PubMed Health⌕ Search

Biomedical subjects

Charis Roussos

Publications and source records attributed to Charis Roussos.

At least 55 records · Page 3Linked to original sources
PubMed2005

Perinuclear antineutrophil cytoplasmic antibody myeloperoxidase-positive vasculitis in association with ulcerative colitis.

We describe a patient with ulcerative colitis (UC) who developed small vessel vasculitis. Perinuclear antineutrophil cytoplasmic antibody myeloperoxidase (p-ANCA-MPO) positivity was detected along with a highly elevated titer of anticardiolipin antibodies. A total proctocolectomy was undertaken and the patient, more than 5 years later, remains in very good condition. The possible causative association between the UC, the p-ANCA-MPO-positive small vessel vasculitis, and the anticardiolipin antibodies is discussed.

Antibodies, Anticardiolipin↗
PubMed2005

Non-random structural chromosomal changes in primary gastric cancer.

Gastric cancer is of major importance world-wide representing the second most common cause of cancer related death in the world. Data concerning the chromosomal changes in gastric cancer are limited and no specific change has been identified to date. We have studied cytogenetically 15 cases of primary gastric cancer by direct culture of tumors cells and G-banding technique. We focused on structural aberrations observed in order to identify non-random aberrations presenting common chromosomal breakpoints. Chromosomes most commonly involved were according to frequency 1,11,14,7,17,6,8 and 13. Chromosome 11 was involved as add(11)(p15), while the pericentromeric area of chromosome 14 was constantly participated in aberrations. Isochromosomes i(1q), i(8q), i(13q), i(14q) and i(17q) were constantly found. Furthermore translocations t(1;7), t(7;14), t(6;17) and t(5;14) were identified. Conventional cytogenetics continues to be valuable in cancer study detecting genomic areas potentially candidate for the isolation of genes related to carcinogenesis.

Chromosome Aberrations↗
PubMed2005

Is loaded breathing an inflammatory stimulus?

PURPOSE OF REVIEW: To summarize recent data indicating that loaded breathing generates an inflammatory response. RECENT FINDINGS: Loaded breathing initiates an inflammatory response consisting of elevation of plasma cytokines and recruitment and activation of lymphocyte subpopulations. These cytokines do not originate from monocytes but are instead produced within the diaphragm secondary to the increased muscle activation. Oxidative stress is a major stimulus for the cytokine induction secondary to loaded breathing. The production of cytokines within the diaphragm may mediate the diaphragm muscle fiber injury that occurs with strenuous contractions, or contribute to the expected repair process. These cytokines may also compromise diaphragmatic contractility or contribute to the development of muscle cachexia. They may also have systemic effects, mobilizing glucose from the liver and free fatty acids from the adipose tissue to the strenuously working respiratory muscles. At the same time, they stimulate the hypothalamic-pituitary-adrenal axis, leading to the production of adrenocorticotropic hormone and beta-endorphins. The adrenocorticotropic hormone response may represent an attempt of the organism to reduce the injury occurring in the respiratory muscles through the production of glucocorticoids and the induction of the acute-phase response proteins. The beta-endorphin response would decrease the activation of the respiratory muscles and change the pattern of breathing, which becomes more rapid and shallow, possibly in an attempt to reduce and/or prevent further injury to the respiratory muscles. SUMMARY: Loaded breathing is an immune challenge for the body, initiating an inflammatory response. Further studies are needed to elucidate the role of this response in the development of ventilatory failure.

Airway Resistance↗
PubMed2005

The effects of nebulized salbutamol, external positive end-expiratory pressure, and their combination on respiratory mechanics, hemodynamics, and gas exchange in mechanically ventilated chronic obstructive pulmonary disease patients.

