Asthma or bronchial asthma is a disease which is characterized by airways narrowing. It happens because of some agents provoke the airways making them inflamed. This disorder gains more and more scope nowadays making asthma one of the most widespread disorder nowadays. The evidence has proved that the amount of asthma sufferers grows rapidly.
This 72-year-old man with longstanding chronic asthmatic bronchitis and Kaposis sarcoma, involving only the integument, was admitted on July 12,1982 for evaluation of a new pulmonary infiltrate. The patient had been on prednisone at varying dosages (5-20 mg) for two years, in addition to oral terbutaline, aminophylline, inhaled isoetharine, and chlorprom-pamide. One year previously, he developed histologically proven Kaposi s sarcoma involving both lower extremities up to the lower thighs. Because of progressive bilateral leg edema and severe paresthesias, he underwent radiotherapy (Cobalt-60) treatment, to these areas for a total midline dosage of 2,500 rads.
Twin studies and studies of familial aggregation have demonstrated a significant genetic contribution to asthma. Estimates of the heritability of asthma in twin studies have ranged from 36 to 79%.
To date, 15 groups have reported results of genome-wide linkage analysis for asthma and/or its intermediate phenotypes in 17 distinct populations. Several of these groups have published second-generation surveys with larger numbers of subjects and markers. One of these genome-wide linkage studies for asthma reported only partial results. Fourteen chromosomal regions have shown significant evidence of linkage to asthma or its intermediate phenotypes in at least one genome scan, as follows: chromosomes 2p1658 and 2p2551 (to increased airway responsiveness); 2q32 (to FEV1/FVC ratio); 2q33 (to eosinophil count); 5q31-q33 (to mite-sensitive asthma); 7p14-p1550 and 7q21 (to total serum IgE level); 11q12-q13 (to atopy)-; 6p21, 12q24,14q24, and 20p1355 (to asthma); and 19p13 and 20q13 (to dust mite allergy).
Many studies of the genetic association for asthma phenotypes have been conducted, often yielding inconsistent results. The potential reasons for the conflicting findings of studies of genetic association in asthma include small sample sizes, a failure to correct for multiple comparisons, genetic and environmental heterogeneity, publication bias, the inadequate assessment of asthma and/or its intermediate phenotypes, and (for case-control studies) population stratification. To date, there have been reports of association between variants in > 100 genes and asthma phenotypes. Of these, 25 genes (eg, ADRB2 and IL10) had variants that were associated with asthma phenotypes in at least six popu-lations, suggesting that alleles in or near these genes influence the pathogenesis of asthma. Data from studies in experimental models and/or functional studies in humans are needed to firmly identify the functional variants responsible for the observed genetic associations.
We found that low therapeutic concentrations of theophylline significantly increased aerosol penetration in the lung of healthy subjects based on the finding of significantly lower mean skew with theophylline. Neither mucociliary clearance nor tracheal mucociliary transport rate was different between theophylline and placebo trials. When aerosol deposition is taken into consideration, the data suggest that theophylline may have increased mucociliary transport rates.
Delivery of aerosolized bronchodilator agents through metered-dose inhalers (MDI) has enjoyed wide popularity because these devices are portable and convenient, require minimum time for administration, and have the potential for effecting rapid relief of bronchospasm. More recently, it has been shown that MDI-delivered corticosteroids may reduce oral corticosteroid requirements in asthmatic patients who are chronically steroid dependent. Depression of the MDI canister by the fingers to actuate a valve mechanism for release of a puff of aerosolized drug appears to be a simple procedure. However, this must be coordinated with a slow, deep inhalation, a hand-breath maneuver which as many as 70 percent of adults find impossible to perform correctly. Patients often are unable to depress the canister as they inhale and even may actuate the MDI during exhalation, thereby receiving none of the drug. Further, the recommended techniques for administration include various combinations of inspiratory flow rate, breath-holding times, and actuation of MDI at different lung volumes, creating confusion both to patients and physicians.
