Asthma

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Ventolin Inhaler or Advair Diskus: What Asthma Medication to Choose?

Ventolin and Advair Diskus are the most popular inhalers at the moment, they are both maintenance inhalers for asthma and are often compared, so which one is right for you? You should know that they are both used to treat asthma and COPD, but are Advair and Ventolin the same? The website administration addressed the online company specialized on asthma inhalers for sale onlineasthmainhalers.com to find out the differences between these medications.

Ventolin Inhaler

Ventolin is an anti-asthmatic drug that is used to treat various diseases of the bronchi and lungs.

The medication is used for inhalation only.

Ventolin composition:

Active substance – Salbutamol, which inhibits the reactivity of the bronchi and helps eliminate or prevent asthma attacks;

Auxiliary substances – facilitate administration of Salbutamol and its distribution.

Ventolin acts on the smooth muscles of the bronchi: ensures their complete relaxation, lowers the resistance of the airways and increases the amount of inhaled air. In addition, the active ingredient of Ventolin – Salbutamol – is able to stimulate the secretion of the bronchial glands and activate the ciliary epithelium of the bronchi, which ensures the excretion of mucus during coughing. Salbutamol in therapeutic doses can cause increased heartbeat and lowered blood pressure. Make sure to read the detailed Ventolin instructions before use.

Advair Diskus

Advair Diskus is a combined medication with bronchodilator, anti-inflammatory, anti-asthmatic, glucocorticoid, beta-adrenomimetic action. This medication is used to control and prevent asthma or CORD symptoms.

Advair contains 2 active ingredients:

Fluticasone – belongs to the group of drugs known as corticosteroids. It reduces irritation and swelling of the airways;

Salmeterol belongs to the group of drugs known as long-acting beta agonists. It opens airways in the lungs and makes breathing easier.

Advair Diskus should be used regularly to be effective. It is not used to relieve sudden shortness of breath or asthma attacks. If you experience sudden breathing problems, you need to use other inhaler. Before using the drug, make sure you know how to use Advair Diskus correctly.

Difference between Advair and Ventolin

Comparative unit Ventolin Inhaler Advair Diskus Visual appearance Components Albuterol Fluticasone Propionate/Salmeterol Xinafoate Indications for use Asthma, Wheezing, Shortness of Breath, Asthma Attack, COPD. Ventolin is mostly prescribed for Asthma and Wheezing Asthma, Emphysema. Advair is mostly prescribed for Asthma Minimum price per unit $25.95 $34.95 Package type Inhaler Diskus Dosages available 100mcg/100mcg 50mcg/500mcg; 50mcg/250mcg; 50mcg/100mcg; 25mcg/250mcg; 25mcg/125mcg; 25mcg/50mcg Min/max dosage 100mcg only 25mcg/50mcg / 50mcg/500mcg Maximum dosage per day 100mcg 6 times a day 500mcg/50mcg 2 times a day Onset of action In 75% of cases the maximal effect is achieved within 5 minutes About 30 minutes after the initial dose Duration of action Bronchodilation lasts up to 6 hours Bronchodilation lasts at least 12 hours Possible side effects Chest Tightness, Itching, Shaking, Weight Gain, Headaches, Runny Nose, Depression, Weight Loss, Cramping, Chest Pain Weight Gain, Weight Loss, Thrush, Tiredness, Insomnia, Hoarseness, Anxiety, Depression, Chest Pain Contraindications Hypersensitivity to the components of the drug, Age under 2 years, Threat of miscarriage or premature birth Wide-Angle Glaucoma, Cataracts, High Blood Pressure, Abnormal Heart Rhythm, Herpes Simplex Infection of the Eye, Osteoporosis, active tuberculosis, Diabetes Alcohol interaction There may be a negative interaction between Ventolin and alcohol There may be a negative interaction between Advair Diskus and alcohol Food interaction No food instructions No food instructions Use in children Can be used to treat and prevent asthma bronchospasm in children, starting from the age of 2. At an earlier age, Ventolin is used in rare cases, as the possible negative effects of the drug on children under 2 have not been sufficiently studied. Can be used in children 4 to 11 years old for asthma treatment that isn’t adequately controlled by inhaled corticosteroid therapy

Ventolin Inhaler reviews

The following Ventolin Inhaler reviews are taken from the well-known, authoritative websites and medical Internet forums. According to patients’ reviews, Ventolin is well tolerated and very effective in asthma treatment. When used correctly, side effects are rare. Only a small percentage of the reviews mention such side effects as: skeletal muscle tremors, headache or tachycardia. Ventolin inhaler price is described as “affordable” and “not high.”

