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PubMed2002

Cicatricial alopecia; a dermatopathologic and immunopathologic study of 33 patients (pseudopelade of Brocq is not a specific clinico-pathologic entity).

BACKGROUND: Pseudopelade of Brocq (PB) is a permanent progressive scarring alopecia characterized by numerous alopecic patches localized only in the scalp, that tend to coalesce into larger, irregular plaques with policyclic borders. PB can be considered either the final atrophic stage of several scarring disorders such as lichen planus pilaris (LPP) and discoid lupus erythematosus (DLE) (secondary PB) or an autonomous disease (primary PB). The aim of this study was to assess the incidence of primary vs. secondary PB by a combined histopathological and immunopathological study in a series of patients who fulfilled the clinical diagnostic criteria for PB set forth by Braun Falco et al. METHODS: We studied 33 patients (5 males and 28 females, whose age ranged from 24 to 75 years). The duration of the disease (from onset to biopsy) ranged from 3 months to 8 years. Serum samples were tested for circulating auto-antibodies (antinuclear antibodies anti ENA, anticentromere, anti-Scl70, antithyroid, antigastric parietal cells) circulating immune complexes, total and single fraction (C3, C4) complement activity. The skin biopsies taken from the active advancing margin of the more recent alopecic patch were bisected vertically, one was sent for histopathological examination, and the other for the immunofluorescence studies. RESULTS: In all patients the serum tests above were found to be negative or normal. Histopathologically, 11 biopsies (33.3%) displayed findings typical for LPP whereas seven cases (21.2%) showed typical DLE features. In the remaining 15 cases (45.5%) histopathological findings were not suggestive of any specific dermatosis. DIF investigations showed findings typical of LPP in six cases (18.1%) and typical of DLE in seven cases (21%). In three cases we did not find findings typical of LPP, DLE, or any other specific dermatitis. In 11 cases no immunological deposits could be detected and therefore were classified as negative. CONCLUSION: In conclusion, PB is a type of scarring alopecia of the scalp associated with a peculiar clinical presentation and evolution, which cannot be considered an autonomous nosologic entity because in 66.6% of patients it is the end stage of other inflammatory chronic diseases such as LPP and DLE. It is conceivable that even in those cases in which the histopathological and immunopathological findings did not allow for a specific diagnosis, LPP and DLE were also involved. It is noteworthy that in our study the histopathological and the immunopathological examinations did not conflict and often the results were even coincidental, thus confirming the compatibility of the combined histo-immunopathological approach in the diagnostic evaluation of PB.

Adult↗
PubMed2000

Association of a promoter polymorphism of tumor necrosis factor-alpha with subacute cutaneous lupus erythematosus and distinct photoregulation of transcription.

Ultraviolet irradiation stimulates keratinocytes and dermal fibroblasts to release cytokines involved in apoptosis and immunomodulation, such as tumor necrosis factor-alpha and interleukin-1alpha. Recent work has associated the -308A polymorphism of the human tumor necrosis factor-alpha promoter with systemic lupus erythematosus and adverse outcomes in several infectious diseases. To explore the role of this polymorphism in ultraviolet-induced disease, we used two approaches. First, we examined its prevalence in individuals with different ultraviolet sensitivity. Compared with healthy controls, there was a substantially increased prevalence of -308A in subacute cutaneous lupus erythematosus, an extremely photosensitive form of cutaneous lupus erythematosus, but not in discoid lupus erythematosus, a less photosensitive form. Next, to examine molecular regulation by tumor necrosis factor -308A, cultured 3T3 fibroblasts were transiently transfected with chloramphenicol acetyl transferase reporter constructs under the control of either -308A or the wild-type -308G promoter. Without added interleukin-1alpha the two constructs produced similar baseline chloramphenicol acetyl transferase activity and similar responses to ultraviolet. The responses to interleukin-1alpha, a photoinduced cytokine, were markedly different: interleukin-1alpha without ultraviolet produced a 15-fold increase in chloramphenicol acetyl transferase transcription from the -308A construct without affecting the wild-type -308G. Interleukin-1alpha plus ultraviolet B caused a remarkable 300-fold increase in -308A chloramphenicol acetyl transferase transcription over baseline, while increasing the wild type to <15% of this level. These results indicate a clear difference between the two promoters, including a striking synergy between ultraviolet B and added interleukin-1alpha in the induction of transcription by the tumor necrosis factor-alpha -308A promoter. Overall, our findings indicate a strong linkage between the -308A polymorphism and subacute systemic lupus erythematosus, which is likely to directly contribute to the photosensitivity of these patients.

