Tunnel of Inflammation in Obstructive Airway Diseases

The use of macrolides for asthma must be put in context of the apparent beneficial affects also observed in complex lung diseases with features of chronic inflammation plus infection such as cystic fibrosis and diffuse panbronchiolitis. It is difficult to determine if this improvement is related to a distinct antiinflammatory property because concurrent bacterial infection or colonization may be present, which has also been implicated in asthma. However, a previous trial12 evaluated the role of clarithromycin in asthma patients that had no evidence of airway colonization with either Mycoplasma pneumoniae or Chlamydia pneumoniae.

In this cohort, clarithromycin treatment decreased BAL fluid IL-12 and tumor necrosis factor-а expression but did not improve in FEV1. In the future, separating the microbial and nonmicrobial properties of the macrolides would assist in determining if the nonmicrobial properties of macrolides could produce the desired antiinflammatory effects in subjects with asthma. Canadian Health and Care Mall treatment your asthma with Canadian medications online. Order asthma medications with 10% discount you can on Canadian Health and Care Mall Shop.

In summary, our results demonstrated that azithromycin possesses antiinflammatory properties in an in vivo noninfectious model of allergic airway inflammation. These observations suggest azithromycin may be beneficial in the treatment of inflammatory conditions, such as asthma, and support the rationale for future prospective randomized clinical trials.

Chronic and persistent airway inflammation is one of the main driving forces in the obstructive airway diseases. It is proving increasingly useful to classify the pattern of inflammation based on the dominant granulocyte present, and there is great potential to use markers of inflammation serially to monitor disease activity and assist in treatment selection and dose adjustment. In asthma, this approach is well developed, particularly for eosinophilic forms of the disease.

The pathway leading to eosinophilic inflammation in asthma is well understood and effectively targeted by treatment. In sensitized individuals, allergen exposure leads to activation of T-helper type 2 lymphocytes, and the resulting cytokine response involving interleukin-5 promotes eosinophilic airway inflammation.

Health and Care: Respiratory research

Respiratory research
Respiratory research

We found that neither SGRQ total nor dimensional score were affected by sex. There was no statistically significant correlation between age and SGRQ dimensions and total scores. SGRQ total and activity dimension scores were slightly skewed and therefore presented as median and interquartile ranges (IQRs); moreover, the median, IQR, and minimum and maximum ranges of SGRQ dimensions and total scores are also illustrated.

Using Cronbach a for measuring internal consistency for the total score and each dimension (symptom, activity, and impact), we found a values of 0.94, 0.77, 0.91, 0.86, respectively. Total SGRQ had a highly statistically significant correlation with SGRQ symptoms, activity, and impact domains (0.64, 0.82, and 0.96, respectively). Symptoms domain had mild correlation with activity domain (0.41) and a moderate correlation with impact domain (0.61).

However, a better correlation was seen between activity and impact domains (0.7) (P < . 0001 for all these correlations). For test-retest reliability, the intraclass correlation coefficients for the total SGRQ and its dimensions (symptom, activity, and impact) were 0.97, 0.92, 0.94 and 0.95, respectively. There were small and statistically insignificant mean differences between scores at both completions, and the 95% limits of agreement of repeatability as shown in Bland-Altman plot.

The SGRQ total and dimensional scores showed high convergent validity correlating with different objective and subjective measures in respiratory research. The MRC dyspnea score, SF-36 PCS score, and SF-36 PCM score had the highest correlation with total and dimensional SGRQ scores. The maximum correlation was with both SF-36 scores and greater than the MRC dyspnea score (R2 = 0.5), suggesting that other important elements of ill health in these patients are being captured by the SGRQ.

Worse health status was associated with increasing severity of CPA; patients with severe CPA had worse health status than patients with mild or moderate disease. Moreover, the SGRQ showed significant discriminating ability in differentiating between all grades of shortness of breath. In addition, patients with more disease severity as justified by the respiratory physician scored consistently higher total and dimensional SGRQ scores.