We hypothesized that combined salbutamol and external positive end-expiratory pressure (PEEPe) may present additive benefits in chronic obstructive pulmonary disease (COPD) exacerbation. In 10 anesthetized, mechanically ventilated, and bronchodilator-responsive COPD patients exhibiting moderate intrinsic PEEP (PEEPi), we assessed respiratory system (rs) mechanics, hemodynamics, and gas exchange at (a) baseline (zero PEEPe [ZEEPe]), (b) 30 min after 5 mg of nebulized salbutamol administration (ZEEPe-S), (c) 30 min after setting PEEPe at baseline PEEPi level (PEEPe), and (d) 30 min after 5 mg of nebulized salbutamol administration with PEEPe maintained unchanged (PEEPe-S). Return of determined variable values to baseline values was confirmed before PEEPe application. Relative to ZEEPe, (a) at ZEEP-S, PEEPi (4.8 +/- 0.7 versus 7.0 +/- 1.1 cm H(2)O), functional residual capacity change (115.6 +/- 23.1 versus 202.1 +/- 46.0 mL), minimal rs (airway) resistance (9.3 +/- 1.4 versus 11.8 +/- 2.2 cm H(2)O.L(-1).s(-1)), and additional rs resistance (5.2 +/- 1.4 versus 7.2 +/- 1.3 cm H(2)O.L(-1).s(-1)) were reduced (P < 0.01), and hemodynamics were improved; (b) at PEEPe, PEEPi (3.7 +/- 1.3 cm H(2)O) was reduced (P < 0.01), and gas exchange was improved; and (c) at PEEPe-S, PEEPi (2.0 +/- 1.2 cm H(2)O) was minimized, and rs mechanics (static rs elastance included), hemodynamics, and gas exchange were improved. Conclusively, in carefully preselected COPD patients, bronchodilation/PEEPe exhibits additive benefits.

Aerosols↗
PubMed2005

Relationship of BAL and lung tissue CD4+ and CD8+ T lymphocytes, and their ratio in idiopathic pulmonary fibrosis.

BACKGROUND: Surgical biopsy specimens have shown that T lymphocytes (TLs) infiltrate lung parenchyma in patients with idiopathic pulmonary fibrosis (IPF) and might play a pathogenetic role. BAL, a far less invasive technique, has also been used for the investigation of IPF pathogenesis. However, controversy exists whether the BAL fluid cellular profile reflects the cellular composition of the lung parenchyma. STUDY OBJECTIVE: To compare infiltrating TLs subpopulations (CD4+, CD8+, and CD4+/CD8+ ratio) in lung tissue and BAL fluid. PATIENTS AND METHODS: Immunohistochemistry was performed according to the streptavidin-biotin method on the surgical biopsy specimens of 12 untreated patients with IPF. The number of CD3+, CD4+, and CD8+ TLs was determined by observer-interactive computerized image analysis (SAMBA microscopic image processor; Meylan, France). In BAL fluid, the same TLs subpopulations were evaluated by flow cytometry. RESULTS: In lung tissue, CD3+ TLs accounted for a mean (+/- SEM) of 28.8 +/- 7% of total cells, CD4+ TLs accounted for 14.5 +/- 4% of total cells (50.1 +/- 4% of CD3+ TLs), and CD8+ TLs accounted for 13.8 +/- 4% of total cells (47.4 +/- 4% of CD3+ TLs). In BAL fluid, lymphocytes accounted for 9.8 +/- 2.5% of total cells, CD4+ TLs accounted for 51.8 +/- 4% of CD3+ TLs, and CD8+ TLs accounted for 42.2 +/- 4% of CD3+ TLs. Tissue CD4+ and CD8+ TLs (expressed as a percentage of CD3+ TLs) correlated significantly with the number of CD4+ and CD8+ TLs in BAL fluid (r = 0.846 and p = 0.001 vs r = 0.692 and p = 0.013, respectively). A significant positive correlation was also found between the mean CD4+/CD8+ ratio found in tissue and BAL fluid (1.05 +/- 0.21 and 1.5 +/- 0.27, respectively; r = 0.832; p = 0.01). CONCLUSION: The results suggest that in patients with IPF, the TL subpopulations in BAL fluid reflect the pattern of lymphocytic infiltration in pulmonary parenchyma.

Bronchoalveolar Lavage Fluid↗
PubMed2005

Skeletal muscle adaptations to interval training in patients with advanced COPD.