Chloramphenicol O-Acetyltransferase↗
PubMed2001

Dermal fibroblasts sustain proliferation of activated T cells via membrane-bound interleukin-15 upon long-term stimulation with tumor necrosis factor-alpha.

In chronic inflammatory conditions, mononuclear cells infiltrate the connective tissue attracted by fibroblast-secreted chemokines. The role of fibroblasts in sustaining the lymphocyte immune response upon cellular infiltration is so far unresolved. We here report that, upon prolonged stimulation with tumor necrosis factor-alpha, dermal fibroblasts enhance proliferation of activated T cells whereas unstimulated fibroblasts do not. T cell growth stimulation requires cell contact of tumor necrosis factor-alpha stimulated fibroblasts to T cells and is not due to soluble factors. Growth stimulation is substantially blocked by neutralizing antibodies to interleukin-15. Fluorescence-activated cell sorter analyses revealed that tumor necrosis factor alpha stimulated fibroblasts expose interleukin-15 in a membrane-bound form on the cell surface whereas nonstimulated fibroblasts and interferon-gamma treated fibroblasts do not. The amount of membrane interleukin-15 increases with the duration of tumor necrosis factor-alpha stimulation for at least 3 d. Unstimulated fibroblasts, however, accumulate interleukin-15 in the cytoplasm. No interleukin-15 could be detected in the culture supernatant. Immunohistochemical analyses confirmed membrane interleukin-15 on dermal fibroblasts in discoid lupus erythematosus skin lesions whereas no membrane interleukin-15 was found on the surface of fibroblasts in healthy skin. We conclude that dermal fibroblasts upon long-term tumor necrosis factor-alpha stimulation during chronic inflammation are involved via membrane-bound interleukin-15 in stimulating proliferation of accumulated, activated T cells.

Antibodies↗
PubMed2001

Atrophic facial scars secondary to discoid lupus erythematous: treatment using the Erbium:YAG laser.

BACKGROUND: Discoid lupus erythematosus (DLE) is a chronic inflammatory skin condition notorious for causing disfiguring scars and alopecia. We describe the case of a 66-year-old woman with a 25-year history of relapsing DLE who developed extensive cribriform scarring on her face. OBJECTIVE: To assess the safety and efficacy of laser resurfacing in the treatment of facial scars in DLE. METHODS: One patient was treated with an Er:YAG laser and followed for more than 2 years. RESULTS: The patient showed remarkable cosmetic improvement with no hypertrophic scarring and no reactivation of her disease. CONCLUSION: Er:YAG laser resurfacing may be safe and effective in the treatment of patients with DLE-induced atrophic scars.

Aged↗
PubMed1975

[Unusual clinical forms of pseudo-LE syndrome: an induced immune-complex disease? (author's transl)].

Two of nine patients with pseudo-LE syndrome had previously undescribed organ manifestations. In one there was the full-blown picture of cutaneous lupus erythematodes, with renal and CNS involvement, ending fatally. Immunohistologically there was severe vasculitis and nephritis, histologically generalised necrotizing angitis. It is possible that the dramatic clinical picture was due to alpha-methyldopa. In the second case lymphadenopathy with bihilar involvement and splenomegaly predominated. Histologically there was no evidence of Boeck's sarcoid. Further studies revealed systemic involvement with immune-complex nephritis, electron-dense deposits in the glomerular basal membrane, and the typical changes of lupus erythematodes in the marrow. In a third case there were similar changes in kidney and marrow. These findings support the view of an immune-complex disease which can be fatal. An unusual feature in seven of the nine patients was the proven intake of Venopyronum¿ coated tablets in temporal relationship to the manifestation of the disease. It is possible that the described cases of pseudo-LE syndrome were drug-induced. The immunological mechanism of the disease would, in that case, be analogous to penicillamine nephropathy.

