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This article reviews inflammatory and infectious diseases and unusual benign lesions that may be seen on the hands.
Inflammatory diseases
Psoriasis
Psoriasis affects 2% of the U.S. population and shows no gender predilection. The age of onset has a bimodal peak, in the third and sixth decades of life. The disease tends to run a chronic course. A family history of psoriasis is seen in 7% of patients.
The mode of inheritance is multilocus, and HLA types-B13, -B17, -Bw57, -B27, and -Cw6 have been associated with psoriasis. In particular, HLA-B27 has been associated with generalized pustular psoriasis and psoriatic arthritis.
Clinical manifestations
Psoriasis can be divided into psoriasis vulgaris, inverse psoriasis, guttate psoriasis, psoriatic erythroderma, generalized pustular psoriasis, and localized pustular psoriasis. The koebner phenomenon is seen in psoriasis, whereby psoriatic lesions follow areas of trauma to the skin or preexisting scars. We discuss psoriasis vulgaris and localized pustular psoriasis that can be seen on the hands.
Psoriasis vulgaris presents with round, well-circumscribed, pink papules and plaques with overlying silvery scale. Auspitz sign is present, which is shown by removing the overlying scale with resultant bleeding. The lesions have a predilection for the scalp, elbows, knees, lumbosacral area, buttocks, umbilicus, and extensor surfaces of the extremities. Lesions may become circinate (psoriasis gyrate) or ring-like with central clearing (annular psoriasis).
Localized pustular psoriasis can be divided into pustulosis palmaris et plantaris and acrodermatitis continua of Hallopeau. Pustulosis palmaris et plantaris is a chronic condition affecting middle-aged adults. Over the palms and soles symmetrically, more than the digits, are multiple yellow pustules over psoriatic plaques (Fig 1). In contrast, acrodermatitis continua of Hallopeau begins with pustules at the distal tips of the fingers and toes, progressing proximally (Fig 2). Generalized pustular psoriasis may result. Osteolysis of the distal phalanx occasionally is present.
Fig. 1Pustular psoriasis. Multiple discrete pustules with surrounding erythema and crust.
Psoriatic arthritis is seen in 5% of patients with psoriasis, most commonly between the ages of 35 and 45. It is more prevalent in patients with severe psoriasis vulgaris or pustular psoriasis. Patients have an asymmetric seronegative spondyloarthropathy affecting the hands, feet, and large joints. Distal interphalangeal involvement is almost pathognomonic for psoriatic arthritis and Reiter's syndrome. Contractures can lead to claw-hand deformities.
Guttate or eruptive psoriasis is seen in young adults with psoriasis vulgaris and often preceded by a streptococcal throat infection. Psoriatic lesions are 0.5 to 1.5 cm in diameter and distributed over the trunk and proximal extremities. The lesions often respond to treatment of the underlying streptococcal infection, but may have a chronic course.
Histopathologic findings
Psoriasis vulgaris shows acanthosis of the epidermis with regular elongation of the rete ridges and thinning of the suprapapillary plates. Parakeratosis with a diminished or absent granular layer is observed. The dermal papillae are edematous. Neutrophils may accumulate in the epidermal spinous layer as sponIMAGEorm pustules of Kogoj, or in the parakeratotic mounds as Munro's microabscesses. In pustular psoriasis, the sponIMAGEorm pustule of Kogoj occurs as a macropustule.
The treatment of psoriasis depends on the extent of body surface area involvement, as well as the patient's response to different treatment modalities. Topical calcipotriene, a vitamin D derivative, often is used in combination with topical steroids. Tar, anthralin, and tazarotene are other topical treatments. Some patients with diffuse involvement respond well to phototherapy with ultraviolet B light. Systemic treatments for recalcitrant psoriasis include methotrexate, cyclosporine, retinoids, and hydroxyurea. Patients must be monitored closely for hematologic and other systemic side effects. New immunomodulators currently are undergoing trials in psoriasis.
Psoriatic arthritis, in particular, may be treated with nonsteroidal anti-inflammatory agents, methotrexate, etretinate, cyclosporine, or phototherapy with psoralens.
Vesiculobullous hand eczemas can be divided into 3 groups: pompholyx or acute eruptions, chronic vesiculobullous hand eczema, and hyperkeratotic hand eczema. These groups show considerable overlap between them.
