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Other papulosquamous disorders

The document covers various papulosquamous disorders, focusing on conditions such as pityriasis rosea and pityriasis rubra pilaris, detailing their definitions, epidemiology, clinical pictures, differential diagnoses, histological features, and treatments. Pityriasis rosea is characterized by a herald patch and self-limiting course, while pityriasis rubra pilaris is a rare chronic skin disease with distinct lesions. It also discusses parapsoriasis, outlining its classifications and clinical characteristics, with some cases linked to T-cell dysregulation.

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Other Papulosquamous Disorders
Psoriasis Pityriasis rosea Lichen Planus Lichen nitidus Seborrheic dermatitis Pityriasis rubra pilaris Exfoliative dermatitis Lichen striatus Parapsoriasis, small / large plaque Pityriasis lichenoides
Other important papulosquamous diseases 1. Mycosis fungoides (cutaneous T-cell lymphoma) 2. Discoid lupus erythematosus 3. Subacute cutaneous lupus erythematosus 4. Tinea corporis 5. Nummular eczema 6. Secondary syphilis 7. Drug eruptions 8. Erythema dyschromicum perstans 9. Keratosis lichenoides chronica 10. Lichen sclerosus 11. Lichenoid dermatitis 12. Lichenoid reaction of graft-versus-host disease 13. Extramammary Paget’s disease
Today’s Topics • Pityriasis Rosea • Pityriasis Rubra Pilaris (PRP) • Parapsoriasis • Pityriasis Lichenoides (Acute and chronic)
Pityriasis Rosea
Pityriasis Rosea (PR) • Definition • Epidemiology • Etiology • Clinical Picture • Differential Diagnoses • Histological features • Treatment
Definition • IT is common, self limited acute papulosquamous disorder often with distinctive and constant course lasting from 4-10 weeks. • Pityriasis: Any of several skin diseases marked by the formation and desquamation of fine scales. • Rosea: rose colored or pink. • Benign Self limiting but associated with increased miscarriage in first 15 wks. of pregnancy.
Epidemiology • Worldwide distribution. • AGE: Predominantly occur in adolescents and young adults 10-35 years but can occur rarely in infants and old persons. • SEX: F>M. • SEASON: more in spring & autumn. • Most cases of pityriasis rosea (PR) are sporadic.
Etiology Exact cause unknown but may be due to; i. INFECTIONS: HHV-6, HHV-7 infections but viral DNA couldn’t be detected from the lesion. Not contagious & gives life long immunity after outbreak. ii. DRUGS: Arsenic, Adalimumab, Barbiturates, Bismuth, Captopril, Clonidine, D-penicillamine, Etanercept, Gold, Isotretinoin, Ketotifen, Lithium, Metronidazole, Nortriptyline, Omeprazole, Terbinafine.
Clinical Picture
Clinical Picture I. PRODROME • May or may not be present only 5% of patients. • Fever • Malaise • Headache • Mild constitutional symptoms • Respiratory infection
Clinical Picture II. “HERALD PATCH” OR MOTHER PATCH • Seen in 50-80% of cases. • Preceding exanthem. • Raised plaque or patch. • Large (2 – 10 cm). • Usually single but may be multiple. • Usually oval. • Pink or salmon pink. • Collarette scales points inwards just inside the well-demarcated border. • Central clearing occasionally & slightly raised advancing margin (mimic tinea). • Usually on the trunk.
Herald Patch
Herald Patch
Clinical Picture III. SECONDARY ERUPTION (EXANTHEM) • Appear within 1-2 weeks. • May be asymptomatic or pruritic 25-75%. • Mainly of 2 types: 1. Small rounded papules with or w/o fine scaling that ↑ in number & spread peripherally. 2. Similar lesions to herald patch but smaller (1-2 cm): • Appear as discrete bilateral symmetrical oval salmon pink in color on the trunk and proximal aspects of the extremities with peripheral collarette scales. • Run along lines of cleavage (Langer’s lines) /parallel to the ribs giving fir tree or Christmas tree pattern.
Secondary eruption
Secondary eruption
Langer’s Lines
Christmas tree pattern
Christmas tree pattern
Clinical Picture IV. FADING OF THE LESIONS: • Spontaneous remission occurs within 4 to 8 weeks. • Occasionally lasts for 5 months or more. • Postinflammatory pigment changes can be observed. Both hypopigmentation and hyperpigmentation can follow the rash. • Recurrences are uncommon.
Mnemonic
Atypical Variants of Pityriasis Rosea • 20% of patients. • Atypical morphology, distribution, or both.
Atypical Variants of Pityriasis Rosea 1. Inverse PR: Involving the axilla, groin, hands, feet & may the face. It is more common in younger children & in those with darkly pigmented skin. 2. Drug-induced PR: herald patch may be absent. 3. Oral lesions of various types, including erythemato us plaques, punctate hemorrh-age, and ulcers. 4. Pityriasis rosea irritata: usually results from irritation and sweating, often as a consequ-ence of inadequate treatment. 5. Abortive: herald patch may be the sole manifestati on of the disease and is not followed by the typical rash. 6. Vesicular PR. 7. Erythema multiform e–like.
Atypical Variants of Pityriasis Rosea 8. Papular PR: scaling papules in the normal distribution; more common in young children, pregnant women, & black people (central Hyperpigmen tation & follicular papules). 9. Pustular PR. 10. Purpuric PR. 11. Photosensi tive PR. 12. Urticarial PR. 13. Unilateral PR: in which the lesions do not cross the midline. 14. limb-girdle PR: atypical large patches that tend to be fewer in number and coalescent.
