LEVERS HISTOPATHOLOGY OF THE SKIN PDF
Library of Congress Cataloging-in-Publication Data. Lever's histopathology of the skin / editor in chief, David E. Elder ; associate editors. Download the Medical Book: Lever's Histopathology of the Skin 11th Edition For Free. This Website we Provide Free Medical Books for all Students. Lever's Histopathology of the Skin, 10th edition. David E. Elder, Editor‐in‐Chief, Philadelphia: Wolters Kluwer/Lippincott Williams & Williams.
|Language:||English, Spanish, Dutch|
|ePub File Size:||30.48 MB|
|PDF File Size:||13.10 MB|
|Distribution:||Free* [*Regsitration Required]|
Remains your authoritative source for comprehensive coverage of those skin Lever's Histopathology of the Skin. Lever's Histopathology of the Skin View PDF. Lever's Histopathology of the Skin, 10th ed. David E. Elder, Rosalie Elenitsas, Bernett L. Johnson,. Jr, George F. Murphy, and Xiaowei Xu, editors,. Rely on Lever's for more accurate, more efficient diagnoses! Continuously in publication for more than 65 years, Lever's Histopathology of the Skin remains your.
Bhutani et al. Hence, this entity was termed LPP, and it was considered a macular variant of lichen planus. All the cases showed pigment incontinence and perivascular lymphocytic infiltrate in the dermis with thinning of the epidermis in the majority of the cases [Figure 2]. Most of the changes noted in the biopsies were identical to those reported in the previous studies. Click here to view Hypertrophic lichen planus HLP is a variant of Lichen planus which is generally confined to the shins and is rarely generalized.
Most striking feature is raised extensive hypertrophic hyperpigmented pruritic plaques.
Histopathologically, HLP showed moderate to marked hyperkeratosis and basal cell degeneration in epidermis with band-like infiltrate of lymphoplasmacytic at the dermoepidermal junction. Clinical and histopathological features correlated with other studies.
Ulcerative HLP of the soles may develop into squamous cell carcinoma. Lichen amyloidosis is a primary localized cutaneous amyloidosis.
Clinically, lesions consist of pruritic, small discrete, hyperkeratotic, hyperpigmented, waxy papules in rippled pattern, usually on the extensor surface of the lower limbs, pretibial areas shin being the most common site of involvement with a female preponderance.
Chronic irritation to the skin e. Amyloid deposits were restricted to papillary dermis. Most common sites are the neck, ankles, scalp, vulva, pubis, scrotum, and extensor aspect of forearms. The peak incidence is between 35 and 50 years of age and women are more affected than men. Severe intractable pruritus is the hallmark of LSC in almost all patients. The histopathological features are similar to those mentioned in other studies. Histopathologically, differentiating features of lichenoid eruptions include focal parakeratosis and mild basal vacuolar changes with a few eosinophils and plasma cells [Figure 3].
The degree of melanin incontinence is higher, and dermal infiltrate is less dense and less band like than that of lichen planus. Skin insults that result in inflammation can induce PIH, particularly in people with dark skin, such insults are acne lesions, ingrown hairs, scratches, and insect bites. Histologically, the sun exposed skin has elevated inflammatory cell count. Epidermal PIH involves increased melanin pigment in the basal cell layer of the epidermis. Dermal PIH involves the upper dermis, with pigment incontinence due to increased numbers of melanophages in the papillary dermis.
Another study by Ortonne and Bissett found similar results comparable to our present study. Click here to view Prurigo nodules Prurigo nodular is a dermatologic condition which can occur at all ages and equally in both sexes. It presents with hard nodule s 1—5 cm in diameter, with a warty, excoriated, pigmented dark red surface with central crusts, usually surrounded by an irregular hyperpigmented ring.
The extensor area of the limbs, face, and trunk are usually affected by the lesions, which may leave scars. The characteristic neurological changes include hypertrophy and proliferation of dermal nerves. Click here to view Polymorphic light eruption PLE is thought to be caused by an immune reaction to a compound in the skin, which is altered by exposure to ultraviolet UV radiation resulting in an inflammatory rash.
Very early lesions show either a normal epidermis or mild spongiosis with focal lymphocyte exocytosis and mild to moderate lymphohistiocytic perivascular or periadnexal infiltration. Histologically, PLE must be differentiated from lupus erythematosus, the porphyrias, actinic prurigo, and Jessners lymphocytic infiltrate.
