Massive compaction of horny material on the entire scalp.
Macerated, bright red, and fissured, usually not scaly.
Types 1, 2, 3, 5, and 6.
Scaling papules of reddish-brown color with a central mica-like scale.
Lesions in LPP are oval or irregularly shaped patches and >5 cm, with minimal scaling, with and without atrophy, and may be poikilodermatous.
Acral pustule formation, subungual lakes of pus, and destruction of nail plates, which may lead to permanent loss of nails and scarring.
Burning, fiery-red erythema topped by pinpoint sterile yellow pustules, spreading rapidly over the entire body, with fever, malaise, and leukocytosis.
With topical fluorinated glucocorticoid covered with plastic wrap, and glucocorticoid-impregnated tape.
Methotrexate (MTX) and systemic retinoids.
Generalized, classically beginning on the head and neck, then spreading caudally.
Localized orange plaque.
Pityriasis lichenoides chronica (PLC).
Plaques with thick adherent scales, often very pruritic, and does not lead to hair loss.
Plaques are sharply marginated with thick adherent scales, often very pruritic, and do not lead to hair loss.
Enthesitis, tenosynovitis, dactylitis ('sausage' digit), bone erosions, osteolysis, or ankylosis.
Tinea, candidiasis, intertrigo, extramammary Paget disease.
Sharp demarcation of the plaques.
These lesions must be carefully followed, and repeated biopsies are necessary to detect mycosis fungoides. It may be considered as a prestage of mycosis fungoides but not all patients progress to MF.
Small (<5 cm), round to oval, or linear mostly on the trunk, slightly infiltrated, yellowish, or fawn-colored patches with minimal scaling, asymptomatic, or mild pruritus.
Massive silvery white or yellowish hyperkeratosis, sharply demarcated inflammatory plaque, cracking, painful fissures, and bleeding.
Creamy yellow pustules that are partially confluent on the palm, sterile, pruritic, and become painful when larger.
A type of arthritis with the ICD10 code L40.5.
Ten to 43 years, but can occur rarely in infants and old persons.
Tar or ketoconazole shampoos followed by betamethasone valerate, 1% lotion.
L44.4.
Combination therapy with 311nm UVB or PUVA.
A socially and psychologically disabling condition. Long duration; type 3 often resolves after 2 years; type 4 may clear. Type 5 has a very chronic course. Type 6 may respond to highly active antiretroviral therapy (HAART).
By pustules, not papules, arising on normal or inflamed, erythematous skin.
Asymptomatic, well-defined, rounded, slightly scaly, thin plaques or patches. They can be larger than 10 cm and are light red-brown or salmon-pink. Atrophy may be present in some areas.
Generalized, classically beginning on the head and neck, then spreading caudally.
Erythematous plaques with thick, yellowish, lamellar scale and desquamation on sites of pressure, with a sharp demarcation of the inflammatory lesion on the arch of the foot.
One to two weeks after the herald patch.
Systemic administration of MTX or retinoids.
Oval, slightly raised plaque or patch 2 to 5 cm, salmon-red, with fine collarette scale at the periphery.
Multiple large scaling plaques on the trunk, buttock, and legs. Lesions are round or polycyclic and confluent forming geographic patterns.
Seborrheic dermatitis, tinea capitis.
It forms a 'Christmas tree' pattern on the back.
KOH examination.
Drug eruptions, secondary syphilis, guttate psoriasis, small plaque parapsoriasis, erythema migrans, erythema multiforme, and tinea corporis.
Spontaneous remission in 6 to 12 weeks or less, with uncommon recurrences.
Sudden onset of psoriasis may be associated with HIV infection.
Asymptomatic, yellowish or fawn-colored, very thin, well-defined, slightly scaly, and superficially wrinkled patches. Oval in shape, following the lines of cleavage of the skin, often reaching more than 5 cm in length.
Randomly arranged bright red edematous papules, vesicles, central necrosis with hemorrhagic crusting.
Showers of creamy-white coalescing pustules on a fiery-red base.
Emollients, keratolytic agents, vitamin D3 (calcipotriol), glucocorticoids, and vitamin A analogs (tazarotene).