Atypical Variants of PR
In dark individuals
Differential Diagnoses 1. Guttate psoriasis 2. Small plaque parapsoriasis 3. PLEVA 4. PLC (especially if persistent) 5. PRP 6. P. alba 7. Tinea corporis 8. Tinea Versicolor 9. Seborrhoeic dermatitis 10. Discoid dermatitis 11. Viral Exanthems 12. Drug eruptions 13. Secondary syphilis 14. Erythema multiforme
Histological features
Histological features 1. Patchy epidermal spongiosis & lymphocytes 2. Lymphocytes surrounding dermal vessels 3. Extravasated red blood cells 4. Patchy hyperkeratosis & parakeratosis
Histological features
Histological features
Histological features 1. Focal (Patchy) or diffuse parakeratosis. 2. Absence of granular layer. 3. Mild acanthosis. 4. Focal spongiosis. 5. Occasional dyskeratotic cells with an eosinophilic homogeneous appearance. 6. Exocytosis. 7. Perivascular dermal infiltration with lymphocytes. 8. Edema of dermis. 9. Often some extravasated red blood cells. 10. Increase in eosinophils in drug induced PR.
Treatment 1. Assurance: Since it is self limited no treatment is required. 2. Antipruritic lotions. 3. Antihistamines: Symptomatic relief from itching. 4. Topical steroids: Low-mid strength. 5. Systemic steroids: Short course. 6. Erythromycin: 1 gm q.i.d for 2 weeks. 7. Phototherapy: NB-UVB light may hasten the disappearance or natural sunlight if treatment is begun in the first week of eruption. 8. Acyclovir: Standard dose  not effective. High dose 800 mg five times/d for 1 week may give rapid clearance of the lesions.
Pityriasis Rubra Pilaris
Pityriasis Rubra Pilaris (PRP) • Definition • Epidemiology • Etiology • Clinical Picture • Classification • Differential Diagnoses • Histological features • Treatment
Definition • A rare chronic papulosquamous skin disease characterized by the appearance of keratotic follicular papules, salmon-colored erythematous plaques interspersed with distinct islands of uninvolved skin, and palmoplantar keratoderma.
Epidemiology • Rare. • M=F. • Nearly all cases are acquired sporadic, with occasional reports of a familial inherited form. • Familial cases show autosomal dominant inheritance with incomplete penetrance and variable expression. Familial PRP usually presents at birth or appears during the first years of life and runs a chronic course.
Etiology • The actual cause of PRP is unknown. • May be due to: 1. Dysfunction in keratinization or vitamin A metabolism. 2. An autoimmune pathogenesis 3. An abnormal immunologic response to particular antigens. 4. Physical trigger.
Clinical Picture CRITERIA FOR SPOT DIAGNOSIS: 1. Coalescence scaling orange–red )salmon color) plaques with sharp borders covered with fine powdery scales & islands of sparing (nappes claires) in-between. 2. Follicular papules with an erythematous base especially on the dorsal aspect of the proximal fingers (nutmeg grater appearance). 3. An orange–red waxy keratoderma of the palms and soles in most patients.
Clinical Picture • The plaques may progress to an erythroderma with varying degrees of exfoliation. • Erythema with a fine diffuse scale is often seen on the scalp. • Nail changes include 1. Distal yellow-brown discoloration 2. Subungual hyperkeratosis 3. Longitudinal ridging 4. Nail plate thickening 5. Splinter hemorrhages 6. Nail dystrophy and shedding may occur. • The mucous membranes are rarely involved, but they may show features similar to oral lichen planus. • Pruritus and burning in 20% of cases. • Mild ectropion may develop when the face becomes uniformly erythematous. • Both photoaggravated and phototriggered forms of PRP can also occur.
Classification • According to Griffiths classification there are 6 types of PRP. • According to age group and typicality of clinical presentation.
Type I/Classic adult PRP
Type I/Classic adult PRP
Type I/Classic adult PRP
Type I/Classic adult PRP
Type I/Classic adult PRP
Type I/Classic adult PRP
Type I/Classic adult PRP
Type I/Classic adult PRP
Type II/Atypical adult PRP
Type III/Classic juvenile PRP
Type III/Classic juvenile PRP
Type IV/Circumscribed juvenile PRP
Type V/Atypical juvenile PRP
Clinical type % of patients Age at onset Distribution Skin findings Course I (classical adult) 50 Peak in the 6th decade Generalized, beginning on the head & neck then spreading caudally •Red-orange plaques, confluent with islands of sparing •Perifollicular papules with keratotic plugs •Diffuse, waxy PPK Often resolves within 3 years II (atypical adult) 5 Adults of various ages Generalized •Areas of eczematous dermatitis •Ichthyosiform scale on the lower extremities •PPK with lamellated scale •Alopecia Chronic intractable III (classic juvenile) 10 Peaks in the first few years of life and the late teens Generalized •Similar to type I (see above) •<50% have palmoplantar involvement Often resolves within 3 years IV (circumscribed juvenile) 25 Prepubertal Focal, favoring the elbows and knees •Well-circumscribed, scaly, erythematous plaques •Perifollicular papules with keratotic plugs Variable Some cases clear in the late teens V (atypical juvenile) 5 First few years of life Generalized •Ichthyosiform dermatitis •Perifollicular papules with keratotic plugs •Scleroderma-like appearance of hands & feet •Accounts for most familial cases of PRP Chronic intractable VI (HIV-associated) NA Variable Generalized •Similar to type I (see above) •Associated with acne conglobata, hidradinitis suppurativa, and lichen spinulosus Refractory May respond to HAART
Differential Diagnoses 1. Psoriasis. 2. Erythroderma. 3. Seborrheic dermatitis (Early cases). 4. Dermatomyositis. 5. Cutaneous T-cell lymphoma. 6. Erythrokeratodermia variabilis 7. Kawasaki disease (Children with acute-onset PRP).
