Dermatopathologic diagnosis of Lyme Borreliosis
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Abstract:
The goal of this study was to determine the general light microscopic findings which lend support to the histopathologic diagnosis of the main cutaneous manifestations of Lyme Borreliosis. Their diagnostic criteria are delineated and illustrated. In culminating lesions of erythema migrans and acrodermatitis chronica atrophicans, a peculiar connective tissue reaction includes an increase in the number of fibroblasts, proliferation of collagen fibers, and interstitial mucinous edema. The cellular infiltrates are patchy perivascular in erythema migrans and either patchy and/or band-like in acrodermatitis chronica atrophicans. They consist of lymphohistiocytic cells with a variable admixture of plasma cells. The damage to elastic (and even collagen) fibers occurs in early acrodermatitis chronica atrophicans and is reflected by the phenomenon of elastophagocytosis. Reduction or lack of pilosebaceous units is a constant finding. In advanced lesions of acrodermatitis chronica atrophicans, a thinning of the dermal breadth is noticed, resulting from a decrease in collagen and elastic fibers. Fibrous nodules and morphea-like conditions are characterized by excessive formation of collagen. Borrelial lymphocytoma exhibits two different patterns of infiltration, accompanied by dermal fibrosis and increased numbers of fibroblasts. Recent tick bites show a predominantly neutrophilic infiltrate. By applying the results of this synoptic study, histopathologic diagnosis of dermatoborrelioses should be possible without the absolute necessity of clinical correlation.Keywords:
Erythema migrans
Acrodermatitis
Morphea
Erythema
Infiltration (HVAC)
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Erythema elevatum diutinum (EED) is a chronic cutaneous disease characterized by nodules and plaques in an acral and symmetrical location. Histologically, the earliest findings are a vasculitis in the dermis associated with an inflammatory-cell infiltrate and a tinctorial change in the vessel wall and adjacent perivascular fibers. The histologic findings are thought to be highly characteristic. Extracellular cholesterosis (EC) most likely represents a variant in which lipids are secondarily deposited between the collagen bundles. The earlier division of EED into the Hutchinson and Bury types is no longer thought to be warranted. A patient is presented with clinical and histological features of EED; an elevation of several amino acids in the urine with essentially normal plasma levels was revealed. Elevations of IgG and IgA, and a mild elevation in leukocyte alkaline phosphatase were present.
Erythema
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Light and electron microscopical studies of erythema multiforme showed two types of tissue changes with the bullae forming at a different location in each type. (a) Erythematous papular lesions revealed primarily dermal edema resulting in intradermal bulla formation, with the basal lamina at the top of the blister. (b) "Target" lesions showed primarily epidermal damage resulting in bulla formation at the dermal-epidermal junction, with the basal lamina, if preserved, at the floor of the bulla. Vascular changes were encountered in both types. These findings show that analogous to the multiform clinical appearance of erythema multiforme, the type of bulla that develops in a given case depends on whether the dermis or the epidermis is primarily involved.
Bulla (seal)
Epidermis (zoology)
Erythema multiforme
Erythema
Lamina densa
Basal (medicine)
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Abstract Reticulate pigmentation with or without skin atrophy, depigmentation and telangiectasia is frequently encountered on the neck of severe cases of adult type atopic dermatitis. These skin changes were graded clinically into 3 stages. Based on histological features, hyperplasia of the sebaceous gland, dilated tortuous capillaries, and mild degeneration of elastic fibers were noted in stage I lesions. Lesions of both stages II and III contained increased melanin in the basal cell layer with incontinence of pigment, remarkable destruction and degeneration of elastic fibers, proliferated and dilated capillaries, and deposition of mucinous substances. The numbers of mast cells in papillary dermis were significantly increased in late stage I and stage II lesions. Poikiloderma‐like lesions on the neck could be attributable to chronic inflammation and delay of wound healing process, possibly caused by long‐standing topical corticosteroid therapy.
