PITYRIASIS ROSEA / CHRISTMAS TREE- VIRAL SKIN DISEASE

www.centromedicodecaracas.com.ve
www.infoguia.com
www.paginasamarillascantv.com.ve
www.alergiascaracasmarketing.blogspot.com
@carlosmixares
www.facebook.com/Alergologos.Asma y Alergias
google+CarlosMijares

Carlos E Mijares,MD. Former Fellow in Allergy & Immunology, pediatrics. University of Kansas. USA.
Comment: Differential Diagnosis: Seborrheic Dermatitis, Pityriasis Versicolor, Lichen Dermatosis.

Mancha como chocolate o sello de corcho rojo, prurito intenso y malestar general, con faringitis y estress, simulando urticaria...Puede ser asintomática. El paciente muchas veces no lo puede creer y en emergencias han  inyectado esteroides y antihistaminicos, que ayudan pero confunden. Es una virosis, benigna, limitada.

carlosmixares@gamil.com

Pityriasis rosea

Authors
Adam O Goldstein, MD, MPH
Beth G Goldstein, MD

Section Editors
Robert P Dellavalle, MD, PhD, MSPH
Moise L Levy, MD

Deputy Editor
Abena O Ofori, MD

Disclosures: Adam O Goldstein, MD, MPH Nothing to disclose. Beth G Goldstein, MD Nothing to disclose. Robert P Dellavalle, MD, PhD, MSPH Nothing to disclose. Moise L Levy, MD Grant/Research/Clinical Trial Support: Anacor [atopic dermatitis (investigational drug)]; Stiefel/GlaxoSmithKline [psoriasis (calcipotriene foam)]. Consultant/Advisory Boards: Galderma [acne (adapalene/benzoyl peroxide)]; Anacor [atopic dermatitis (investigational drug)]; Promius [atopic dermatitis (investigational drug)]. Patent Holder: Incontinentia pigmenti (NEMO gene mutations). Abena O Ofori, MD Nothing to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Sep 2015. | This topic last updated: Aug 06, 2015.

INTRODUCTION — Pityriasis rosea (PR) is an acute, self-limited, exanthematous skin disease characterized by the appearance of slightly inflammatory, oval, papulosquamous lesions on the trunk and proximal areas of the extremities (picture 1A-E). The diagnosis and management of this disorder are reviewed here.

ETIOLOGY — A viral etiology for pityriasis rosea (PR) has been hypothesized based upon the following observations:

●PR is sometimes preceded by a prodrome.

●It occasionally occurs in small case clusters.

●It has not been shown to be associated with bacterial or fungal organisms.

This supposition is reinforced by the finding of viral-like particles in PR biopsy specimens examined with the electron microscope [1]. A significant literature supports the hypothesis that PR is a manifestation of human herpesvirus 7 (HHV-7) reactivation [2,3]. However, others have failed to detect HHV-7 DNA sequences and antigens in a significant number of PR cases, arguing against a causative role for this agent [4]. Some studies have also implicated HHV-6 in the pathogenesis of PR [3,5,6]. Possible associations with HHV-8 and 2009-2010 pandemic H1N1 influenza A virus have also been reported [7-9].
More study is needed before this issue can be definitively resolved.

CLINICAL FEATURES — PR is largely a disease of older children and young adults. It is slightly more common in women than men. A prodrome of headache, malaise, and pharyngitis may occur in a small number of cases, but except for itching, the condition is usually asymptomatic.