Trunk and proximal aspects of the arms and legs, rarely on the face.
Unknown, but fever and leukocytosis result from the release of cytokines and chemokines into circulation.
Topical fluorinated glucocorticoid covered with plastic wrap.
Pruritus is relatively common, especially in scalp and anogenital psoriasis.
Hepatic toxicity, especially in patients with diabetes and/or obesity.
Disseminated, generalized, mainly on the trunk.
3 to 5 mg/kg per day.
Tuberculosis, consider HIV.
Topical glucocorticoids, phototherapy, narrowband 311nm UV phototherapy, and PUVA.
They are usually not scaly but macerated, bright red, and fissured.
Asymptomatic, well-defined, rounded, slightly scaly, thin plaques or patches. Light red-brown or salmon-pink in color, can be larger than 10 cm, and may show atrophy in some areas.
Bilateral, often symmetric; often spares exposed areas.
Varicella, guttate psoriasis, and lymphomatoid papulosis.
Diffuse, waxy, yellowish/orange hyperkeratosis.
A condition where psoriasis involves the entire skin.
Impetigo herpetiformis, Annular type, Psoriasis cum pustulatione, Acrodermatitis continua of Hallopeau.
Cleared by acitretin /PUVA combination treatment within 4 weeks.
Keratoses and squamous cell carcinomas in some patients.
Glucagonoma syndrome.
Combination of 311nm UVB or PUVA (rePUVA).
It appears rapidly, sometimes disappears spontaneously, and more often evolves into chronic plaque psoriasis.
Low.
On clinical grounds.
Progression to erythroderma (except for types 2 and 4).
Pityriasis lichenoides et varioliformis acuta (PLEVA).
Lacks bright red color, lesions are brown to black with similar morphology as in lighter skin.
L40.
It can present as distal arthritis, asymmetric oligoarthritis, symmetric polyarthritis, arthritis mutilans, sacroiliitis, and spondylitis.
Age, type of psoriasis, site and extent of involvement, previous treatment, and associated medical disorders.
Potassium hydroxide (KOH) examination.
Distal yellow-brown discoloration, nail plate thickening, subungual hyperkeratosis, and splinter hemorrhages.
Treat streptococcal infection with antibiotics, narrowband UVB phototherapy (311 nm) is very effective.
Methotrexate (MTX) and biologics.
Emollients, keratolytic agents, vitamin D3 (calcipotriol), glucocorticoids, and vitamin A analogs (tazarotene).
Pitting, oil spots, and onycholysis.
It is increased in 50% of patients, usually correlated with the extent of the disease, and there is an increased risk of gouty arthritis.
Papules are brown.
Acute form (PLEVA) and chronic form (PLC).
An erythematous (salmon-red) plaque with a collarette scale on the trailing edge of the advancing border.
Similar to psoriasis, often leading to asbestoslike accumulation of scale.
SPP does not progress to mycosis fungoides (MF), while LPP exists on a continuum with patch-stage MF and can progress to overt MF.
Uncommon but usually associated with a refractory type of psoriasis.
Reactivation of human herpesvirus 7 (HHV7) and HHV6.
Mycosis fungoides.
PUVA soaks and glucocorticosteroids are effective, systemic treatment for recalcitrant cases.
Psoriatic Arthritis.
Scalp and face involvement in children, inverse pattern in axillary and inguinal areas, purpuric, papular, urticarial, and vesicular variants.
Blood pressure and serum creatinine due to the known nephrotoxicity of the drug.
Oral antihistamines, phototherapy, topical glucocorticoids for relief of pruritus, oral erythromycin, and acyclovir if prescribed early in the course.
Any maculopapular drug eruption, secondary syphilis, pityriasis rosea.
Sharp demarcation and the absence of scales.
To detect mycosis fungoides.
Localized orange/red plaques.
Expanding ring-like micropustular eruptions on a highly inflammatory base, resulting in a collarette-like scaling at the margin.
Massive compaction of horny material on the entire scalp, with thick asbestoslike scales compacting hairs but not leading to alopecia, and involvement of the forehead.