STUDY OBJECTIVES: To investigate the response to interval exercise (IE) training by looking at changes in morphologic and biochemical characteristics of the vastus lateralis muscle, and to compare these changes to those incurred after constant-load exercise (CLE) training. DESIGN: Randomized, controlled, parallel, two-group study (IE vs CLE training). SETTING: Multidisciplinary, outpatient, hospital-based, pulmonary rehabilitation program. PATIENTS: Nineteen patients with stable advanced COPD (mean +/- SEM FEV1, 40 +/- 4% predicted). INTERVENTIONS: Patients (n = 10) assigned to IE training exercised at a mean intensity of 124 +/- 15% of baseline peak exercise capacity (peak work rate [Wpeak]) with 30-s work periods interspersed with 30-s rest periods for 45 min/d. Patients (n = 9) allocated to CLE training exercised at a mean intensity of 75 +/- 5% Wpeak for 30 min/d. Patients exercised 3 d/wk for 10 weeks. MEASUREMENTS AND RESULTS: Needle biopsies of the right vastus lateralis muscle were performed before and after rehabilitation. After IE training, the cross-sectional areas of type I and IIa fibers were significantly increased (type I before, 3,972 +/- 455 microm2; after, 4,934 +/- 467 microm2 [p = 0.004]; type IIa before, 3,695 +/- 372 microm2; after, 4,486 +/- 346 microm2 [p = 0.008]), whereas the capillary-to-fiber ratio was significantly enlarged (from 1.13 +/- 0.08 to 1.24 +/- 0.07 [p = 0.013]). Citrate synthase activity increased (from 14.3 +/- 1.4 to 20.5 +/- 4.2 micromol/min/g), albeit not significantly (p = 0.097). There was also a significant improvement in Wpeak (by 19 +/- 5%; p = 0.04) and in lactate threshold (by 17 +/- 5%; p = 0.02). The magnitude of changes in all the above variables was not significantly different compared to that incurred after CLE training. During training sessions, however, ratings of dyspnea and leg discomfort, expressed as fraction of values achieved at baseline Wpeak, were significantly lower (p < 0.05) for IE training (73 +/- 9% and 60 +/- 8%, respectively) compared to CLE training (83 +/- 10% and 87 +/- 13%, respectively). CONCLUSIONS: High-intensity IE training is equally effective to moderately intense CLE training in inducing peripheral muscle adaptations; however, IE is associated with fewer training symptoms.

Adaptation, Physiological↗
PubMed2005

Reducing ventilation frequency during cardiopulmonary resuscitation in a porcine model of cardiac arrest.

INTRODUCTION: American Heart Association/American College of Cardiology guidelines recommend a compression-to-ventilation ratio (C/V ratio) of 15:2 during cardiopulmonary resuscitation (CPR) for out-of-the-hospital cardiac arrest. Recent data have shown that frequent ventilations are unnecessary and may be harmful during CPR, since each positive-pressure ventilation increases intrathoracic pressure and may increase intracranial pressure and decrease venous blood return to the right heart and thereby decrease both the cerebral and coronary perfusion pressures. HYPOTHESIS: We hypothesized that reducing the ventilation rate by increasing the C/V ratio from 15:2 to 15:1 will increase vital-organ perfusion pressures without compromising oxygenation and acid-base balance. METHODS: Direct-current ventricular fibrillation was induced in 8 pigs. After 4 min of untreated ventricular fibrillation without ventilation, all animals received 4 min of standard CPR with a C/V ratio of 15:2. Animals were then randomized to either (A) a C/V ratio of 15:1 and then 15:2, or (B) a C/V ratio of 15:2 and then 15:1, for 3 min each. During CPR, ventilations were delivered with an automatic transport ventilator, with 100% oxygen. Right atrial pressure, intratracheal pressure (a surrogate for intrathoracic pressure), aortic pressure, and intracranial pressure were measured. Coronary perfusion pressure was calculated as diastolic aortic pressure minus right atrial pressure. Cerebral perfusion pressure was calculated as mean aortic pressure minus mean intracranial pressure. Arterial blood gas values were obtained at the end of each intervention. A paired t test was used for statistical analysis, and a p value < 0.05 was considered significant. RESULTS: The mean +/- SEM values over 1 min with either 15:2 or 15:1 C/V ratios were as follows: intratracheal pressure 0.93 +/- 0.3 mm Hg versus 0.3 +/- 0.28 mm Hg, p = 0.006; coronary perfusion pressure 10.1 +/- 4.5 mm Hg versus 19.3 +/- 3.2 mm Hg, p = 0.007; intracranial pressure 25.4 +/- 2.7 mm Hg versus 25.7 +/- 2.7 mm Hg, p = NS; mean arterial pressure 33.1 +/- 3.7 mm Hg versus 40.2 +/- 3.6 mm Hg, p = 0.007; cerebral perfusion pressure 7.7 +/- 6.2 mm Hg versus 14.5 +/- 5.5 mm Hg, p = 0.008. Minute area intratracheal pressure was 55 +/- 17 mm Hg . s versus 22.3 +/- 10 mm Hg . s, p < 0.001. End-tidal CO(2) with 15:2 versus 15:1 was 24 +/- 3.6 mm Hg versus 29 +/- 2.5 mm Hg, respectively, p = 0.001. Arterial blood gas values were not significantly changed with 15:2 versus 15:1 C/V ratios: pH 7.28 +/- 0.03 versus 7.3 +/- 0.03; P(aCO(2)) 37.7 +/- 2.9 mm Hg versus 37.6 +/- 3.5 mm Hg; and P(aO(2)) 274 +/- 36 mm Hg versus 303 +/- 51 mm Hg. CONCLUSIONS: In a porcine model of ventricular fibrillation cardiac arrest, reducing the ventilation frequency during CPR by increasing the C/V ratio from 15:2 to 15:1 resulted in improved vital-organ perfusion pressures, higher end-tidal CO(2) levels, and no change in arterial oxygen content or acid-base balance.

