Pityriasis rosea

For patient information, click here Template:DiseaseDisorder infobox

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [3]

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]

Overview

Pityriasis rosea is a skin disease marked by patches of pink, oval rash. Although its exact cause is unknown and its onset is not linked to food, medicines or stress, it is thought that this essentially non-contagious condition is set off by a virus. Pityriasis rosea can affect members of either sex of any age. However, it is most common in females and those between the ages of 8 and 35. Symptoms only recur in 3% of the affected.

Risk Factors

Although pityriasis rosea may occur in more than one person in a household at a time, it is not thought to spread from one person to another.

Natural History, Complications and Prognosis

Pityriasis rosea usually lasts between 8 to 10 weeks — the rashes disappear without scarring. In people with dark complexions, however, hyperpigmented discolorations may last for several months afterwards. Although Pityriasis rosea may occur in more than one person in a household at a time, it is not thought to be highly contagious. Dogs and bears are known to be afflicted by Pityriasis rosea quite frequently

References

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Historical Perspective

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References

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Classification

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References

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Pathophysiology

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References

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Causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]

Overview

Pityriasis rosea is believed to be caused by a virus and it occurs most often in the fall and spring.

References

Template:WikiDoc Sources

Differentiating Pityriasis rosea from other Diseases

Overview

Differential Diagnosis

Syphilis
- After 4-10 weeks of primary syphilis, secondary syphilis can occur affecting skin, mucous membrane and lymph nodes. They can present with fever, malaise, sore throat, weight loss, headache, and hair loss.^[1]^[2]