Anna (27): “My child suffered from hereditary allergy to certain foods in the form of a rash, sometimes puffiness. Every viral disease resulted in obstructive bronchitis due to constant allergic attacks. When my baby fell ill for the first time, he was 10 months. So we ha to get acquainted with Ventolin inhaler bought online. When the baby had seizures, it was really scary. Ventolin relieved the attacks of suffocation quickly – within 3-5 minutes, and my child began to smile again. We are happy to have this medication, we will use it as necessary.”

Adam (34): “I’ve never suffered from bronchial asthma, but, unfortunately, I had to experience bronchospasm attacks. Such phenomena are typical for allergies that I have. Use of Ventolin inhaler was my rescue during asthma attacks, especially at work, when it is necessary to concentrate as much as possible. I do not recommend using the medication too often, because it is addictive, only if you really need it.”

David (25): “Once I saw my college using Ventolin inhaler. I was very surprised when she said that she was suffering from asthma since childhood. I did not notice any signs of her disease before. The college admits that she can’t do without Ventolin – inhalation aerosol for asthma.”

Martin (37): “Ventolin (also known as Albuterol / Salbutamol) helps me every autumn. I suffer from chronic bronchitis, I smoke a lot and begin coughing at the slightest hypothermia, sometimes even have suffocating seizures. Of course, I understand that I have to quit smoking, but I can not make myself do it so far. The doctor advised to buy Ventolin inhaler, but said that examination is necessary – I plan to do it in the nearest future. The medication always helps me, there are no special contraindications, so it suits me. Besides, I have not experienced any side effects. Tip: taking Advair and Ventolin together allows you to control asthma perfectly.”

Advair Diskus reviews

The following Advair Diskus reviews are taken from the well-known, authoritative websites and medical Internet forums.

George (55): “I was smoking all my life and my respiratory tract became really bad. I was hospitalized many times. It helped for a while. I started using Ventolin inhaler in December 2013 under medical supervision. The doctor prescribed Ventolin maximum dosage of 500 mcg, as I “swallowed the air like a fish”. The effect was immediate, from the first night, what really surprised me. A month later I switched to Ventolin 250 mcg. Soon my dose will be reduced even more. Guys, it’s nice to breathe deeply! Thanks to the Fluticasone and Salmeterol oral inhaler, I feel healthy again. Thank you!”

Dean (35): “I had been suffering from asthma for 10 years. When I was looking for asthma inhalers online, the disease was too bad and nothing helped me. I came across Advair Diskus. I was able to fall asleep without suffering on the first night, so I refused other asthma inhalers almost immediately. I used the medication according to the instructions for a month, then I reduced the dose to 1 inhalation in the morning and at night. I always buy asthma inhalers online – I guess it’s the easiest way to save your time.”

Arthur (16): “Advair Diskus is an excellent drug, which relieves asthma attacks quickly and effectively, although doctors say it does not relieve attacks but only prevents them. False. I am 16 years old, use Advair for 3 years and feel excellent. But the most important thing is that the medication is not additive! I recommend Advair to all asthmatics.”

Monika (25): “I have suffered from asthma since I was 2, even had seven clinical deaths, nothing helped me…. The doctor persuaded me buying Advair Diskus. I have been using the medication for 5 years and managed to forget about asthma, cold, etc. So, I advise it!”

Trisha (33): “My nephew has been suffering from bronchial asthma since the age of 6. Nothing would help him, cough did not want to retreat. He felt really bad, especially at night closer to 4-5 am. At the age of 8, they changed a doctor. The new physician prescribed Advair Diskus (Fluticasone and Salmeterol oral inhaler). It is quite expensive. They use it for a month, as there is a shift. That is, they got rid of a painful cough at night. So I can say Advair really works! But do not forget to consult your doctor on how often to use Advair first.”

Conclusion

So what inhaler to choose to treat asthma? Both the medications have positive reviews and high efficiency. The thing is what purpose you need an inhaler for: to prevent asthma or stop sudden asthma attacks. Advair Diskus copes well with the first task, while Ventolin is a rescue inhaler.

Besides, you may combine Ventolin and Advair to control asthma. Ventolin or Advair first? Ventolin inhaler is short-acting and its bronchodilating properties are more important. Using Ventolin first allows the brochioles to dilate which in turn allows Advair to get deeper into the lungs and make the treatment more effective.