Animals↗
PubMed2004

Respiratory kinematics by optoelectronic plethysmography during exercise in men and women.

Gender differences in resting pulmonary function are attributable to the smaller lung volumes in women relative to men. We sought to investigate whether the pattern of response in operational lung volumes during exercise is different between men and women of similar fitness levels. Breath-by-breath volume changes of the entire chest wall ( V(.)( CW)) and its rib cage ( V(.)( Rc)) and abdominal ( V(.)( Ab)) compartments were studied by optoelectronic plethysmography in 15 healthy subjects (10 men) who underwent a symptom-limited ( W (peak)) incremental bicycle test. The pattern of change in end-inspiratory and end-expiratory V(.)( CW) ( V(.)( CW,EI) and V(.)( CW,EE), respectively) did not differ between the sexes. With increasing workload the decrease in V(.)( CW,EE) was almost entirely attributable to a reduction in end-expiratory V(.)( Ab), whereas the increase in V(.)( CW,EI) was due to the increase in end-inspiratory V(.)( Rc) in both sexes. In men, at W (peak) tidal volume [ V(.)( T), 2.7 (0.2) l] and inspiratory capacity [IC, 3.4 (0.2) l] were significantly greater than in women [1.8 (0.2) and 2.6 (0.2) l, respectively]. However, after controlling for lung size using forced vital capacity (FVC) as a surrogate, the differences between men and women were eliminated [ V(.)( T) /FVC 49 (3) and 45 (3) respectively, and IC/FVC 63 (2) and 65 (3) respectively]. All data are presented as mean (SE). In both men and women the contribution of the rib cage compartment to V(.)( T) expansion was significantly greater than that of the abdominal compartment. We conclude that gender differences in operational lung volumes in response to progressive exercise are principally attributable to differences related to lung size, whereas compartmental chest wall kinematics do not differ among sexes.

Adult↗
PubMed2004

The Medical Research Council dyspnea scale in the estimation of disease severity in idiopathic pulmonary fibrosis.

BACKGROUND: Medical Research Council (MRC) chronic dyspnea scale, used for the estimation of disability due to dyspnea, may serve as a simple index of disease severity and extent in patients with idiopathic pulmonary fibrosis (IPF). However, its relationship with other commonly used measures has not been evaluated. METHODS: The association of MRC chronic dyspnea scale with lung function indices and high-resolution computerized tomography (HRCT) scores such as the total interstitial disease score (TIDs) and the fibrosis score (Fs) was examined in 26 untreated patients with IPF sequentially recruited over a period of 3 years. The aim of this observational study was to explore the relationship between dyspnea, impairment of lung function and CT estimation of disease severity in patients with IPF. RESULTS: The MRC dyspnea score was significantly associated with FVC, FEV1, TLC, DLCO, PaO2, and PaCO2 and with both HRCT scores. In multiple regression analysis only the FVC (OR = 0.85, 95% CI = 0.75-0.95, P = 0.004) and PaCO2 (OR = 0.69, 95% CI = 0.50-0.95, P = 0.02) correlated with dyspnea. Furthermore, both TIDs and Fs were negatively associated with FVC, FEV1, TLC and PaO2. In multiple regression analysis only the FVC correlated with both TIDs (r2 = 0.57, P = 0.0001) and Fs (r2 = 0.46, P = 0.0005). CONCLUSIONS: These observations suggest that the MRC dyspnea scale could offer useful information about the estimation of severity in patients with IPF. Furthermore among functional indices the FVC seems to be the best estimator of disease severity and extent.