Histological features
Histological features
Histological features
Histological features
Histological features
Histological features
Histological features PSORIASIFORM DERMATITIS: 1. Biopsy from non-follicular lesion consists of distinctive orthokeratosis and parakeratosis alternating in both vertical and horizontal directions (checkerboard pattern). 2. The hair follicles are dilated and filled with a keratinous plug, while the “shoulder effect” of stratum corneum surrounding the follicular opening frequently shows parakeratosis. 3. Focal or confluent hypergranulosis. 4. Thick suprapapillary plate. 5. Occasionally, mild spongiosis. 6. Scattered intraepidermal lymphocytes. 7. Acantholysis and focal acantholytic dyskeratosis, may be present. 8. Broad slightly elongated epidermal rete ridges, narrow dermal papillae. 9. Perivascular lymphohistiocytic infiltrate in the superficial dermis. 10. Small numbers of plasma cells and eosinophils may be present.
Treatment • Empiric as the actual cause of PRP is unknown & in many patients there is spontaneous resolution. • The goals of treatment are to reduce morbidity and to prevent complications. • Consider combination treatment.
FIRST LINE SECOND LINE Topical 1.Emollients reduce fissuring and dryness. 2.Keratolytics (salicylic acid, urea). 3.Vitamin D3 (calcipotriol). 1.Glucocorticoids (medium to high potency). 2.Topical retinoids (tazarotene). 3.Calcineurin inhibitors. Photo(chemo)therapy (May respond well or may flare) 1.Narrowband UVB. 2.Extracorporeal photopheresis. 1.Topical or Systemic PUVA. 2.Ultraviolet A1. 3.Broadband UVB. Systemic 1.Oral retinoids: Currently they are the first line of therapy. Isotretinoin (1 to 1.5 mg/kg/day for 3–6 months), although acitretin (0.5 to 0.75 mg/kg per day) may be more effective in clearing lesions. 2.Methotrexate (10 to 25 mg weekly, IM or orally, once a week) has shown variable rates of success may be combination with a systemic retinoid. 3.Triple antiretroviral therapy (for HIV-associated variant). 1.Oral vitamin A: sometimes in combination with vitamins B and D. 2.Azathioprine (100 to 150 mg/day) but its effect is also inconsistent. 3.Cyclosporine (5 mg/kg/day) Several cases of adult-type PRP showed significant clearance in 2-4 wks. 4.Fumaric acid esters. 5.Biological agents: TNF-αinhibitors and Ustekinumab.
Treatment Erythroderma with islands of sparing on the chest and abdomen and yellow palmar keratoderma with fissuring Erythema and scaling subsided following 3 infusions of infliximab.
Parapsor ias i s
Parapsoriasis • Definition • Classification • Epidemiology • Etiology • Clinical Picture • Differential Diagnoses • Histological features • Treatment • Prognosis
Definition • Group of idiopathic chronic cutaneous diseases that can be characterized by scaly patches or slightly elevated papules and/or plaques that have a resemblance to psoriasis.
Classification A. Small plaque parapsoriasis B. Large plaque parapsoriasis
Epidemiology • Presentation most frequently is in middle age; peak incidence is in the fifth decade of life. • Small plaque parapsoriasis the male-to-female ratio is 3:1.
Etiology • Exact cause is unknown. • T-cell–predominantly CD4+ infiltrates in the skin. • Small plaque parapsoriasis shows multiple dominant clones. • Large plaque parapsoriasis is a may be due to long-term antigen stimulation & it is associated with a dominant T-cell clone, one that may represent up to 50% of the T-cell infiltrate. • Human herpesvirus type 8 may be detected in skin lesions of large plaque parapsoriasis and the significance is unclear.
Clinical Picture • Onset of parapsoriasis is indolent. • Asymptomatic or mildly pruritic. • Composed of patches rather than plaques. • Typically persistent and can slowly progress to become more extensive. • Favor more sun-protected sites.
Clinical Picture SMALL PLAQUE PARAPSORIASIS • Can last months to several years; the disease often resolves spontaneously. • Lesions are well-circumscribed, round–oval slightly scaly, light salmon-colored patches that measure <5 cm in diameter and are scattered over the trunk and extremities.
Clinical Picture SMALL PLAQUE PARAPSORIASIS • Digitate pattern “Digitate Dermatosis” is a distinctive form of small plaque disease that consists of palisading elongated fingerlike patches that follow the dermatome and are most prominently displayed symmetrically on the lateral flank and abdomen. • They may measure 10 cm or more along their long axis.
Digitate dermatosis
Clinical Picture LARGE PLAQUE PARAPSORIASIS • It is chronic and progresses over many years, sometimes decades. It may progress to CTCL. • Manifests as faint erythematous patches with arcuate geographic borders. Each lesion often is >5 cm in diameter. • Lesions are scattered on the proximal extremities and the trunk and often show a bathing-suit distribution. • Surfaces of the lesions have a faint red-to-salmon color; show flaky thin scales; and have an atrophic, cigarette-paper or tissue-paper, wrinkling quality or may show poikiloderma or retiform (all retiform cases progress to overt MF).
Large plaque parapsoriasis
Retiform parapsoriasis
Differential Diagnoses SMALL PLAQUE PARAPSORIASIS 1. Pityriasis rosea 2. Drug eruption, esp. PR-like 3. Guttate psoriasis 4. PLC 5. MF 6. 2ry syphilis 7. Nummular dermatitis LARGE PLAQUE PARAPSORIASIS 1. MF 2. Drug eruption, esp. MF-like 3. Psoriasis 4. Causes of Poikiloderma a. Poikilodermatous autoimmune connective tissue disease (e .g . dermatomyositis) b. Poikilodermatous genodermatoses c. Chronic radiodermatitis
Laboratory studies • Complete blood cell count with differential should be performed, and a high lymphocyte count or the presence of Sézary cells suggests mycosis fungoides.
Histological features SMALL PLAQUE PARAPSORIASIS • Exhibit a mild, nonspecific spongiotic dermatitis, focal hyperkeratosis, parakeratosis mild superficial perivascular lymphocytic infiltrate, scale crust, and occasional exocytosis. • Lymphocytes are small and do not show atypical features. do not show histologic atypia to suggest malignant transformation. LARGE PLAQUE PARAPSORIASIS • May have similar histologic findings or an interface lymphocytic infiltrate with a variable degree of lichenoid features. • Blood vessels are dilated, and melanophages can be present. • The epidermis shows flattening of the rete ridges when epidermal atrophy is prominent on clinical examination. • Acanthosis of the epidermis and irregular hyperkeratosis of the cornified layer are present. • In contrast to small plaque parapsoriasis, spongiosis is absent.