There is no epidermal spongiosis or exocytosis. No Inflammation There is hyperkeratosis and the upper dermis contains only sparse perivascular lymphocytes.
It is only rarely present at birth. Although female heterozygotes are frequently affected, male gender has a more severe form of the disorder. The thickness of the adherent scales increases during childhood. In contrast to ichthyosis vulgaris, the flexural creases may be involved. Histopathology There is hyperkeratosis. The granular layer is normal or slightly thickened but not thinned as in dominant ichthyosis vulgaris. The epidermis may be slightly thickened.
Epidermolytic Hyperkeratosis Clinical Summary This rather striking histologic reaction pattern is also known as granular degeneration of the epidermis. It is seen in some linear epidermal nevi and in bullous congenital ichthyosiform erythroderma.
The disease results from mutations in the K1 and K10 keratin genes chromosomes 12 and 17, respectively , which encode the keratins in the suprabasal epidermis.
These mutations cause faulty assembly of keratin tonofilaments and impair their insertion into desmosomes. These flaws prevent normal development of the cytoskeleton, resulting in epidermal lysis and a tendency to form vesicles 4. Similar changes are also seen as one of the reaction patterns in Grover's disease, and the same pattern is commonly observed as P.
Histopathology The salient histologic features are a perinuclear vacuolization of the cells in the stratum spinosum and the stratum granulosum; b irregular cellular boundaries peripheral to the vacuolization; 3 an increased number of irregularly shaped, large keratohyalin granules; and 4 compact hyperkeratosis in the stratum corneum.
Large dirty scales on the ankle are characteristic. At scanning power, the epidermis appears normal, except for uniform thickening of the stratum corneum. The thickened stratum corneum contains no parakeratotic nuclei, constituting orthokeratosis. A normal granular layer is present. Epidermodysplasia Verruciformis Clinical Summary Epidermodysplasia verruciformis EV is a genetic disease characterized by human papillomavirus HPV infection with types not seen in otherwise healthy individuals 6.
It usually begins in childhood and is characterized by a generalized infection by HPV, frequent association with cutaneous carcinomas, and abnormalities of cellmediated immunity. Two forms of EV are recognized.
Popliteal flexures are involved with keratotic, almost verrucous, malodorous scale. Erosions appear in sites of bullae. The sole of the same patient's foot shows characteristic symptomatic yellow keratoderma. The patient's son shares this autosomal dominant condition. The epidermis is thickened and there is papillomatosis these changes are not usually seen in focal acantholytic dyskeratoses.
There is compact hyperkeratosis in the stratum corneum. The epidermis shows vacuolated keratinocytes with large keratohyalin granules. There is orthokeratotic hyperkeratosis. The keratohyalin granules are irregular and cell borders are ill defined. Sections show hyperkeratosis, vacuolar change of superficial keratinocytes, and hypergranulosis.
The superficially located affected keratinocytes are swollen and irregularly shaped. There are a few lymphocytes in the upper dermis. The nuclei are enlarged, with open chromatin, and there are prominent basophilic keratohyalin granules. Some of the cases are familial.
There is no tendency for malignant transformation in this form. The second form is primarily related to HPV5. There is often a familial history with an autosomal recessive or X-linked recessive inheritance. In addition to the plane warts, irregularly outlined, slightly scaling macules of various shades of brown, red, and white; tinea versicolor-like lesions; and seborrheic keratosis-like lesions have been noted.
Development of Bowen's disease squamous cell carcinoma in situ within lesions in exposed areas is a common occurrence, and invasive lesions of squamous cell carcinoma are occasionally found. EV-like lesions can develop in renal transplantation patients and human immunodeficiency virus HIV -infected persons. The underlying defect in EV is not clear but may involve oncogene or immunologic dysfunction.
Histopathology The epidermal changes, although similar to those observed in verruca plana, often differ by being more pronounced and more extensive. The affected keratinocytes are swollen and irregularly shaped. They show abundant, slightly basophilic cytoplasm and contain numerous round, basophilic keratohyalin granules. A few dyskeratotic cells may be seen in the lower part of the epidermis. Although some nuclei appear pyknotic, others appear large, round, and empty owing to marginal distribution of the chromatin.