Adult↗
PubMedDate not supplied

[Lupus erythematodesus profundus].

A 4 year old boy with lupus panniculitis since the third month is presented. Typical discoid lupus erythematosus lesions were also present. There were no signs of systemic involvement. Lupus panniculitis is an uncommon subtype of cutaneous lupus erythematosus. Our case is very unusual as the lesions developed already 3 month after birth. Clinical manifestation, therapy and histopathology of lupus panniculitis are discussed.

Adipose Tissue↗
PubMed2001

SET-related cell division autoantigen-1 (CDA1) arrests cell growth.

We used an autoimmune serum from a patient with discoid lupus erythematosus to clone a cDNA of 2808 base pairs. Its open reading frame of 2079 base pairs encodes a predicted polypeptide of 693 amino acids named CDA1 (cell division autoantigen-1). CDA1 has a predicted molecular mass of 79,430 Daltons and a pI of 4.26. The size of the cDNA is consistent with its estimated mRNA size. CDA1 comprises an N-terminal proline-rich domain, a central basic domain, and a C-terminal bipartite acidic domain. It has four putative nuclear localization signals and potential sites for phosphorylation by cAMP and cGMP-dependent kinases, protein kinase C, thymidine kinase, casein kinase II, and cyclin-dependent kinases (CDKs). CDA1 is phosphorylated in HeLa cells and by cyclin D1/CDK4, cyclin A/CDK2, and cyclin B/CDK1 in vitro. Its basic and acidic domains contain regions homologous to almost the entire human leukemia-associated SET protein. The same basic region is also homologous to nucleosome assembly proteins, testis TSPY protein, and an uncharacterized brain protein. CDA1 is present in the nuclear fraction of HeLa cells and localizes to the nucleus and nucleolus in HeLa cells transfected with CDA1 or its N terminus containing all four nuclear localization signals. Its acidic C terminus localizes mainly to the cytoplasm. CDA1 levels are low in serum-starved cells, increasing dramatically with serum stimulation. Expression of the CDA1 transgene, but not its N terminus, arrests HeLa cell growth, colony numbers, cell density, and bromodeoxyuridine uptake in a dose-dependent manner. The ability of CDA1 to arrest cell growth is abolished by mutation of the two CDK consensus phosphorylation sites. We propose that CDA1 is a negative regulator of cell growth and that its activity is regulated by its expression level and phosphorylation.

Amino Acid Sequence↗
PubMed1999

Fibromyalgia in lupus erythematosus.

Fibromyalgia has been reported to occur with high prevalence in systemic lupus erythematosus. Data on fibromyalgia in other subsets of lupus erythematosus are not available. Risk factors for fibromyalgia have not been defined. We investigated 60 patients with different subsets of lupus erythematosus for the presence of fibromyalgia, association with clinical and laboratory parameters and disease activity. Our data were compared with the multicentre lupus erythematosus registry at the Free University of Berlin. Ten out of 60 patients with more than 11 tender points and widespread pain for more than 3 months were classified as positive for fibromyalgia. All of them were female. Fibromyalgia-positive patients suffered significantly more often from headache, morning stiffness, diffuse alopecia, muscle pain, arthralgia, renal involvement, and disclosed peripheral blood cell cytopenia, rheumatoid factor, hypergammaglobulinaemia and intake of corticosteroids and azathioprine. Fibromyalgia was more frequent in systemic lupus than in other lupus subsets. Evaluation of fibromyalgia symptoms and lupus disease activity was performed in 30 patients in a 1-year (range 9-13 months) follow-up. These 30 patients consisted of 9 fibromyalgia-positive and 21 fibromyalgia-negative patients. Both groups were characterized by stable clinical features such as number of tender points and ECLAM index. Fibromyalgia did not show a correlation with lupus activity. We suggest that fibromyalgia and lupus erythematosus are distinct complaints. Patients with lupus are at risk of developing secondary fibromyalgia. The clinical features of fibromyalgia-positive patients may contribute to misinterpretation of lupus activity.

Adult↗