In 50 to 90 percent of cases, the eruption begins with a "herald" or "mother" patch, a single round or oval, sharply delimited, pink or salmon-colored lesion on the chest, neck, or back (picture 1C, 1F) [10]. The herald patch is usually 2 to 5 cm in diameter. The lesion soon becomes scaly and begins to clear centrally, leaving the free edge of the cigarette paper-like scale directed inwards toward the center. This clinical finding is often described as a "collarette" of scale.
A few days or one to two weeks later, oval lesions similar in appearance to the herald patch, but smaller, appear in crops on the trunk and proximal areas of the extremities (picture 1A-E, 1G). The long axes of these oval lesions tend to be oriented along the lines of cleavage of the skin. This characteristic arrangement is most evident on the back, where it is emphasized by the oblique direction of the cleavage lines in that location. This morphologic pattern has been referred to as a "fir tree" or "Christmas tree" distribution.
The eruption spreads centrifugally or from the top down over the course of a few days. Erythema gradually subsides, desquamation is completed, and the eruption fades, leaving few residual changes, except postinflammatory dyspigmentation. In most cases the papules and plaques resolve in four to six weeks; occasionally the disease will persist for several months. Postinflammatory hyperpigmentation is a common sequela in dark-skinned individuals and often takes several months or longer to resolve.
In children, the distribution of the lesions is often atypical, involving the scalp and face; it may be completely "inverse," affecting the face and distal extremities, while sparing the trunk, or may be concentrated in the pubic, inguinal, and axillary regions (picture 1G-J) [11]. The lesions themselves also are sometimes atypical in children; they may be folliculo-papular, vesicular, pustular, urticarial, or purpuric. PR generally has only mild effects on quality of life in children [12].

DIAGNOSIS — The presence of a herald patch by history or on examination, the characteristic morphology and distribution of the lesions, and the absence of symptoms other than pruritus combine to make PR an easy diagnosis in most instances. However, the herald patch can resemble tinea corporis so closely that potassium hydroxide (KOH) examination of scales for dermatophyte hyphae may be necessary to distinguish these conditions. (See "Dermatologic procedures", section on 'Potassium hydroxide (KOH) prep'.)

There are typically no laboratory abnormalities with PR. Skin biopsy is rarely necessary, but when performed shows focal parakeratosis with or without acanthosis, spongiosis, a perivascular infiltrate of lymphocytes and histiocytes, and occasionally extravasation of red cells (picture 2). The biopsy picture is characteristic, but not pathognomonic. A 3 mm or 4 mm punch biopsy typically provides an adequate specimen for analysis. (See "Skin biopsy techniques", section on 'Punch biopsy'.)
In doubtful cases, signs, symptoms, and laboratory abnormalities relevant to the conditions listed in the differential diagnosis list will assist in proper identification.

Differential diagnosis — The possibility of other disorders should be considered in patients who present with lesions that are suspicious for PR [13]. When the diagnosis is in question, a skin biopsy can be performed. A potassium hydroxide preparation is useful for ruling out fungal infections. (See "Skin biopsy techniques", section on 'Punch biopsy' and "Dermatologic procedures", section on 'Potassium hydroxide (KOH) prep'.)

●Secondary syphilis – The papulosquamous eruption of secondary syphilis can closely resemble PR; however, unlike the latter, secondary syphilis often presents with red-brown macules on the palms and soles (picture 3). Patients with secondary syphilis also may recall the appearance of a chancre and will lack a history of a herald patch. In patients in whom secondary syphilis is suspected, appropriate serologic testing should be performed. (See "Pathogenesis, clinical manifestations, and treatment of early syphilis", section on 'Secondary syphilis' and "Diagnostic testing for syphilis".)

●Guttate psoriasis – Guttate psoriasis is a variant of psoriasis that most frequently affects children and young adults. Small, erythematous, scaly plaques are distributed primarily on the trunk (picture 4). The scale tends to be coarser than the scale associated with PR, and a herald patch does not precede the eruption. Guttate psoriasis frequently is associated with a preceding streptococcal infection. (See "Guttate psoriasis".)

●Tinea corporis – The herald patch of PR may be mistaken for tinea corporis, which may also present with an annular plaque with peripheral scale (picture 5). A KOH preparation from a lesion of tinea corporis will reveal fungal hyphae. (See "Dermatophyte (tinea) infections", section on 'Tinea corporis'.)

●Tinea versicolor – Tinea versicolor presents with hypopigmented or hyperpigmented macules that are most commonly located on the neck and trunk (picture 6A-B). Unlike in PR, erythema is absent or minimal. The scale in tinea versicolor is fine, and lesions lack the peripheral rim of scale that is often seen in PR. A KOH preparation easily confirms a diagnosis of tinea versicolor. (See "Tinea versicolor (Pityriasis versicolor)".)

●Nummular eczema – Nummular eczema presents with intensely pruritic, coin-shaped plaques that may range in size from 2 to 10 cm (picture 7A-B). Involvement of the extremities is more common in nummular eczema than in PR. Serous exudate may be visible in acute lesions of nummular eczema. (See "Overview of dermatitis", section on 'Nummular dermatitis'.)