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Deliberations about Chronic Asthma Due to Toluene Diisocyanate

In the present study, 12 workers with suspected TDI asthma were evaluated by bronchial challenge to TDI. Seven persons demonstrated sensitivity to low levels of TDI (reactors), confirming isocyanate sensitization. Six of these TDI reactors were challenged months to years after removal from their workplace exposure, demonstrating that isocyanate sensitization may persist for years in the absence of further occupational exposure. These six persons had chronic asthma symptoms reduced by flovent and pulmonary disability despite long-term removal from exposure. Four workers have had persistent asthma for one to three years, and two workers have had asthma for nine and 12 years, respectively, after removal from the workplace.

The persistent asthma caused by TDI seems related to the presence of nonspecific bronchial hyperreactivity. Five of the TDI reactors had a positive methacholine challenge, one case showed a positive cold air challenge, and all of them required medication for daily control of respiratory symptoms. All six symptomatic TDI reactors with bronchial hyperreactivity showed late occurring responses to TDI challenge testing. It has been reported that antigen-induced late occurring asthmatic responses are associated with induction of nonspecific bronchial hyperreactivity. The present cases suggest that occupational exposure to TDI may result in a prolonged state of hyperreactive airways.

Five persons with consistent histories for TDI asthma had negative TDI challenge studies. Three demonstrated bronchial hyperreactivity by metha-choline challenge and may represent sensitized individuals tested with an insufficient TDI challenge dose. For example, worker 9 experienced prominent cough symptoms after his TDI challenge unaccompanied by significant airway obstruction. A longer TDI challenge exposure might have elicited bronchospasm, though this remains unconfirmed since further testing was not performed. The recent demonstration that a greater percentage of the 2,6 TDI isomer is released into the ambient air than the corresponding 2,4 TDI isomer in a polyurethane foam industry (though the original composition contained a minority of 2,6 TDI) raises the possibility that isomers of TDI may have different potentials for respiratory sensitization. Future inhalation challenge testing to TDI in the clinical laboratory may need to include a mixture of isomers to improve test sensitivity. Alternatively, the TDI nonreactors may have lost their sensitivity to TDI after removal from the workplace. If bronchial hyperreactivity persists after loss of TDI sensitivity, the worker may develop respiratory symptoms due to the presence of nonspecific airway hyperreactivity unrelated to isocyanate exposure. Some TDI nonreactors may not have been originally sensitized to TDI though their medical histories strongly suggested this diagnosis. These individual may have been sensitized to other agents in the workplace such as amines added to isocyanate mixtures as catalysts in polyurethane foam manufacturing, or to other non-cross-reactive isocyanates. Of course, individuals with pre-existing hyperreactive airways may respond to a variety of nonspecific irritants in the workplace environment without sensitization to specific workplace agents. Buy asthma inhalers online to prevent asthma development.

The persistence of pulmonary complaints eventually led the worker to recognize an association between symptoms and job exposure. Despite the association between the workplace environment, all but one worker continued their employment before increasing symptom severity, or employer recognition resulted in a change of job. Continued TDI exposure after symptom onset could be important in the persistence of bronchial sensitization in the TDI reactors, but further longitudinal studies will be needed to demonstrate this in isocyanate workers. In another occupational disease, studies of Western Red Cedar workers have shown that persons with a delayed identification of cedar asthma, and hence, continued occupational exposure, were more likely to have persistent disease following their removal from the workplace.

The form of TDI exposure may be an important factor in the sensitization process and in the general prognosis. Our previous studies have indicated that workers with asthma or bronchitis symptoms were more likely to have past exposure to multiple isocyanate spills. In the current study, four workers with positive bronchial challenges to TDI reported exposure to TDI spills. Worker 6 was drenched with TDI following an industrial accident. This one and only exposure was followed by at least 12 years of respiratory symptoms. Three TDI reactors worked with polyurethane foam injection processes using TDI or other isocyanates. The development of their pulmonary disease may have occurred after unknowingly high exposure to TDI.

Workers in the present study were forced to leave their jobs because of progressive respiratory symptoms. This finding supports reports which indicate industries using isocyanates have a high turnover rate of employees. A survey of a plant using TDI in a polyurethane foam process found over 16 percent of workers reporting previous job transfers out of an isocyanate work area because of respiratory problems believed to be due to the job. Future epidemiologic studies which do not have identification and follow-up of persons leaving or transferring out of the isocyanate work area may miss affected individuals.

In summary, six reported cases of TDI asthma documented by TDI bronchial challenge testing represent a subset of isocyanate workers who experienced persistent disease associated with nonspecific bronchial hyperreactivity and isocyanate sensitization despite removal from occupational exposure. This suggests the prognosis in TDI asthma remains guarded in some workers. Long-term prospective studies of symptomatic isocyanate workers are needed in order to fully define the extent of this problem.