Disease	Rash Characteristics	Signs and Symptoms	Associated Conditions
Cutaneous T cell lymphoma/Mycosis fungoides^[3]	Premycotic phase: A scaly, red rash in areas of the body that usually are not exposed to the sun. This rash does not cause symptoms and may last for months or years. Patch phase: Thin, reddened, eczema -like rash. Plaque phase: Small raised bumps (papules) or hardened lesions on the skin, which may be reddened. Tumor phase: Tumors form on the skin. These tumors may develop ulcersand the skin may get infected.	Epidermal atrophy or poikiloderma Generalized itching (pruritus) Pain in the affected area of the skin. Insomnia Red (erythematous) patches scattered over the skin of the trunk and the extremities Tumor-like lobulated outgrowths form on the skin in the latter part of the disease Weight loss Lymphadenopathy Malaise and fatigue Anemia May progress to Sezary syndrome (Skin involvement plus hematogenous dissemination)	Sezary syndrome
Pityriasis rosea^[4]	Pink or salmon in colour, which may be scaly, termed as “herald patch” Oval in shape Long axis oriented along the clevage lines Distributed on the trunk and proximal extremities Squamous marginal collarette and a “fir-tree” or “Christmas tree” distribution on the posterior trunk Develops after viral infection Resolves spontaneously after 6-8 weeks	Preceded by a prodrome of: Sore throat Gastrointestinal disturbance Fever Arthralgia	Infection by any of the following:^[5] HHV-6 HHV-7 HHV-8
Pityriasis lichenoides chronica	Recurrent lesions are usually less evenly scattered than psoriasis Brownish red or orange-brown color Lesions are capped by a single detachable opaque mica-like scale Often leave hypopigmented macules	High fever Malaise Myalgias Skin burning Pruritis	Infection by any of the following:^[6] Epstein-Barr virus (EBV) Toxoplasma gondii Human immunodeficiency virus (HIV)
Nummular dermatitis^[7]	Multiple coinshaped eczematous lesions Commonly affecting the extremities (lower>upper) and trunk May ooze fluid and become dry and crusty	Often appears after a skin injury, such as a burn, abrasion (from friction), or insect bite Lesions commonly relapse after occasional remission or may persist for long periods Pruritis	Associated with: Dry skin Emotional stress Allergens(rubber chemicals, formaldehyde, neomycin, chrome, mercury and nickel) Staphylococcus infection Seasonal variation Alcohol Drugs Atopy
Secondary syphilis^[8]	Round coppery red color lesions on palms and soles Papules with collarette of scales	Fever Generalized lymphadenopathy Sore throat Patchy hair loss Headaches Weight loss Myalgia Fatigue	Associated with: Condylomata lata Corona verinata Positive VDRL test
Bowen’s disease^[9]	Erythematous little scaly plaque, which enlarges over time in an erratic manner Scale is usually yellow or white and it is easily detachable without producing any bleeding Well defined margins	Pruritis Pain Bleeding lesions	Associated with:^[10] Erythroplasia of Queyrat (Bowen’s disease of the penis) Squamous cell carcinoma Solar radiation and ultraviolet (UV) exposure Radiotherapy Immunosuppression Arsenic exposure Human papilloma virus (HPV) type 16 Merkel cell polyomavirus Sjögren’s syndrome
Exanthematous pustulosis^[11]	Numerous small, primarily non-follicular, sterile pustules, arising within large areas of edematous erythema	Fever Leukocytosis Intracorneal, subcorneal, and/or intraepidermal pustules with papillary dermal edema containing neutrophils and eosinophils	Associated with:^[12] Antibiotics(penicillins, sulfonamides, tetracyclines) Carbamazepine Calcium channel blockers(Diltiazem) Hydroxychloroquine
Hypertrophic lichen planus^[13]	Classically involves shin and ankles and is characterized by hyperkeratotic plaques and nodules covered by a scale Lesions may transform into hyperkeratotic thickened elevated purplish or reddish plaques and nodules	Chronic pruritis Scaling May be asymptomatic	Associated with Hepatitis C virus infection^[14]
Sneddon–Wilkinson disease^[15]	Flaccid pustules that are often generalized and have a tendency to involve the flexural areas Have an annular configuration	Pruritis May be asymptomatic	Associated with: Monoclonal gammopathy, usually an IgA paraproteinemia^[16] Crohn’s disease^[17] Osteomyelitis Adalimumab^[18]
Small plaque parapsoriasis^[19]	Erythematous plaques which are covered with fine scale. May present with elongated, finger-like patches symmetrically distributed on the flanks, also known as digitate dermatosis	Lesions may be asymptomatic May be mildly pruritic May fade or disappear after sun exposure during the summer season, but typically recur during the winter	May progress to mycosis fungoides^[20]
Intertrigo^[21]	Red and fleshy looking lesion in skin folds Itching oozing May be sore	Pruritis Musty odor	Associated with: Infections (Fungal, bacterial, viral) Allergies Diabetes Obesity
Langerhans cell histiocytosis^[22]	Scaling and crusting of the scalp	Pathological fractures^[23] Visceromegaly (hepatomegaly, spleenomegaly) Chronic cough Dyspnea^[24] Lymphadenopathy	Associated with: Diabetes insipidus^[25] Pancytopenia
Tinea manuum/pedum/capitis^[26]	scaling, flaking, and sometimes blistering of the affected areas Hair loss with a black dot on scalp in case of tinea capitis	Pruritis KOH preparation of the lesions confirms fungal infection	Associated with: Diabetes Immunosupression Intimate contact with infected person May lead to asthma exacerbation
Seborrheic dermatitis	Papulosquamous, scaly, flaky, itchy, and red rash found particularly at sebaceous gland-rich areas of the body		Associated with:^[27] AIDS Stress^[28] Fungal infection Fatigue Sleep deprivation Change of season Parkinson’s disease Biotin deficiency