●Pityriasis lichenoides chronica – Pityriasis lichenoides chronica (PLC) is an uncommon condition that is characterized by recurrent crops of erythematous to brown scaly papules on the trunk and proximal extremities. Lesions may be asymptomatic or pruritic, and spontaneously regress over the course of weeks to months. PLC most commonly occurs in children and young adults. The disorder may persist for years. (See "Pityriasis lichenoides chronica".)

Other disorders that should be considered in the differential diagnosis of PR include Lyme disease, human immunodeficiency virus (HIV) seroconversion illness, and drug eruptions. Testing for HIV should be performed in patients with risk factors for or symptoms suggestive of HIV infection. (See "Acute and early HIV infection: Pathogenesis and epidemiology" and "Screening and diagnostic testing for HIV infection".)
Therapeutic gold injections also can cause eruptions that mimic PR closely; these eruptions do not represent allergic reactions, but are dose-related and can be managed safely by reduction in dose size and the frequency of administration [14]. Other medications and procedures suspected of producing PR-like reactions are omeprazole [15], terbinafine [16], bone marrow transplantation [17], interferon alpha 2A [18], naproxen [19], captopril [20], isotretinoin [21], and bacillus Calmette-Guerin therapy [22].

TREATMENT

General approach — Education, reassurance, and interventions for pruritus are sufficient for the management of most patients with PR.

Patient/parent education — Patients with PR and parents of children with PR typically want information about clinical course, infectivity, and relapse. We reassure patients and parents that PR typically spontaneously resolves within two to three months, is thought to have a low likelihood for transmission, and does not recur in most patients. (See 'Prognosis' below.)

Pruritus — Clinical experience has shown that topical corticosteroids in the medium potency range (group 4 or group 5) are helpful in the control of itching (table 1). They can be applied to the pruritic areas two or three times daily for two to three weeks. Long-term use of topical corticosteroids without medical supervision should be avoided because of risk for corticosteroid-induced skin atrophy. (See "General principles of dermatologic therapy and topical corticosteroid use", section on 'Side effects'.)

Topical antipruritic lotions that contain pramoxine or menthol and oral antihistamines may also be helpful for reducing symptoms of pruritus [13].

Severe cases — Although the vast majority of patients with PR require no treatment or only treatment to control pruritus, there is some evidence that oral acyclovir and ultraviolet light may accelerate clinical improvement. Routine treatment with these interventions is not recommended because efficacy data are limited and PR typically resolves without treatment. We reserve trials of acyclovir or ultraviolet light therapy for patients with severe symptoms associated with a significant negative effect on quality of life.

Acyclovir — The proposed link between PR and human herpesvirus led to trials of antiviral therapy in patients with this disorder. (See 'Etiology' above.)

●Efficacy – The results of a few small trials suggest that oral acyclovir therapy (400 to 800 mg five times per day for one week) may accelerate resolution of the clinical manifestations of PR. Larger, high-quality trials would be useful for confirming these findings.

•In a randomized trial without a placebo-control arm in which the evaluators were unaware of treatment assignment, 64 patients with PR (ages 10 to 60 years) received either acyclovir 400 mg five times per day for one week or no treatment [23]. Treatment with acyclovir significantly accelerated improvement in erythema; after two weeks, the percentage of patients with a reduction in erythema was 79 percent in the acyclovir group versus 27 percent in the group that was not treated. By the fourth week, a reduction in erythema was seen in 93 versus 61 percent of patients, respectively. Scale also resolved more quickly in the acyclovir group, but the difference between the groups was no longer statistically significant at the four-week time-point.

•In a randomized trial in which 38 patients with PR were treated with a seven-day course of high-dose oral acyclovir (800 mg given five times per day for adults, 20 mg/kg given four times per day for children) and 35 patients with PR were given vitamin C tablets as placebo, rapid reductions in erythema were significantly more frequent in the acyclovir group compared with the placebo group [24]. By day 7, 53 percent of the 30 acyclovir-treated patients who returned for reevaluation compared with only 10 percent of the 30 vitamin C recipients who returned showed decreased or absent erythema in all skin lesions. After 14 days, this endpoint occurred in 87 and 33 percent of patients in the acyclovir and vitamin C groups, respectively.