In immunocompromised patients, EV often lacks the histologic features of verruca plana, a focally thickened granular layer is a marker for viral detection, and the risk for dysplasia in such lesions is much higher than that in cases of EV not associated with acquired immunosuppression. Conditions to consider in the differential diagnosis: lamellar ichthyosis X-linked ichthyosis epidermolytic hyperkeratosis epidermolytic acanthoma oculocutaneous tyrosinosis tyrosinemia acanthosis nigricans large cell acanthoma EV hyperkeratosis lenticularis perstans Flegel's disease IB2.
Scant Inflammation There is hyperkeratosis and lymphocytes are minimally increased around the superficial plexus. There may be a few neutrophils in the stratum corneum. At scanning magnification, there is slight hyperkeratosis with minimal inflammation.
At this power, the epidermis appears normal, except for slight uniform acanthosis. Subtle deposits of pink amorphous material amyloid are seen in dermal papillae. The granular layer is normal. There are deposits of amyloid filling the papillary dermis. Patient presented with pruritic papules on the pretibial areas. Pigmented discrete papules resulting from deposition of amyloid derived from keratinocytes.
Lever's Histopathology of the Skin
In contrast to macular amyloidosis, lichen amyloidosis reveals irregular acanthosis, papillomatosis, and hyperkeratosis. The papillary dermis is expanded and there is a mild perivascular inflammatory infiltrate. At higher magnification, the amorphous deposits of amyloid are seen in the papillary dermis associated with pigment-laden macrophages.
Lichen amyloidosis is characterized by closely set, discrete, brown-red pruritic, often somewhat scaly papules and plaques that are most commonly located on the legs, especially the shins. The plaques often have verrucous surfaces and then resemble hypertrophic lichen planus or lichen simplex chronicus. It is assumed by some that the pruritus leads to damage of keratinocytes by scratching and to subsequent production of amyloid.
Histopathology Lichen and macular amyloides show deposits of amyloid that are limited to the papillary dermis. Most of the amyloid is situated within the dermal papillae. Although the deposits are usually smaller in macular amyloidosis than in lichen amyloidosis, differentiation of the two on the basis of the amount of amyloid is not possible. The two conditions actually differ only in the appearance of the epidermis, which is hyperplastic and hyperkeratotic in lichen amyloidosis.
Occasionally, the amount of amyloid in macular amyloidosis is so small that it is missed, even when special stains are used on frozen sections. In such instances, more than one biopsy may be necessary to confirm the diagnosis.
Conditions to consider in the differential diagnosis of this category: dermatophytosis lichen amyloidosis and macular amyloidosis IC.
Hyperkeratosis with Parakeratosis The stratum corneum is thickened, the granular cell layer is reduced, and there is parakeratosis.
The dermis may show only sparse perivascular lymphocytes, although some of the conditions listed here may in other instances show more substantial inflammation. Some neoplastic disorders e. Scant or No Inflammation IC1. Scant or No Inflammation Lymphocytes are minimally increased around the superficial plexus.
Dermatophytosis is prototypic 8. Dermatophytosis Clinical Summary Fungal infections of seven anatomical regions are commonly recognized: tinea capitis including tinea favosa or favus of the scalp , tinea barbae, tinea faciei, tinea corporis including tinea imbricata , tinea cruris, tinea of the hands and feet, and tinea unguium.
Tinea corporis may be caused by any dermatophyte, but by far the most common cause in the United States is Trichophyton rubrum, followed by Microsporum canis and Trichophyton mentagrophytes.
IC1 Tinea pedis. A leading edge of scale and erythema in a moccasin distribution characterizes this infection, most commonly caused by the dermatophyte Trichophyton rubrum. There is slight uniform thickening of the stratum corneum. At high magnification, there is mixed orthokeratotic hyperkeratosis often sandwiched above a layer of parakeratosis and with focal collections of neutrophils.
PAS stain highlights fungal hyphae in the stratum corneum. These are likely to be most numerous in areas away from the collections of neutrophils. There is acanthosis of the epidermis with little to no spongiosis.
There is a markedly thickened and compacted stratum corneum. The superficial dermis reveals mild perivascular inflammation. The stratum corneum is markedly thickened and compacted. It is basophilic in appearance. Within the thickened stratum corneum, there is retention of the basophilic granules of the granular cell layer.