When the above considerations are taken into account, it seems that for aerosol therapy we require as ideals: (1) aerosol MMAD <5 to minimize oropharyngeal deposition, (2) slow, steady inhalation, and (3) a period of breath-holding on completion of inhalation. These ideals are hard to achieve for metered-dose inhalers (MDIs), partly because of the nature of the spray itself, and partly because of the difficulties many patients have in using MDIs.
The spray released from an MDI consists of large droplets of propellant within which the drug itself is enclosed either as a solid crystal or as a liquid. Although the drug particles or droplets have MMADs between 2 and 5 y,, the effective MMAD may exceed 40 \i at the actuator orifice. Although the propellants evaporate as the droplets move away from the canister, evaporation is not instantaneous, and some unevaporated propellant may coat the drug even after several seconds. Further, the initial velocity of the propellant droplets exceeds 30 nrsec, although they slow down on encountering air resistance. Because of the large effective aerosol size and the rapid droplet velocity, most of the spray (^80 percent of the dose) impacts in the oropharynx, and only about 10 percent of the dose penetrates to the lungs.
The ihalation therapy has several well-established advantages over the oral and intravenous (IV) routes: (1) A small dose of drug can be used; a few hundred micrograms of inhaled (3-agonist may be as effective as a 10-mg oral dose. (2) There is a rapid onset of action; an inhaled bronchodilator is effective within 5 minutes and reaches peak effect in 15 to 30 minutes compared to 2 to 3 hours for an oral dose. (3) There is a low incidence of systemic side effects; inhaled corticosteroids control asthma in doses far lower than those required to cause adrenal suppression.
With the exception of several preparations that can be given as sublingual sprays for systemic therapy, it is a general rule that therapeutic aerosols should reach the lungs to be effective. A small part of the effect of inhaled E-agonists or corticosteroids may arise from drug either deposited in the oropharynx and absorbed locally or swallowed and absorbed from the gastrointestinal (GI) tract. Bearing in mind the small amounts of drug conventionally used, though, the majority of the effect arises from drug deposited directly in the lungs. For instance, 500 xg of terbutaline sulfate (the usual therapeutic dose) deposited in the upper airways gave rise to no significant bronchodilatation, and gargling with the same amount of fenoterol solution was also ineffective. Inhaled bronchodilators produce their maximum effect when plasma levels of drug are negligible.
This study shows that in elderly asthmatics, death from all causes was increased compared to control subjects. However, asthma perse was not recognized among factors associated with death in pooled asthma and control subjects. Furthermore, the sets of risk factors identified in asthmatics and control subjects substantially differed. Thus, clustering of selected risk factors in asthmatics rather than asthma as a respiratory disease seems relevant to explain the excess mortality rate in asthmatics.
The high proportion of deaths attributed to respiratory nonneoplastic causes confirms an American survey of asthma-related death in the period from 1990 to 2001. Interestingly, the observed trend toward lower mortality rate from cancer confirms results of a very large epidemiologic study showing that both overall cancer mortality rate and colorectal cancer mortality rate were lower in subjects with asthma or hay fever. However, another study failed to support this observation.
We found that predictors of death in asthmatics were mainly nonrespiratory: depression, age, and smoking habit. On the contrary, Dantzer et al failed to recognize risk factors for death in elderly asthmatics followed up for 5 years. This difference between the two studies may be due to different methods used to assess the presence of asthma (self-reported in the Dantzer et al study, and based on objective methods in our study) and to differences in the array of collected variables. Furthermore, the French study did not evaluate predictors of survival within an asthma population; rather, it aimed at assessing whether asthma affects survival in an heterogeneous population of 2,348 elderly subjects including 206 asthmatics.
People with and without asthma were similar with respect to demographic characteristics. Physical performance was, as expected, slightly worse in the group with asthma, and in this group we also found a higher prevalence of depressed mood. No difference was found, instead, with regard to cognitive performance. Eversmokers were more prevalent in the group with asthma (56.2% vs 47.8%). We found only minimal difference between groups in the prevalence of cerebrovascular disease and diabetes, while cardiovascular diseases (including heart failure) were more prevalent in the group with asthma (Table 1).
Asthma Inhaler List