Adult↗
PubMed2004

Perillyl alcohol is an angiogenesis inhibitor.

Aberrant angiogenesis is essential for the progression of solid tumors and hematological malignancies. Thus, antiangiogenic therapy is one of the most promising approaches to control cancer. In the present work, we examined the ability of perillyl alcohol (POH), a dietary monoterpene with well-established tumor chemopreventive and chemotherapeutic activity, to interfere with the process of angiogenesis. POH remarkably prevented new blood vessel growth in the in vivo chicken embryo chorioallantoic membrane assay and proved to be effective in inhibiting the morphogenic differentiation of cultured endothelial cells into capillary-like networks both in collagen gel and Matrigel models. In addition, POH reduced the cell number in a proliferation assay and induced apoptosis of endothelial cells as indicated by the POH-mediated increase of caspase-3 activity and DNA fragmentation. Consistent with the observed antisurvival effect, POH treatment resulted in a significant inhibition of Akt phosphorylation in endothelial cells. Finally, POH was able to differentially modulate the release of two important angiogenic regulators: vascular endothelial growth factor (VEGF) and angiopoietin 2 (Ang2). POH decreased the release of VEGF from cancer cells but stimulated the expression of Ang2 by endothelial cells, indicating that it might suppress neovascularization and induce vessel regression. Overall, these data underscore the antiangiogenic potential of POH and suggest that POH, in addition to its anticancer activity, may be an effective agent in the treatment of angiogenesis-dependent diseases.

Angiogenesis Inhibitors↗
PubMed2004

The low-dose corticotropin stimulation test in acute traumatic and non-traumatic brain injury: incidence of hypo-responsiveness and relationship to outcome.

OBJECTIVE: To investigate adrenal responses to the low-dose corticotropin (ACTH) stimulation test in acute traumatic or non-traumatic brain injury (BI) and to assess its value in predicting outcome. DESIGN: Prospective study. SETTING. Intensive care unit (ICU) in a university hospital. PATIENTS AND PARTICIPANTS: Seventy-five patients with acute BI, with a median age of 45 years were investigated. BI was due to trauma ( n=51), ischemic stroke ( n=17), subarachnoid hemorrhage ( n=4) or intracerebral hemorrhage (n=3). INTERVENTIONS: Blood was taken on day 16 (median) after admission to the ICU to determine baseline cortisol and ACTH. Thereafter, a low-dose stimulation test (LDST) was performed: 1 microg of tetracosactrin was injected and 30 min later a second blood specimen was obtained to measure stimulated cortisol. Patients having a stimulated cortisol below 500 nmol/l were defined as non-responders to the LDST. MEASUREMENTS AND RESULTS: Median baseline and stimulated cortisol were 491 nmol/l and 690 nmol/l, respectively. The median increment in cortisol was 154 nmol/l (range 5-579 nmol/l). Mean ACTH was 46+/-21 pg/ml. Ten (13%) patients were non-responders to the LDST; these had a higher mortality rate compared to patients with adequate cortisol production (70 vs 32%, p=0.034). Logistic regression analysis revealed that APACHE II ( p<0.001), Glasgow Coma Scale (GCS) ( p=0.04) and age ( p=0.02) were independent outcome predictors. In contrast, the increment in cortisol ( p=0.26) did not add to outcome prediction. CONCLUSIONS: Adrenal hypo-responsiveness in the setting of acute traumatic or non-traumatic BI is not an independent outcome predictor in the presence of high APACHE II, low GCS and older age.

Adolescent↗
PubMed2004

Endocrine abnormalities in critical care patients with moderate-to-severe head trauma: incidence, pattern and predisposing factors.