Papillary dermis
Depigmentation
Poikiloderma
Melanosis
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Abstract Histopathology is a major diagnostic tool in dermatology, particularly in psoriasiform diseases. Morphological studies showed that the initial event in psoriatic lesions is perivascular infiltrate, followed by dilatation of superficial papillary vessels. Proliferation of keratinocytes and neutrophil exocytosis are secondary events. Fully developed psoriasis has a very characteristic pattern, which includes elongation of rete ridges leading to regular acanthosis, oedema of the papillary dermis associated with tortuous dilated vessels, thinning of suprapapillar area, decreased thickness of granular layer, and exocytosis of neutrophils in the spinous layer (Kogoj's pustule) or in the cornified parakeratotic layer (Munro microabscesses). Pustular psoriasis is characterized by large or confluent intra‐epidermal multilocular pustules. Whatever the clinical variant of psoriasis, common morphological signs suggest that it is basically a unique pathological process, with many possible presentations according to various factors such as age, size and localization of lesions, or therapy. Similar microscopic elementary lesions indicate that Hallopeau's acrodermatitis continua, Reiter's disease and geographical tongue are variants of psoriasis. Because of the many faces of the disease, psoriasis can resemble many other squamous or pustular disorders. Differential diagnosis by microscopic analysis is based on pattern analysis, PAS (Periodic Acid Schiff) staining to rule out fungal infection, and immunohistochemistry to characterize lymphocytic infiltrate. Psoriasis is one of the most common inflammatory skin diseases. In its characteristic presentation, psoriasis comprises well‐circumscribed red scaly papules and plaques. In this form, the disease is generally easy to identify, especially when the elbows, knees and scalp are affected. Nevertheless, the term ‘psoriasis’ includes more clinical variants than any other inflammatory dermatosis: psoriasis vulgaris vs. pustular, localized vs. generalized, topographic variants, mucous membranes involvement, hair and nail lesions. Although some of these conditions might be extremely different from psoriasis vulgaris, common pathological findings can be identified in all of them. Microscopic analysis of psoriatic lesions may therefore help clinicians to make the diagnosis and to understand that, whatever the clinical presentation, signs and symptoms are mainly due to a unique pathological process.
Acanthosis
Papillary dermis
Parakeratosis
Histopathology
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The human progenitor-cell antigen CD34 is expressed in dermal dendritic cells and is lost in several disorders affecting dermal collagen. The loss of CD34 immunohistochemical staining has been demonstrated to be helpful in the histologic diagnosis of morphea, lichen sclerosus, and the classic pattern of granuloma annulare. This study characterized CD34 expression in 2 sclerosing disorders affecting the subcutis: lipodermatosclerosis (LDS) and the sclerodermoid form of chronic graft-versus-host disease (ScGVHD). In addition, we applied CD34 staining to the interstitial pattern of granuloma annulare (IGA), which is a diagnostically challenging entity with subtle amounts of dermal collagen degeneration. Fifteen cases of LDS, 6 cases of ScGVHD, and 4 cases of IGA were identified and stained with CD34. All cases of LDS showed loss of CD34 within subcutaneous septa, and 9 cases (60%) also exhibited full-thickness dermal loss of interstitial staining. All 6 cases of ScGVHD showed varying degrees of CD34 loss within the dermis and/or subcutaneous septa. The normal subcutis showed diffuse septal staining with CD34, with a density equal to that seen in the dermis. CD34 staining was lost in areas of dermal inflammation in half of the IGA cases. We conclude that CD34 staining is a useful ancillary test in disease processes affecting the subcutaneous collagen such as LDS and ScGVHD. Its utility also extends to diagnostically challenging disorders of dermal collagen degeneration such as IGA.
Granuloma Annulare
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Jessner’s lymphocytic infiltrate of skin, reticular erythematous mucinosis and lupus tumidus are the group of rare, insufficiently explored dermatosis with common clinical and histological features, whose nosology is controversial today. Plasmacytoid dendritic cells play the key role in autoimmune disease induction The target of our study was the analysis of pathomorphological features of lesional skin and the research of plasmacytoid dendritic cells in the skin of patients with Jessner’s lymphocytic infiltrate of skin, reticular erythematous mucinosis and lupus tumidus. Material and methods. Histological and indirect immunohistochemistry examination (anti-CD123 antibodies) of lesional skin of 36 patients was held (JLIS - 12, REM - 10, LT - 14) and 10 healthy people. Result. The main pathomorphological changes of skin in all groups were found in dermis: dense perivascular and perifollicular infiltration and deposit of mucin between collagen fibers. Deposits of mucin in papillary dermis were found between patients with JLIS, REM and LT in 10/12 (83%), 7/10 (70%) and 12/14 (86%) of cases, there were no mucin found in skin of healthy people 0/10 (0%) In all dermatosis the distribution of CD123 cells in lesional skin, in immunohistochemistry study, was corresponded clusters model of infiltrate - plasmacytoid DC concentrate in groups around vessels of superficial and profundus networks and perivascular. The comparative analysis of density and localization of perivascular infiltration, number of CD123-cells and their correspondence in dermis perivascular infiltrates didn’t reveal statistically significant differences between JLIS, REM and LT. Results. Our results allow us to consider JLIS and LT as identical decease, and REM as similar in clinical-pathomorphological features dermatosis.
