] have used low dose UVA1
phototherapy (starting with 10–20 J/cm2 and increasing
to 30 J/cm2 given 2–3 times a week till improvement)
to treat PR with significant improvement in severity
score after 2–3 treatments. There was also improvement
in pruritus. Based on the results of above studies,
phototherapy has a conflicting role in PR and thus,
further studies are needed to fully establish its role.
The following table enlists the level of evidence for
various interventions tried in PR [Table 6].
Pregnancy and Pityriasis Rosea
This topic needs special mention as lately, there are
conflicting reports about adverse pregnancy outcomes
in females developing PR during pregnancy, and most of
the clinicians are unaware about this fact. The incidence
of PR in pregnancy has been reported to be 18% versus
6% in general population.[69] Drago et  al. studied 38
women who developed PR during pregnancy out of which
9 had premature delivery and 5 miscarried. They found
the rate of abortion was 62% in women who developed
PR within 15 weeks of gestation. Six cases showed
neonatal hypotonia, weak motility, and hyporeactivity;
however, all neonates eventually followed normal growth
trends. All patients showed high immunoglobulin G (IgG)
Table 6: Level of evidence for treatment options in
pityriasis rosea
Level I Level II‑1 Level II‑2 Level II‑3 Level III
Acyclovir Phototherapy Corticosteroids
Macrolides Emollients
(not effective)
Indian Journal of Dermatology 2016; 61(4)
antibody titers for HHV 6 and 7 and negative IgM
antibodies. Embryonic tissue obtained from one female
showed signs of viral cytopathic damage pointing toward
the fact that PR is actually a systemic HHV infection
leading to intraplacental transmission of virus. Thus,
authors postulated that PR occurring in pregnancy,
especially in the first trimester, may be a marker of
possible adverse pregnancy outcome.[70] Authors further
extended their study to include 61 pregnant patients
with PR and found similar results.[71] However, this has
been refuted by other authors.[72] Chuh et  al. reported
two pregnant patients with PR whose pregnancies and
delivery were uneventful and bore healthy normal
children.[73] Thus, further studies are needed to establish
the causal relation between PR and adverse pregnancy
outcome and till then, all pregnant females developing
PR should be kept under strict follow‑up. All pregnant
females with PR, however, should undergo serological
screening for syphilis. They should be managed with
emollients and antihistaminics, and systemic therapy
should be avoided.
Conclusion
Although lot is known about PR, there are still a lot of
gray areas which need to be addressed in future studies.
Through this article, we have tried to bring together
the literature published for the same. We conclude that
viral etiology is probably the most likely cause of PR,
and thus, antivirals should be given in early stages of PR
itself. All recurrent cases should be worked up properly,
and all pregnant females developing PR should be kept
under close follow‑up.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
What is new?
• Human herpes virus is the most likely etiological agent causing PR
• Although the diagnostic criteria are available and verified in Indian population,
its validity in atypical cases still needs to be established
• Erythromycin is ineffective in PR whereas acyclovir is a promising therapy
• A careful history of drugs or chemical exposure should be taken in all cases of
recurrent PR
• All pregnant females developing PR should be kept under strict follow‑up.
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