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Results for “Scleroderma, Localized”

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At least 631 records · Page 35Linked to original sources
PubMed2004

Increased prevalence of human parvovirus B19 DNA in systemic sclerosis skin.

BACKGROUND: Human parvovirus B19 is a small, single-stranded DNA virus encoding two structural capsid proteins and a nonstructural protein. It is the aetiological agent of erythema infectiosum and transient aplastic crisis in patients with haemolytic anaemia, and has been associated with fetal death, arthritis and chronic anaemia. In recent years, the possible involvement of parvovirus B19 in systemic sclerosis (SSc) has been reported. OBJECTIVES: To determine whether human parvovirus B19 DNA can be detected in SSc skin tissue specimens. METHODS: Normal subjects (n = 97) and patients with SSc (n = 48), systemic lupus erythematosus (n = 16), dermatomyositis (n = 8), morphoea (n = 6) and graft-versus-host disease (n = 8) were studied. Crude DNA was extracted from skin tissue specimens. We attempted to determine whether human parvovirus B19 could be detected in the skin of SSc using nested polymerase chain reaction (PCR). PCR amplification was performed with specifically designed first and second primer pairs for parvovirus B19 DNA. RESULTS: After the first PCR, the occurrence rate of parvovirus B19 DNA in SSc skin tissues (36 of 48, 75%) was significantly elevated in comparison with that in normal controls (50 of 97, 52%) (P < 0.01). After the second PCR, the occurrence rate of parvovirus B19 DNA in SSc skin tissues (36 of 48, 75%) was significantly elevated compared with that in normal controls (53 of 97, 55%) (P < 0.02). The occurrence rates in the other diseases showed no significant difference from that in normal controls. CONCLUSIONS: The increased prevalence of human parvovirus B19 DNA in SSc skin showed the possibility that the virus may be involved in the formation of skin tissue abnormalities in the disease.

Adult↗
PubMed2004

High plasminogen activator inhibitor type 2 expression is a hallmark of scleroderma fibroblasts in vitro.

Systemic scleroderma is a chronic disease, which leads to fibrosis of the skin and internal organs. Fibroblasts obtained from patients with this disease demonstrate an activated state in culture. We, in this study, report strong, constitutive overexpression of plasminogen activator inhibitor type-2 (PAI-2) in scleroderma fibroblasts and demonstrate that this induction observed at the mRNA and protein level is dependent on serum addition. Induced PAI-2 protein levels were restricted to the non-glycosylated 47-kDa form, which is located intracellularly. Induction was stable for at least 12 passages. No modulation by fibrogenic cytokines--for example, transforming growth factor-beta1 or connective tissue growth factor--or by antagonizing IL-1 receptors was observed. The data indicate that scleroderma fibroblasts are more sensitive to the induction of PAI-2 expression than control fibroblasts by a presently unknown factor in serum.

Adult↗
PubMed1992

Palindromic morphea: multiple recurrence of morphea lesions in a case of systemic sclerosis.

We report an unusual scleroderma case. A 45-year-old woman had recurrent morphea lesions over 10 times in 6 years. She had had preceding inactive systemic scleroderma. New morphea lesions developed cyclically on various portions of her body and improved within 2 years. Interestingly, new lesions have developed on once involved skin as well as uninvolved skin. No exacerbation of systemic scleroderma was induced by outbreaks of new morphea lesions. We could not find a similar case in the literature and named it "Palindromic morphea" because of its unique clinical course. D-penicillamine treatment had a limited effect. Minimal oral prednisolone (5 mg/day) completely suppressed the multiple recurrence of the morphea lesions and enhanced improvement of the sclerosis.

Female↗
PubMed1994

Nodular scleroderma in a worker using a silica-containing abrasive.

A patient with progressive systemic sclerosis and high levels of serum IgE developed multiple papules at/on an area of non-sclerotic skin. Histologic examination of the papule revealed the typical features of scleroderma. For several years, the patient had been working on polishing watches with an abrasive agent composed mainly of aluminum, chromium dioxide, and silica. An association of the abrasive agent, especially of the silica component, with the scleroderma was circumstantially suspected. To the best of our knowledge, this is the first report of nodular scleroderma which occurred in the course of PSS being associated with chemical agents.