•In a nonrandomized single-blind trial of 87 adults with PR, high-dose acyclovir (800 mg five times daily for one week) was beneficial [25]. Patients treated with acyclovir had more rapid resolution of lesions (mean time to clearance 19 versus 38 days) and fewer new lesions after one week of therapy.

•An unblinded randomized trial performed with 42 children and adults with PR found that a one-week course of acyclovir (800 mg five times per day for adults and 20 mg/kg per day given in five divided doses for children) was more effective than a one-week course of erythromycin (500 mg four times daily in adults and 40 mg/kg per day in four divided doses for children) for reducing the severity and duration of PR [26].

The rationale for efficacy for acyclovir therapy remains unclear. In vitro studies demonstrating that acyclovir has poor antiviral activity against HHV-6 and HHV-7 raise questions about the etiology of PR and the reasons for the efficacy of acyclovir [27,28].

●Administration – Doses for adults with PR range from 400 to 800 mg of acyclovir given five times per day for one week. Improvement is expected within one to two weeks.

Acyclovir therapy is generally well tolerated. Acute renal failure is a potential severe adverse effect. Adverse effects of acyclovir are reviewed separately. (See "Acyclovir: An overview", section on 'Toxicity'.)

Phototherapy — Phototherapy has an extensive history of use for a variety of papulosquamous and inflammatory disorders of the skin as well as for pruritus. Although clinical experience suggests that ultraviolet (UV) light from natural sunlight or phototherapy devices may have benefit in PR, data on efficacy are limited. No randomized trials have been performed, leaving uncertainty about the impact of this therapy. (See "UVB therapy (broadband and narrowband)".)

●Efficacy – Three split-body studies in which one-half of the body was treated with broadband UVB suggest beneficial effects of phototherapy [29-31]. As an example, a study of 101 children and adults with PR found statistically significant reductions in PR severity scores on the side of the body treated with broadband UVB four times per week, but not on the side treated with a very low dose of UVA as a control [31]. Patients received a mean of five treatments. In addition, in a study in which broadband UVB was used to treat one-half of the body for 10 treatments over two weeks in 17 patients with extensive PR, and a very low dose of UVA was given contralaterally as a control, UVB significantly decreased disease severity during the treatment period. However, the difference in effect was no longer present two weeks after the completion of treatment [29]. UVB had no effect on pruritus in this study. In contrast, a split-body study of 20 patients with PR found that broadband UVB therapy decreased the extent of disease and pruritus [30].

Narrowband UVB devices, which emit UVB in the range of 311 to 313 nm rather than the 290 nm to 320 nm range emitted by broadband UVB devices, are now commonly used for the treatment of skin diseases previously treated with broadband UVB. Narrowband UVB has not been specifically studied for PR, but is presumed to have at least similar efficacy. Worsening of PR following narrowband UVB phototherapy has been reported in one patient [32]; however, it is unclear whether the exacerbation of disease was secondary to phototherapy or the natural course of the disease [33]. (See "UVB therapy (broadband and narrowband)".)

UVA1 phototherapy also may have some benefit for the treatment of PR, although it has much more limited availability. In an uncontrolled study of patients with extensive PR, UVA1 was associated with improvements in disease severity, and 12 out of 15 patients noted improvement in pruritus (mean number of treatments = 6.5 ± 1.8) [34]. (See "UVA1 phototherapy".)

In clinical practice, exposure to outdoor sunlight is sometimes suggested to patients with PR. However, data on the efficacy of this mode of exposure to ultraviolet light are lacking.

●Administration – The best regimen for phototherapy is unclear. When treating PR with phototherapy, we most frequently treat with broadband or narrowband UVB two to three times per week. Improvement is expected within the first two to three weeks of treatment. Additional studies are necessary to confirm the efficacy of phototherapy for PR and to determine the optimal regimen for phototherapy.

Short-term side effects of phototherapy include erythema, pruritus, dry skin, and blistering. Side effects of phototherapy are reviewed in detail separately. (See "UVB therapy (broadband and narrowband)", section on 'Short- and long-term adverse effects' and "UVA1 phototherapy", section on 'Adverse effects'.)

