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PubMed1989

[Scleroderma and HLA antigens].

A possible HLA disease association was investigated in 40 patients (38 female, 2 male) with progressive systemic scleroderma (PSS), and 42 patients (32 female, 10 male) with morphea. HLA ABCDR/DQ, glyoxalase and properdin factor B (GLO and BF) phenotypes of patients were compared with 193 healthy controls. Four PSS family studies were performed. The following relative risk (rR) values were determined in PSS: A1 (1.38), A2 (1.39), B8 (1.67), B15 (3.22) and in morphea: A3 (1.43), B7 (1.39), B40 (1.81), BW60 (2.49), DR2 (2.38) and DRW8 (2.55), indicating a relatively weak, HLA-linked genetic predisposition for the manifestation of these dermatological disorders. The HLA "risk" antigens for the two clinically different subtypes of the disease are also different: raised A1/B8 frequencies such as those in our PSS group are related to high (or pathologic) immune response (autoimmune disorders). In contrast, A3 B7 DR2 elevations such as those recorded in our morphea group correlate with low immune response. Following exposition to certain suspected environmental factors (quartz, chemical solvents, drugs, viral fragments), the HLA phenotype may thus predipose some individuals--predominantly women--to different clinical patterns of the disease. HLA typing may thus be useful in clinical differential diagnosis (recent subtyping protocols) and possibly also for determination of the prognosis, i.e. HLA-B8 seems to be related to an acute, inflammatory course of PSS, and HLA-B7/DR2, to rather mild morphea patterns.

Adult↗
PubMed1989

[Studies on stimulating circulation to end stasis in scleroderma].

Of 725 cases of scleroderma, 265 were of systemic type (the sex ratio being 1M:6F) and 460 of circumscribed type (the sex ratio being 1M:9F). The patients were divided into three groups and treated with three different stimulating circulation to end stasis (SCES) prescriptions. Satisfactory therapeutic effects were obtained in all. According to the clinical practice and laboratory findings, although SCES therapy exerted manifold actions on the disease, it not only softened the indurated connective tissues, tonified the body and improved the symptoms, but also improved laboratory indexes as follows: nailfold bed capillary, parameter of the peripheral blood stream in patients, content of urinary 2-ketol, 17-KS, free corten, serum joint-hexose, amino-hexose and histopathology including ultrastructure of the skin. The main effect was the improvement of circulation, especially the microcirculation and regulation of the metabolism of the connective tissues. Great attention should be paid to the drug's function of softening the indurated connected tissues. For further investigation, the authors have stressed three important points: screening of clinical symptoms and signs, examination of blood circulatory disturbances, and examination of pathological changes of the connective tissue. The necessity of developing new criteria for judging the therapeutic effects was emphasized.

Drugs, Chinese Herbal↗
PubMed1986

[Increased retraction of collagen lattices by fibroblasts from patients with scleroderma].

Skin fibroblasts from eight scleroderma patients were seeded in collagen lattices, and their capacity of retraction was compared to that of fibroblasts from normal volunteers. In all cases, pathological fibroblasts retracted collagen lattices earlier and more intensively than controls. This in vitro feature may be related to the cutaneous retraction which characterizes scleroderma lesions in vivo.

Adult↗
PubMed1977

[Scleroderma].

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Collagen Diseases↗
PubMed1988

[Trigeminus neuropathy as a rare main symptom of progressive systemic sclerosis].

In addition to the habitual skin manifestations, the following forms of organic involvement were found (with decreasing frequency) in 33 patients with progressive systemic sclerosis treated from 1972-1986 at the Clinic of Rheumatology, University Hospital of Zürich: blood vessels 29, lungs 18, digestive system 11, joints 11, bones 8, lacrimal and salivary glands 7, musculature 3, heart 3, kidneys 2, cranial nerves 1 and peripheral neuropathy 1.-A 65-year-old patient with classic progressive systemic sclerosis and visceral involvement of the esophagus and the lungs showed, as a principal sign, unilateral neuropathy of the trigeminal nerve involving all three branches as well as absent corneal reflex. Electromyographic examination afforded evidence of a sensory neuropathy of the trigeminal nerve. Chemical laboratory tests revealed a typical high titre of antinuclear antibodies. In addition to autoimmunological causes, proliferation of fibrous structures of the perineurium and vascular lesions are discussed in connection with these complications.-The subsequent history of 37 patients with localized scleroderma and 4 patients suffering from progressive systemic sclerosis, treated at the Clinic of Dermatology, University Hospital of Zürich from 1980-1985 provided no evidence of a cranial nerve involvement. The fact that during the period 1975 to 1985 only one patient treated at the Clinic of Neurology of Zürich University Hospital showed signs of disturbances of pupil motility confirms the very rare involvement of the nervous system in progressive systemic sclerosis.

Aged↗
PubMed1988

Esophageal motor abnormalities in children and adolescents with scleroderma and mixed connective tissue disease.

To determine the frequency and nature of esophageal motor abnormalities in children and adolescents with scleroderma syndromes and mixed connective tissue disease, esophageal manometry was performed on seven patients with progressive systemic sclerosis, four patients with mixed connective tissue disease, and two patients with linear scleroderma. A total of 73% of patients with progressive systemic sclerosis and mixed connective tissue disease had symptoms of esophageal dysfunction. A significant association between the presence of Raynaud phenomenon and esophageal symptoms was noted. Esophageal motor abnormalities were detected in 73% of patients with progressive systemic sclerosis and mixed connective tissue disease; these abnormalities were characterized by decreased lower esophageal sphincter pressure and abnormal peristalsis in the distal two thirds of the esophageal body. They resemble those described among adults with progressive systemic sclerosis and mixed connective tissue disease but were not related to disease duration or to the presence of Raynaud phenomenon. Patients with linear scleroderma did not have esophageal symptoms and demonstrated only nonspecific motor abnormalities that did not worsen during several years of follow-up.

Adolescent↗
PubMed1978

Is vitamin E involved in the autoimmune mechanism?

Autoimmune diseases are characterized by an alteration of the body's defense mechanism, designed for protection against infections and toxic injuries, which for unknown reasons attacks and destroys normal tissue. Some evidence strongly suggests that such diseases are the result of hydrolytic enzymes that escape from lysosomes whose membranes have been damaged by lipid peroxidation or other causes and that combine with and denature normal tissue proteins--in effect converting them into foreign proteins--to which the body then reacts by producing antibodies. During the past ten years, in a private dermatologic practice, we have conducted clinical investigations on the possible therapeutic value of vitamin E in the management of a number of disabling skin diseases of unknown etiology as well as several muscular disorders. Among the diseases that were successfully controlled were a number in the autoimmune category, including scleroderma, discoid lupus erythematosus, porphyria cutanea tarda, several types of vasculitis, and polymyositis. Since vitamin E is a physiologic stabilizer of cellular and lysosomal membranes, and since some autoimmune diseases respond to vitamin E, we suggest that a relative deficiency of vitamin E damages lysosomal membranes, thus initiating the autoimmune process.

Aged↗