Asthma is a serious health problem throughout the world During the past two decades, many scientific advances have improved our understanding of asthma and ability to manage and control it effectively However, recommendations for asthma care need to be adapted to local conditions, resources and services Since it was formed in 1993, the Global Initiative for Asthma, a network of individuals, organisations and public health officials, has played a leading role in disseminating information about the care of patients with asthma based on a process of continuous review of published scientific investigations A comprehensive workshop report entitled "A Global Strategy for Asthma Management and Prevention", first published in 1995, has been widely adopted, translated and reproduced, and forms the basis for many national guidelines The 2006 report contains important new themes First, it asserts that "it is reasonable to expect that in most patients with asthma, control of the disease can and should be achieved and maintained," and recommends a change in approach to asthma management, with asthma control, rather than asthma severity, being the focus of treatment decisions The importance of the patient-care giver partnership and guided self-management, along with setting goals for treatment, are also emphasised

https://erj.ersjournals.com/content/erj/31/1/143.full.pdf

Global strategy for asthma management and prevention: GINA executive summary.

These guidelines have been replaced by British Guideline on the Management of Asthma. A national clinical guideline. Superseded By 2012 Revision Of 2008 Guideline: British Guideline on the Management of Asthma. Thorax 2008 May; 63(Suppl 4): 1–121.

/pdf/british-guideline-on-the-management-of-asthma-a-national-3q1wreyszl.pdf

British guideline on the management of asthma: A national clinical guideline

http://www.johnsonupdaydowndaydiet.samsbiz.com/content/00/01/53/97/83/userimages/ADCR%20article.pdf

Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma.

Background Psychologic stress modifies immune function and cytokine production. Objective We examined relationships between caregiver stress on the following markers of early childhood immune response: (1) IgE expression (n = 215); (2) mitogen-induced and allergen-specific ( Dermatophagoides farinae [Der f 1] and cockroach [Bla g 2]) proliferative response (n = 114); and (3) subsequent cytokine expression (INF-γ, TNF-α, IL-10, and IL-13) in a prospective birth cohort predisposed to atopy. Methods Caregiver stress was measured at 2-month intervals for the first 2 years of life and yearly thereafter by using the Perceived Stress Scale. A subsequent blood sample obtained from the children (median age, 2.1 years; range, 18-32 months) was analyzed for total serum IgE level and allergen-induced proliferation quantified as the stimulation index (SI; mean thymidine incorporation of the stimulated sample divided by that of the unstimulated sample). The relationship between stress and the proliferative response (SI >3 vs SI ≤3), and total IgE level (≤100 IU/mL vs >100 IU/mL) was examined by using logistic regression. The relationship between cytokine levels and stress was analyzed by using linear regression. Results In adjusted analyses higher caregiver stress in the first 6 months after birth was associated with a Der f 1 SI of greater than 3 (odds ratio [OR], 1.5; 95% CI, 1.0-2.3) and nominally associated with a Bla g 2 SI of greater than 3 (OR, 1.13; 95% CI, 0.7-1.8). Higher stress between ages 6 and 18 months was associated with a high total IgE level (OR, 2.03; 95% CI, 1.1-3.6). Higher stress was significantly associated with increased production of TNF-α, with a suggested trend between higher stress and reduced INF-γ production. Conclusion Increased stress in early childhood was associated with an atopic immune profile in these children predisposed to atopy-asthma.

https://www.jacionline.org/article/S0091-6749(04)01164-9/pdf

Chronic caregiver stress and IgE expression, allergen-induced proliferation, and cytokine profiles in a birth cohort predisposed to atopy

The pharmacokinetic and pharmacodynamic effects of inhaled corticosteroids (ICS) have shaped the efficacy and safety of these agents in the treatment of asthma. Important pharmacokinetic and pharmacodynamic characteristics that can enhance the efficacy of ICS include small particle size, high glucocorticoid-receptor-binding affinity, long pulmonary residence time and lipid conjugation. These characteristics can increase or prolong the anti-inflammatory effects of an ICS. Important pharmacokinetic characteristics that can enhance the safety of ICS include on-site activation in the lung, low oropharyngeal exposure, negligible oral bioavailability, high protein-binding and rapid systemic clearance. The degree of oropharyngeal exposure is relevant to local side-effects, such as oropharyngeal candidiasis, dysphonia and coughing. Pharmacokinetic properties that influence the degree of systemic exposure are relevant to the pharmacodynamic effect of ICS-induced hypothalamic-pituitary-adrenal axis suppression and cortisol suppression, an indicator of potential long-term systemic side-effects, such as reduced growth velocity and bone density, fractures, and skin bruising and thinning. Therefore, significant differences in the pharmacokinetic and pharmacodynamic characteristics of the currently available inhaled corticosteroids warrant careful consideration when used in clinical practice as they may result in differences in efficacy and local and systemic safety profiles.

https://erj.ersjournals.com/content/erj/28/5/1042.full.pdf

Relevance of pharmacokinetics and pharmacodynamics of inhaled corticosteroids to asthma

Comparative efficacy of once-daily ciclesonide and budesonide in the treatment of persistent asthma.

Role of TNF-α and its 55 and 75 kDa receptors in bronchial hyperreactivity

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Comparative efficacy of once-daily ciclesonide and budesonide in the treatment of persistent asthma.

Role of TNF-α and its 55 and 75 kDa receptors in bronchial hyperreactivity