Other therapy

Macrolide antibiotics — The efficacy of oral erythromycin for PR is uncertain based upon conflicting efficacy data for erythromycin and the failure of randomized trials of other macrolides to find benefit in PR. Given the uncertain benefit of erythromycin and the common gastrointestinal side effects associated with the drug, we do not use erythromycin for the treatment of PR.

Controlled trials evaluating erythromycin therapy include:

●A blinded, controlled trial that alternately assigned 90 patients to treatment or placebo found that erythromycin (250 mg four times daily for 14 days) was effective in reducing both the duration and the severity of the disease [35]. In this report, a complete response at six weeks of follow-up was noted in 73 percent of patients in the treatment group compared with none in the placebo group.

●A systematic review identified a small (n = 40) unpublished randomized trial of erythromycin (250 mg every six hours for fourteen days), which the authors of the systematic review felt to be a good quality trial [36]. Among the 34 evaluable patients, a higher percentage of those treated with erythromycin achieved complete cure of rash at two weeks (77 versus 6 percent). Patients treated with erythromycin also had greater improvements in itching.

●In contrast to the above results, a trial of 184 patients with PR published after the above systematic review found no benefit with two weeks of oral erythromycin (200 mg four times daily in adults; 20 to 40 mg/kg daily in four divided doses in children) started within seven days of the appearance of secondary lesions of PR [37]. The trial was not randomized, evaluators were not blinded, and the placebo was an emollient cream rather than a pill. No patient in either arm of the trial achieved complete clearance of lesions at two weeks, and there were also no differences in complete clearance between the arms at weeks 4, 6, or 8. Despite the methodologic issues with this trial, it is difficult to reconcile these results with the beneficial outcomes discussed above. The authors argue that earlier trials did not adequately identify a group of patients with a clear diagnosis of early PR.

Also in contrast to the trials that support efficacy of erythromycin, trials of azithromycin and clarithromycin for PR have yielded unfavorable results. For example, a blinded randomized trial in 49 children with PR found no statistically significant benefit to five days of treatment with azithromycin (12 mg/kg per day, up to 500 mg per day) [38]. At four weeks, there were similar percentages of complete (60 versus 42 percent) and partial (28 versus 29 percent) responses with azithromycin and placebo. A randomized trial in 70 children and adults with PR also failed to find superiority of a five-day course of azithromycin (12 mg/kg per day) over a multivitamin placebo [39]. Similarly, clarithromycin was ineffective in a randomized trial in which 60 children and adults with PR were given one-week courses of clarithromycin (200 or 250 mg twice daily) or placebo pills [40].

PROGNOSIS — Patients should be advised that the rash may persist for two to three months; no follow-up is necessary as long as it resolves within this time. New lesions may occur during this period but should disappear spontaneously. Relapse after resolution is uncommon [3].

PREGNANCY — An analysis of a case series of 61 women who developed PR during pregnancy suggests that PR increases the risk for spontaneous abortion [41]. Spontaneous abortions occurred in 8 of 61 women (13 percent) who developed PR during pregnancy and 8 of 14 women (57 percent) who developed PR within the first 15 weeks of gestation. Further studies are necessary to clarify the impact of PR on pregnancy.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient information: Pityriasis rosea (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Pityriasis rosea is an acute, self-limited, exanthematous skin disease felt most likely to be due to a viral etiology. (See 'Introduction' above and 'Etiology' above.)

●The eruption commonly begins with a "herald" or "mother" patch, a single round or oval, rather sharply delimited pink or salmon-colored lesion on the chest, neck, or back, 2 to 5 cm in diameter. A few days or a week or two later, oval lesions similar in appearance to the herald patch, but smaller, appear in crops on the trunk and proximal areas of the extremities (picture 1A-E). The long axes of these oval lesions tend to be oriented along the lines of cleavage of the skin. (See 'Clinical features' above.)

●A prodrome of headache, malaise, and pharyngitis may occur in a small number of cases, but except for itching, the condition is usually asymptomatic. (See 'Clinical features' above.)

●The diagnosis of pityriasis rosea is typically made based on the history of a herald patch and the clinical appearance of the rash. Laboratory testing is sometimes needed to exclude other conditions such as secondary syphilis. (See 'Differential diagnosis' above.)