The etiology of vesiculobullous hand eczema is largely unknown. Patients typically have an atopic background and the hands may flare with stress or irritants, such as chemicals or occlusive gloves. Palmoplantar hyperhidrosis is a common finding. Gender predilection varies with the disease group. In chronic vesiculobullous hand eczema, the female to male ratio is 3 to 1. In contrast, males outnumber females in hyperkeratotic dermatitis of the palms by 2 to 1.
Pompholyx is a rare condition characterized by the sudden appearance of pruritic, deep-seated vesicles on the palms, soles, and sides of the fingers. Vesicles may coalesce to form bullae. Lesions last several weeks and then resolve spontaneously.
Chronic vesiculobullous hand eczema (dyshidrotic eczema) is common and characterized by pruritic or burning vesicles on the palms and soles with weeping patches (Fig 3). Again, the lesions have a predilection for the sides of the fingers and are symmetric. Bullae may form and the condition may resolve and relapse frequently. Fifteen percent of patients have atopic dermatitis.
Fig. 3Chronic vesiculobullous hand eczema. Multiple deep-seated tapioca-colored vesicles with surrounding erythema, fissures, and scale.
Hyperkeratotic dermatitis of the palms presents as pruritic hyperkeratotic papules and plaques on the palmar surface with fissuring.
Histopathologic findings
A nonspecific spongiotic dermatitis, exocytosis of lymphocytes into the epidermis, and intraepidermal vesicles or bullae are seen. A mixed superficial perivascular inflammatory infiltrate may be present.
Pompholyx usually resolves spontaneously. However, acute cases may require symptomatic treatment with soaks, compresses, and emollients. The patient must be monitored for superinfection with Staphylococcus or Streptococcus species. Potent topical glucocorticoids may decrease inflammation. Severe attacks can be shortened with systemic gluococorticoids.
Chronic vesiculobullous hand eczema is exceedingly difficult to treat. Topical glucocorticoids, systemic antihistamines, and phototherapy commonly are used.
Hyperkeratotic eczema may benefit from superpotent topical or intralesional glucocorticoids, keratolytics, and oral retinoids. Emollients to wet skin are vital in controlling all types of hand eczema.
Allergic contact dermatitis accounts for 7% of all occupation-related illnesses. The physiology behind allergic contact dermatitis is that of a delayed-type hypersensitivity reaction. On initial exposure, the patient experiences no reaction. On repeat exposure, however, a cutaneous reaction is seen in 24 to 72 hours.
In acute eruptions, vesicles, bullae, and erythema are seen on the hands. However, in chronic cases of repeated allergic contact, the reaction presents as plaques with overlying lichenification, scale, and fissures. Vesiculation may be present in chronic cases. The presentation may mimic that of hand eczema. Common allergens include sesquiterpene lactones present in oil-soluble plant oleoresins of certain plants such as daisies, dandelions, chamomiles, and chrysanthemum, nickel, chromate, and paraphenylenediamine found in hair dyes and causing an allergic contact dermatitis of the hands in hair dressers. In patients with hand eczema not responding to conventional treatments, patch testing must be performed.
Histopathologic findings
By histology, an acute, spongiotic dermatitis is seen. Vesicles may contain collections of Langerhans cells. In chronic cases, a chronic spongiotic dermatitis is seen. Eosinophils may be present.
The allergen causing the hypersensitivity reaction must be identified and contact avoided through a thorough history and patch testing. High-potency topical steroids may be used on the palms, combined with oral antihistamines. Acute lesions may require soaks. In chronic cases with unidentified allergens, phototherapy may be implemented.
Palmoplantar keratoderma
Palmoplantar keratoderma (PPK) encompasses a multitude of both acquired and inherited disorders characterized by thickening of the palmar and plantar surfaces. These keratodermas are classified according to their inheritance patterns, morphology and distribution of the specific lesions, other ectodermal or systemic manifestations, age of onset, and histopathologic findings. Acquired PPK may be secondary to acquired immune deficiency syndrome, keratoderma blenorrhagicum in Reiter's disease, corns, calluses, keratoderma climactericum, psoriasis, secondary syphilis, lichen planus, or arsenic with arsenical keratoses. Inherited keratodermas without associated systemic manifestations include diffuse epidermolytic and nonepidermolytic PPK (Fig 4), erythrokeratoderma variabilis, PPK of Sybert, striate PPK, keratosis punctata palmaris et plantaris, spiny keratoderma (Fig 5), and focal acral hyperkeratosis. Inherited PPK with systemic manifestations include pachyonychia congenita type I and II, focal PPK with oral mucosa hyperkeratosis, PPK associated with esophageal cancer, Papillon-Lefevre syndrome, oculocutaneous tyrosinaemia, Olmsted syndrome, Vohwinkel's syndrome, Mal de Meleda, Huriez syndrome, hidrotic ectodermal dysplasia, and keratitis-icthyosis-deafness syndrome.
