1. by
Layth Tameem
Bristol Med School

2. Outline
Why I chose this topic
Classical Presentations
Epidemiology
Aetiology
Treatments
Outcomes
Summary

3. Why I chose this topic…

4. Clinical Presentation 1
First – A Herald Patch
2-5 cm in diameter
A scale trailing just inside
edge of lesion
Pink
Not itchy
Usually on trunk but can be
seen on neck or extremities
Can be mistaken for ring
worm

5. Clinical Presentation 2
Then after 1 week – 10 days…
Eruption of a smaller similar
scaly rash over trunk and
sometimes legs and neck
Lasts for 4-10 weeks
Symmetric – ‘Fir tree’ pattern
Dry
Inner circle of scale
Faint pink to deep red
Follow the lines of the ribs
Sometimes Itchy

6. Clinical Presentation 3
Can occur with a prodromal
phase…
Malaise
Anorexia
Nasuea
Fever
Joint pain
Lymph node enlargement
Head ache

7. Epidemiology
Herald Patch is seen in 50%-90% of cases at least a
week before onset of smaller lesions
Almost equal amongst M:F at 1:1.43
Prevalence rises during childhood
Most common between 15-40 y/o.
Rare in infants and elderly

8. Aetiology – Infective Theory
Cause currently unknown
The Pathogenesis of PR suggests a virus:
 Average affected age is 15-40
 Appears in clusters (not epidemics and only in women so far!)
 Seems to be related to respiratory tract infections in some
 Reported associations with unfavourable socioeconomic backgrounds
 Reports of infection after contact with other PR patients
 Very rare for recurrence of infection
 Programmed course of events
 Increased incidence around winter and spring time
Currently virus implicated is the Human Herpes
virus 6 and 7 but the evidence is controversial
Enterovirus Infection has been linked recently

9. Aetiology – Non Infective Theory
 After generations of research, still no infective agent has been found
 Real epidemics have not been found, only small clusters, and only in
women – reason unknown
 Autoimmunity and genetic predisposition
 An auto-aggressive disease affecting genetically susceptible people.
 Burch et al found that 28% of their test group had T-lymphcyte antibodies, the
same found in 82% of patients with SLE
 Another theory proposed by Chuh et al is patients with PR share the same HLA –
DR haplotypes as those with a high incidence of autoantibodies and autoimmune
diseases. This is yet to be research though.
 Atopy
 Chuang et al reported a high incidence of atopy among PR sufferers.
 However, this was then further studied by Chuang et al and found that there was
no significant link between atopy and PR and control groups (P=0.29)

10. Treatment - UVB
Potential benefit was first reported by Hazen in 1928
and supported in 1983 by Arndt.
This does not support the infection theory as an
infection would not respond to UVB.
However, in 1995, Leenutaphong et al found no
significant difference between those treated with UVB
and those without.
It is still used as a treatment though because in some
patients there appears to be a positive response to
UVB treatment.

11. Treatment –
Systemic Corticosteroids
There have been reports of clinical improvement with
oral prednisolone. (Tay et al)
However, there have also been reports of
exacerbation of the rash. (Leonforte et al)

12. Treatment –
Erythromycin
Reported to benefit as early as 1954.
Sharma et al reported significant benefit for patients
with PR on oral erythromycin.
This however cannot be relied upon for evidence that
this is an infective condition as it is known that
erythromycin has immunomodulating effects as well
as antimicrobial elements.