L42.
By a dermatologist.
Diffuse, waxy, yellowish/orange hyperkeratosis.
Salmonpink papules (guttate: Latin gutta, “drop”), 2.0 mm to 1.0 cm with or without scales. Scales may not be visible but become apparent upon scraping.
Psoriasis, follicular ichthyosis, erythrokeratodermia variabilis, and ichthyosiform erythrodermas.
Single lesion or lesions localized to one or more predilection sites: elbows, knees, sacral gluteal region, scalp, and palm/soles. Sometimes only regional involvement (scalp), often generalized.
Patchy or diffuse parakeratosis, absence of granular layer, slight acanthosis, focal spongiosis, microscopic vesicles, occasional dyskeratotic cells, edema of dermis, and perivascular infiltrate of mononuclear cells.
Marked overall thickening of the epidermis, increased mitosis of keratinocytes, fibroblasts, and endothelial cells, parakeratotic hyperkeratosis, and inflammatory cells in the dermis and epidermis.
Seborrheic dermatitis, lichen simplex chronicus, psoriasiform drug eruptions, and tinea corporis.
Pitting, subungual hyperkeratosis, onycholysis, and oil spots (yellowish-brown spots under the nail plate).
Adherent scales with fissures, erythematous base, and sharp margin on the wrist.
Oval, scattered, with characteristic distribution following the lines of cleavage in a “Christmas tree” pattern.
Ultraviolet radiation (natural sunlight or broadband UVB), 311nm UVB, and PUVA.
Topical glucocorticoids, phototherapy, narrowband 311nm UV phototherapy, PUVA.
Ionizing radiation, systemic glucocorticoids, photochemotherapy (PUVA), cyclosporine (CS), and methotrexate (MTX).
By using hydrocolloid dressing left on for 24 to 48 hours.
Type 1: Classic Adult, Type 2: Atypical Adult, Type 3: Classic Juvenile, Type 4: Circumscribed Juvenile, Type 5: Atypical Juvenile, Type 6: HIV Associated.
Scales are lamellar, loose, and easily removed by scratching. Removal of scale results in the appearance of minute blood droplets (Auspitz sign).
Hyperkeratosis, acanthosis with broad short rete ridges, alternating orthokeratosis, and parakeratosis. Keratinous plugs of follicular infundibula and perifollicular areas of parakeratosis. Prominent granular layer may distinguish PRP from psoriasis. Superficial perivascular lymphocytic infiltrate.
Unknown.
Infliximab, adalimumab, etanercept, and certolizumab.
Throat culture for group A β hemolytic streptococcus infection.
Multiple large scaling plaques on the trunk, buttock, and legs. Lesions are round or polycyclic and confluent forming geographic patterns.
Oral PUVA treatment.
Ichthyosiform lesions on legs in type 2, sclerodermalike appearance of hands and feet in type 5, acne conglobata, hidradenitis suppurativa, and lichen spinulosus in type 6.
Proximal aspects of the arms and legs.
Increased morbidity and mortality from cardiovascular events, metabolic syndrome, hypertension, and hyperlipidemia.
Insidious and rapid onset, skin lesions including follicular hyperkeratotic papules of reddish-orange color, and a psoriasiform, scaling dermatitis with sharply demarcated islands of unaffected skin.
Small plaque PP (SPP) and large plaque PP (LPP).
Seborrheic dermatitis and tinea capitis.
Once-weekly dosing starting at 5 to 7.5 mg.
Oral retinoids as in von Zumbusch pustular psoriasis; MTX, CS, and biologics are other treatment options.
Systemic administration of MTX or retinoids (both as in psoriasis). In type 6: HAART. The anti-TNF agents, for example, infliximab and etanercept, are effective.
It is a human IgG1 κ monoclonal antibody that binds to the common p40 subunit of human IL12 and IL23, preventing its interaction with its receptor.
Tinea corporis and mycosis fungoides.
It indicates an antecedent streptococcal infection.
Tinea, candidiasis, intertrigo, extramammary Paget disease, glucagonoma syndrome, Langerhans cell histiocytosis, and Hailey–Hailey disease.
