A Clinical, Histological, and Immunohistochemical Comparison of Acrodermatitis Chronica Atrophicans and Morphea

Aberer, Elisabeth; Klade, H; Hobisch, G

doi:10.1097/00000372-199108000-00003

Cited by 55 publications

(34 citation statements)

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“…Remarkably, these clinical entities can occur at the same time in the same patient, and coexisting morphea has been described in patients with EM, BL, ACA and Lyme arthritis [56][57][58][59][60]. There are also similarities in the histopathological findings between EM, ACA and morphea [61]. These include the following: variable infiltration of lymphocytes, macrophages and plasma cells; slight vacuolar degeneration of the basal layer in the late stages; and an increase of fibrocytes/ fibroblasts with variable fibrosis to sclerosis.…”

Section: Reviewmentioning

confidence: 99%

Cutaneous and systemic Lyme disease

Deluca¹,

Eisendle²,

Zelger

2013

Expert Review of Dermatology

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Section: Reviewmentioning

confidence: 99%

Cutaneous and systemic Lyme disease

Deluca¹,

Eisendle²,

Zelger

2013

Expert Review of Dermatology

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“…The percentage of CD4 / T lymphocytes, however, seen in patients in the United States and Europe. Several recent articles have described the symptoms of CLB increases up to 90% [8][9][10]. Although the presence of many plasma cells is histologically pathognomonic, the predomi- [1][2][3][4][5][6][7].…”

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confidence: 99%

“…Although the presence of many plasma cells is histologically pathognomonic, the predomi- [1][2][3][4][5][6][7]. Studies of CLB in the rhesus monkey model have revealed characteristic clinical, histopathologic, and laboratory nance of CD22 / /CD20 / B cells varies [9,10]. But what happens as a consequence of this active inflammafindings [3].…”

mentioning

confidence: 99%

“…Nevertheless, the erythema can either smooth muscle actin [12]. Deposition of immunocomplexes in dermal vessel walls as well as granular IgM or C3 deposits can sometimes be seen at the dermoepidermal junction [10]. The inflammatory infiltrate S65 CID 1997;25 (Suppl 1) Chronic Lyme Borreliosis tinocytes show vacuolization, as also seen in lichen planus or early stage of borreliosis suggests that their function might be altered in Lyme borreliosis.…”

mentioning

confidence: 99%

“…The inflammatory infiltrate S65 CID 1997;25 (Suppl 1) Chronic Lyme Borreliosis tinocytes show vacuolization, as also seen in lichen planus or early stage of borreliosis suggests that their function might be altered in Lyme borreliosis. graft-versus-host disease of the skin [10,13,14].…”

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confidence: 99%

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Why Is Chronic Lyme Borreliosis Chronic?

1997

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Chronic Lyme borreliosis (CLB) can present not only in different organs but also in different patterns. Although many theories exist about the mechanisms leading to CLB, it is known that viable Borrelia burgdorferi can persist for decades and cause late skin manifestations of acrodermatitis chronica atrophicans (ACA). Thus, the immunopathogenetic findings in ACA can serve as a model for studying the chronic course of Lyme borreliosis. Recent findings indicate that the most important cell for antigen presentation, the epidermal Langerhans cell (LC), is invaded by B. burgdorferi in early Lyme borreliosis. Therefore, LCs were stained immunohistochemically with different markers to investigate their functional activity. Numbers of CD1a+ LCs were reduced in erythema migrans but normal or slightly elevated in ACA. In both diseases there was also a marked downregulation of major histocompatibility complex class II molecules on LCs, as measured by staining of human leukocyte antigen DR. This phenomenon might be a mechanism that protects against the presentation of autoantigens and may be the cause of the impaired capacity of LCs to eliminate B. burgdorferi antigens, thus explaining why CLB is chronic.

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