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Details about Chronic Asthma Due to Toluene Diisocyanate

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Output Concerning Chronic Asthma Due to Toluene Diisocyanate

In seven cases, TDI asthma was documented by a positive inhalation challenge to TDI (Table 1). Results of baseline pulmonary function tests were generally normal (FEV1 and FVC 80 percent predicted and FEV1/FVC 70 percent) or perhaps mildly decreased in the study population as follows: spirometric findings were normal in five of seven reactors and four of five nonreactors. One reactor had a FEV1 of 73 percent predicted (and FEV/FVC of 33 percent); the second reactor had FEV1 of 69 percent and FVC of 74 percent predicted. One nonreactor had FEV/FVC of 67 percent. Four of the seven workers demonstrated a dual asthmatic response, two had isolated late bron-chospastic responses, and another had an immediate bronchospastic response to TDI (Fig 1). The six patients with dual or late bronchospasm on TDI challenge testing had nonspecific bronchial hyperreactivity as shown by a positive methacholine challenge (five cases) or a positive cold air challenge (one case). The worker with an immediate asthmatic response to TDI had a negative methacholine challenge on three occasions before and after a positive TDI inhalation test.

The seven TDI reactors reported being exposed to TDI for one day to ten years (mean, 1.9 years) prior to the onset of their asthma symptoms. Four were exposed to TDI for less than four months before developing asthma cured successfully by advair. The subject with only one day of known TDI exposure was exposed to very high concentrations during a spill when a hose coupling became loose and drenched him with TDI. Three additional TDI reactors gave a history of past exposure to TDI spill?.

The TDI reactors with bronchial hyperreactivity had been removed from isocyanate exposure for intervals as long as 12 years (mean 4.5 years, Table 2). The six TDI reactors with bronchial hyperreactivity related persistent respiratory symptoms and required bronchodilator. therapy during the interval of absent occupational exposure to TDI. These six individuals had been exposed to TDI for periods ranging from six weeks to two years before symptom severity or management recognition resulted in a change of job with removal from exposure. The TDI reactor with an isolated immediate bronchospastic response to TDI was removed from the workplace one week prior to inhalation testing.

Five workers showed no significant bronchospasm to TDI inhalation challenges at either the low or high dose (Table. 3). These nonreactors had been exposed to TDI for intervals ranging from one month to 16 years (mean five years). The time from TDI exposure until bronchial inhalation challenge testing was 1.2 years (range one week to three years). One of them gave a history of past exposure to TDI spills. Methacholine challenges were positive in three of these five workers. Two of these TDI nonreactors with bronchial hyperreactivity had respiratory symptoms at the time of TDI challenge testing. One of them reported experiencing protracted coughing when exposed to multiple irritants. This worker had prominent coughing but no demonstrable bronchospasm in response to his TDI inhalation challenge test. Three of the five patients were asymptomatic and were not receiving any medication at the time of their negative result on TDI challenge test.

Eight of the 12 workers had serologic measurements of specific IgE to TDI-HSA, MDI-HSA, or HDI-HSA performed by RAST testing. No significant levels of specific IgE to isocyanate-protein conjugate were demonstrated in any of these workers.

Table 1—Clinical Summary of Seven Workers with Suspected TDI Asthma and Positive TDI Bronchoprovocation Test

WorkerNo. Age Job Form of TDI Exposure Past TDI Spill AtopicStatus PulmonaryFunctionTests MethacholineChallenge Type of Response to TDI Challenge 1 61 Structuralengineer Spraying polyurethane paint containing TDI Yes No FEV-73% predicted FEV/FVC 63% Positive Late 2 44 Assembly line worker Polyurethane foam seats, dashboards, steering wheels No No Normal Positive Immediate and late 3 31 Refrigeratorassembler Polyurethane foam injection process No No Normal Positive* Immediate and late 4 37 Millwright TDI spills, clean up Yes No FEVj 69% Positive Immediate and late 5 24 Refrigerator Polyurethane foam injection process Possible (dog, cat milk allergies) Normal Positive Late 6 58 Airconditionerworker TDI spill Yes No Normal Positive Immediate and late 7 43 Molder Polyurethane paint containing TDI No No Normal Negative Immediate

Table 2—Clinical Course of Workers with TDI Asthma Documented by a Positive Inhalation Challenge Test to TDI