Histological features
Histological features
Histological features
Treatment FIRST LINE 1. Assurance (small plaque parapsoriasis) 2. Emollients 3. Topical corticosteroids (mid- to high-potency) 4. Topical coal tar products 5. Phototherapy: Sunlight, Broadband or Narrowband ultraviolet B 6. Antihistamines (If there is pruritus) SECONDLINE (Mainly for large-plaque parapsoriasis cases considered to be early MF & must be treated) 1. Topical bexarotene 2. Topical imiquimod 3. PUVA 4. Topical mechlorethamine (nitrogen mustard) 5. Topical carmustine (BCNU) 6. Subcutaneous interferon-α
Prognosis SMALL PLAQUE PARAPSORIASIS • Is a stable benign disorder that rarely if ever progresses. It lasts several months to years and can spontaneously resolve. LARGE PLAQUE PARAPSORIASIS • Is chronic & more ominous in that approximately 10-35% of patients progress to CTCL. • It does not enter remission without treatment & requires closer follow-up. • Induration or epidermal atrophy should prompt a repeat skin biopsy to consider a diagnosis of MF in evolution. The 5-year survival rate, however, still remains high and is greater than 90%.
Pityriasis Lichenoides
Pityriasis Lichenoides • Definition • Types • Epidemiology • Etiology • Clinical Picture • Differential Diagnoses • Histological features • Treatment
Definition • They are papular clonal T-cell disorders characterized by recurrent crops of spontaneously regressing erythematous papules.
Types I. Pityriasis lichenoides et varioliformis acuta (PLEVA/Mucha–Habermann disease) II. Pityriasis lichenoides chronica (PLC)
Epidemiology • Both are more prevalent in the pediatric population, but it affects patients in all age groups, races and geographic regions. • There is a male predominance.
Etiology • The exact etiology is unknown. • May be response to foreign antigens such as infectious agents or drugs. • The infiltrate is predominantly T cells (CD8+) that are often monoclonal thus they are lymphoproliferative disorders.
Clinical Picture • The acute and chronic forms of pityriasis lichenoides exist on a disease spectrum with variable presentations so many patients have intermediate or mixed manifestations, either serially or concurrently. • Can resolve spontaneously after weeks to months or it may pursue a chronic relapsing course.
Clinical Picture PLEVA PLC Lesions • Vesicular, ulcerative, crusted or pustular. • Scaly erythematous to red–brown papules. Course • Rapid. • More indolent. Resolution • Within weeks may  varioliform scars if dermal damage is extensive. • Over weeks to months  hypopigmented macules (more obvious in darkly pigmented individuals and may be the presenting C/O). Extracut. manifestation • Malaise, fever, lymphadenopathy, arthritis and/or bacteremia. • “Febrile ulceronecrotic Mucha–Habermann disease (FUMHD)” severe variants with mucosal, gastrointestinal and pulmonary involvement. • Absent.
PLEVA
PLEVA
PLEVA
PLEVA
PLC
PLC
PLC
PLC
PLC
Differential Diagnoses PLEVA 1. Lymphomatoid papulosis 2. Cutaneous small vessel vasculitis 3. Lichenoid drug eruption 4. Arthropod reactions 5. Varicella, enteroviral exanthems 6. Folliculitis 7. Erythema multiforme 8. Dermatitis herpetiformis PLC 1. Small plaque parapsoriasis 2. Guttate psoriasis 3. Lichen planus 4. Pityriasis rosea 5. Secondary syphilis 6. Lymphomatoid papulosis 7. Papular dermatitis 8. Lichenoid drug eruption
Histological features • Pityriasis lichenoides exhibits a superficial perivascular interface dermatitis in all cases.
Histological features PLEVA PLC S. corneum • Hyperkeratosis • Foci of parakeratosis • Few neutrophils • Laminated Hyperkeratosis • Foci of thin flat parakeratosis • w/o neutrophils Granular cell layer • Deficient beneath mound of parakeratosis • Well formed Prickle cell layer • From edema to extensive epidermal necrosis in well-developed lesions. • No or focal necrotic keratinocytes Basal cell layer & dermo-epidermal junction. • Marked vacuolar changes • Denser interface lymphocytic infiltrate. • Very focal mild basal cell vacuolization which may not be evident in well-developed or resolving lesions. • Milder interface lymphocytic infiltrate. Dermis • Shows denser superficial &deep perivascular wedge-shaped lymphocytic infiltrates. • Numerous erythrocyte extravasation. • Only a superficial perivascular lymphocytic infiltrate. • Mild erythrocyte extravasation.
PLEVA
PLC
Treatment FIRST LINE 1. Topical corticosteroids 2. Topical coal tar preparations 3. Antibiotics (erythromycin 500 mg PO 2-4× daily; azithromycin; tetracycline 500 mg PO 2-4× daily, minocycline 100 mg PO twice daily) 4. Phototherapy (Sunlight, ultraviolet A, broadband or narrowband UVB) SECOND LINE 1. Topical tacrolimus 2. Methotrexate (10-25 mg PO weekly) 3. Phototherapy (ultraviolet AI, PUVA) 4. Cyclosporine 5. Biological agents: etanercept 6. IVIg
Treatment • If a drug association is suspected, stop the offending drug. • SPECIAL TREATMENTS: 1. Prednisone: (60/40/20 mg PO taper, 5 days each) If there is fever, arthritis or other systemic findings. 2. Antihistamines: if pruritus is present. 3. Other Systemic antibiotics: If there is secondary infection.
REFERENCES • Bolognia 3rd ed • http://dermnetnz.org • Google images • Husein Oozeerally (Presentation) • Jonathan Faulkner (Presentation) • emdicine.com • dermis.net
THANK YOU

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Other papulosquamous disorders

  • 1.