References

↑ Mullooly C, Higgins SP (2010). “Secondary syphilis: the classical triad of skin rash, mucosal ulceration and lymphadenopathy”. Int J STD AIDS. 21 (8): 537–45. doi:10.1258/ijsa.2010.010243. PMID 20975084.
↑ Kent ME, Romanelli F (2008). “Reexamining syphilis: an update on epidemiology, clinical manifestations, and management”. Ann Pharmacother. 42 (2): 226–36. doi:10.1345/aph.1K086. PMID 18212261.
↑ “Mycosis Fungoides and the Sézary Syndrome Treatment (PDQ®)—Patient Version – National Cancer Institute”.
↑ Mahajan K, Relhan V, Relhan AK, Garg VK (2016). “Pityriasis Rosea: An Update on Etiopathogenesis and Management of Difficult Aspects”. Indian J Dermatol. 61 (4): 375–84. doi:10.4103/0019-5154.185699. PMC 4966395. PMID 27512182.
↑ Prantsidis A, Rigopoulos D, Papatheodorou G, Menounos P, Gregoriou S, Alexiou-Mousatou I, Katsambas A (2009). “Detection of human herpesvirus 8 in the skin of patients with pityriasis rosea”. Acta Derm. Venereol. 89 (6): 604–6. doi:10.2340/00015555-0703. PMID 19997691.
↑ Smith KJ, Nelson A, Skelton H, Yeager J, Wagner KF (1997). “Pityriasis lichenoides et varioliformis acuta in HIV-1+ patients: a marker of early stage disease. The Military Medical Consortium for the Advancement of Retroviral Research (MMCARR)”. Int. J. Dermatol. 36 (2): 104–9. PMID 9109005.
↑ Jiamton S, Tangjaturonrusamee C, Kulthanan K (2013). “Clinical features and aggravating factors in nummular eczema in Thais”. Asian Pac. J. Allergy Immunol. 31 (1): 36–42. PMID 23517392.
↑ “STD Facts – Syphilis”.
↑ Neagu TP, Ţigliş M, Botezatu D, Enache V, Cobilinschi CO, Vâlcea-Precup MS, GrinŢescu IM (2017). “Clinical, histological and therapeutic features of Bowen’s disease”. Rom J Morphol Embryol. 58 (1): 33–40. PMID 28523295.
↑ Murao K, Yoshioka R, Kubo Y (2014). “Human papillomavirus infection in Bowen disease: negative p53 expression, not p16(INK4a) overexpression, is correlated with human papillomavirus-associated Bowen disease”. J. Dermatol. 41 (10): 878–84. doi:10.1111/1346-8138.12613. PMID 25201325.
↑ Szatkowski J, Schwartz RA (2015). “Acute generalized exanthematous pustulosis (AGEP): A review and update”. J. Am. Acad. Dermatol. 73 (5): 843–8. doi:10.1016/j.jaad.2015.07.017. PMID 26354880.
↑ Schmid S, Kuechler PC, Britschgi M, Steiner UC, Yawalkar N, Limat A, Baltensperger K, Braathen L, Pichler WJ (2002). “Acute generalized exanthematous pustulosis: role of cytotoxic T cells in pustule formation”. Am. J. Pathol. 161 (6): 2079–86. doi:10.1016/S0002-9440(10)64486-0. PMC 1850901. PMID 12466124.
↑ Ankad BS, Beergouder SL (2016). “Hypertrophic lichen planus versus prurigo nodularis: a dermoscopic perspective”. Dermatol Pract Concept. 6 (2): 9–15. doi:10.5826/dpc.0602a03. PMC 4866621. PMID 27222766.
↑ Shengyuan L, Songpo Y, Wen W, Wenjing T, Haitao Z, Binyou W (2009). “Hepatitis C virus and lichen planus: a reciprocal association determined by a meta-analysis”. Arch Dermatol. 145 (9): 1040–7. doi:10.1001/archdermatol.2009.200. PMID 19770446.
↑ Lutz ME, Daoud MS, McEvoy MT, Gibson LE (1998). “Subcorneal pustular dermatosis: a clinical study of ten patients”. Cutis. 61 (4): 203–8. PMID 9564592.
↑ Kasha EE, Epinette WW (1988). “Subcorneal pustular dermatosis (Sneddon-Wilkinson disease) in association with a monoclonal IgA gammopathy: a report and review of the literature”. J. Am. Acad. Dermatol. 19 (5 Pt 1): 854–8. PMID 3056995.
↑ Delaporte E, Colombel JF, Nguyen-Mailfer C, Piette F, Cortot A, Bergoend H (1992). “Subcorneal pustular dermatosis in a patient with Crohn’s disease”. Acta Derm. Venereol. 72 (4): 301–2. PMID 1357895.
↑ Sauder MB, Glassman SJ (2013). “Palmoplantar subcorneal pustular dermatosis following adalimumab therapy for rheumatoid arthritis”. Int. J. Dermatol. 52 (5): 624–8. doi:10.1111/j.1365-4632.2012.05707.x. PMID 23489057.
↑ Lambert WC, Everett MA (1981). “The nosology of parapsoriasis”. J. Am. Acad. Dermatol. 5 (4): 373–95. PMID 7026622.
↑ Väkevä L, Sarna S, Vaalasti A, Pukkala E, Kariniemi AL, Ranki A (2005). “A retrospective study of the probability of the evolution of parapsoriasis en plaques into mycosis fungoides”. Acta Derm. Venereol. 85 (4): 318–23. doi:10.1080/00015550510030087. PMID 16191852.
↑ Janniger CK, Schwartz RA, Szepietowski JC, Reich A (2005). “Intertrigo and common secondary skin infections”. Am Fam Physician. 72 (5): 833–8. PMID 16156342.
↑ Satter EK, High WA (2008). “Langerhans cell histiocytosis: a review of the current recommendations of the Histiocyte Society”. Pediatr Dermatol. 25 (3): 291–5. doi:10.1111/j.1525-1470.2008.00669.x. PMID 18577030.
↑ Stull MA, Kransdorf MJ, Devaney KO (1992). “Langerhans cell histiocytosis of bone”. Radiographics. 12 (4): 801–23. doi:10.1148/radiographics.12.4.1636041. PMID 1636041.
↑ Sholl LM, Hornick JL, Pinkus JL, Pinkus GS, Padera RF (2007). “Immunohistochemical analysis of langerin in langerhans cell histiocytosis and pulmonary inflammatory and infectious diseases”. Am. J. Surg. Pathol. 31 (6): 947–52. doi:10.1097/01.pas.0000249443.82971.bb. PMID 17527085.
↑ Grois N, Pötschger U, Prosch H, Minkov M, Arico M, Braier J, Henter JI, Janka-Schaub G, Ladisch S, Ritter J, Steiner M, Unger E, Gadner H (2006). “Risk factors for diabetes insipidus in langerhans cell histiocytosis”. Pediatr Blood Cancer. 46 (2): 228–33. doi:10.1002/pbc.20425. PMID 16047354.
↑ Al Hasan M, Fitzgerald SM, Saoudian M, Krishnaswamy G (2004). “Dermatology for the practicing allergist: Tinea pedis and its complications”. Clin Mol Allergy. 2 (1): 5. doi:10.1186/1476-7961-2-5. PMC 419368. PMID 15050029.
↑ Schwartz RA, Janusz CA, Janniger CK (2006). “Seborrheic dermatitis: an overview”. Am Fam Physician. 74 (1): 125–30. PMID 16848386.
↑ Misery L, Touboul S, Vinçot C, Dutray S, Rolland-Jacob G, Consoli SG, Farcet Y, Feton-Danou N, Cardinaud F, Callot V, De La Chapelle C, Pomey-Rey D, Consoli SM (2007). “[Stress and seborrheic dermatitis]”. Ann Dermatol Venereol (in French). 134 (11): 833–7. PMID 18033062.

