|
#31
25.08.2006, 22:09
|
||||
|
||||
|
Цитата:
некоторые важные (на мой взгляд) дополнения из полного текста Biol Psychiatry. 2005 Dec 1;58(11):865-70. FEV1 измерялось: The Asthma Control Questionnaire (ACQ) is a 6-item self-report tool that has been shown to be highly reliable and sensitive to changes in asthma symptomatology over time, including FEV1% Predicted (Juniper et al 1999b). Airway obstruction was assessed with a portable spirometer, which provided forced expiratory volume (FEV)1% Predicted values. По кортикостероидам следующее: However, during the study period analysis revealed the citalopram group had significantly fewer follow-up assessments in which they were receiving systemic corticosteroids than the placebo group (3% vs. 12% of total assessments in which participants answered yes to current oral corticosteroid use, treatment group by time interaction: F1,273 = 6.26, p = .013). Исходные данные: на системных кортикостероидах были 16%(6) на циталопраме и 20% (8) на плацебо, а стали 1 и 5 соответственно. Вот что пишут сами авторы в дискуссии об этом: Changes in asthma-related outcomes were similar between groups. However, the citalopram group required less systemic corticosteroids during the trial. This finding is of clinical importance as systemic corticosteroid therapy is associated with numerous side effects and is a marker for severe asthma exacerbations. Thus, similar clinical asthma outcomes were achieved in the citalopram group but with less use of oral corticosteroids. Citalopram may increase glucocorticoid negative feedback on the hypothalamic-pituitary-adrenal axis (Pariante et al 2004), through enhancement of glucocorticoid receptor function through modulation of membrane steroid transporters (Pariante et al 2001), and changes in glucocorticoid receptor binding sites (Hery et al 2000), Thus, citalopram could potentially have a direct effect at the receptor level on prescription corticosteroid requirements in asthma patients. Remission from depression, whether in citalopram or placebo groups, was associated with greater improvement in asthma symptoms than observed in nonremitters. Thus, remission from depression, not merely response, is an outcome associated with improvement in asthma. The findings are important as they suggest that effective treatment of depression can result in improvement in a general medical condition. The correlation between change in depressive symptom severity and change in asthma symptoms and functioning is also noteworthy, and suggest that improvement in depression is associated with improvement in asthma. Our findings suggest that change in depressive symptom severity is associated with change in asthma-specific measures. The reasons for this association between change in depression and change in asthma are not clear. Improvement in depression could lead to better asthma medication adherence or result in a subjective improvement in asthma symptoms. As we did not assess asthma medication adherence, we cannot determine its impact on our findings. The ACQ assesses both subjective symptoms (e.g. awakening at night with asthma) which may be influenced by depressive symptoms and objective measures (e.g. bronchodilator use, forced expiratory volume in 1-second), which may be less influenced by bias due to a depressed mood. Although highly speculative, the relationship between improvement in asthma and depression could be related to biological similarities. For example, glucocorticoid resistance is found in some patients with asthma (Lane et al 1997) and in some with depression (Lowy et al 1984). Neuroendocrine abnormalities in MDD tend to normalize with improvement in depressive symptoms (Greden et al 1983). As discussed above, citalopram appears to enhance glucocorticoid receptor functioning in animal models, which could, in part, explain the relationship between improvement in asthma and depression. 
