Biomedical subjects

Yvonne F Heijdra

Publications and source records attributed to Yvonne F Heijdra.

8 recordsLinked to original sources

PubMed2006

Supplemental oxygen prevents exercise-induced oxidative stress in muscle-wasted patients with chronic obstructive pulmonary disease.

RATIONALE: Although oxygen therapy is of clear benefit in patients with severe chronic obstructive pulmonary disease (COPD), recent studies have shown that short-term supplementary oxygen may increase oxidative stress and inflammation within the airways. OBJECTIVE: We investigated whether systemic inflammation and oxidative stress at rest and during exercise in patients with COPD are influenced by supplemental oxygen. METHODS: Nine normoxemic, muscle-wasted patients with moderate to very severe COPD were studied. Plasma markers of systemic inflammation (leukocyte counts, interleukin 6 [IL-6]) and oxidative stress (lipid peroxidation, protein oxidation, antioxidant capacity) were measured after treatment with either supplemental oxygen (nasal, 4 L . min(-1)) or compressed air, both at rest (1 h treatment) and after submaximal exercise (40 W, constant work rate). In addition, free-radical production by neutrophils and ATP-degradation products were determined before and after exercise. RESULTS: Short-term oxygen breathing at rest did not influence systemic low-grade inflammation and oxidative stress. The IL-6 response to exercise was attenuated during cycling with supplemental oxygen. Exercise-induced lipid and protein oxidation were prevented by treatment with supplemental oxygen. This was associated with both decreased free-radical production by neutrophils and reduced formation of (hypo)xanthine and uric acid. CONCLUSION: Short-term supplementary oxygen does not affect basal systemic inflammation and oxidative stress but prevents exercise-induced oxidative stress in normoxemic, muscle-wasted patients with COPD, and attenuates plasma IL-6 response. Inhibition of neutrophil activation and ATP degradation appears to be involved in this effect.

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PubMed2006

Exercise-induced systemic effects in muscle-wasted patients with COPD.

PURPOSE: Physical exercise is known to induce an acute inflammatory response and oxidative stress in healthy subjects and patients with chronic obstructive pulmonary disease (COPD). Increasing evidence associates systemic inflammation and oxidative stress with muscle wasting and muscle dysfunction in COPD. In the present study, it was hypothesized that exercise-induced systemic inflammatory and oxidative responses in muscle-wasted COPD patients are increased compared with non-muscle-wasted patients and healthy subjects. METHODS: Pulmonary function, body composition, and quadriceps muscle strength were measured in 10 muscle-wasted (fat-free mass index (FFMI) < 16 kg x m(-2) (men), < 15 kg x m(-2) (women)), 10 non-muscle-wasted COPD patients, and 10 healthy subjects. Systemic inflammation (C-reactive protein (CRP), leukocytes, cytokines) and oxidative stress (production of reactive oxygen species (ROS) by neutrophils, plasma antioxidant capacity, protein oxidation, lipid peroxidation, oxidized to reduced glutathione ratio (GSSG/GSH)) were determined before and after maximal and submaximal (50% of maximal work rate) cycle ergometry. RESULTS: Low-grade systemic inflammation was significantly (P < 0.05) elevated in all COPD patients and tended to be highest in muscle-wasted patients. A decreased antioxidant status (plasma antioxidant capacity, P < 0.05; GSH, P < 0.05) and increased protein oxidation (P < 0.001) reflected increased basal oxidative stress in muscle-wasted COPD patients compared with both other groups. Both maximal and submaximal exercise caused increased inflammatory (IL-6, +1.1 pg. x mL(-1) vs rest, P < 0.05) and oxidative responses (ROS release by neutrophils, + 32%; GSSG/GSH + 29%; lipid peroxidation, + 30% vs rest) in muscle-wasted COPD patients, which were less pronounced or not observed in non-muscle-wasted patients and healthy subjects. CONCLUSIONS: These data indicate that both maximal and submaximal exercise induce increased systemic inflammatory and oxidative responses in muscle-wasted COPD patients compared with non-muscle-wasted patients and healthy subjects.

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PubMed2005

Systemic inflammatory response to exhaustive exercise in patients with chronic obstructive pulmonary disease.