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Epidemiology and Demographics

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References

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Risk Factors

Please help WikiDoc by adding content here. It’s easy! Click here to learn about editing. Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]

Overview

Although pityriasis rosea may occur in more than one person in a household at a time, it is not thought to spread from one person to another.

References

Template:WikiDoc Sources

Natural History, Complications and Prognosis

Please help WikiDoc by adding more content here. It’s easy! Click here to learn about editing.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]

Overview

Pityriasis rosea usually lasts between 8 to 10 weeks — the rashes disappear without scarring. In people with dark complexions, however, hyperpigmented discolorations may last for several months afterwards. Although Pityriasis rosea may occur in more than one person in a household at a time, it is not thought to be highly contagious. Dogs and bears are known to be afflicted by Pityriasis rosea quite frequently

References

Template:WikiDoc Sources

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Other Imaging Findings | Other Diagnostic Studies

Treatment

Medical Therapy | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case #1

Related Chapters

Ringworm
Pityriasis – for list of similarly named flaky skin conditions

External Links

Template:DermNet

Template:WikiDoc Sources

[pmid20975084-1] Mullooly C, Higgins SP (2010). “Secondary syphilis: the classical triad of skin rash, mucosal ulceration and lymphadenopathy”. Int J STD AIDS. 21 (8): 537–45. doi:10.1258/ijsa.2010.010243. PMID 20975084.

[pmid18212261-2] Kent ME, Romanelli F (2008). “Reexamining syphilis: an update on epidemiology, clinical manifestations, and management”. Ann Pharmacother. 42 (2): 226–36. doi:10.1345/aph.1K086. PMID 18212261.