|
|
#32
25.08.2006, 22:27
|
||||
|
||||
|
Еще "писча" к размышлениям или нелегок путь от гипотез к лечению:
Med Hypotheses. 2005;64(5):938-40. Therapeutic value of antidepressants in asthma. Krommydas G, Gourgoulianis KI, Karamitsos K, Krapis K, Kotrotsiou E, Molyvdas PA. Department of Internal Medicine, General Hospital of Larissa, Greece. Introduction Antidepressants may be of therapeutic value in asthma. Tricyclic antidepressants have been tested in asthma therapy in the past. The beneficial effect of amitryptiline was observed since 1965, while doxepine, a tricyclic antidepressant might actually have a bronchodilator effect [1] and [2]. There is increasing evidence that a biological linkage may exist between asthma and depression. Even patients with mild asthma exhibit relatively high rates of anxiety and depression [1], [3], [4], [5] and [6].Children with asthma have higher rates of depression than children with certain other chronic medical conditions [7]. Defects in the function of the autonomic nervous system such as (a) adrenergic and cholinergic hyperresponsiveness and (b) adrenergic hyporesponsiveness even distal from the airways has been demonstrated in asthmatic patients, as well as in depression [4]. Antidepressants seem to have some interesting anti-inflammatory properties, that make them promising drugs in the treatment of many inflammatory conditions such as rheumatic diseases [8] and [9]. According to its definition, asthma is a chronic inflammatory disorder, in which many cells and cellular elements play a role. If antidepressants suppress inflammatory mediators, then they may be useful in treating asthma as well as other conditions in which inflammation has a central role. The keynote of this hypothesis is that antidepressants may have a therapeutic role in asthma by suppressing proinflammatory cytokines and preventing their brain effects. Possible mechanisms by which antidepressants may exert their beneficial action are presented. Asthma pathophysiology and cytokines Leukotrienes (LTs) and cytokines are important molecules that promote allergic reaction, airway inflammation and modulate airway smooth muscle (ASM) cell function [10] and [11]. T1-helper (Th1) cell derived cytokines such as interferon (IFN)-γ and Th2 cell derived cytokines – interleukines (IL) IL4, IL5 and cysteinyl leukotrienes (CysLTs) are the main mediators in the inflammation process.This cascade of reactions finally leads to smooth muscle mass increasing, airway narrowing and hyperresponsiveness. Prostanoids (PGs), especially PG E2 and nitric oxide (NO) also have a special role in airway function and epithelium defence [12]. However, despite the fact that NO may actually have beneficial bronchodilatation effects, increased production of NO has a deleterious effect on airways [13]. Immune effects of antidepressants and possible mechanisms In the last decades, accumulating evidence have revealed intriguing analogies between symptoms of the host response to infection, which are mediated by the brain effects of cytokines and many features of depression. These analogies include stress like alterations of central neurotransmission systems, activation of the hypothalamic–pituitary–adrenocortical (HPA) axis and profound behavioral modifications such as anhedonia, anorexia, depressed activity [8]. Indeed, IL-1, IL-6 and interferons (IFNs) given to experimental animals may produce behavioral alterations and symptoms similar to those observed in major depression. The tricyclicantidepressants (TCA)-induced reduction of the stimulated production of pro-inflammatory cytokines (particularly TNF-a, IL-1β, and IFN-γ) is usually associated with an increase in the production of the anti-inflammatory cytokine IL-10 [8] and [14]. SSRI antidepressants also reduced the production of IL-1, IL-4, and increased the production of IL-10 [15]. A recent in vitro study has shown that TCA and SSRI antidepressants also attenuate cytokine-induced PGE2 and NO production by inflammatory cells from synovial tissue [16]. Most antidepressants also induce adaptive changes in central monoaminergic neurotransmission, which itself might modulate immune reactivity and central actions of cytokines [14]. On the other hand, lymphocytes and macrophages are innervated by the sympathetic and parasympathetic nervous system and this innervation modulates immune reactivity. Furthermore, immune cells are known to have receptors for neurotransmitters and antidepressants may modify the activity of immune cells by acting at the level of these receptors [17]. Antidepressants may also have direct effects on the immune cells. (rolipram suppresses the production of TNF and to a lesser extent that of IFNγ in human and rat specific T lines) [14] and [18]. The effect of antidepressants on the HPA axis is also noteworthy, since they favor the negative feedback of cortizone, thus suppressing the axis [19]. A suppressed HPA axis has been associated with atopic manifestations [20]. However, in certain local responses and under certain conditions, stress hormones actually may boost regional immune responses through induction of TNF-a, IL-1 and other molecules [21]. Despite the fact that antidepressants inhibit the production of NO and PGE and possibly HPA axis, their primary effect on the production of cytokines is expected to terminate the cascade of inflammatory events in asthma as well as in other inflammatory diseases. Main points and future research The main points of this hypothesis could be summarized as follows: 1. Antidepressants are expected to modify inflammation process in asthma. 