  • 3.
    Psoriasis Pityriasis rosea Lichen Planus Lichen nitidus Seborrheic dermatitis Pityriasis rubra pilaris Exfoliative dermatitis Lichen striatus Parapsoriasis, small / large plaque Pityriasis lichenoides
  • 4.
    Other important papulosquamousdiseases 1. Mycosis fungoides (cutaneous T-cell lymphoma) 2. Discoid lupus erythematosus 3. Subacute cutaneous lupus erythematosus 4. Tinea corporis 5. Nummular eczema 6. Secondary syphilis 7. Drug eruptions 8. Erythema dyschromicum perstans 9. Keratosis lichenoides chronica 10. Lichen sclerosus 11. Lichenoid dermatitis 12. Lichenoid reaction of graft-versus-host disease 13. Extramammary Paget’s disease
  • 5.
    Today’s Topics •Pityriasis Rosea • Pityriasis Rubra Pilaris (PRP) • Parapsoriasis • Pityriasis Lichenoides (Acute and chronic)
  • 6.
  • 7.
    Pityriasis Rosea (PR) • Definition • Epidemiology • Etiology • Clinical Picture • Differential Diagnoses • Histological features • Treatment
  • 8.
    Definition • ITis common, self limited acute papulosquamous disorder often with distinctive and constant course lasting from 4-10 weeks. • Pityriasis: Any of several skin diseases marked by the formation and desquamation of fine scales. • Rosea: rose colored or pink. • Benign Self limiting but associated with increased miscarriage in first 15 wks. of pregnancy.
  • 9.
    Epidemiology • Worldwidedistribution. • AGE: Predominantly occur in adolescents and young adults 10-35 years but can occur rarely in infants and old persons. • SEX: F>M. • SEASON: more in spring & autumn. • Most cases of pityriasis rosea (PR) are sporadic.
  • 10.
    Etiology Exact causeunknown but may be due to; i. INFECTIONS: HHV-6, HHV-7 infections but viral DNA couldn’t be detected from the lesion. Not contagious & gives life long immunity after outbreak. ii. DRUGS: Arsenic, Adalimumab, Barbiturates, Bismuth, Captopril, Clonidine, D-penicillamine, Etanercept, Gold, Isotretinoin, Ketotifen, Lithium, Metronidazole, Nortriptyline, Omeprazole, Terbinafine.
  • 11.
  • 12.
    Clinical Picture I.PRODROME • May or may not be present only 5% of patients. • Fever • Malaise • Headache • Mild constitutional symptoms • Respiratory infection
  • 13.
    Clinical Picture II.“HERALD PATCH” OR MOTHER PATCH • Seen in 50-80% of cases. • Preceding exanthem. • Raised plaque or patch. • Large (2 – 10 cm). • Usually single but may be multiple. • Usually oval. • Pink or salmon pink. • Collarette scales points inwards just inside the well-demarcated border. • Central clearing occasionally & slightly raised advancing margin (mimic tinea). • Usually on the trunk.
  • 14.
  • 15.
  • 16.
    Clinical Picture III.SECONDARY ERUPTION (EXANTHEM) • Appear within 1-2 weeks. • May be asymptomatic or pruritic 25-75%. • Mainly of 2 types: 1. Small rounded papules with or w/o fine scaling that ↑ in number & spread peripherally. 2. Similar lesions to herald patch but smaller (1-2 cm): • Appear as discrete bilateral symmetrical oval salmon pink in color on the trunk and proximal aspects of the extremities with peripheral collarette scales. • Run along lines of cleavage (Langer’s lines) /parallel to the ribs giving fir tree or Christmas tree pattern.
  • 17.
  • 18.
  • 19.
  • 20.
  • 21.
  • 22.
    Clinical Picture IV.FADING OF THE LESIONS: • Spontaneous remission occurs within 4 to 8 weeks. • Occasionally lasts for 5 months or more. • Postinflammatory pigment changes can be observed. Both hypopigmentation and hyperpigmentation can follow the rash. • Recurrences are uncommon.
  • 23.
  • 24.
    Atypical Variants ofPityriasis Rosea • 20% of patients. • Atypical morphology, distribution, or both.
  • 25.
    Atypical Variants ofPityriasis Rosea 1. Inverse PR: Involving the axilla, groin, hands, feet & may the face. It is more common in younger children & in those with darkly pigmented skin. 2. Drug-induced PR: herald patch may be absent. 3. Oral lesions of various types, including erythemato us plaques, punctate hemorrh-age, and ulcers. 4. Pityriasis rosea irritata: usually results from irritation and sweating, often as a consequ-ence of inadequate treatment. 5. Abortive: herald patch may be the sole manifestati on of the disease and is not followed by the typical rash. 6. Vesicular PR. 7. Erythema multiform e–like.
  • 26.
    Atypical Variants ofPityriasis Rosea 8. Papular PR: scaling papules in the normal distribution; more common in young children, pregnant women, & black people (central Hyperpigmen tation & follicular papules). 9. Pustular PR. 10. Purpuric PR. 11. Photosensi tive PR. 12. Urticarial PR. 13. Unilateral PR: in which the lesions do not cross the midline. 14. limb-girdle PR: atypical large patches that tend to be fewer in number and coalescent.
  • 27.
  • 28.
  • 29.
    Differential Diagnoses 1.Guttate psoriasis 2. Small plaque parapsoriasis 3. PLEVA 4. PLC (especially if persistent) 5. PRP 6. P. alba 7. Tinea corporis 8. Tinea Versicolor 9. Seborrhoeic dermatitis 10. Discoid dermatitis 11. Viral Exanthems 12. Drug eruptions 13. Secondary syphilis 14. Erythema multiforme
  • 30.
  • 32.