Abdomen↗
PubMed1995

Human type VI collagen: purification from human subcutaneous fat tissue and an immunohistochemical study of morphea and systemic sclerosis.

Collagen was isolated from human placenta by pepsin digestion and salt precipitation. This collagen was similar in its electrophoretic mobility and immunological reactivity with monoclonal antibody to form B of type VI collagen in the literature (Trueb B, Schreier T, Bruckner P and Winterhalter K. 1987. Eur. J. Biochem. 166: 699-703). We prepared polyclonal rabbit antiserum against alpha 2 chain of type VI collagen and performed an immunohistochemical study using this polyclonal antibody. It reacted in fat tissue and around vessels and peripheral nerves in normal human skin. To confirm the presence of type VI collagen in fat tissue, we isolated collagen from human subcutaneous tissue. This collagen showed a similar pattern in polyacrylamide gel electrophoresis with that from human placenta and cross-reacted with monoclonal or polyclonal antibody against type VI collagen. By immunohistochemical staining, abundant type VI collagen was observed in the septum of subcutaneous fat tissue in morphea or systemic sclerosis. In the mild hyalinizing areas or after treatment with 6M urea or hyaluronidase in highly hyalinized areas, the staining of type VI collagen increased. These data suggest that the amount of type VI collagen in subcutaneous tissue is involved in the early phases of these fibrosing disorders and that type VI collagen accumulates even more in hyalinizing tissue in late phases of these diseases.

Adipose Tissue↗
PubMed1996

Successful treatment of scleroderma with PUVA therapy.

PUVA therapy was carried out on four patients with scleroderma; three of them had cutaneous manifestations of progressive systemic sclerosis and one other exhibited generalized morphea. PUVA therapy was given with daily doses of 0.25J/cm2 or 0.4J/cm2 for 3-8 weeks, resulting in total doses between 3.5J/cm2 and 9.6J/cm2. All four patients responded well to this treatment; improvements of hand closure, skin sclerosis index, and flexion of fingers or knee joints were obtained. Thus, PUVA appeared to be beneficial for treating scleroderma.

Adult↗
PubMed1999

Topical tocoretinate improved hypertrophic scar, skin sclerosis in systemic sclerosis and morphea.

Four patients with systemic scleroderma (SSc), 4 patients with morphea, and 4 patients with hypertrophic scar were treated with topical tocoretinate for 6 months to 3 years and studied clinically and histopathologically. Clinically, all of the lesions responded to this therapy. The stiffness of the skin lesions, glossy appearance of the lesions, and telangiectasia improved. Histopathologically, the proliferated collagen fibers decreased in thickness, and the inter-fiber spaces increased. Immunoreactive tenascin-C expressed in the proliferated deep dermal fibers of the SSc and hypertrophic scar lesions was markedly decreased compared with the level before the topical tocoretinate therapy. Topical tocoretinate has been used for the treatment of ulcers; it is also a potent treatment for sclerotic skin diseases.

Administration, Topical↗
PubMed2005

A case of nodular scleroderma.

Nodular scleroderma is a rare complication of systemic sclerosis; the pathogenetic implications are still unknown, although many factors are supposed to play a role in lesion development. We report the case of a young woman suffering from systemic sclerosis, who developed nodular lesions during therapeutic management with D-penicillamine and plasmapheresis. In order to better understand the essence of this disease, we examined all the possible pathogenetic mechanisms that could be implicated in nodular lesion development.

Adult↗
PubMed1984

Anaesthesia and severe skin disease.

A review of the anaesthetic management of severe skin disease is presented. Erythroderma, urticaria pigmentosa, hereditary angioedema, epidermolysis bullosa, pemphigus, pemphigoid, the Stevens-Johnson syndrome, Behcet's syndrome, scleroderma, Ehlers-Danlos syndrome and congenital anhidrotic ectodermal defect are discussed.

Adult↗