2. Antidepressants modifies the control of CNS over respiratory and immune system. 3. A model for a beneficial role of antidepressants in many disorders is proposed. Possible further in vitro experiments may include intubation of human bronchoalveolar lavage cells or animal damaged tracheal epithelium with antidepressants in tissue therapeutic concentrations as achieved in depression. Moreover, antidepressants could be used in experimental clinical trials in asthmatic patients. Acknowledgement We are indebted to Lilly pharmaceuticals for the financial support of this paper. References [1] P. Yellowlees and R. Kalucy, Psychobiological aspects of asthma and consequent research implications, Chest 97 (1990), pp. 628–634. [2] Sugihara H, Ishihara K, Nogughi H. Clinical experience with amitriptyline (tryptanol) in the treatment of bronchial asthma 1965;23:422–9. [3] T. Ritz and A. Steptoe, Emotion and pulmonary function in asthma: reactivity in the field and relationship with laboratory induction of emotion, Psychosom Med 62 (2000), pp. 808–815. [4] J.R. Wright, M. Rodriguez and S. Cohen, Review of psychosocial stress and asthma: an integrated biopsychosocial approach, Thorax 53 (1998), pp. 1066–1074. [5] G. Krommydas, K.I. Gourgoulianis, N.V. Angelopoulos, G. Andreou and P.A. Molyvdas, Left-handedness and parental psychopathology in the course of bronchial asthma in childhood, Pediatr Asthma Aller Immunol 15 (2002), pp. 145–152. [6] G. Krommydas, K.I. Gourgoulianis, N. Angelopoulos, E. Kotrotsiou, V. Raftopoulos and P.-A. Molyvdas, Depression and pulmonary function in outpatients with asthma, Resp Med 98 (2004), pp. 220–224. [7] G. Vila, C. Nollet-Clemenson and M. Vera et al., Prevalence of DSM-IV disorders in children and adolescents with asthma v. diabetes, Can J Psychiat 44 (1999), pp. 562–569. [8] N. Castanon, B. Leonard, P. Neveu and R. Yirmira, Effects of antidepressants on cytokine production and actions, Brain Behav Immun 16 (2002), pp. 569–574. [9] D.L. Goldenberg, M. Mayskiv, C. Mossey, R. Ruthazer and C. Schmidt, A randomized, double-blind crossover trial of fluoxetine and amitriptyline in the treatment of fibromyalgia, Arthritis Rheum 39 (1996), pp. 1852–1859. [10] S. Holgate, M. Peters-Golden, R.A. Panettieri and W.R. Henderson, Roles of cysteinyl leukotrienes in airway inflammation, smooth muscle function, and remodeling, J Allergy Clin Immunol 111 (2003), pp. S18–S36. [11] D. Chantry and L. Burgess, Chemokines in allergy, Current Drug Targets-Inflammation Allergy 1 (2002), pp. 109–116. [12] C. Vancheri, C. Mastruzzo, M.A. Sortino and N. Crimi, The lung as a priviledged site for the beneficial actions of PGE2, Trends Immunol 25 (2004), pp. 40–46. [13] F.L.M. Ricciardolo, Multiple roles of nitric oxide in the airways, Thorax 58 (2002), pp. 175–182. [14] PJ Neveu and N Castanon, Is there evidence for an effect of antidepressant drugs on immune function?. In: Danzer et al., Editors, Cytokines, stress and depression, Kluwer Academic/Plenum Publishers, New York (1999). [15] M. Kubera, S. Andrew, R. Mathison and M. Maes, Effects of repeated fluoxetine and citalopram administration on cytokine release in C57BL/6 mice, Psychiat Res 96 (2000), pp. 255–266. [16] I. Yaron, I. Shirazi, R. Judovich, D. Levartovsky, D. Caspi and M. Yaron, Fluoxetine and amitriptyline inhibit nitric oxide, prostaglandine E2, and hyaluronic acid production in human synovial cells and synovial tissue cultures, Arthritis Rheum 42 (1999), pp. 2561–2568. [17] M. Frieri, Neuroimmunology and inflammation: implications for therapy of allergic and autoimmune diseases, Ann Allerg Asthma Immunol 90 (2003) (Suppl 3), pp. 34–40. [18] T.E. Renau, The potential of phosphodiesterase 4 inhibitors for the treat of depression: opportunities and challenges, Curr Opin Investig Drugs 5 (2004), pp. 34–39. [19] N. Barden, Regulation of corticosteroid receptor gene expression in depression and antidepressant action, J Psychiatr Neurosci 24 (1999), pp. 25–39. [20] E.M. Sternberg, Neuroendocrine regulation of autoimmune/inflammatory disease, J Endocrinol 169 (2001), pp. 429–435. [21] I.J. Elenkov and G.P. Chrousos, Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity, Ann N Y Acad Sci 966 (2002), pp. 290–303.