Systemic inflammation may be present in patients with chronic obstructive pulmonary disease (COPD). Exercise is known to elicit an inflammatory response. We hypothesized that the systemic inflammatory response to exercise might be exaggerated in COPD patients compared to healthy subjects. Sixteen COPD patients and 11 healthy subjects performed a maximal incremental bicycle test. Before and at maximal exercise arterial blood samples were taken to determine circulating catecholamines, (subsets of) leukocytes, acute phase proteins, creatine kinase and myoglobin. At rest, increased levels of norepinephrine and systemic inflammation were present in COPD. The response of catecholamines to exercise was lower in COPD patients (P<0.01), which in part was due to the lower maximal exercise capacity of these patients (P<0.01). Exercise-induced leukocytosis showed similar responses in both groups, but occurred at higher levels in COPD. Although patients had increased levels of CRP at rest (P<0.001), exercise did not affect acute phase proteins. No systemic signs of muscle damage were found. The present study shows that COPD patients are exposed to systemic inflammation that is intensified by exhaustive exercise. The inflammatory response in COPD is not exaggerated compared to healthy subjects but occurs at a higher level and is observed at lower external workload.

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PubMed2005

Extrapulmonary small cell carcinoma.

This article reviews the recent literature on extrapulmonary small cell carcinomas. Until now, only four cases have been published in the English literature, two of those in the Southern Medical Journal. Sharing the information on diagnosis and treatment of these cases is important for better understanding and treatment of these patients. The differential diagnosis of pleural masses and the relation to asbestos exposure is briefly discussed. In addition, the available literature on other extrapulmonary localizations of small cell carcinoma is reviewed. The focus is on the available larger series of patients. Small cell carcinoma of the skin is included. This form of small cell carcinoma is often excluded from the larger review series, but can be an important alternative in the diagnostic process of patient evaluation.

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PubMed2005

Survival of chronic hypercapnic COPD patients is predicted by smoking habits, comorbidity, and hypoxemia.

STUDY OBJECTIVES: Chronic hypercapnia in patients with COPD has been associated with a poor prognosis. We hypothesized that, within this group of chronic hypercapnic COPD patients, factors that could mediate this hypercapnia, such as decreased maximum inspiratory mouth pressure (P(I(max))), decreased maximum expiratory mouth pressure (P(E(max))), and low hypercapnic ventilatory response (HCVR), could be related to survival. Other parameters, such as arterial blood gas values, airway obstruction (FEV1), body mass index (BMI), current smoking status, and the presence of comorbidity were studied as well. METHODS: A cohort of 47 chronic hypercapnic COPD patients recruited for short-term trials (1 to 3 weeks) in our institute was followed up for 3.8 years on average. Survival was analyzed using a Cox proportional hazards model. The risk factors considered were analyzed, optimally adjusted for age and gender. RESULTS: At the time of analysis 18 patients (10 male) were deceased. After adjusting for age and gender, P(I(max)), P(E(max)), and HCVR were not correlated with survival within this hypercapnic group. Current smoking (hazard ratio [HR], 7.0; 95% confidence interval [CI], 1.4 to 35.3) and the presence of comorbidity (HR, 5.5; 95% CI, 1.7 to 18.7) were associated with increased mortality. A higher Pa(O2) affected survival positively (HR, 0.6 per 5 mm Hg; 95% CI, 0.4 to 1.0). Pa(CO2) tended to be lower in survivors, but this did not reach statistical significance (HR, 2.0 per 5 mm Hg; 95% CI, 0.9 to 4.3). FEV1 and BMI were not significantly related with survival in hypercapnic COPD patients. CONCLUSION: In patients with chronic hypercapnia, only smoking status, the presence of comorbidity, and Pa(O2) level are significantly associated with survival. Airway obstruction, age, and BMI are known to be predictors of survival in COPD patients in general. However, these parameters do not seem to significantly affect survival once chronic hypercapnia has developed.

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PubMed2003

Muscle strength and exercise kinetics in COPD patients with a normal fat-free mass index are comparable to control subjects.

STUDY OBJECTIVE: This study was designed to investigate the extent of clinical muscle dysfunction in stable patients with COPD who were attending an out-patient pulmonary clinic compared with that of age-matched control subjects without COPD. DESIGN AND SUBJECTS: Respiratory muscle and hand grip strength, steady-state O(2) kinetics, and body composition were measured in 32 patients with COPD (19 women) [mean (+/- SD) FEV(1), 38 +/- 11% predicted] and 36 age-matched control subjects (13 women). RESULTS: Measurements of handgrip force (mean, 97 +/- 32% vs 106 +/- 26% predicted, respectively), maximal expiratory pressure (mean, 57 +/- 33% vs 61 +/- 22% predicted, respectively), steady-state O(2) kinetics (mean tau, 72 +/- 34 s vs 78 +/- 37 s, respectively) and steady-state CO(2) kinetics (mean tau, 77 +/- 38 s vs 65 +/- 32 s, respectively) at submaximal exercise were similar in patients and control subjects. All the subjects, except for one female COPD patient, had a normal fat-free mass index (FFMI), although on average the FFMI was lower in male patients (19.8 +/- 2.8) than in male control subjects (23.0 +/- 2.8; p < 0.01). CONCLUSIONS: In patients with COPD who were attending a regular outpatient pulmonary clinic, there was no evidence of reduced upper extremity and expiratory muscle strength or prolonged O(2) and CO(2) kinetics during isowork submaximal cardiopulmonary exercise compared to healthy, age-matched control subjects. Also, a normal body composition was found in nearly all COPD patients. This argues against the existence of a clinically significant systemic myopathy in most stable patients with severe COPD and normal FFMI.