A thorough discussion of the earlier-named diseases is beyond the scope of this review. The most characteristic conditions and findings are discussed later.
Fig. 4Palmoplantar keratoderma. Sharply demarcated pink-red hyperkeratotic plaques involving the entire palmar surfaces, characteristic of nonepidermolytic PPK.
This is one of the most common forms of PPK and is inherited in an autosomal-dominant fashion. Diffuse epidermolytic PPK may be caused by keratin 9 (K9) mutations, although a few families have not shown a mutation in K9.
Diffuse epidermolytic PPK presents in the first few months of life with well-demarcated thickening of the palms and soles. The underlying epidermolysis may give the skin a ″dirty snakeskin appearance.”
Elbows and knees may show minimal involvement. No associated systemic manifestations have been reported.
Histopathologic findings
The thickened palms and soles show marked hyperkeratosis, papillomatosis, and acanthosis. Epidermolysis is seen in the spinous and granular cell layers.
Treatment
Topical keratolytics may decrease hyperkeratosis. Systemic retinoids often are used. However, painful erosions may result.
Erythrokeratoderma variabilis
Etiology and epidemiology
This form of PPK is inherited in an autosomal-dominant fashion and has been linked to the Rhesus blood group locus at 1p36.2-p34.
Erythrokeratoderma variabilis presents in early infancy and increases in severity in childhood. Initially, symmetric geographic areas of erythrokeratoderma are seen over the body with desquamation and hyperhidrosis of the palms and soles. The erythrokeratoderma usually spreads to the palms and soles.
Histopathologic findings
Orthohyperkeratosis and acanthosis are seen in erythrokeratoderma variabilis.
Treatment
Systemic retinoids are the treatment of choice.
Keratosis punctata palmaris et plantaris
Etiology and epidemiology
Keratosis punctata palmaris et plantaris is inherited in an autosomal-dominant manner with variable penetrance.
Clinical manifestations
The lesions present between the ages of 15 to 30, with a male predominance.
Multiple 1- to 5-mm punctuate keratoses begin on the lateral digits and evolve to cover the entire palms and soles. The keratoses are more diffuse over pressure points. Lesions occur secondary to trauma. There is questionably an increased risk for lung and colon cancer.
Histopathologic findings
Hyperkeratosis, parakeratosis, and spongiosis are seen with dilatation of blood vessels.
Treatment
These lesions are exceedingly difficult to treat. Surgical excision or mechanical debridement have been used.
Granuloma annulare
Etiology and epidemiology
The etiology of granuloma annulare largely is unknown. It has been reported to follow sun exposure, insect bites, or trauma, but not in a consistent fashion. In general, granuloma annulare typically is seen in children and young adults with a 2 to 1 female to male predominance. However, generalized lesions are seen in patients younger than 10 or older than 40 years old.
Clinically, granuloma annulare can be divided into localized, generalized, subcutaneous, and perforating lesions. Localized lesions present with the characteristic findings of granuloma annulare. An annular skin-colored to pink plaque is seen on the dorsa of the hands or feet most commonly (Fig 6). The upper and lower extremities may be affected as well. In half of patients, only one lesion is noted. Generalized lesions present with hundreds to thousands of 1- to 2-mm skin-colored papules with a predilection for the trunk, neck, forearms, legs, and extensor elbows. Lesions are symmetric in distribution and papules may form annular plaques, usually smaller in diameter than localized granuloma annulare. Subcutaneous lesions consist of one to multiple large, skin-colored subcutaneous nodules. The lesions are seen on the palms, soles, buttocks, toes, and eyelids. Lesions may ulcerate on occasion. Perforating lesions consist of superficial papules with central umbilication. These lesions are seen on the hands and fingers.
Fig. 6Granuloma annulare. Discrete pink annular plaque without scales.
