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Results for “FIBROSITIS”

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PubMed1978

[Roentgenological morphology and clinical signs for the differential diagnosis of pulmonary fibroses (author's transl)].

The clinician usually determines the measures to be taken on the basis of clear symptomatics represented by more or less pronounced cyanosis. The author is able to show that the negative roentgenogram is not a reliable means of excluding pulmonary fibrosis, in contrast to functional pulmonary studies. If breathing physiology is normal and the roentgenogram does not reveal any abnormal findings, further invasive procedure will not be required. However, if functional investigations are positive and indicate a diffuse pulmonary disease, then our criteria point to open pulmonary biopsy, since prognosis and possible causal treatment largely depend on the histology.

Adult↗
PubMed1988

[Pathophysiology of fibroses. Progressive systemic scleroderma as a model disease].

Fibrosis is characterized by excessive deposition of connective tissue in the involved organs. Although the prime event in the pathogenesis is still poorly understood, several mechanisms are discussed, which finally result in the activation of fibroblasts. Recent studies have demonstrated that immunocompetent cells play a crucial role during the initial phases of the development of fibrosis. Therefore, several mediators have been characterized, which are secreted by platelets, lymphocytes and macrophages and which can attract fibroblasts, induce proliferation and collagen synthesis in mesenchymal cells. These include PDGF, EGF, TGF--beta and many others. In addition, gamma-interferon has been shown to inhibit chemotaxis of fibroblasts and to reduce collagen mRNA levels. A controlled interaction of all the different mediators is required to guarantee a normal functioning of connective tissue. Alterations in these regulation steps can result in excessive deposition of connective tissue and the development of fibrotic processes.

Collagen↗
PubMed1986

Sleep related myoclonus in rheumatic pain modulation disorder (fibrositis syndrome).

Thirty-three patients with rheumatic pain modulation disorder (RPMD) were divided into 2 groups: RPMD with sleep related myoclonus (RPMD-SM) (n = 12) and RPMD only (n = 21). Both groups showed chronic nonarticular musculoskeletal pain, fatigue, tender points, and nonrestorative sleep with alpha (7.5-11 Hz) EEG sleep anomaly. RPMD-SM patients were older, had later onset of illness, showed disrupted sleep with periodic involuntary leg movements that were related to fatigue, and alpha EEG sleep related to fatigue and pain.

Adult↗