Clin Exp Rheumatol
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Nintedanib is approved for the treatment of idiopathic pulmonary fibrosis (IPF) and was demonstrated to slow disease progression in patients with IPF by reducing decline in forced vital capacity by 50%. Recently, nintedanib has been reported to exert anti-fibrotic activity on systemic sclerosis (scleroderma, SSc) skin fibroblasts and to diminish skin and lung fibrosis in mouse models. The goal of the present study was to determine the effects of nintedanib on a cellular model of SSc-associated interstitial lung disease (ILD). ⋯ Our data demonstrate significant antifibrotic efficacy of nintedanib in SSc-ILD LF suggesting that nintedanib has the potential not only to prevent but also to reverse the increased activity of LF consequently attenuating excessive lung fibrosis observed in SSc-ILD.
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We investigated whether serum soluble programmed cell death protein 1 (sPD-1) could predict the current activity and severity of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) based on Birmingham vasculitis activity score (BVAS) in patients with AAV. ⋯ Serum sPD-1 could predict the current activity and severity of AAV.
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To investigate the in-situ expression of acetylcholinesterase (AChE) in the inflamed vessel wall of patients with biopsy-positive giant cell arteritis (GCA) as compared to biopsy-negative non-GCA patients, and to evaluate the in-vivo expression of AChE in patients with large-vessel GCA (LVGCA) by 11C-donepezil (AChE inhibitor) positron emission tomography/computed tomography (PET/CT). ⋯ AChE is highly expressed in the inflamed vessel wall of patients with GCA. Although, 11C-donepezil PET/CT showed no vascular uptake in the FDG PET/CT verified LV-GCA patients, histological findings raise the possibility that AChE can be used in the development of new diagnostic and disease monitoring tools for GCA.
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Neuromuscular efficiency (NME) is impaired in fibromyalgia (FM). Hyperbaric oxygen therapy (HBOT) is a medical treatment using 100% of oxygen through an oxygen mask. HBOT in FM induces changes in cortical excitability and a secondary reduction in pain and muscle fatigue. However, there are still no direct data indicating changes in muscle fatigue. The aim of this study was to assess whether the reduction in muscle fatigue so far attributed to a central effect of HBOT can be directly detected by means of non-invasive sEMG as a change in NME. ⋯ HBOT did not improve muscle strength or change muscle fibre content, but improved the ability of the central motor command to generate the same effort (MVC) with fewer recruited fibres. Our sEMG findings underlined a modified central mechanism related to fibre type recruitment order, thus suggesting that muscle fatigue is not primarily a muscular problem, as also demonstrated by other authors with different methods.
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Fibromyalgia (FM) is defined as a severe, chronic, non-articular rheumatic condition characterised by widespread musculoskeletal pain, hyperalgesia and generalised tender points, in the absence of inflammatory or structural musculoskeletal abnormalities. Pain is the predominant symptom, allodynia and hyperalgesia are common signs. Extreme fatigue, impaired cognition and non-restorative sleeping difficulties coexist in addition to other somatic symptoms. Several studies suggest there is a meaningful relationship between FM and the psychological symptoms of depression and post-traumatic stress disorder (PTSD). PTSD is a mental disorder that can develop after a person has been exposed to a traumatic event, characterised by a specific set of symptoms including re-experiencing of the event, avoidance and numbing and arousal. The present study investigates the impact of lifetime potentially traumatic events, including losses, and of post-traumatic stress symptoms on the severity of illness in patients with fibromyalgia (FM). ⋯ The results of the study show that fibromyalgic patients with PTSD report more potentially traumatic events, avoidance symptoms, numbing, arousal, maladaptive coping and personality characteristics compared to patients with partial or without PTSD; these results could indicate that loss and/or trauma events represent a risk factor for the development of symptoms of FM in genetically predisposed individuals.