Reticular Dermis
Reticular connective tissue
Mucinosis
Papillary dermis
Dermal papillae
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A study of the cutaneous eruptions of eight patients with mixed connective tissue disease (MCTD) was performed to better characterize its dermatopathology and to explore a role for the membrane attack complex of complement C5b-9 in lesional pathogenesis. Nine lesional skin biopsies were obtained from eight patients with MCTD and analyzed by conventional light microscopy. Direct immunofluorescence (IF) and indirect IF using a monoclonal antibody to C5b-9 were applied in six and five cases respectively. The biopsied cutaneous eruptions were characterized clinically as photodistributed erythematous annular and/or papulosquamous lesions mimicking subacute cutaneous lupus erythematosus (SCLE) in five of eight patients as an ill-defined, telangiectatic, scaly patch on the face in one patient, palpable purpura in one patient, and dorsal hand blisters resembling porphyria cutanea tarda (PCT) in another. With the exception of the latter two patients, the histology appeared similar, comprising a cell poor and/or lichenoid interface dermatitis with suprabasilar exocytosis around necrotic keratinocytes in the absence of deep periadnexal or perivascular extension or conspicuous follicular plugging, a pattern similar to that of SCLE. However, the lesions differed from SCLE by virtue of vasculopathic alterations comprising vascular ectasia, hypovascularity, and/or luminal thrombosis confined to the superficial vascular plexus and a sclerodermoid tissue reaction, the latter seen in two cases. One biopsy showed a pustular leukocytoclastic vasculitis (LCV). In another case, a biopsied hand blister demonstrated a PCT-like appearance histologically, namely, pauci-inflammatory subepithelial blister formation with hyalinization of dermal papillae capillaries accompanied by an LCV. There was nuclear keratinocyte decoration with IgG and C5b-9 in all cases studied, accompanied by a positive lupus band test in two cases and homogenous deposition of immunoreactants along the dermoepidermal junction and within vessels in the PCT-like eruption. Granular vascular decoration with immunoreactants including C5b-9 was seen in two LCV cases and in two biopsies from rashes clinically mimicking SCLE. Although the epidermal pathology of MCTD mimicks that of SCLE, a concomitant vasculopathy paralleling that seen in skin lesions of dermatomyositis distinquishes the dermatopathology of MCTD from that of SCLE. Corroborating the role of microangiopathy in the pathogenesis of the skin lesions of MCTD was the demonstration of C5b-9 in blood vessels. The deposition of C5b-9 in keratinocytes may explain the pattern of IgG decoration of keratinocytes; the formation of plasmalemmal pores may permit binding of immunoglobulin to antigens in the nucleus and/or cytosol. The C5b-9 complex may be the effector mechanism of epithelial and/or endothelial cell injury in MCTD or may serve to augment the effects of antibody-dependent cellular cytotoxicity.
Skin biopsy
Papillary dermis
Hyaline
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The authors describe a 58-year-old woman who experienced an erythema multiforme-like reaction following therapy with cefamandole naftate. Histologically, findings were consistent with erythema multiforme, but diffuse linear deposition of IgA was demonstrated at the dermo-epidermal junction by direct immunofluorescence. Ultrastructurally, deposits were located beneath the basal lamina, around the anchoring fibrils. These observations illustrate that adult linear IgA bullous dermatosis can mimic the clinical and histological features of erythema multiforme and suggest the possibility of drug-induced pathogenesis.
Erythema multiforme
Hypersensitivity reaction
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The lichenoid tissue reaction in which epidermal basal cell damage gives rise to a cascade of histologic events that produce lichenoid or poikilodermatous clinical pictures is outlined. Histologic features in the epidermis are degeneration of basal cells, preservation or increase of granular layer, orthokeratosis, and damage to melanocytes. In the dermis, lymphocytic infiltrate with tendency to invade the lower epidermal layers, capillary proliferation, and participation of histiocytes with formation of pigmented macrophages are characteristic. To the lichenoid and poikilodermatous groups of lesions is added a relatively new subgroup, exemplified by erythema dyschromicum perstans and lichen pigmentosus. The question is raised, whether the recent increase of pigmenting dermatitis of various type is due to the reaction of the skin of predisposed individuals to some as yet unknown environmental contaminant.
Erythema
Basal (medicine)
Epidermis (zoology)
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Morphea (localized scleroderma) is a disease of unknown etiology, presenting as circumscribed areas of indurated skin. Histologically, most cases of morphea feature thickened collagen bundles in the deep reticular dermis, sometimes also extending into the superficial dermis or into the subcutis. We present six cases of morphea in which typical histologic features were restricted to the superficial dermis and contrast these with 27 additional biopsies of conventional morphea seen during the same time period. Sections were stained for elastic fibers, and dermal dendritic cells were labeled with antibodies to CD34 and Factor XIIIa. All six cases showed thickened collagen bundles restricted to the superficial dermis, sparing the deep dermis and without associated evidence of lichen sclerosus et atrophicus (LSA). Dermal elastic fibers were not appreciably decreased in number. There was loss of CD34-positive dermal spindle cells in each of our six superficial examples of morphea, which was restricted to the area of altered collagen in four of the six cases. This report highlights the distinctly uncommon phenomenon of morphea presenting solely as alteration of the superficial reticular dermis, without features of LSA. The selective loss of CD34-labeled spindle cells may provide information regarding the role of these putative immune accessory cells in morphea. Recognition of this manifestation of morphea may be helpful diagnostically.
Morphea
Reticular Dermis
Reticular connective tissue
Dermoepidermal junction
Localized Scleroderma
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Citations (61)