Posted by: Indonesian Children | April 14, 2010

Abstract Watch : Allergy Asthma-Hormone

Abstract Watch : Allergy Asthma-Hormone

 

Probl Tuberk Bolezn Legk. 2005;(8):57-60. Links

[Endocrine mechanisms of the pathogenesis of nocturnal asthma]

The parameters of external respiration function and the peripheral blood concentration of cortisol, testosterone, estradiol, and progesterone were determined in 28 male patients with nocturnal asthma every 6 hours during two days running. There was a shift in the maximum secretion of estradiol from daylight to night hours, which may contribute to enhanced bronchospasm in the presence of hypoprogesteronemia, hypoandrogynemism, and absolute and relative adrenal cortical glucocorticoid

J Allergy Clin Immunol. 2003 Jul;112(1):52-7.   Links

Altered pituitary-adrenal interaction in nocturnal asthma.

Department of Medicine, National Jewish Medical and Research Center, University of Colorado Health Sciences Center, Denver, USA.

BACKGROUND: Increased airway inflammation at night contributes to the nocturnal worsening of asthma, but the mechanisms regulating circadian variations in airway inflammation are unknown. OBJECTIVE: We hypothesized that altered hypothalamic-pituitary-adrenal axis function serves as an endogenous controller of inflammation in nocturnal asthma. METHODS: Patients with nocturnal asthma (n = 7), patients with nonnocturnal asthma (n = 13), and healthy control subjects (n = 11) adhered to a regular sleep-wake cycle for 1 week. Corticotropin and cortisol levels were assayed every 2 hours for 24 hours. Low-dose corticotropin stimulation was performed. Circadian hormonal flux was analyzed by means of cosinor modeling and calculation of the area under the 24-hour curve. RESULTS: Corticotropin peak levels and areas under the 24-hour curve were significantly increased in patients with nocturnal asthma versus values in patients with nonnocturnal asthma and control subjects. Patients with nonnocturnal asthma demonstrated significantly increased areas under the 24-hour cortisol curve when compared with control subjects, but peak cortisol levels did not differ between groups. Cortisol levels after low-dose corticotropin stimulation did not differ between groups. Corticotropin and cortisol levels were not correlated with the degree of physiologic impairment. CONCLUSION: Nocturnal asthma is marked by increased corticotropin levels that are not accompanied by commensurate increases in cortisol levels. This observation might indicate blunted adrenal responsiveness in the nocturnal asthma phenotype. Conversely, adrenal response to corticotropin might be enhanced in nonnocturnal asthma, attenuating nocturnal worsening of airway inflammation.

J Allergy Clin Immunol. 2003 Sep;112(3):513-7.   Links

Elevated serum melatonin is associated with the nocturnal worsening of asthma.

Department of Pediatrics, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206, USA.

BACKGROUND: Increased airway inflammation at night contributes to the nocturnal worsening of asthma. In vitro studies have shown exogenous melatonin to be pro-inflammatory in asthma, but it is unknown whether endogenous melatonin levels are a controller of airway inflammation in nocturnal asthma. OBJECTIVE: Our aim was to determine 24-hour patterns of serum melatonin and their relationship to overnight decline in physiology in subjects with nocturnal asthma, non-nocturnal asthma, and in healthy controls. METHODS: Observational study of pulmonary physiology and melatonin levels in patients with nocturnal asthma (n = 7), non-nocturnal asthma (n = 13), and healthy controls (n = 11). Subjects maintained a constant sleep-wake regimen for 7 days. On day 8, serum melatonin was measured every 2 hours by radioimmunoassay and analyzed by cosinor modeling. The correlation between serum melatonin levels and overnight change in spirometry was evaluated by Spearman’s rank correlation analysis. RESULTS: In subjects with nocturnal asthma, peak melatonin levels were significantly elevated compared with healthy controls (67.6 +/- 5.0 pg/mL versus 53.5 +/- 4.0 pg/mL, P =.03). Melatonin acrophase was delayed in nocturnal asthma (02:54 versus 01:58 in healthy controls, P =.003, and 02:15 in non-nocturnal asthma, P =.01). In subjects with nocturnal asthma, increasing melatonin levels were significantly and inversely correlated with overnight change in FEV(1) (r = -.79, P =.04), a relationship that was not observed in non-nocturnal asthma or healthy controls. CONCLUSIONS: Nocturnal asthma is associated with elevation and phase delay of peak serum melatonin levels. Elevated melatonin levels might contribute to the pathogenesis of nocturnal asthma.

Thorax. 1994 Mar;49(3):257-62. Links

Role of inflammation in nocturnal asthma.