A clear relationship of granuloma annulare to any systemic disease has not been established. There may be an association with diabetes mellitus.
Histopathologic findings
A palisaded granuloma is seen at the level of the subpapillary plexus of blood vessels or lower. Necrobiosis with prominence of mucin is noted in the center of the granulomas. The granulomas are palisaded by histiocytes and a mixture of a few inflammatory cells. Multinucleated giant cells may be present. In subcutaneous granuloma annulare, granulomas are seen in the deep dermis or subcutaneous tissue. In perforating granuloma annulare, central ulceration with a channel forming between the necrobiotic center and the surface epidermis is seen.
Lesions may spontaneously regress within 2 years. Intralesional triamcinolone injections greatly hasten resolution. Potent topical glucocorticoids also can be used. For generalized lesions, patients respond remarkably to psoralen plus ultraviolet light therapy.
T. manus refers to a dermatophyte infection involving the hands and interdigital spaces. It is extremely common worldwide, particularly in the summer months in tropical climates. The most common infecting dermatophytes are T. rubrum and T. mentagrophytes.
T. rubrum produces a dry, erythematous, scaly eruption on the hands. On the dorsal aspect of the hands, an annular configuration with scales commonly is seen (Fig 7). Rarely, T. rubrum may produce verrucous lesions resembling tuberculosis verrucosa cutis. T. mentagrophytes, however, produces a moist, vesicular eruption with possible bullae.
Typically, with any dermatophyte infection of the hands, tinea of the feet, groin, or other areas on the body is seen. T. manus often presents with 2 feet, 1 hand involvement, in which dermatophytes and a typical scaly eruption are seen on both feet and the dominant hand. Often, on the hands, a dermatophytid reaction is seen with multiple minute vesicles and intense pruritus. A dermatophytid reaction is immunologic in nature and does not involve an actual dermatophyte infection of the hands. The vesicles are sterile. The patient does have a dermatophyte infection in a distinct location, typically of the feet or groin areas. The hands will clear when the distant infection is cleared.
Fig. 7T. manus. Well-demarcated pink plaque with central clearing and scale.
Potassium hydroxide examination reveals septate, branching hyphae, and is diagnostic. If potassium hydroxide examination is negative and there continues to be a high suspicion of T. manus, a biopsy procedure may be performed. Pathology reveals the sandwich sign, showing fungal hyphae between parakeratosis below and orthokeratosis above. Periodic acid-Schiff staining reveals hyphae.
Treatment
T. manus usually is treated with topical antifungal creams such as clotrimazole, ketoconazole, terbinafine, or miconazole. The treatment regimen is to apply the cream twice a day for 2 weeks longer than required for complete clinical clearance. Recurrences are common.
For 2 feet, 1 hand involvement and severe or recalcitrant infections, oral therapy may be implemented with griseofulvin, terbinafine, itraconzaole, fluconazole, or ketoconazole.
Herpetic whitlow
Etiology and epidemiology
Twenty percent of cases of herpetic whitlow are seen in children under 10, whereas 55% are seen in adults 20 to 40 years of age. In adults, there is a 2 to 1 female to male predominance. The causative organisms are herpes simplex viruses 1 and 2. Herpes simplex virus 1 accounts for all cases seen in children and one quarter of those cases seen in adults. Herpes simplex virus 2 accounts for the remainder of adult cases, approximately 75%.
Lesions often are seen on the hands of medical and dental personnel, who encounter the virus by direct inoculation from infected patients' mouths. Lesions in children are caused by biting or thumbsucking during an active oral outbreak.
Clinical manifestations
A superficial abrasion is required on the skin for direct inoculation with the virus. After inoculation, in 2 to 6 weeks a painful red vesicle is noted on the lateral nail fold or fingertip. Axillary lymphadenopathy and erythematous streaks on the forearm may be noted. The vesicle may progress to a punched-out–appearing ulcer.
Laboratory and histopathologic findings
A Tzanck smear, direct fluorescent antibody examination, or viral culture may be performed by unroofing a vesicle and scraping the base. A Tzanck smear shows multinucleated giant cells in both herpes simplex and varicella zoster infections. Histopathologic findings on hematoxylin-eosin reveal an intraepidermal vesicle with molded multinucleated giant cells with steel-gray nuclei. Acantholysis and ballooning degeneration of the epidermal cells is seen.