OBJECTIVE: To investigate the incidence and type of endocrine abnormalities in critical care patients with traumatic brain injury (TBI) and to examine their relationships to possible predisposing factors. DESIGN: Prospective study. SETTING: General intensive care unit in a university hospital. PATIENTS AND PARTICIPANTS: Thirty-four TBI patients (27 men, 7 women), having a mean age of 37+/-16 years, were studied after weaning from mechanical ventilation. INTERVENTIONS: Baseline endocrine assessment was carried out by measuring cortisol, corticotropin, dehydroepiandrosterone sulfate, free thyroxine, thyrotropin (TSH), testosterone, oestradiol, follicle stimulating hormone (FSH), luteinizing hormone, prolactin, growth hormone and insulin-like growth factor I. Dynamic evaluation was performed by human corticotropin releasing hormone and growth hormone releasing hormone in all patients. Male patients underwent additional investigation with gonadotropin-releasing hormone. Severity of neurological derangement was graded according to Glasgow Coma Scale (GCS), Marshall Computerized Tomographic Classification and intracranial pressure (ICP) levels. MEASUREMENTS AND RESULTS: Eighteen of the 34 patients (53%) had an abnormal result in at least one hormonal axis tested, with cortisol hyporesponsiveness and gonadal dysfunction being equally common, affecting 24% of patients. Endocrine abnormalities were associated with a higher brain CT-scan classification score ( p=0.02). The GCS on admission correlated positively with baseline FSH (r=0.37, p=0.03), peak FSH (r=0.41, p=0.03), testosterone (r=0.44, p=0.02) and TSH (r=0.39, p=0.03). There were no relations between ICP(max) and any baseline or dynamic hormone measurements. CONCLUSIONS: Patients with TBI receiving critical care show changes in their neuroendocrine responses, which depend upon clinical and radiological measures of head injury severity. Most common abnormalities include cortisol hyporesponsiveness and hypogonadism.

Adult↗
PubMed2004

Structural and functional characterization of the dimerization region of soluble guanylyl cyclase.

Soluble guanylyl cyclase (sGC) is a ubiquitous enzyme that functions as a receptor for nitric oxide. Despite the obligate heterodimeric nature of sGC, the sequence segments mediating subunit association have remained elusive. Our initial screening for relevant interaction site(s) in the most common sGC isoenzyme, alpha(1) beta(1), identified two regions in each subunit, i.e. the regulatory domains and the central regions, contributing to heterodimer formation. To map the relevant segments in the beta(1) subunit precisely, we constructed multiple N- and C-terminal deletion variants and cotransfected them with full-length alpha(1) in COS cells. Immunoprecipitation revealed that a sequence segment spanning positions 204-408 mediates binding of beta(1) to alpha(1) The same region of beta(1)[204-408] was found to promote beta /beta(1) homodimerization. Fusion of [204 beta(1)-408] to enhanced green fluorescent protein conferred binding activity to the recipient protein. Coexpression of beta(1)[204-408] with alpha(1) or beta(1) targeted the sGC subunits for proteasomal degradation, suggesting that beta(1)[204-408] forms structurally deficient complexes with alpha(1) and beta(1). Analysis of deletion constructs lacking portions of the beta(1) dimerization region identified two distinct segments contributing to alpha(1) binding, i.e. an N-terminal site covering positions 204-244 and a C-terminal site at 379-408. Both sites are crucial for sGC function because deletion of either site rendered sGC dimerization-deficient and thus functionally inactive. We conclude that the dimerization region of beta(1) extends over 205 residues of its regulatory and central domains and that two discontinuous sites of 41 and 30 residues, respectively, facilitate binding of beta(1) to the alpha(1) subunit of sGC.

Amino Acid Sequence↗
PubMed2004

Huge biatrial primary cardiac B-cell lymphoma resulting in bilateral atrioventricular valve obstruction.

We report the case of a 48-year-old man with a clinical syndrome caused by both pulmonary and systemic venous congestion. Echocardiography indicated a huge tumor occupying both dilated atria almost completely, seeming to invade from the atrial septum. A test for HIV was negative. Our primary diagnosis was a biatrial myxoma. Urgent surgery was performed disclosing large cell B-cell primary cardiac lymphoma. The patient died 8 days later. Primary cardiac lymphoma is extremely rare in immunocompetent patients. Its rarity and heterogenous clinical presentation make diagnosis difficult. As tissue characterization is still beyond the capabilities of currently available echocardiography, a combination of examinations are indicated, when the clinical condition is relatively stable, in order to reach the exact diagnosis.