    Histological features 1.Patchy epidermal spongiosis & lymphocytes 2. Lymphocytes surrounding dermal vessels 3. Extravasated red blood cells 4. Patchy hyperkeratosis & parakeratosis
  • 33.
  • 34.
  • 35.
    Histological features 1.Focal (Patchy) or diffuse parakeratosis. 2. Absence of granular layer. 3. Mild acanthosis. 4. Focal spongiosis. 5. Occasional dyskeratotic cells with an eosinophilic homogeneous appearance. 6. Exocytosis. 7. Perivascular dermal infiltration with lymphocytes. 8. Edema of dermis. 9. Often some extravasated red blood cells. 10. Increase in eosinophils in drug induced PR.
  • 36.
    Treatment 1. Assurance:Since it is self limited no treatment is required. 2. Antipruritic lotions. 3. Antihistamines: Symptomatic relief from itching. 4. Topical steroids: Low-mid strength. 5. Systemic steroids: Short course. 6. Erythromycin: 1 gm q.i.d for 2 weeks. 7. Phototherapy: NB-UVB light may hasten the disappearance or natural sunlight if treatment is begun in the first week of eruption. 8. Acyclovir: Standard dose  not effective. High dose 800 mg five times/d for 1 week may give rapid clearance of the lesions.
  • 38.
  • 39.
    Pityriasis Rubra Pilaris(PRP) • Definition • Epidemiology • Etiology • Clinical Picture • Classification • Differential Diagnoses • Histological features • Treatment
  • 40.
    Definition • Arare chronic papulosquamous skin disease characterized by the appearance of keratotic follicular papules, salmon-colored erythematous plaques interspersed with distinct islands of uninvolved skin, and palmoplantar keratoderma.
  • 41.
    Epidemiology • Rare. • M=F. • Nearly all cases are acquired sporadic, with occasional reports of a familial inherited form. • Familial cases show autosomal dominant inheritance with incomplete penetrance and variable expression. Familial PRP usually presents at birth or appears during the first years of life and runs a chronic course.
  • 42.
    Etiology • Theactual cause of PRP is unknown. • May be due to: 1. Dysfunction in keratinization or vitamin A metabolism. 2. An autoimmune pathogenesis 3. An abnormal immunologic response to particular antigens. 4. Physical trigger.
  • 43.
    Clinical Picture CRITERIAFOR SPOT DIAGNOSIS: 1. Coalescence scaling orange–red )salmon color) plaques with sharp borders covered with fine powdery scales & islands of sparing (nappes claires) in-between. 2. Follicular papules with an erythematous base especially on the dorsal aspect of the proximal fingers (nutmeg grater appearance). 3. An orange–red waxy keratoderma of the palms and soles in most patients.
  • 44.
    Clinical Picture •The plaques may progress to an erythroderma with varying degrees of exfoliation. • Erythema with a fine diffuse scale is often seen on the scalp. • Nail changes include 1. Distal yellow-brown discoloration 2. Subungual hyperkeratosis 3. Longitudinal ridging 4. Nail plate thickening 5. Splinter hemorrhages 6. Nail dystrophy and shedding may occur. • The mucous membranes are rarely involved, but they may show features similar to oral lichen planus. • Pruritus and burning in 20% of cases. • Mild ectropion may develop when the face becomes uniformly erythematous. • Both photoaggravated and phototriggered forms of PRP can also occur.
  • 45.
    Classification • Accordingto Griffiths classification there are 6 types of PRP. • According to age group and typicality of clinical presentation.
  • 46.
  • 47.
  • 48.
  • 49.
  • 50.
  • 51.
  • 52.
  • 53.
  • 54.
  • 55.
  • 56.
  • 57.
  • 58.
  • 59.
    Clinical type %of patients Age at onset Distribution Skin findings Course I (classical adult) 50 Peak in the 6th decade Generalized, beginning on the head & neck then spreading caudally •Red-orange plaques, confluent with islands of sparing •Perifollicular papules with keratotic plugs •Diffuse, waxy PPK Often resolves within 3 years II (atypical adult) 5 Adults of various ages Generalized •Areas of eczematous dermatitis •Ichthyosiform scale on the lower extremities •PPK with lamellated scale •Alopecia Chronic intractable III (classic juvenile) 10 Peaks in the first few years of life and the late teens Generalized •Similar to type I (see above) •<50% have palmoplantar involvement Often resolves within 3 years IV (circumscribed juvenile) 25 Prepubertal Focal, favoring the elbows and knees •Well-circumscribed, scaly, erythematous plaques •Perifollicular papules with keratotic plugs Variable Some cases clear in the late teens V (atypical juvenile) 5 First few years of life Generalized •Ichthyosiform dermatitis •Perifollicular papules with keratotic plugs •Scleroderma-like appearance of hands & feet •Accounts for most familial cases of PRP Chronic intractable VI (HIV-associated) NA Variable Generalized •Similar to type I (see above) •Associated with acne conglobata, hidradinitis suppurativa, and lichen spinulosus Refractory May respond to HAART
  • 60.
    Differential Diagnoses 1.Psoriasis. 2. Erythroderma. 3. Seborrheic dermatitis (Early cases). 4. Dermatomyositis. 5. Cutaneous T-cell lymphoma. 6. Erythrokeratodermia variabilis 7. Kawasaki disease (Children with acute-onset PRP).
  • 61.
  • 62.
  • 63.
  • 64.
  • 65.
  • 66.
  • 67.
    Histological features PSORIASIFORMDERMATITIS: 1. Biopsy from non-follicular lesion consists of distinctive orthokeratosis and parakeratosis alternating in both vertical and horizontal directions (checkerboard pattern). 2. The hair follicles are dilated and filled with a keratinous plug, while the “shoulder effect” of stratum corneum surrounding the follicular opening frequently shows parakeratosis. 3. Focal or confluent hypergranulosis. 4. Thick suprapapillary plate. 5. Occasionally, mild spongiosis. 6. Scattered intraepidermal lymphocytes. 7. Acantholysis and focal acantholytic dyskeratosis, may be present. 8. Broad slightly elongated epidermal rete ridges, narrow dermal papillae. 9. Perivascular lymphohistiocytic infiltrate in the superficial dermis. 10. Small numbers of plasma cells and eosinophils may be present.