Herpetic whitlow infections resolve spontaneously, but recurrences are common. There has been anecdotal evidence that oral acyclovir may shorten the course of a herpetic whitlow and can be used as prophylaxis to decrease recurrences.
Blistering distal dactylitis
Etiology and epidemiology
Blistering distal dactylitis is secondary to infection with group A β-hemolytic streptococcus, Staphylococcus aureus, or, on rare occasions, group B streptococcus.
A large tense blister on a tender erythematous base with seropurulent fluid is seen on the volar fat pads of the distal phalanx. The lesion may involve the nail folds.
Laboratory and histopathologic findings
Bacterial culture reveals the causative organism. Uncommonly, a biopsy examination may be performed. Biopsy examination reveals massive subepidermal edema. There is a subcorneal pustule filled with neutrophils. Gram stain reveals gram-positive cocci.
Treatment
The lesions are responsive to oral erythromycin or penicillin. Antibiotic choice may be guided by culture and sensitivities.
Secondary syphilis
Etiology and epidemiology
The incidence of syphilis has decreased remarkably owing to public health surveillance methods. Syphilis occurs secondary to Treponema pallidum infection. It can be seen through all age groups, particularly sexually active young adults.
Secondary syphilis usually develops 3 to 12 weeks after the primary chancre appears. It is marked by proliferation of spirochetes and systemic involvement with the spirochete. In response to spirochete numbers, antibodies are produced, but cell-mediated immunity remains deficient. Therefore, the organisms continue to proliferate.
Clinical manifestations
Secondary syphilis has long been termed the great mimicker. Skin lesions have a wide morphology, including macular, papular, maculopapular, annular, nodular, and pustular. Lesions of secondary syphilis tend to be asymptomatic and resolve in 2 to 10 weeks without scarring, regardless of treatment.
Mucous membrane lesions present as condyloma lata and mucous patches. Scalp lesions classically present as moth-eaten alopecia, with scattered areas of ill-defined nonscarring alopecia, most prominent on the occipital and parietal regions.
Of the many morphologic forms of secondary syphilis, the palms and soles are affected by macular, maculopapular, and papular lesions classically. These lesions are pink- to copper-colored macules and papules involving the palms and soles. In papular eruptions, a thin, white ring of scale may be present, known as Biette's collarette.
Systemic manifestations of secondary syphilis are multifold and beyond the scope of this discussion. However, almost every organ system in the body may be affected.
Laboratory and histopathologic findings
Serologic testing for secondary syphilis includes nontreponemal and treponemal tests. Nontreponemal tests include rapid plasma reagin test and Venereal Disease Research Laboratory (VDRL), and are screening tests using a cardiolipin-lipoprotein complex to which antibodies in syphilis react. VDRL may be followed to monitor therapeutic response rates. Treponemal tests include fluorescent treponemal antibody absorption test and microhemagglutination assay with T. pallidum antigen. These tests use T. pallidum as the antigen, allowing greater specificity. The treponemal tests are used as confirmatory tests in the case of a positive rapid plasma reagin test or VDRL.
Histopathology reveals a superficial and deep perivascular dermal infiltrate with abundant plasma cells. The infiltrate may be lichenoid and obscure the dermal-epidermal junction. Impregnated silver stains, such as Warthin-Starry, reveal intracellular and extracellular gray spirochetes.
Treatment
Benzathine penicillin G, 2.4 million units, is given intramuscularly as a single dose. In patients who are allergic to penicillin, doxycycline 100 mg twice a day for 2 weeks is used. Patients need to have close follow-up evaluation at 6 and 12 months, for a physical examination and serologic testing.
Verruca or warts are caused by the human papilloma viruses (HPV). Many different types of HPV have been identified and associated with various forms of warts. Verruca vulgaris are caused by HPV types 1, 2, 4, and 7. Verruca plana occur owing to HPV types 3, 10, 27, and 41.
Verrucae may be seen in any age population and ethnic background. Lesions tend to be much more severe and widespread in immunosuppressed patients.
Clinical manifestations
Verruca vulgaris present commonly on the hands, especially the fingers, periungual areas, and palms. Lesions appear as skin-colored to gray papules and plaques with a rough, verrucous surface (Fig 8). Under close inspection, black dots are commonly visible in the wart, representing thrombosed, dilated capillaries.
Fig. 8Verruca vulgaris, partially treated. Multiple discrete verrucous papules and plaques with surrounding pigmentary changes.
