Biomedical subjects

Piotr Rozentryt

Publications and source records attributed to Piotr Rozentryt.

4 recordsLinked to original sources

PubMed2006

[Cachexia in chronic pulmonary obstructive disease].

Weight loss is a characteristic feature of chronic obstructive pulmonary disease (COPD) and a negative, independent predictor of outcome. It is a consequence of a misbalance between protein synthesis and breakdown resulting from increased energy requirement unbalanced by dietary intake. A depletion of fat-free mass is seen, especially in muscles (up to 60% of their mass) and leads to the loss of their power and endurance. The impairment of quality of life is very distinct. So far, there is no systemic treatment in cachectic patients with COPD, anti-catabolic treatment by polyunsaturated fatty acid may be of significance but needs further investigation.

Cachexia↗

PubMed2005

[Pathomechanism of cachexia in chronic obstructive pulmonary disease].

Weight loss is a characteristic for advanced chronic obstructive pulmonary disease (COPD), but its mechanism remains unexplained. The decrease of lean body mass is due to a negative energy balance with a noncatabolic hypermetabolic state. Pulmonary inflammation or tissue hypoxia might contribute to it, the decrease in protein content is accompanied by an increase in reactive oxygen forms. Tumor necrosis factor (TNF) has been implicated, other candidates are cytokines IL-1B and IL-6. Activation of apoptosis may be noticed. Pulmonary inflammation and changes in serum leptin may be interrelated. Other hormonal disturbances involve serum IGF-1 level decrease, increase of insulin resistance, raised catecholamine and cortisol levels and other mechanisms which need further investigations. Up to now the attempts undertaken to counteract the observed hormonal changes failed to success.

Apoptosis↗

PubMed2002

[Tumor necrosis factor receptors sTNF-RI and sTNF-RII in advanced chronic heart failure].

UNLABELLED: The inflammatory process in chronic heart failure (CHF) is the result of dysbalance between the function of inflammatory and natural antiinflammatory mediators. Tumor necrosis factor alpha (TNF-alpha) is increased in patients with severe CHF. Two soluble proteins, the extracellular domains of the TNF receptors (sTNF-RI and sTNF-RII) inhibit the TNF-alpha biological effect. The aim of the study was to examine the plasma levels of sTNF-RI and sTNF-RII in patients with CHF and its relation to clinical, biochemical parameters of CHF severity. 41 patients with CHF (NYHA III and NYHA IV) and 18 control subjects were enrolled in this study. Plasma levels of sTNF-RI and sTNF-RII were analyzed by immunosorbent assay (ELISA) kits R&D (Research and Diagnostics Systems) (pg/ml). RESULTS: CHF patients had significantly increased receptor plasma levels compared to controls (p < 0.001). Soluble sTNF-RI and sTNF-RII receptors levels were similar in class NYHA III and NYHA IV. Receptor sTNF-RII correlated negatively with sodium plasma levels (p < 0.001), and sTNF-RI positively correlated with urice acid plasma level (p < 0.05). No statistically significant correlations were found between those receptors and age and gender etiology and severity of CHF, body weight (BMI) or other examined parameters (clinical, hemodynamic, echocardiographic, holter). CONCLUSIONS: Plasma level of sTNF-RI and sTNF-RII are increased in patients with CHF.

Adult↗

PubMed2002

[Concentration of nitric oxide in exhaled air in patients with sarcoidosis--pilot study].

Exhaled nitric oxide (eNO) concentration measurement may allow for noninvasive estimation of severity of airways inflammation in asthma and other airways diseases. The purpose of this study was to evaluate usefulness of eNO concentration measurements in patients with pulmonary sarcoidosis. Study group consisted of 22 patients with sarcoidosis (8 women, 14 men aged 26-46). They included 11 patients with radiographically stage I and II and 11 patients with stage III of disease. Sixteen patients had active pulmonary sarcoidosis and 6 had nonactive disease. Ten patients had indications for treatment, 12 patients had not any. Exhaled NO was measured by means of SIEVERS 280 Nitric Oxide Analyser (USA). There was no significant difference in mean eNO concentration in study group (6.91 +/- 0.60 ppb) and in normal control (5.2 +/- 0.73 ppb, p = 0.10). Exhaled NO concentration was similar in patients with sarcoidosis stage I and II (7.5 +/- 1.08 ppb) and in patients with stage III disease (6.2 +/- 0.51 ppb, p = 0.27). We failed to found significant difference in eNO concentration between patients with active (6.7 +/- 0.71 ppb) and nonactive sarcoidosis (7.5 +/- 1.1 ppb; p = 0.57). Neither did eNO concentration differ between patients with and without indications for therapy (5.77 +/- 0.50 ppb vs. 7.8 +/- 0.95 ppb; p = 0.08). In conclusion our pilot study results indicate that measurement of eNO concentrations may be of little value in patients with sarcoidosis.

Adult↗