  • 68.
    Treatment • Empiricas the actual cause of PRP is unknown & in many patients there is spontaneous resolution. • The goals of treatment are to reduce morbidity and to prevent complications. • Consider combination treatment.
  • 69.
    FIRST LINE SECONDLINE Topical 1.Emollients reduce fissuring and dryness. 2.Keratolytics (salicylic acid, urea). 3.Vitamin D3 (calcipotriol). 1.Glucocorticoids (medium to high potency). 2.Topical retinoids (tazarotene). 3.Calcineurin inhibitors. Photo(chemo)therapy (May respond well or may flare) 1.Narrowband UVB. 2.Extracorporeal photopheresis. 1.Topical or Systemic PUVA. 2.Ultraviolet A1. 3.Broadband UVB. Systemic 1.Oral retinoids: Currently they are the first line of therapy. Isotretinoin (1 to 1.5 mg/kg/day for 3–6 months), although acitretin (0.5 to 0.75 mg/kg per day) may be more effective in clearing lesions. 2.Methotrexate (10 to 25 mg weekly, IM or orally, once a week) has shown variable rates of success may be combination with a systemic retinoid. 3.Triple antiretroviral therapy (for HIV-associated variant). 1.Oral vitamin A: sometimes in combination with vitamins B and D. 2.Azathioprine (100 to 150 mg/day) but its effect is also inconsistent. 3.Cyclosporine (5 mg/kg/day) Several cases of adult-type PRP showed significant clearance in 2-4 wks. 4.Fumaric acid esters. 5.Biological agents: TNF-αinhibitors and Ustekinumab.
  • 70.
    Treatment Erythroderma withislands of sparing on the chest and abdomen and yellow palmar keratoderma with fissuring Erythema and scaling subsided following 3 infusions of infliximab.
  • 72.
  • 73.
    Parapsoriasis • Definition • Classification • Epidemiology • Etiology • Clinical Picture • Differential Diagnoses • Histological features • Treatment • Prognosis
  • 74.
    Definition • Groupof idiopathic chronic cutaneous diseases that can be characterized by scaly patches or slightly elevated papules and/or plaques that have a resemblance to psoriasis.
  • 75.
    Classification A. Smallplaque parapsoriasis B. Large plaque parapsoriasis
  • 76.
    Epidemiology • Presentationmost frequently is in middle age; peak incidence is in the fifth decade of life. • Small plaque parapsoriasis the male-to-female ratio is 3:1.
  • 77.
    Etiology • Exactcause is unknown. • T-cell–predominantly CD4+ infiltrates in the skin. • Small plaque parapsoriasis shows multiple dominant clones. • Large plaque parapsoriasis is a may be due to long-term antigen stimulation & it is associated with a dominant T-cell clone, one that may represent up to 50% of the T-cell infiltrate. • Human herpesvirus type 8 may be detected in skin lesions of large plaque parapsoriasis and the significance is unclear.
  • 78.
    Clinical Picture •Onset of parapsoriasis is indolent. • Asymptomatic or mildly pruritic. • Composed of patches rather than plaques. • Typically persistent and can slowly progress to become more extensive. • Favor more sun-protected sites.
  • 79.
    Clinical Picture SMALLPLAQUE PARAPSORIASIS • Can last months to several years; the disease often resolves spontaneously. • Lesions are well-circumscribed, round–oval slightly scaly, light salmon-colored patches that measure <5 cm in diameter and are scattered over the trunk and extremities.
  • 80.
    Clinical Picture SMALLPLAQUE PARAPSORIASIS • Digitate pattern “Digitate Dermatosis” is a distinctive form of small plaque disease that consists of palisading elongated fingerlike patches that follow the dermatome and are most prominently displayed symmetrically on the lateral flank and abdomen. • They may measure 10 cm or more along their long axis.
  • 81.
  • 82.
    Clinical Picture LARGEPLAQUE PARAPSORIASIS • It is chronic and progresses over many years, sometimes decades. It may progress to CTCL. • Manifests as faint erythematous patches with arcuate geographic borders. Each lesion often is >5 cm in diameter. • Lesions are scattered on the proximal extremities and the trunk and often show a bathing-suit distribution. • Surfaces of the lesions have a faint red-to-salmon color; show flaky thin scales; and have an atrophic, cigarette-paper or tissue-paper, wrinkling quality or may show poikiloderma or retiform (all retiform cases progress to overt MF).
  • 83.
  • 84.
  • 85.
    Differential Diagnoses SMALLPLAQUE PARAPSORIASIS 1. Pityriasis rosea 2. Drug eruption, esp. PR-like 3. Guttate psoriasis 4. PLC 5. MF 6. 2ry syphilis 7. Nummular dermatitis LARGE PLAQUE PARAPSORIASIS 1. MF 2. Drug eruption, esp. MF-like 3. Psoriasis 4. Causes of Poikiloderma a. Poikilodermatous autoimmune connective tissue disease (e .g . dermatomyositis) b. Poikilodermatous genodermatoses c. Chronic radiodermatitis
  • 86.
    Laboratory studies •Complete blood cell count with differential should be performed, and a high lymphocyte count or the presence of Sézary cells suggests mycosis fungoides.
  • 87.
    Histological features SMALLPLAQUE PARAPSORIASIS • Exhibit a mild, nonspecific spongiotic dermatitis, focal hyperkeratosis, parakeratosis mild superficial perivascular lymphocytic infiltrate, scale crust, and occasional exocytosis. • Lymphocytes are small and do not show atypical features. do not show histologic atypia to suggest malignant transformation. LARGE PLAQUE PARAPSORIASIS • May have similar histologic findings or an interface lymphocytic infiltrate with a variable degree of lichenoid features. • Blood vessels are dilated, and melanophages can be present. • The epidermis shows flattening of the rete ridges when epidermal atrophy is prominent on clinical examination. • Acanthosis of the epidermis and irregular hyperkeratosis of the cornified layer are present. • In contrast to small plaque parapsoriasis, spongiosis is absent.