Verruca plana present as 2- to 4-mm, flat-topped, skin-colored to hyperpigmented papules and tend to be grouped. Autoinoculation and spreading of lesions is common, especially with shaving in the beard area of men or on the legs of women.
Verruca vulgaris show a thickened, acanthotic epidermis with papillomatosis, hyperkeratosis, and parakeratosis. Koilocytes, which are large keratinocytes with an eccentric, pyknotic nucleus and perinuclear halo are seen. Verruca plana show less acanthosis, hyperkeratosis, and no parakeratosis or papillomatosis. Koilocytes, however, are abundant, allowing for the diagnosis.
Many verrucae show spontaneous resolution. It is estimated that over half of all verruca vulgaris resolve in 1 year, and two-thirds resolve in 2 years. Verruca plana show an even higher rate of regression.
Treatment modalities include cryotherapy with liquid nitrogen. The possibility of scarring with hypo- or depigmentation must be discussed before treatment. Other modalities include curettage or surgical excision, carbon dioxide laser, imiquimod cream, salicylic acid, and cantharidin. Most over-the-counter wart compounds contain salicylic acid.
Orf
Etiology and epidemiology
Orf virus is a member of the Poxviridae family endemic to sheep, goats, and musk oxen and causes a condition termed contagious pustular dermatitis or ecthyma contagiosum. It commonly is found near the nose or mouth of infected animals and may survive on barn doors, feeding troughs, and fences. Humans acquire the virus through direct contact with infected animals or through contact with an infected object.
Farmers and veterinarians are at the highest risk, however, the infection also can be acquired at petting zoos. The disease has only been seen in Caucasians, but has no age predilection.
Clinical manifestations
A typical lesion usually is solitary and located on the dorsal right index finger. The exact appearance of the lesion depends on the stage of the disease. There are 6 stages, progressing from a papular stage with a red, elevated lesion, to a target stage with a red center, white middle ring, and peripheral ring of red (Fig 9). In the acute stage, a serosanguinous exudates is seen and the lesion may increase in size. After the acute stage, a regenerative stage is seen with a thin crust over the nodule with black dots. In the papillomatous stage, small papillomas appear over the surface of the lesion. Finally, in the regressive stage, a thick crust develops, papillomas resolve, and the elevation of the lesion subsides. Lesions last 35 days and heal uneventfully.
Patients also may have regional lymphadenopathy, lymphangitis, fever, erythema multiforme, and a widespread papulovesicular eruption of the skin.
Histopathologic findings
Findings largely depend on the stage of the lesion. In the target stage, vacuolated epidermal cells migrate peripherally, with epidermal thickening centrally. A mixed infiltrate is seen. In the acute stage, a superficial ulceration is seen over the central lesion. The black dots seen in the regenerative stage correspond to cellular debris that has collected in the follicles. In the papillomatous stage, papillary elevations and downward finger-like projections are noted. The regressive stage is marked by decreased inflammation and resolution of papillary elevations.
No treatment is necessary, however, lesions may be excised and cauterized, and heal without complication. Compresses and bacterial culture and sensitivity are performed for superinfections. Appropriate antibiotics may be administered if a bacterial superinfection is detected.
No residual disease is seen after lesions resolve.
Unusual benign neoplasms
Infantile digital fibromatosis
Etiology and epidemiology
The etiology of infantile digital fibromatosis is unknown. Lesions may be present at birth, but usually occur in the first year of life. No ethnic predilection has been observed.
Clinical manifestations
On the fingers or toes, a less than 2-cm pink to skin-colored asymptomatic nodule is seen. Lesions have been seen rarely on extradigital sites such as the breast and tongue.
Histopathologic findings
Within the dermis and extending to the subcutaneous tissue, a benign-appearing spindle cell proliferation is seen without atypia. Eosinophilic cytoplasmic inclusion bodies are characteristic, measuring 3 to 10 μm. These inclusion bodies stain a deep red color with Masson trichrome and purple with phosphotungstic acid-hematoxylin.
Treatment
Lesions typically are excised, but recurrence is common. Lesions may spontaneously resolve after a few years.
References
References
Christophers E
Mrowietz U
Psoriasis.
in: 5th ed. Fitzpatrick's Dermatology in General Medicine. McGraw-Hill,
New York1999: 495-519
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