Histopathology Fungi may present as filamentous hyphae, arthrospores, yeast forms, or pseudohyphae. Hyphae are threadlike structures that may be septate or nonseptate. Arthrospores are spores formed by fragmentation of septate hyphae at the septum, usually appearing as rounded, boxlike, or short cylindrical forms. Yeasts are single-celled forms that appear as round, elongated, or ovoid bodies; they grow by budding, and their progeny may adhere to each other and form elongated chains called pseudohyphae.
If fungi are present in the horny layer, they are usually sandwiched between two zones of cornified cells, the upper being orthokeratotic and the lower partially consisting of parakeratotic cells.
This sandwich sign should prompt the performance of a stain for fungi for verification.
The presence of neutrophils in the stratum corneum is another valuable diagnostic clue. In the absence of demonstrable fungi, the histologic picture of fungal infections of the glabrous skin is not diagnostic. Depending on the degree of reaction of the skin to the presence of fungi, there may be histologic features of an acute, a subacute, or a chronic spongiotic dermatitis. Granular Parakeratosis Clinical Summary Granular parakeratosis was initially described as axillary granular parakeratosis because all the original patients presented with lesions confined to the axillae.
Subsequent reports described lesions in inguinal creases, inframammary folds, and other nonintertriginous areas 9. It occurs in both men and women, with predominance in the female gender. The characteristic clinical findings are erythematous or hyperpigmented plaques that may be crusted or verrucous.
There may be associated pruritus or burning. The total number of lesions is usually small and there are no oral lesions. Because of the clinical presentation, the clinical differential diagnosis usually includes HaileyHailey disease, Darier's disease, acanthosis nigricans, or contact dermatitis.
In the original descriptions, an unusual contact reaction to deodorants was hypothesized; however, with subsequent reports, this is felt to be less likely. The current hypothesis is that granular parakeratosis is a disorder of keratinization, possibly an abnormality of filaggrin processing.
Lever's Histopathology of the Skin, 2nd Edition
Histopathology The histopathology of granular parakeratosis is distinct. There is a markedly thickened stratum corneum with parakeratosis and retention of multiple basophilic granules.
The epidermis may be normal or slightly thickened. The dermis shows either absent inflammation or mild perivascular mononuclear cell infiltrate.
Lever’s Histopathology of the Skin 10th Edition PDF
Except for one reported case of granular parakeratosis associated with tinea, special stains for fungi are negative. Conditions to consider in the differential diagnosis of this category: dermatophytosis granular parakeratosis pityriasis rubra pilaris ichthyosis seborrheic dermatitis P.
A benign acquired macule with irregular borders and uniform brown pigmentation developed near the vermilion border in a middle-aged woman. Melanoma is considered in the differential diagnosis. At this magnification, the epidermis may appear completely normal, unless the difference in melanin pigment content between the lesion and the adjacent skin can be appreciated.
Often, however, there is slight acanthosis, as in this example. There may be patchy lymphocytes and melanophages in the papillary dermis, or inflammatory cells may be completely absent, as shown here.
There is increased melanin pigment in basal keratinocytes. Melanocyte content may be slightly increased, but there is no contiguous melanocytic proliferation as in nevi and melanomas. A few melanophages are present in the papillary dermis. Localized or Diffuse Hyperpigmentations Increased melanin pigment is present in basal keratinocytes, without melanocytic proliferation.
No Inflammation The upper dermis contains only sparse perivascular lymphocytes. Mucosal melanotic macule melanosis is the prototype Mucosal Melanotic Macules Clinical Summary These benign lesions present as a pigmented patch on a mucous membrane.
Common locations P. The lesions may be synonymously referred to as mucosal lentigo or mucosal melanotic macule. In the common location on the vulva vulvar lentigo , this process may present as a broad, irregular, and asymmetric patch of brown to blue-black hyperpigmentation, resembling a melanoma.
The lesions are entirely macular, unlike most invasive melanomas. The so-called labial lentigo labial melanotic macule , a hyperpigmented macule of the lower lip, is uniformly pigmented brown, usually completely macular, and usually less than approximately 6 mm in diameter. Fair-complexioned man has prominent brown macule that darkens in sunlight. Melanocytes are not increased in number.