Department of Medicine (RIE), University of Edinburgh, UK.

BACKGROUND–Nocturnal airway narrowing is a common problem for patients with asthma but the role of inflammation in its pathogenesis is unclear. Overnight changes in airway inflammatory cell populations were studied in patients with nocturnal asthma and in control normal subjects. METHODS–Bronchoscopies were performed at 0400 hours and 1600 hours in eight healthy subjects and in 10 patients with nocturnal asthma (> 15% overnight fall in peak flow plus at least one awakening/week with asthma). The two bronchoscopies were separated by at least five days, and both the order of bronchoscopies and site of bronchoalveolar lavage (middle lobe or lingula with contralateral lower lobe bronchial biopsy) were randomised. RESULTS–In the normal subjects there was no difference in cell numbers and differential cell counts in bronchoalveolar lavage fluid between 0400 and 1600 hours, but in the nocturnal asthmatic subjects both eosinophil counts (median 0.11 x 10(5) cells/ml at 0400 hours, 0.05 x 10(5) cells/ml at 1600 hours) and lymphocyte numbers (0.06 x 10(5) cells/ml at 0400 hours, 0.03 x 10(5) cells/ml at 1600 hours) increased at 0400 hours, along with an increase in eosinophil cationic protein levels in bronchoalveolar lavage fluid (3.0 micrograms/ml at 0400 hours, 2.0 micrograms/l at 1600 hours). There were no changes in cell populations in the bronchial biopsies or in alveolar macrophage production of hydrogen peroxide, GM-CSF, or TNF alpha in either normal or asthmatic subjects at 0400 and 1600 hours. There was no correlation between changes in overnight airway function and changes in cell populations in the bronchoalveolar lavage fluid. CONCLUSIONS–This study confirms that there are increases in inflammatory cell populations in the airway fluid at night in asthmatic but not in normal subjects. The results have also shown a nocturnal increase in eosinophil cationic protein levels in bronchoalveolar lavage fluid, but these findings do not prove that these inflammatory changes cause nocturnal airway narrowing.

J Allergy Clin Immunol. 2003 Jul;112(1):52-7.   Links

Altered pituitary-adrenal interaction in nocturnal asthma.

Department of Medicine, National Jewish Medical and Research Center, University of Colorado Health Sciences Center, Denver, USA.

BACKGROUND: Increased airway inflammation at night contributes to the nocturnal worsening of asthma, but the mechanisms regulating circadian variations in airway inflammation are unknown. OBJECTIVE: We hypothesized that altered hypothalamic-pituitary-adrenal axis function serves as an endogenous controller of inflammation in nocturnal asthma. METHODS: Patients with nocturnal asthma (n = 7), patients with nonnocturnal asthma (n = 13), and healthy control subjects (n = 11) adhered to a regular sleep-wake cycle for 1 week. Corticotropin and cortisol levels were assayed every 2 hours for 24 hours. Low-dose corticotropin stimulation was performed. Circadian hormonal flux was analyzed by means of cosinor modeling and calculation of the area under the 24-hour curve. RESULTS: Corticotropin peak levels and areas under the 24-hour curve were significantly increased in patients with nocturnal asthma versus values in patients with nonnocturnal asthma and control subjects. Patients with nonnocturnal asthma demonstrated significantly increased areas under the 24-hour cortisol curve when compared with control subjects, but peak cortisol levels did not differ between groups. Cortisol levels after low-dose corticotropin stimulation did not differ between groups. Corticotropin and cortisol levels were not correlated with the degree of physiologic impairment. CONCLUSION: Nocturnal asthma is marked by increased corticotropin levels that are not accompanied by commensurate increases in cortisol levels. This observation might indicate blunted adrenal responsiveness in the nocturnal asthma phenotype. Conversely, adrenal response to corticotropin might be enhanced in nonnocturnal asthma, attenuating nocturnal worsening of airway inflammation

J Allergy Clin Immunol. 2005 Dec;116(6):1179-86; quiz 1187. Epub 2005 Nov 8.   Links

Nocturnal asthma.