●Most patients do not require therapy. For patients with mild itching who desire therapy, we suggest treatment with medium-potency topical corticosteroids (table 1) (Grade 2C). (See 'Pruritus' above.)

●For patients with severe presentations resulting in a significant negative impact on quality of life, limited data suggest that oral acyclovir may be useful for shortening the course of pityriasis rosea. Phototherapy is an additional treatment option. We suggest not treating such patients with oral erythromycin (Grade 2C). Additional studies will be useful for confirming the efficacy of PR therapies. (See 'Severe cases' above and 'Other therapy' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. el-Shiemy S, Nassar A, Mokhtar M, Mabrouk D. Light and electron microscopic studies of pityriasis rosea. Int J Dermatol 1987; 26:237.
2. Drago F, Ranieri E, Malaguti F, et al. Human herpesvirus 7 in patients with pityriasis rosea. Electron microscopy investigations and polymerase chain reaction in mononuclear cells, plasma and skin. Dermatology 1997; 195:374.
3. Drago F, Broccolo F, Rebora A. Pityriasis rosea: an update with a critical appraisal of its possible herpesviral etiology. J Am Acad Dermatol 2009; 61:303.
4. Kempf W, Adams V, Kleinhans M, et al. Pityriasis rosea is not associated with human herpesvirus 7. Arch Dermatol 1999; 135:1070.
5. Watanabe T, Kawamura T, Jacob SE, et al. Pityriasis rosea is associated with systemic active infection with both human herpesvirus-7 and human herpesvirus-6. J Invest Dermatol 2002; 119:793.
6. Broccolo F, Drago F, Careddu AM, et al. Additional evidence that pityriasis rosea is associated with reactivation of human herpesvirus-6 and -7. J Invest Dermatol 2005; 124:1234.
7. Mubki TF, Bin Dayel SA, Kadry R. A case of Pityriasis rosea concurrent with the novel influenza A (H1N1) infection. Pediatr Dermatol 2011; 28:341.
8. Kwon NH, Kim JE, Cho BK, Park HJ. A novel influenza a (H1N1) virus as a possible cause of pityriasis rosea? J Eur Acad Dermatol Venereol 2011; 25:368.
9. Prantsidis A, Rigopoulos D, Papatheodorou G, et al. Detection of human herpesvirus 8 in the skin of patients with pityriasis rosea. Acta Derm Venereol 2009; 89:604.
10. Blauvelt A. Pityriasis rosea. In: Fitzpatrick's Dermatology in General Medicine, 7th ed, Wolf K, Goldsmith LA, Katz SI, et al. (Eds), McGraw Hill, New York 2008. p.362.
11. Trager JD. What's your diagnosis? Scaly pubic plaques in a 2-year-old girl--or an "inverse" rash. J Pediatr Adolesc Gynecol 2007; 20:109.
12. Chuh AA. Quality of life in children with pityriasis rosea: a prospective case control study. Pediatr Dermatol 2003; 20:474.
13. Browning JC. An update on pityriasis rosea and other similar childhood exanthems. Curr Opin Pediatr 2009; 21:481.
14. Wilkinson SM, Smith AG, Davis MJ, et al. Pityriasis rosea and discoid eczema: dose related reactions to treatment with gold. Ann Rheum Dis 1992; 51:881.
15. Buckley C. Pityriasis rosea-like eruption in a patient receiving omeprazole. Br J Dermatol 1996; 135:660.
16. Gupta AK, Lynde CW, Lauzon GJ, et al. Cutaneous adverse effects associated with terbinafine therapy: 10 case reports and a review of the literature. Br J Dermatol 1998; 138:529.
17. Spelman LJ, Robertson IM, Strutton GM, Weedon D. Pityriasis rosea-like eruption after bone marrow transplantation. J Am Acad Dermatol 1994; 31:348.
18. Durusoy C, Alpsoy E, Yilmaz E. Pityriasis rosea in a patient with Behçet's disease treated with interferon alpha 2A. J Dermatol 1999; 26:225.