13. Treatment – Acyclovir
A recent study performed in Italy by Drago et al
reported that 79% of the patients treated with oral
acyclovir (800mg 5 times daily) fully regressed after 14
days of treatment compared to 4% in the control
group.
However, a limitation to this study is that it was not
performed double blind or randomized. It is reported
that objectivity was achieved by counting the lesions.
No other information could be found at this time

14. Other Treatments
Supportive treatment
Avoid irritating substances
like soap, shower gels etc
Calamine lotion
Topical zinc oxide

15. Outcome
Since this is a self limiting disease, it resolves over 6-
12 weeks with no treatment.
With treatment, this time can be reduced a little but
this varies from patient to patient.
Recurrence rate is very low, almost 1 %

16. DifferentialsGuttate Psoriasis
 Type of psoriasis that looks like small salmon-
pink drops on the skin. Usually occurs 2-3
weeks post sore throat
 Can’t be treated, but the cause of the sore
throat can be treated with antibiotics to
prevent furst recurrence
Secondary Syphilis
 Important as is the 2nd
stage in untreated
Syphilis
 Commonly presents as a rash that involving
small red lesions the size of a penny
 Must test for with a blood test in suspected
individuals

17. SummarySelf limiting disease
Herald patch appears for 7-10 days
Then a ‘fir tree’ patterned small oval pink rash
appears with a scaly ring for ~ 4-10 weeks
Cause is unknown as yet. Possible theories include
HHV 6 and 7 infection.
Treatment is purely supportive. UVB and
erythromycin can help. Recently, Acyclovir has been
shown to help.
Full recovery is expected by 12 weeks
Chance of recurrence is roughly 1%

18. References Chuh et al: Is human herpesvirus 7 the causative agent of pityriasis rosea? – a
critical review : Int Journ Derm Volume 43, Number 12, December 2004, pp. 870-
875
 Amer et al : Azithromycin Does Not Cure Pityriasis Rosea : PEDIATRICS Vol.
117 No. 5 May 2006, pp. 1702-1705
 Chuh et al : Pityriasis rosea – evidence for and against an infectious
aetiology
 Messenger AG, Knox EG, Summerly R, et al. Case clustering in pityriasis rosea:
support for role of an infective agent. Br Med J (Clin Res Ed) 1982; 284:371–373.
 Arndt KA, Paul BS, Stern RS, Parrish JA. Treatment of pityriasis rosea with UV
radiation. Arch Dermatol 1983; 119: 381–382.
 Leenutaphong V, Jiamton S. UVB phototherapy for pityriasis rosea: a bilateral
comparison study. J Am Acad Dermatol 1995; 33: 996–999.
 Tay YK, Goh CL. One-year review of pityriasis rosea at the National Skin
Centre, Singapore. Ann Acad Med Singapore 1999; 28: 829–831.
 Leonforte JF. Pityriasis rosea: exacerbation with corticosteroid treatment.
Dermatologica 1981; 163:480–481.

19. References 2 White W. Pityriasis rosea in sisters. Br Med J 1973; 2:245.
 Burch PRJ, Rowell NR. Pityriasis rosea – an autoaggressive disease? Br J
Dermatol 1970; 82: 549–560.
 Durusoy C, Alpsoy E, Yilmaz E. Pityriasis rosea in a patient with Behcet’s
disease treated with interferon alpha 2A. J Dermatol 1999; 26: 225–228.
 Chuang TY, Ilstrup DM, Perry HO, Kurland LT. Pityriasis rosea in Rochester,
Minnesota, 1969 to 1978. J Am Acad Dermatol 1982; 7: 80–89.
 Chuang TY, Perry HO, Ilstrup DM, Kurland LT. Recent upper respiratory tract
infection and pityriasis rosea: a case-control study of 249 matched pairs. Br J
Dermatol 1983; 108: 587–591.
 Sharma PK, Yadav TP, Gautam RK, et al. Erythromycin in pityriasis rosea: a
double-blind, placebo controlledclinical trial. J Am Acad Dermatol 2000;
42:241–244. 63
 Labro MT, Anti-inflammatory activity of macrolides: a new therapeutic
potential? J Anti microb Chemother1998; 41 (Suppl B): 37–46.
 Drago et al, Use of high-dose acyclovir in pityriasis rosea : J Am Acad
Dermatol 2006; 54: 82-85
 Antonio Chuh, Narrow band UVB phototherapy and oral acyclovir for
pityriasis rosea Photodermatology, Photoimmunology & Photomedicine 2004; 20
(1), 64–65