Echocardiography↗
PubMed2004

Hypothalamic-pituitary-adrenal axis dysfunction in critically ill patients with traumatic brain injury: incidence, pathophysiology, and relationship to vasopressor dependence and peripheral interleukin-6 levels.

OBJECTIVE: To investigate hypothalamic-pituitary-adrenal axis function in patients requiring mechanical ventilation for traumatic brain injury and to assess the relation of hypothalamic-pituitary-adrenal axis abnormalities with vasopressor dependence and peripheral cytokine levels. DESIGN: Prospective study. SETTING: General intensive care unit in a university teaching hospital. PATIENTS: Forty patients (33 men and 7 women) with moderate to severe traumatic brain injury (mean age, 37 +/- 16 yrs) were studied the day after termination of mechanical ventilation (7-60 days after trauma). INTERVENTIONS: First, a morning blood sample was obtained to measure baseline cortisol, corticotropin, interleukin-6, and tumor necrosis factor alpha. Subsequently, 1 microg of synthetic corticotropin was injected intravenously, and 30 mins later, a second blood sample was drawn to determine stimulated plasma cortisol. Based on data derived from healthy volunteers, patients having stimulated cortisol levels <18 microg/dL were defined as nonresponders to the low-dose stimulation test. Thirty-one patients underwent also a human corticotropin releasing hormone test. MEASUREMENTS AND MAIN RESULTS: In traumatic brain injury patients, mean baseline and low-dose stimulation test-stimulated cortisol levels were 17.2 +/- 5.4 microg/dL and 24.0 +/- 6.6 microg/dL, respectively. The median increment in cortisol was 5.9 microg/dL. Basal corticotropin levels ranged from 3.9 to 118.5 pg/mL. Six of the 40 patients (15%) failed the low-dose stimulation test. The human corticotropin releasing hormone test (performed in 26 responders and five nonresponders) revealed diminished cortisol release only in the low-dose stimulation test nonresponder patients. Corticotropin responses to corticotropin releasing hormone were consistent with both primary (three patients) and/or secondary (two patients) adrenal dysfunction. In retrospect, nonresponders to the low-dose stimulation test more frequently required vasopressors (6/6 [100%] vs. 16/34 [47%]; p =.02) and for a longer time interval (median, 0 vs. 293 hrs; p =.006) compared with responders. Furthermore, nonresponders had higher interleukin-6 levels compared with responders (56.03 vs. 28.04 pg/mL; p =.01), whereas tumor necrosis factor alpha concentrations were similar in the two groups (2.42 vs. 1.55 pg/mL; p =.53). CONCLUSIONS: Adrenal cortisol secretion after dynamic stimulation is deficient in a subset of critically ill patients with moderate to severe head injury. This disorder is associated with prior vasopressor dependency and higher interleukin-6 levels.

Adrenocorticotropic Hormone↗
PubMed2004

Airway obstruction and acute respiratory failure due to Aspergillus tracheobronchitis.

OBJECTIVE: To report a patient with lymphoma who developed Aspergillus tracheobronchitis resulting in airway obstruction and acute respiratory failure. DESIGN: Case report. SETTING: Intensive care unit of a tertiary care hospital. PATIENT: A 22-yr-old female with lymphoma who developed a respiratory infection 3 months after completing immunosuppressive therapy. She was treated empirically with broad spectrum antibiotics and subsequently received a supplementary chemotherapeutic course. Soon afterward she developed severe respiratory failure. Chest radiograph showed atelectasis of the right upper and lower lobes. INTERVENTIONS: Emergent mechanical ventilation; fiberoptic bronchoscopy. MEASUREMENTS AND MAIN RESULTS: Fiberoptic bronchoscopy revealed extensive obstruction of both main and subsegmental bronchi with a solid mass strongly adhered to the bronchial wall; both histologic examination and culture of that mass revealed Aspergillus. The patient died of refractory hypoxemia a few days later. CONCLUSIONS: Aspergillus tracheobronchitis should be considered in immunocompromised patients with suspected lung infection even when the main radiographic finding is atelectasis. Bronchoscopy and histologic examination of identified intraluminal material should be performed as soon as possible.

Acute Disease↗