19. Yosipovitch G, Kuperman O, Livni E, et al. [Pityriasis rosea-like eruption after anti-inflammatory and antipyretic medication]. Harefuah 1993; 124:198.
20. Ghersetich I, Rindi L, Teofoli P, et al. [Pityriasis rosea-like skin eruptions caused by captopril]. G Ital Dermatol Venereol 1990; 125:457.
21. Helfman RJ, Brickman M, Fahey J. Isotretinoin dermatitis simulating acute pityriasis rosea. Cutis 1984; 33:297.
22. Honl BA, Keeling JH, Lewis CW, Thompson IM. A pityriasis rosea-like eruption secondary to bacillus Calmette-Guérin therapy for bladder cancer. Cutis 1996; 57:447.
23. Rassai S, Feily A, Sina N, Abtahian S. Low dose of acyclovir may be an effective treatment against pityriasis rosea: a random investigator-blind clinical trial on 64 patients. J Eur Acad Dermatol Venereol 2011; 25:24.
24. Ganguly S. A Randomized, Double-blind, Placebo-Controlled Study of Efficacy of Oral Acyclovir in the Treatment of Pityriasis Rosea. J Clin Diagn Res 2014; 8:YC01.
25. Drago F, Vecchio F, Rebora A. Use of high-dose acyclovir in pityriasis rosea. J Am Acad Dermatol 2006; 54:82.
26. Amatya A, Rajouria EA, Karn DK. Comparative study of effectiveness of oral acyclovir with oral erythromycin in the treatment of Pityriasis rosea. Kathmandu Univ Med J (KUMJ) 2012; 10:57.
27. Zhang Y, Schols D, De Clercq E. Selective activity of various antiviral compounds against HHV-7 infection. Antiviral Res 1999; 43:23.
28. De Clercq E, Naesens L, De Bolle L, et al. Antiviral agents active against human herpesviruses HHV-6, HHV-7 and HHV-8. Rev Med Virol 2001; 11:381.
29. Leenutaphong V, Jiamton S. UVB phototherapy for pityriasis rosea: a bilateral comparison study. J Am Acad Dermatol 1995; 33:996.
30. Arndt KA, Paul BS, Stern RS, Parrish JA. Treatment of pityriasis rosea with UV radiation. Arch Dermatol 1983; 119:381.
31. Valkova S, Trashlieva M, Christova P. UVB phototherapy for Pityriasis rosea. J Eur Acad Dermatol Venereol 2004; 18:111.
32. Castanedo-Cazares JP, Lepe V, Moncada B. Should we still use phototherapy for Pityriasis rosea? Photodermatol Photoimmunol Photomed 2003; 19:160.
33. Chuh A. Narrow band UVB phototherapy and oral acyclovir for pityriasis rosea. Photodermatol Photoimmunol Photomed 2004; 20:64.
34. Lim SH, Kim SM, Oh BH, et al. Low-dose Ultraviolet A1 Phototherapy for Treating Pityriasis Rosea. Ann Dermatol 2009; 21:230.
35. Sharma PK, Yadav TP, Gautam RK, et al. Erythromycin in pityriasis rosea: A double-blind, placebo-controlled clinical trial. J Am Acad Dermatol 2000; 42:241.
36. Chuh AA, Dofitas BL, Comisel GG, et al. Interventions for pityriasis rosea. Cochrane Database Syst Rev 2007; :CD005068.
37. Rasi A, Tajziehchi L, Savabi-Nasab S. Oral erythromycin is ineffective in the treatment of pityriasis rosea. J Drugs Dermatol 2008; 7:35.
38. Amer A, Fischer H. Azithromycin does not cure pityriasis rosea. Pediatrics 2006; 117:1702.
39. Pandhi D, Singal A, Verma P, Sharma R. The efficacy of azithromycin in pityriasis rosea: a randomized, double-blind, placebo-controlled trial. Indian J Dermatol Venereol Leprol 2014; 80:36.
40. Ahmed N, Iftikhar N, Bashir U, et al. Efficacy of clarithromycin in pityriasis rosea. J Coll Physicians Surg Pak 2014; 24:802.
41. Drago F, Broccolo F, Javor S, et al. Evidence of human herpesvirus-6 and -7 reactivation in miscarrying women with pityriasis rosea. J Am Acad Dermatol 2014; 71:198.

Topic 5665 Version 17.0