Evenly tan-colored macules can be seen in normal individuals. Multiple caf au lait changes raise suspicion for neurofibromatosis. Teenaged boy acquired an enlarging tan macule with scalloped borders on his shoulder and chest.
Hypertrichosis may develop. Histopathology At first glance, a biopsy specimen may appear normal. The findings include mild acanthosis without elongation of rete ridges, and hyperpigmentation of P. Although melanocytes may be normal in number, in most instances the number is slightly increased.
Because of this slight increase in the number of melanocytes, the term genital lentiginosis has recently been proposed for these lesions. Although these lesions may clinically simulate melanoma, histologically there is no contiguous melanocytic proliferation and no significant atypia.
Occasionally, especially in the penile and vulvar lesions, there are prominent dendrites of melanocytes ramifying among the hyperpigmented keratinocytes.
There may be associated mild keratinocytic hyperplasia, and patchy lymphocytes with scattered melanophages in the papillary dermis may account for the blue-black color that may clinically simulate melanoma.
ID2 Pityriasis versicolor. Hyperpigmented patches, commonly, as shown here, present on the trunk, have furfuraceous scale with gentle scraping. Potassium hydroxide examination in this case demonstrated abundant hyphae and spores.
The clinical differential diagnosis for this case would include vitiligo. The epidermis may appear completely normal at scanning magnification. There may be a few perivascular lymphocytes in the papillary dermis or these may be absent. Upon closer inspection, a hyperkeratotic stratum corneum containing organisms can be identified.
The stratum corneum contains abundant yeasts. Hyphae are present in addition, and the classic spaghetti and meatballs appearance results. Ephelides Freckles Clinical Summary Freckles, or ephelides, are small, brown macules scattered over skin exposed to the sun. Exposure to the sun deepens the pigmentation of freckles, in contrast to lentigo simplex, the already deep pigment of which does not change. Freckles, simple lentigines, and solar lentigines are difficult to distinguish from one another clinically and are considered together in most clinical and epidemiologic studies.
Taken together, these lesions constitute a significant risk factor for the development of melanoma In fact, in epidermal spreads of freckled skin, the number of dopa-positive melanocytes within the freckles may appear decreased in comparison with the adjacent epidermis. However, the melanocytes that are present may be larger, and they may show more numerous and longer dendritic processes than the melanocytes of the surrounding epidermis.
Frequently bought together
Conditions to consider in the differential diagnosis: simple ephelis mucosal melanotic macules caf au lait macule actinic lentigo pigmented actinic keratosis melasma Becker's nevus congenital diffuse melanosis reticulated hyperpigmentations Addison's disease alkaptonuric ochronosis hemochromatosis ID2.
Scant Inflammation Lymphocytes are minimally increased around the superficial plexus. Melanophages may be present in the papillary dermis.
Pityriasis tinea versicolor is the prototype Pityriasis Tinea Versicolor Clinical Summary The frequently used term tinea versicolor is not accurate because the causative organism, Malassezia furfur, is not a dermatophyte.
Pityriasis versicolor usually affects the upper trunk, where there are multiple pink to brown papules that may appear hyper- or hypopigmented.
On gentle scraping, the surface of the discolored areas is finely scaled. Histopathology In contrast to other fungal infections of the glabrous skin, the horny layer in lesions of pityriasis versicolor contains abundant amounts of fungal elements, which can often be visualized in sections stained with hematoxylineosin as faintly basophilic structures. Malassezia Pityrosporum is present as a combination of both hyphae and spores, often referred to as spaghetti and meatballs.
The inflammatory response in pityriasis versicolor is usually minimal, although there may occasionally be slight hyperkeratosis, slight spongiosis, or a minimal superficial perivascular lymphocytic infiltrate. Conditions to consider in the differential diagnosis: pityriasis tinea versicolor lichen amyloidosis postinflammatory hyperpigmentation erythema dyschromicum perstans pretibial pigmented patches in diabetes IE.
Localized or Diffuse Hypopigmentations Melanin pigment is reduced in basal keratinocytes, with vitiligo or without early stages of chemical depigmentation a reduction in the number of melanocytes. With or Without Slight Inflammation Lymphocytes may be minimally increased around the dermalepidermal junction, as in the active phase of vitiligo, or may be absent, as in albinism.