|
|
#33
25.08.2006, 22:32
|
||||
|
||||
|
Некоторые суждения "cons":
Med Hypotheses. 2005;65(2):417-8. Asthma, major depression and brain-derived neurotrophic factor. Tsai SJ Division of Psychiatry, School of Medicine, National Yang-Ming University, Taiwan I have read with great interest the recent article, “Therapeutic value of antidepressants in asthma” by Karamitsos et al. [1]. The authors suggested that antidepressants may have a therapeutic role in asthma by suppressing production of proimfammatory cytokines and inducing production of anti-inflammatory ones [1]. However, one should be cautious that antidepressant treatment may increase brain-derived neurotrophic factor (BDNF) which may deteriorate, rather then improve, asthma. BDNF, a member of the neurotrophic factor family, plays an important role in the growth, development, maintenance, and function of several neuronal systems. It has been proposed that BDNF plays an important role in the pathogenesis of major depressive disorder (MDD) and, therefore, in the mechanisms underlying antidepressant action [2]. This proposal was further supported by the finding of increased hippocampal BDNF immunoreactivity in subjects treated with antidepressant medication [3], and the findings that serum BDNF was significantly lower in the antidepressant-naive MDD group than in the treated or in the control group [4]. While BDNF is highly concentrated in the brain, it is also abundantly present in the lung [5]. Utilising a mouse model of asthma, Braun et al. [6] have identified BDNF as a candidate molecule for mediating functional neuronal changes in allergic bronchial asthma. In a later report, the same study group further reported that enhanced platelet BDNF is associated with airflow limitation and airway hyper-responsiveness in asthma patients [7]. From the above findings, it is probable that antidepressant treatment in asthma patients may further worsen asthma condition due to the increase of peripheral BDNF levels. From Medline search, there is still no study of the antidepressant effects on the pulmonary BDNF levels. It should be noted that, in animal studies, the alteration of the central BDNF levels by antidepressants depended on the type of antidepressants, the treatment duration, the drug dosage and the brain regions studied [8] and [9]. Considering the higher rate of depression in asthma, and the potential value of antidepressants in asthma by modulating immune reacting [1], it is suggested that the dose, the duration and the type of antidepressants for such intervention need to be tested in animal model asthma. Furthermore, whether BDNF may play a role in the biological linkage between asthma and major depression may be of interest for further exploration. References [1] G. Krommydas, K.I. Gourgoulianis, K. Karamitsos, K. Krapis, E. Kotrotsiou and P.A. Molyvdas, Therapeutic value of antidepressants in asthma, Med Hypotheses 64 (2005), pp. 938–940. [2] R.S. Duman, G.R. Heninger and E.J. Nestler, A molecular and cellular theory of depression, Arch Gen Psychiatry 54 (1997), pp. 597–606. [3] B. Chen, D. Dowlatshahi, G.M. MacQueen, J.F. Wang and L.T. Young, Increased hippocampal BDNF immunoreactivity in subjects treated with antidepressant medication, Biol Psychiatry 50 (2001), pp. 260–265. [4] E. Shimizu, K. Hashimoto, N. Okamura, K. Koike, N. Komatsu and C. Kumakiri et al., Alterations of serum levels of brain-derived neurotrophic factor (BDNF) in depressed patients with or without antidepressants, Biol Psychiatry 54 (2003), pp. 70–75. [5] M. Lommatzsch, A. Braun, A. Mannsfeldt, V.A. Botchkarev, N.V. Botchkareva and R. Paus et al., Abundant production of brain-derived neurotrophic factor by adult visceral epithelia. Implications for paracrine and target-derived Neurotrophic functions, Am J Pathol 155 (1999), pp. 1183–1193. [6] A. Braun, M. Lommatzsch, A. Mannsfeldt, U. Neuhaus-Steinmetz, A. Fischer and N. Schnoy et al., Cellular sources of enhanced brain-derived neurotrophic factor production in a mouse model of allergic inflammation, Am J Respir Cell Mol Biol 21 (1999), pp. 537–546. [7] M. Lommatzsch, K. Schloetcke, J. Klotz, K. Schuhbaeck, D. Zingler and C. Zingler et al., Brain-derived neurotrophic factor in platelets and airflow limitation in asthma, Am J Respir Crit Care Med 171 (2005), pp. 115–120. [8] H. Xu, J. Steven Richardson and X.M. Li, Dose-related effects of chronic antidepressants on neuroprotective proteins BDNF, Bcl-2 and Cu/Zn-SOD in rat hippocampus, Neuropsychopharmacology 28 (2003), pp. 53–62. [9] J.P. Jacobsen and A. Mork, The effect of escitalopram, desipramine, electroconvulsive seizures and lithium on brain-derived neurotrophic factor mRNA and protein expression in the rat brain and the correlation to 5-HT and 5-HIAA levels, Brain Res 1024 (2004), pp. 183–192.