National Jewish Medical and Research Center and the University of Colorado Health Sciences Center, Denver, CO 80206, USA. sutherlande@njc.org

Nocturnal symptoms and overnight decrements in lung function are a common part of the asthma clinical syndrome. As many as 75% of asthmatic subjects are awakened by asthma symptoms at least once per week, with approximately 40% experiencing nocturnal symptoms on a nightly basis. An extensive body of research has demonstrated that nocturnal symptoms of cough and dyspnea are accompanied by circadian variations in airway inflammation and physiologic variables, including airflow limitation and airways hyperresponsiveness. Alterations in beta2-adrenergic and glucocorticoid receptors and hypothalamic-pituitary-adrenal axis function might play a role in modulating the nocturnal asthma phenotype, and recent studies have suggested that melatonin, a neurohormonal controller of circadian rhythms, might be important as well. Treatment strategies in nocturnal asthma are similar to those used in persistent asthma, although dosing of medications to target optimum effect during periods of nocturnal worsening is beneficial.

Chronobiol Int. 1998 Jan;15(1):85-92. Links

Serum cortisol in asthma: marker of nocturnal worsening of symptoms and lung function?

Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine and University of Colorado Health Sciences Center, Denver 80206, USA. kraftm@njc.org

Changes in the hormone cortisol have been implicated in the pathogenesis of nocturnal worsening of asthma, or nocturnal asthma (NA). We studied 45 patients, 15 with NA, 15 subjects with non-nocturnal asthma (NNA), and 15 controls over a 24h period, measuring forced expiratory volume in 1 second (FEV1) and serum cortisol at 08:00, 12:00, 16:00, 20:00, 23:00, 04:00, and 08:00 the following day. Evaluation of the time response curves for cortisol revealed a significant difference in the shape of the curves (p = 0.04 by mixed-effects model). Evaluation of individual time points revealed that the cortisol levels in the NNA and control groups were significantly lower than in the NA group at 20:00 (NNA: 3.5 +/- 0.8 mg/mL; Controls: 3.4 +/- 0.8 mg/mL; NA: 4.9 +/- 0.8 mg/mL; p = 0.007). The percentage (%) predicted FEV1 was significantly different among the three groups over the 24h period (p < 0.001). The percentage predicted FEV1 was significantly lower in the NA group compared to the control group at all time points and significantly lower than the NNA group at 16:00, 23:00, and 04:00. The difference among the groups was most pronounced at 04:00, when the percentage predicted FEV1 was 58.9 +/- 2.2% in the NA group, 76.8 +/- 2.9% in the NNA group, and 91.6 +/- 2.8% in the control group (p = 0.001, where each group is significantly different from the others). Although the time response curves for cortisol were significantly different among the three groups, the differences in serum levels of cortisol do not appear to be clinically significant. Therefore, serum levels of cortisol may not be the appropriate measurement to assess the role of cortisol in nocturnal asthma.

Am J Respir Crit Care Med. 2002 Mar 1;165(5):708-12.   Links

Role of serum cortisol levels in children with asthma.

Department of Pediatrics, Rijnstate Hospital, P.O. box 9555, 6800 TA Arnhem, The Netherlands. amlandstra@hetnet.nl

Decreased serum cortisol levels have been proposed to contribute to nocturnal airway obstruction. We investigated whether endogenous cortisol levels are lower, and also whether the 24-h cortisol variation is greater, in children with asthma than in control subjects and assessed the relationship between serum cortisol and nocturnal airflow limitation in children with asthma. Cortisol and FEV(1) were measured every 4 h over 24 h; blood eosinophils, airway responsiveness to methacholine and adenosine 5′-monophosphate (AMP) were measured at 0400 and 1600. Children with asthma had lower cortisol levels than did control subjects; at midnight the difference was significant. Subjects with nocturnal asthma (24-h FEV(1) variation > or =15%) had significantly lower cortisol levels than did control subjects at 0000, 0800, and 1200. A higher mean 24-h cortisol level in subjects with asthma was associated with a significantly higher FEV(1) as a percentage of the predicted value (FEV(1) %pred) at 0400, 0800, and 2000, yet not in control subjects. Higher 24-h cortisol variation was associated with lower FEV(1) %pred at all time points in both control subjects and subjects with nonnocturnal asthma. There was no significant association between the level or variation of cortisol and PD(20) methacholine (provocative dose of methacholine causing a 20% fall in FEV(1)), PD(20) AMP, or eosinophils. Our data suggest that lower cortisol levels contribute to both overall lower levels of FEV(1) especially at night. This may be due to a lack of suppression of airway inflamma

Kraft M, Vianna E, Martin RJ, Leung DY. Related Articles, Links Nocturnal asthma is associated with reduced glucocorticoid receptor binding affinity and decreased steroid responsiveness at night.
J Allergy Clin Immunol. 1999 Jan;103(1 Pt 1):66-71.
PMID: 9893187 [PubMed – indexed for MEDLINE]

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  3. […] Abstract Watch : Allergy Asthma-Hormone […]

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