Vitiligo is the prototype 13, Vitiligo Clinical Summary Vitiligo is an acquired, disfiguring condition with patchy, total loss of skin pigment. Stable patches often have an irregular border but are sharply demarcated from the surrounding skin. In expanding lesions, there may rarely be a slight rim of erythema at the border and a thin zone of transitory partial depigmentation.
Histopathology The central process in vitiligo is the destruction of melanocytes at the dermalepidermal junction. With silver stains or the dopa reaction, wellestablished lesions of vitiligo are totally devoid of melanocytes. The peripheries of expanding lesions that are hypopigmented rather than completely depigmented still show a few dopa-positive melanocytes and some melanin granules in the basal layer. In the outer border of patches of vitiligo, melanocytes are often prominent and demonstrate long dendritic processes filled with melanin granules.
Rarely, a superficial perivascular and somewhat lichenoid mononuclear cell infiltrate with vacuolar change is observed at the border of the depigmented areas. Conditions to consider in the differential diagnosis: vitiligo chemical depigmentation idiopathic guttate hypomelanosis albinism tinea versicolor piebaldism ChediakHigashi syndrome hypopigmented mycosis fungoides Clin. IE1 Vitiligo.
Acquired depigmented, well-demarcated patches often appear with striking symmetry. The epidermis may appear completely normal at scanning magnification, unless it is appreciated that melanin pigment is reduced compared to surrounding skin. At high magnification, a careful search reveals the absence of melanocytes from the basal lamina region.
Fontana stain reveals the absence of melanin pigment in basal layer keratinocytes, changes typical of vitiligo.
In contrast, in a biopsy specimen of normal skin, the Fontana stain highlights the melanin pigment, which stains black in the basal layer keratinocytes.
Ichthyosiform dermatoses. Arch Dermatol ; Linkage analysis suggests a locus of ichthyosis vulgaris on 1q J Hum Genet ; Richard G.
Molecular genetics of the ichthyoses. Keratins and skin disorders. J Pathol ; Ackerman AB. Focal acantholytic dyskeratosis. Nuovo GJ, Ishag M. The histologic spectrum of epidermodysplasia verruciformis. Am J Surg Pathol ; Lichen amyloidosis. Am J Dermatopathol ; Medical mycology. Philadelphia, PA: Lea and Febinger, Scheinfeld NS, Mones J. Granular parakeratosis: pathologic and clinical correlation of 18 cases of granular parakeratosis.
J Am Acad Dermatol ;52 5 Maize JC. Mucosal melanosis.
Dermatol Clin ; Pigmentary characteristics and moles in relation to melanoma risk. Int J Cancer ; Tinea versicolor: histologic and ultrastructural investigation of pigmentary changes.
Int J Dermatol ; The genetic concept of vitiligo. J Dermatol Sci ; Fisher AA. Differential diagnosis of idiopathic vitiligo: part III. Occupational leukoderma. Cutis ; The epidermis keratinocytes may proliferate without extension into the dermis, extend into the dermis, and may be squamous or basaloid. Melanocytes within the epidermis may proliferate with or without cytologic atypia nevi, dysplastic nevi, melanoma in situ , in a proliferative epidermis superficial spreading melanoma in situ, Spitz nevi , or in an atrophic epidermis lentigo maligna ; they can also extend into the dermis as proliferative infiltrates invasive melanoma with or without vertical growth phase [VGP].What's your work setting?
Distinction from a dysplastic nevus is based on greater size. Am J Dermatopathol ; Even at scanning magnification. In the most common form of melanoma, the superficial spreading type, the pattern of proliferation is termed pagetoid, with lesional cells extending singly and in groups up into the keratinocytic epithelium, which, as in lentiginous melanomas, tends to be irregularly thickened and thinned.
The rete ridge patterns are incompletely effaced and focally exaggerated. Usually, alterations in the stratum corneum result from inflammatory or neoplastic changes that affect the whole epidermis and, more often than not, the superficial dermis.
At higher magnification, the blue dots are confirmed to be lymphocytes, and one might seek evidence of parakeratosis, atypical keratinocytes, and plasma cells in the lesion, a combination which would rule out lichen planus and establish a diagnosis of actinic keratosis.
During the target stage.