  • 88.
  • 89.
  • 90.
  • 91.
    Treatment FIRST LINE 1. Assurance (small plaque parapsoriasis) 2. Emollients 3. Topical corticosteroids (mid- to high-potency) 4. Topical coal tar products 5. Phototherapy: Sunlight, Broadband or Narrowband ultraviolet B 6. Antihistamines (If there is pruritus) SECONDLINE (Mainly for large-plaque parapsoriasis cases considered to be early MF & must be treated) 1. Topical bexarotene 2. Topical imiquimod 3. PUVA 4. Topical mechlorethamine (nitrogen mustard) 5. Topical carmustine (BCNU) 6. Subcutaneous interferon-α
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    Prognosis SMALL PLAQUEPARAPSORIASIS • Is a stable benign disorder that rarely if ever progresses. It lasts several months to years and can spontaneously resolve. LARGE PLAQUE PARAPSORIASIS • Is chronic & more ominous in that approximately 10-35% of patients progress to CTCL. • It does not enter remission without treatment & requires closer follow-up. • Induration or epidermal atrophy should prompt a repeat skin biopsy to consider a diagnosis of MF in evolution. The 5-year survival rate, however, still remains high and is greater than 90%.
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    Pityriasis Lichenoides •Definition • Types • Epidemiology • Etiology • Clinical Picture • Differential Diagnoses • Histological features • Treatment
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    Definition • Theyare papular clonal T-cell disorders characterized by recurrent crops of spontaneously regressing erythematous papules.
  • 97.
    Types I. Pityriasislichenoides et varioliformis acuta (PLEVA/Mucha–Habermann disease) II. Pityriasis lichenoides chronica (PLC)
  • 98.
    Epidemiology • Bothare more prevalent in the pediatric population, but it affects patients in all age groups, races and geographic regions. • There is a male predominance.
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    Etiology • Theexact etiology is unknown. • May be response to foreign antigens such as infectious agents or drugs. • The infiltrate is predominantly T cells (CD8+) that are often monoclonal thus they are lymphoproliferative disorders.
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    Clinical Picture •The acute and chronic forms of pityriasis lichenoides exist on a disease spectrum with variable presentations so many patients have intermediate or mixed manifestations, either serially or concurrently. • Can resolve spontaneously after weeks to months or it may pursue a chronic relapsing course.
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    Clinical Picture PLEVAPLC Lesions • Vesicular, ulcerative, crusted or pustular. • Scaly erythematous to red–brown papules. Course • Rapid. • More indolent. Resolution • Within weeks may  varioliform scars if dermal damage is extensive. • Over weeks to months  hypopigmented macules (more obvious in darkly pigmented individuals and may be the presenting C/O). Extracut. manifestation • Malaise, fever, lymphadenopathy, arthritis and/or bacteremia. • “Febrile ulceronecrotic Mucha–Habermann disease (FUMHD)” severe variants with mucosal, gastrointestinal and pulmonary involvement. • Absent.
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    Differential Diagnoses PLEVA 1. Lymphomatoid papulosis 2. Cutaneous small vessel vasculitis 3. Lichenoid drug eruption 4. Arthropod reactions 5. Varicella, enteroviral exanthems 6. Folliculitis 7. Erythema multiforme 8. Dermatitis herpetiformis PLC 1. Small plaque parapsoriasis 2. Guttate psoriasis 3. Lichen planus 4. Pityriasis rosea 5. Secondary syphilis 6. Lymphomatoid papulosis 7. Papular dermatitis 8. Lichenoid drug eruption
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    Histological features •Pityriasis lichenoides exhibits a superficial perivascular interface dermatitis in all cases.
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    Histological features PLEVAPLC S. corneum • Hyperkeratosis • Foci of parakeratosis • Few neutrophils • Laminated Hyperkeratosis • Foci of thin flat parakeratosis • w/o neutrophils Granular cell layer • Deficient beneath mound of parakeratosis • Well formed Prickle cell layer • From edema to extensive epidermal necrosis in well-developed lesions. • No or focal necrotic keratinocytes Basal cell layer & dermo-epidermal junction. • Marked vacuolar changes • Denser interface lymphocytic infiltrate. • Very focal mild basal cell vacuolization which may not be evident in well-developed or resolving lesions. • Milder interface lymphocytic infiltrate. Dermis • Shows denser superficial &deep perivascular wedge-shaped lymphocytic infiltrates. • Numerous erythrocyte extravasation. • Only a superficial perivascular lymphocytic infiltrate. • Mild erythrocyte extravasation.
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    Treatment FIRST LINE 1. Topical corticosteroids 2. Topical coal tar preparations 3. Antibiotics (erythromycin 500 mg PO 2-4× daily; azithromycin; tetracycline 500 mg PO 2-4× daily, minocycline 100 mg PO twice daily) 4. Phototherapy (Sunlight, ultraviolet A, broadband or narrowband UVB) SECOND LINE 1. Topical tacrolimus 2. Methotrexate (10-25 mg PO weekly) 3. Phototherapy (ultraviolet AI, PUVA) 4. Cyclosporine 5. Biological agents: etanercept 6. IVIg
  • 117.
    Treatment • Ifa drug association is suspected, stop the offending drug. • SPECIAL TREATMENTS: 1. Prednisone: (60/40/20 mg PO taper, 5 days each) If there is fever, arthritis or other systemic findings. 2. Antihistamines: if pruritus is present. 3. Other Systemic antibiotics: If there is secondary infection.
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    REFERENCES • Bolognia3rd ed • http://dermnetnz.org • Google images • Husein Oozeerally (Presentation) • Jonathan Faulkner (Presentation) • emdicine.com • dermis.net
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