[urlMycosis_Fungoides_and_the_Sézary_Syndrome_Treatment_(PDQ®)—Patient_Version_-_National_Cancer_Institute-3] “Mycosis Fungoides and the Sézary Syndrome Treatment (PDQ®)—Patient Version – National Cancer Institute”.

[pmid27512182-4] Mahajan K, Relhan V, Relhan AK, Garg VK (2016). “Pityriasis Rosea: An Update on Etiopathogenesis and Management of Difficult Aspects”. Indian J Dermatol. 61 (4): 375–84. doi:10.4103/0019-5154.185699. PMC 4966395. PMID 27512182.

[pmid19997691-5] Prantsidis A, Rigopoulos D, Papatheodorou G, Menounos P, Gregoriou S, Alexiou-Mousatou I, Katsambas A (2009). “Detection of human herpesvirus 8 in the skin of patients with pityriasis rosea”. Acta Derm. Venereol. 89 (6): 604–6. doi:10.2340/00015555-0703. PMID 19997691.

[pmid9109005-6] Smith KJ, Nelson A, Skelton H, Yeager J, Wagner KF (1997). “Pityriasis lichenoides et varioliformis acuta in HIV-1+ patients: a marker of early stage disease. The Military Medical Consortium for the Advancement of Retroviral Research (MMCARR)”. Int. J. Dermatol. 36 (2): 104–9. PMID 9109005.

[pmid23517392-7] Jiamton S, Tangjaturonrusamee C, Kulthanan K (2013). “Clinical features and aggravating factors in nummular eczema in Thais”. Asian Pac. J. Allergy Immunol. 31 (1): 36–42. PMID 23517392.

[urlSTD_Facts_-_Syphilis-8] “STD Facts – Syphilis”.

[pmid28523295-9] Neagu TP, Ţigliş M, Botezatu D, Enache V, Cobilinschi CO, Vâlcea-Precup MS, GrinŢescu IM (2017). “Clinical, histological and therapeutic features of Bowen’s disease”. Rom J Morphol Embryol. 58 (1): 33–40. PMID 28523295.

[pmid25201325-10] Murao K, Yoshioka R, Kubo Y (2014). “Human papillomavirus infection in Bowen disease: negative p53 expression, not p16(INK4a) overexpression, is correlated with human papillomavirus-associated Bowen disease”. J. Dermatol. 41 (10): 878–84. doi:10.1111/1346-8138.12613. PMID 25201325.

[pmid26354880-11] Szatkowski J, Schwartz RA (2015). “Acute generalized exanthematous pustulosis (AGEP): A review and update”. J. Am. Acad. Dermatol. 73 (5): 843–8. doi:10.1016/j.jaad.2015.07.017. PMID 26354880.

[pmid12466124-12] Schmid S, Kuechler PC, Britschgi M, Steiner UC, Yawalkar N, Limat A, Baltensperger K, Braathen L, Pichler WJ (2002). “Acute generalized exanthematous pustulosis: role of cytotoxic T cells in pustule formation”. Am. J. Pathol. 161 (6): 2079–86. doi:10.1016/S0002-9440(10)64486-0. PMC 1850901. PMID 12466124.

[pmid27222766-13] Ankad BS, Beergouder SL (2016). “Hypertrophic lichen planus versus prurigo nodularis: a dermoscopic perspective”. Dermatol Pract Concept. 6 (2): 9–15. doi:10.5826/dpc.0602a03. PMC 4866621. PMID 27222766.

[pmid19770446-14] Shengyuan L, Songpo Y, Wen W, Wenjing T, Haitao Z, Binyou W (2009). “Hepatitis C virus and lichen planus: a reciprocal association determined by a meta-analysis”. Arch Dermatol. 145 (9): 1040–7. doi:10.1001/archdermatol.2009.200. PMID 19770446.

[pmid9564592-15] Lutz ME, Daoud MS, McEvoy MT, Gibson LE (1998). “Subcorneal pustular dermatosis: a clinical study of ten patients”. Cutis. 61 (4): 203–8. PMID 9564592.