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PubMed2002

Discontinuation of furosemide decreases PaCO(2) in patients with COPD.

STUDY OBJECTIVE: To evaluate whether the discontinuation of furosemide treatment resulted in a decrease in PaCO(2) and an increase in daytime and nocturnal oxygenation. BACKGROUND: Furosemide is widely prescribed in patients with COPD for the treatment of peripheral edema. It is known that furosemide causes a metabolic alkalosis. A diminished chemoreceptor stimulation may cause a decreased alveolar ventilation. DESIGN: Randomized, double-blind, placebo-controlled, crossover trial. SETTING: Department of Pulmonology, Rijnstate Hospital Arnhem, the Netherlands. PATIENTS: Twenty patients with stable COPD (10 men; median age, 70 years [range, 58 to 81 years]; FEV(1) 35% predicted [range, 19 to 70% predicted]). Subjects were included if they had received furosemide, 40 mg/d, for the treatment of peripheral edema for at least a month and if they had a mean nocturnal arterial oxygen saturation (SaO(2)) < 92%. Patients with cardiac left and/or right ventricular dysfunction, sleep apneas, and patients receiving other diuretics, angiotensin-converting enzyme inhibitors, potassium or chloride replacement therapy, or long-term oxygen treatment were excluded. INTERVENTION: Furosemide was discontinued for 1 week and replaced by placebo treatment in the first or the second week. MEASUREMENTS AND RESULTS: Ventilation, daytime arterial blood gas levels, and nocturnal SaO(2) were measured at baseline, after 1, and after 2 weeks. Sixteen subjects completed the study. Ventilation increased from 10.4 L/min (range, 6.7 to 15.4 L/min) at baseline to 11.6 L/min (range, 8.7 to 14.0 L/min) after discontinuation of furosemide (p < 0.05). PaCO(2) decreased from 45 mm Hg (range, 35 to 64 mm Hg) to 41 mm Hg (range, 32 to 61 mm Hg; p < 0.01). Daytime and nocturnal oxygenation did not improve. CONCLUSIONS: Although it does not improve oxygenation, the discontinuation of furosemide decreases PaCO(2) in patients with COPD.

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PubMed2002

Cough and phlegm are important predictors of health status in smokers without COPD.

STUDY OBJECTIVES: The health-related quality of life of smokers without COPD and that of ex-smokers has not been defined. If abnormal, the role of small airways disease and that of cough and phlegm have never been evaluated. Therefore, the aim of the study was to explore whether the differences in quality of life between smokers and ex-smokers could be explained by cough and phlegm, differences in pulmonary function tests, or exercise capacity. DESIGN: Observational, prospective. SETTING: Pulmonary and Critical Care Division, COPD Center at St. Elizabeth's Medical Center. POPULATION: In 36 smokers, 21 ex-smokers (stopped smoking for > 20 years), 19 never-smokers with normal FVC and FEV(1) values, and 41 patients with COPD (FEV(1) 38 +/- 11% predicted [mean +/- SD]), the St. George's Respiratory Questionnaire (SGRQ), pulmonary function tests, and a 6-min walk distance (6MWD) were performed. RESULTS: The total SGRQ scores were worse in current smokers (15 +/- 15) than in ex-smokers (6 +/- 4) or never-smokers (4 +/- 3) [p < 0.05]. As expected, the worst score was seen in COPD (50 +/- 15). After correcting for cough and phlegm, the difference in SGRQ scores between smokers and ex-smokers disappeared. In current and ex-smokers, the SGRQ score was associated with the exposure to pack-years smoking history (r = 0.45, p < 0.01, and r = 0.83, p < 0.0001, respectively) but independent of lung function or exercise parameters (6MWD). CONCLUSIONS: In smokers without COPD, the abnormal SGRQ score is due to the noxious effect of cigarette smoke, resulting in cough and phlegm, independent of its physiologic effects.

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