|
|
#34
25.08.2006, 22:41
|
||||
|
||||
|
Релевантная корреспонденция:
Am J Respir Crit Care Med. 2005 Oct 15;172(8):1055-6; Where are the guidelines for the treatment of asthma with panic spectrum symptoms? Correspondence Where Are the Guidelines for the Treatment of Asthma with Panic Spectrum Symptoms? To the Editor: Dr. Hasler and colleagues (1) have recently presented the first long-term follow-up study on asthma and panic disorder (PD). They showed dose–response-type relationships between PD and asthma, and bidirectional longitudinal associations between the two conditions. Earlier, Goodwin and colleagues (2) provided information on the association between physician-diagnosed asthma and DSM-IV mental disorders in a representative population sample of adults. Current severe asthma was associated with a significantly increased likelihood of any anxiety disorder, including PD and panic attacks. In patients with asthma, an early identification of PD without restricting the diagnosis to the classification's criteria, allowing a clinical judgment based on symptoms, criteria, and the spectrum concept, could lead to appropriate use of drugs in the absence of any precise psychiatric diagnosis and thus lead to better treatment, improving their health and quality of life (3). We should now start clinical trials with antipanic medication alone and in association with asthma medications, describing the influence of such treatment on respiratory function and daily activities. Nascimento and coworkers (4) evaluated lung function in asymptomatic PD patients without asthma with the goal of investigating the effects of taking antipanic drugs (serotonin selective reuptake inhibitor antidepressants). Lung function evaluation was performed on two different days (taking antipanic drugs and in the washout phase), and included spirometric evaluation and a bronchodilatation test (salbutamol inhalation). Before the bronchodilatation test, forced expiratory volume in 1 second (FEV1) and forced expiratory flow between 25% and 75% of forced vital capacity (FEF25–75) were significantly higher in patients taking antipanic drugs than in the washout period. After salbutamol inhalation, only FEV1 was significantly higher in patients treated with antipanic drugs than when measured during the washout period. A significant increase in FEV1 and FEF25–75 after salbutamol inhalation was observed during a 2-wk drug-free period in PD patients. Follow-up studies with samples of PD patients with asthma may also show the impact of PD treatment on respiratory symptoms. Obstructive pulmonary diseases could trigger panic attacks in predisposed individuals by the stimulation of the central chemoreceptors hypersensitive to PCO2 and/or the locus coeruleus. This hypothesis is reinforced by the hypersensitivity to CO2 false suffocation alarm theory (5). Studies with an enhanced methodology—including laboratory measures relating to asthma—are important to find out if the improvement in lung function in asymptomatic PD patients is due to the antipanic effects in controlling bronchial tone or by decreasing anxiety sensitivity and panic-related cognition. Antonio E. Nardi Federal University of Rio de Janeiro, Rio de Janeiro, Brazil FOOTNOTES Conflict of Interest Statement: A.E.N. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES 1.Hasler G, Gergen PJ, Kleinbaum DG, Ajdacic V, Gamma A, Eich D, Rössler W, Angst J. Asthma and panic in young adults: a 20-year prospective community study. Am J Respir Crit Care Med 2005;171:1224–1230. 2.Goodwin RD, Jacobi F, Thefeld W. Mental disorders and asthma in the community. Arch Gen Psychiatry 2003;60:1125–1130. 3.Nascimento I, Nardi AE, Valença AM, Lopes FL, Mezzasalma MA, Nascentes R, Zin WA. Psychiatric disorders in asthmatic outpatients. Psychiatry Res 2002;110:73–80. 4.Nascimento I, Nardi AE, Valença AM, Cassabian L, Garcia CB, Lopes FL, Zin WA. Effect of antipanic drugs on pulmonary function in patients with panic disorder. Presented at the annual meeting of the American Psychiatric Association; May 21–26, 2005; Atlanta, Georgia. Abstract appears in New Research Abstracts. Arlington, VA: American Psychiatric Association; 2005. p. 174. 5.Klein DF. False suffocation alarms, spontaneous panics and related conditions. Arch Gen Psychiatry 1993;50:306–317
|
|
#35
25.08.2006, 22:45
|
||||
|
||||
|
From the Authors:
Based on the empirical evidence from two longitudinal studies on asthma and panic, Dr. Nardi recommends not restricting panic diagnosis strictly to the DSM classification’s criteria. We agree that a longitudinal perspective is necessary to evaluate panic in asthma, that the temporal criteria in the DSM reflect an arbitrary convention, rather than a frequency threshold based on empirical evidence, and that more research is needed to find meaningful threshold criteria for panic in asthma for clinical use. Nardi points out the next logical step in understanding the interaction of panic and asthma is a clinical trial evaluating the impact of antipanic medication on asthma control. We agree that a clinical trial is necessary, but certain caveats must be kept in mind when designing such a trial. Smoking, for example, appeared to be an important shared risk factor that must be considered in the treatment of both asthma and panic. Nardi suggests looking at antipanic medications alone and in combination with asthmamedication. As demonstrated in our study, asthma and panic are not separate diseases but are actually overlapping and related in certain individuals. This finding suggests that for those individuals, appropriate treatment of their panic attacks will make their asthma easier to control. Once the panic is controlled, it is very likely the majority of these individuals will need to continue their asthma medication but at a lower dose. An individual with chronic asthma and panic should never be treated with antipanic medication alone. In contrast, there are some individuals whose apparent asthma symptoms are actually manifestations of their panic attacks, and these individuals would benefit from treatment of their panic alone. However, at the present time we do not have appropriate diagnostic criteria to identify these individuals with a high degree of precision. Finally, it is noteworthy that certain psychotherapeutic treatments, breathing exercises, and reduction of caffeine consumption may be effective therapeutic elements in reducing panic symptoms. Conflict of Interest Statement : Neither of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. Gregor Hasler National Institute of Mental Health National Institutes of Health Bethesda, Maryland and Psychiatric University Hospital Zurich, Switzerland Peter J. Gergen National Institute of Allergy and Infectious Diseases National Institutes of Health Bethesda, Maryland
|
|
#36
26.08.2006, 00:34
|
||||
|
||||
|
Некоторые публикации, показывающие, что среди больных БА очень высокий уровень невыявленных и нелеченных депрессивных и панических состояний:
Valenca AM, и соавт. The relationship between the severity of asthma and comorbidites with anxiety and depressive disorders. Rev Bras Psiquiatr. 2006 Aug 15; [Ссылки доступны только зарегистрированным пользователям ] Heaney LG и соавт. Prevalence of psychiatric morbidity in a difficult asthma population: relationship to asthma outcome. Respir Med. 2005 Sep;99(9):1152-9 This study demonstrates a high prevalence (49%) of psychiatric morbidity in subjects referred with difficult-to-control asthma, with only 9% of having been previously recognised. Our most common diagnosis was depressive illness (29%), which is consistent with Mancuso and colleagues, who detected depressive symptoms in almost half of subjects with moderate asthma using a variety of screening tools.26 Nascimento, using the Mini-International Neuropsychiatric Interview (MINI) questionnaire, had depression rates of 33.7% and Brown using clinical interview with patients with moderate to severe disease found current depressive disorder of 25% which was again largely undiagnosed.14 and 27 Since depressive illness is common and has been associated with poor medication compliance, loss to follow-up28 and asthma death,5 and 6 identification and treatment of depression is potentially important in this population. а также педиатрические работы, показывающие что уровень депрессии и степень тяжести БА взаимозависимы: Waxmonsky J, и соавт. Association of depressive symptoms and disease activity in children with asthma: methodological and clinical implications. J Am Acad Child Adolesc Psychiatry. 2006 Aug;45(8):945-54. Miller BD, Wood BL. Influence of specific emotional states on autonomic reactivity and pulmonary function in asthmatic children. J Am Acad Child Adolesc Psychiatry (1997), 36:669-677 Рисунок из последней работы:
|
Линейный вид
