BackgroundCryptococcus neoformans is an encapsulated yeast and the most frequent cryptococcal species found in humans. Cryptococcosis is considered an opportunistic infection as it affects mainly immunosuppressed individuals. In humans, C. neoformans causes three types of infections: pulmonary cryptococcosis, cryptococcal meningitis and wound or cutaneous cryptococcosis.Case PresentationAn 81-year-old woman developed severe necrotizing cellulitis on her left arm without any preceding injury. The patient had been treated with systemic corticosteroids over twenty years for rheumatoid arthritis (RA). Skin biopsies of the wound area were initially interpreted as cutaneous vasculitis of unknown etiology. However, periodic acid Schiff staining and smear analysis later revealed structures consistent with Cryptococcus neoformans, and the infection was subsequently confirmed by culture. After the initiation of therapy with fluconazole 400 mg per day the general condition and the skin ulcers improved rapidly and the patient was discharged to a rehabilitation facility. Subsequently surgical debridement and skin grafting were performed.ConclusionsOpportunistic infections such as cryptococcosis can clinically and histologically mimic cutaneous vasculitis and have to be investigated rigorously as a differential diagnosis in immunosuppressed patients.
Objective. Vascular injury and endothelial cell (EC) activation are pathogenic hallmarks of systemic sclerosis (SSc; scleroderma). Human CD90 is highly expressed on activated ECs and can be shed from the cell surface. This study was conducted to examine whether soluble CD90 (sCD90) is elevated in the sera of patients with SSc and linked to pulmonary involvement and in particular, pulmonary arterial hypertension (PAH). Methods. sCD90 serum concentrations were assessed in 76 patients with SSc and related to clinical data, lung function, 6-minute walk distance, echocardiography, bronchoalveolar lavage fluid, and laboratory parameters. Thirty-one healthy volunteers and 29 patients with idiopathic retroperitoneal fibrosis (IRF) served as controls. Results. sCD90 serum concentrations were elevated in patients with SSc compared to healthy volunteers (P ؍ 0.001) and patients with IRF (P ؍ 0.01). SSc patients with pulmonary fibrosis (P ؍ 0.006) and patients with PAH (P < 0.001) had increased sCD90 serum concentrations compared to patients without the respective pulmonary manifestation of SSc. sCD90 levels correlated with diffusing capacity for carbon monoxide (n ؍ 65; r ؍ ؊0.348, P ؍ 0.005) and systolic pulmonary artery pressure (n ؍ 53; r ؍ 0.469, P < 0.001). Receiver operating characteristic curve testing determined an optimal cutoff value of >626 ng/ml with a sensitivity of 68% and a specificity of 83% for PAH (area under the curve 0.773, 95% confidence interval 0.648 -0.898; P < 0.001). Conclusion. sCD90 concentrations were increased in the sera of SSc patients, particularly in patients with vascular involvement of the lungs. These data suggest that sCD90 should be further evaluated as a marker for diagnosis of PAH in SSc.
It is generally known that cigarette smoke alters the activation of alveolar macrophages (AM). CC Chemokine Ligand 18 (CCL18) is a marker of alternatively activated macrophages and is highly expressed in the lung. This study examines the influence of chronic cigarette smoking on the expression of CCL18 by AM. Bronchoalveolar lavage (BAL) and serum were obtained from ten smokers and 14 non-smokers. CCL18 protein concentrations were measured in serum and BAL fluid (BALF) as well as in supernatants from BAL-cells by enzyme-linked immunosorbent assay. In this study we show that the CCL18 production of BAL-cells from smokers was significantly decreased compared to BAL-cells from non-smokers. The BALF CCL18 protein concentration per macrophage cell count was significantly reduced in smokers. Furthermore, we show a decrease in CCL18 production from BAL-cells after stimulation with LPS. This decrease in CCL18 production was only shown in BAL-cells from non-smokers, which is probably due to chronic LPS exposure of smokers, resulting in LPS hypo-responsiveness. No statistically significant difference of CCL18 concentrations was found in BALF or serum of smokers versus non-smokers. CCL18 production by BAL-cells is down-regulated by chronic cigarette smoking and LPS contamination in cigarette smoke might be one factor involved. Thus this article gives further evidence that chronic cigarette smoking alters the phenotype of AM and that the M2 marker CCL18 is down-regulated in smokers macrophages.
Summary Background: In patients with severe chronic obstructive pulmonary disease (COPD), anaemia is common and associated with impaired long‐term survival and quality of life. Whether anaemia is also prevalent in patients with other severe, non‐inflammatory respiratory diseases has not yet been systematically tested. Methods: In 595 patients with obstructive (OD, 54.8%) or restrictive disease (RD, 45.2%) and chronic respiratory failure (CRF), anthropometric data, laboratory parameters, lung function, blood gases and comorbidities were assessed prior to initiation of home mechanical ventilation. Patients were classified as anaemic based on haemoglobin (Hb) levels (Hb < 12/13 g/dl, female patients/male patients). Patients with known causes for anaemia were excluded. Results: In patients with CRF the prevalence of anaemia was 13.3% and not different between RD (11.5%) and OD (14.7%) (p = 0.276). A sex‐related difference occurred only in OD [7.9% (f) vs. 17.3% (m); p = 0.035]. Patients with OD and anaemia presented with higher age (p = 0.003), pH (p = 0.014) and arterial oxygen pressure (PaO2) (p = 0.012), lower body mass index (BMI) (p = 0.011) and total protein (p = 0.012) and higher rates of coronary heart disease (p = 0.01), cardiac arrhythmia (p = 0.014) and diabetes mellitus (p = 0.003) in comparison to non‐anaemic patients. In patients with RD anaemia was associated with higher age, (p = 0.008), pH (p = 0.011) and lower leucocytes numbers (p = 0.006). Conclusions: Anaemia is frequent not only in COPD but also in other severe respiratory diseases combined with CRF. It was associated with advanced age, several comorbidities, impaired nutritional state and elevations of pH and PaO2, probably because of hyperventilation. Its prognostic impact has to be elucidated in future studies.
Serum concentration of CCL18 reflects fibroinflammatory activity and extent of disease in patients with chronic periaortitis.
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