[pmid3056995-16] Kasha EE, Epinette WW (1988). “Subcorneal pustular dermatosis (Sneddon-Wilkinson disease) in association with a monoclonal IgA gammopathy: a report and review of the literature”. J. Am. Acad. Dermatol. 19 (5 Pt 1): 854–8. PMID 3056995.

[pmid1357895-17] Delaporte E, Colombel JF, Nguyen-Mailfer C, Piette F, Cortot A, Bergoend H (1992). “Subcorneal pustular dermatosis in a patient with Crohn’s disease”. Acta Derm. Venereol. 72 (4): 301–2. PMID 1357895.

[pmid23489057-18] Sauder MB, Glassman SJ (2013). “Palmoplantar subcorneal pustular dermatosis following adalimumab therapy for rheumatoid arthritis”. Int. J. Dermatol. 52 (5): 624–8. doi:10.1111/j.1365-4632.2012.05707.x. PMID 23489057.

[pmid7026622-19] Lambert WC, Everett MA (1981). “The nosology of parapsoriasis”. J. Am. Acad. Dermatol. 5 (4): 373–95. PMID 7026622.

[pmid16191852-20] Väkevä L, Sarna S, Vaalasti A, Pukkala E, Kariniemi AL, Ranki A (2005). “A retrospective study of the probability of the evolution of parapsoriasis en plaques into mycosis fungoides”. Acta Derm. Venereol. 85 (4): 318–23. doi:10.1080/00015550510030087. PMID 16191852.

[pmid16156342-21] Janniger CK, Schwartz RA, Szepietowski JC, Reich A (2005). “Intertrigo and common secondary skin infections”. Am Fam Physician. 72 (5): 833–8. PMID 16156342.

[pmid18577030-22] Satter EK, High WA (2008). “Langerhans cell histiocytosis: a review of the current recommendations of the Histiocyte Society”. Pediatr Dermatol. 25 (3): 291–5. doi:10.1111/j.1525-1470.2008.00669.x. PMID 18577030.

[pmid1636041-23] Stull MA, Kransdorf MJ, Devaney KO (1992). “Langerhans cell histiocytosis of bone”. Radiographics. 12 (4): 801–23. doi:10.1148/radiographics.12.4.1636041. PMID 1636041.

[pmid17527085-24] Sholl LM, Hornick JL, Pinkus JL, Pinkus GS, Padera RF (2007). “Immunohistochemical analysis of langerin in langerhans cell histiocytosis and pulmonary inflammatory and infectious diseases”. Am. J. Surg. Pathol. 31 (6): 947–52. doi:10.1097/01.pas.0000249443.82971.bb. PMID 17527085.

[pmid16047354-25] Grois N, Pötschger U, Prosch H, Minkov M, Arico M, Braier J, Henter JI, Janka-Schaub G, Ladisch S, Ritter J, Steiner M, Unger E, Gadner H (2006). “Risk factors for diabetes insipidus in langerhans cell histiocytosis”. Pediatr Blood Cancer. 46 (2): 228–33. doi:10.1002/pbc.20425. PMID 16047354.

[pmid15050029-26] Al Hasan M, Fitzgerald SM, Saoudian M, Krishnaswamy G (2004). “Dermatology for the practicing allergist: Tinea pedis and its complications”. Clin Mol Allergy. 2 (1): 5. doi:10.1186/1476-7961-2-5. PMC 419368. PMID 15050029.

[pmid16848386-27] Schwartz RA, Janusz CA, Janniger CK (2006). “Seborrheic dermatitis: an overview”. Am Fam Physician. 74 (1): 125–30. PMID 16848386.

[pmid18033062-28] Misery L, Touboul S, Vinçot C, Dutray S, Rolland-Jacob G, Consoli SG, Farcet Y, Feton-Danou N, Cardinaud F, Callot V, De La Chapelle C, Pomey-Rey D, Consoli SM (2007). “[Stress and seborrheic dermatitis]”. Ann Dermatol Venereol (in French). 134 (11): 833–7. PMID 18033062.

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Pityriasis rosea

Overview

Risk Factors

Natural History, Complications and Prognosis

References

References

References

References

Overview

References

Overview

Differential Diagnosis

References

References

Overview

References

Overview

References

Diagnosis

Treatment

Case Studies

Related Chapters

External Links

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