Nasal Allergen Challenge: Systemic Effects

Airway inflammation and remodeling can be present in the lower airways of patients with allergic rhinitis, although it is less intense than in patients with asthma. During natural exposure, both the nose and lung come into contact with airborne allergens. Nasal inflammation may influence lower airway inflammatory processes by the release of inflammatory mediators into the circulation or through an effect on BM progenitors or inflammatory cells.  Nasal Allergen Challenge Systemic Effects

As most clinical trials have been performed during natural allergen exposure, studies evaluating the influence of upper airway disease on lower airways cannot properly assess the influence of nasal inflammation on lower airways. Provocative nasal allergen challenge has been used to help sort out the influences of allergic rhinitis on lower airways and specifically determine the influence of the upper airways on lower airway inflammation. Braunstahl performed nasal allergen provocations in allergic rhinitic patients without asthma and in normal control subjects.

An increase of eosinophils as well as increased expression of intercellular adhesion molecule-1 was observed in the nasal and bronchial biopsies of allergic rhinitic patients compared with control subjects. However, Beeh observed no significant difference in sputum eosinophils following nasal allergen provocation, although sputum ECP and intercellular adhesion molecule were increased. In addition, Braunstahl have shown that segmental bronchial allergen challenge can produce nasal eosinophilic inflammation.

Nasal Allergen Challenge: Systemic Effects

In this regard, we recently performed a study using repeated nasal challenges to determine if this can induce lower airway inflammation and to obtain a more accurate model of allergen exposure. Our preliminary results show that a large number of patients with allergic rhinitis with or without asthma can have significant lower airway inflammation after repeated nasal challenge.

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Canadian Health and Care Mall – What is Diabetes?

CAUSES OF DIABETES

Inheritance

CAUSES OF DIABETES

Several members of my family developed diabetes when we were young and most of us are controlled by tablets. I’ve been told we are a MODY family. What does this mean?

MODY stands for Maturity-Onset Diabetes of the Young. (Maturity-onset diabetes is an earlier name for Type 2 diabetes.) In the 1970s, it was noticed that a handful of families seemed to develop diabetes in their teens or twenties and about 50% of family members were affected. This suggests a certain sort of inheritance (autosomal dominant); those family members with diabetes have a specific defect in their insulin-producing cells. Research into these patients has increased our understanding of the causes of diabetes. There are several distinct types of MODY, but generally people in this group can control their diabetes with tablets and do not usually need insulin.

If diabetes is known to be in my family, should I or my children take any preventive action?

The inheritance of diabetes is a complicated subject and different types of diabetes are inherited in different ways. In Type 1 diabetes some family members may carry an increased risk, which can be identified by genetic testing.

However, only a small proportion of the people who inherit this risk will go on to develop diabetes and no one has been able to pin down the factors that cause this to happen.

Type 2 diabetes is more strongly inherited than Type 1, and therefore often affects several members of the same family. It is now clear that a number of different genes are involved. The picture which is slowly emerging suggests that there are several different forms of Type 2 diabetes. The genetics of one rare form of inherited diabetes, called MODY, have been investigated in great detail and have increased our understanding of this condition but these discoveries do not apply to the vast majority of people with Type 2 diabetes (see MODY question above).

There is now evidence that family members who are at risk may put off developing diabetes by regular exercise, losing weight and sometimes by taking medication. They should have a blood glucose test as soon as they develop any relevant symptoms, so that diabetes can be detected and treated early.

I am 16 and have had diabetes for five years. Why has my identical twin brother not got diabetes?

A large 20-year research project has studied examples of identical twins with diabetes. The results show a difference between the way Type 1 and Type 2 diabetes are inherited. If you have an identical twin with Type 1 diabetes, you have only a 50% chance of developing diabetes yourself. On the other hand, if you had Type 2 diabetes (extremely unusual at the age of 11) your twin would be almost certain to get the same sort of diabetes. If your twin brother has not developed diabetes within the last five years, he has a very low risk of developing the condition.