Worker Interval of TDI Exposure Until Symptom Onset Interval of TDI Exposure While Symptomatic Persistent Asthma Symptoms after Removal from TDI Exposure DailyMedications Interval from Termination of TDI Exposure until TDI Challenge Test I 1 mo 6 wk Yes T* + pt 2.5 yr 2 2 wk 3 mo Yes T+p 2.5 yr 3 lyr 1 yr Yes P 8 yr 4 10 yr 2 yr Yes T+p 3 mo 5 2 yr 6 mo Yes T+p 2 yr 6 1 day 1 day Yes P 12 yr 7 4 mo 8 mo No No 1 wk

Table 3—Clinical Summary of Five Workers with Suspected TDI Asthma and Negative TDI Bronchoprovocation Test

WorkerNo. Age Job Form of TDI Exposure Past TDI Spill AtopicHx MethacholineChallengeResults PersistentAsthmaSymptoms* Time Period of TDI Exposure 8 35 Spray painter Polyacrylic paint No No Positive Yes 2 yr 9 28 Assembly line worker Polyurethane foam process Yes No Positive Yes 4 yr(intermittent) 10 56 Spray painter Polyurethane Paint No No Positive No 4 yr 11 18 General plant TDI spill cleanup Yes No Negative No 1 wk 12 58 Transporter Polyurethane foam No (Allergic rhinitis, nasal polyps] Negative) No Not known

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Details about Chronic Asthma Due to Toluene Diisocyanate

Toluene diisocyanate (TDI) is an important cause of occupational respiratory disease with approximately 5 percent of exposed workers developing occupational asthma in industries using TDI. There is uncertainty regarding the long-term prognosis of workers with TDI asthma once they are removed from isocyanate exposure. Recovery of asthma after removal from isocyanate exposure has been reported; however, there are reports documenting airway flow abnormalities for days to weeks after occupational exposure or bronchial challenge to TDI in sensitized individuals. Other clinical studies suggested respiratory symptoms following isocyanate exposure persist for extended periods, but TDI sensitivity was not documented in these cases by inhalation challenge testing. Since clinical history alone may be nondiscriminatory and no in vitro test has sufficient diagnostic sensitivity or specificity, controlled bronchial challenge testing remains the only way to confirm hypersensitivity to TDI. The present report reviews our experience with 12 isocyanate workers who had been removed from their occupational exposure to TDI and who were studied with a TDI inhalation challenge test. A retrospective review of the characteristics of these workers is presented in order to assess the course of their respiratory disease.

Methods and Subjects

Patients

Patients were referred to the Occupational Health Clinic for evaluation of possible TDI asthma over a five-year period from 1980 to 1985. In only 12 workers was the clinical and occupational history consistent with a diagnosis of occupational asthma due to TDI. Approximately 20 other subjects were evaluated, and the history was not consistent with a diagnosis of occupational asthma. Prevent asthma decline with ventolin. The 12 workers reported symptoms consistent with a diagnosis of TDI asthma including cough, shortness of breath, and wheezing which occurred for the first time while working with isocyanates. These symptoms worsened with continued TDI exposure and improved when the workers were completely removed from isocyanate exposure. Three workers reported significant nocturnal asthma symptoms; chest pain was a prominent symptom in one subject (4). The ages of these 12 workers ranged from 18 to 61 years and included ten men and two women. Three workers (4, 8, and 11) were current cigarette smokers; three subjects were past cigarette smokers (1, 4, and 6). There was no personal nor family history of asthma, hayfever, or other allergies prior to the onset of symptoms in ten of the 12 subjects.

Exposure to TDI was substantiated through their employers records. The workers held a wide variety of jobs which required different levels of skills, education, and training, but their exposure to TDI could be classified into three categories. Five individuals performed assembly line work with exposure to TDI used in a polyurethane foam injection process. Four workers were involved in spray painting polyurethane paints containing TDI, and three workers were exposed to TDI spills, often as a member of the cleanup crew.

Eight of these 12 workers reported persistent respiratory symptoms which required daily β-agonist bronchodilators and/or aminophylline despite leaving their occupational exposure to isocyanates. In several cases, intermittent steroids were used for past management of acute asthma during the course of their respiratory disease. No subject was receiving corticosteroids at the time of evaluation nor at any time up to four weeks before admission to the hospital. Buy asthma inhalers to get rid of asthma symptoms (for example: Advair Inhaler, Flovent Inhaler or Ventolin Inhalers)

On their initial evaluation, each worker received a physical examination, pulmonary function tests, and phlebotomy for determination of serum specific IgE to various isocyanate-protein conjugates. Three persons had evidence of mild airway obstruction, and one subject had moderate airway obstruction on their initial spirometric evaluation. The remaining individuals had normal pulmonary function test results when first seen in our clinic.

All patients were admitted to the University of Cincinnati General Clinical Research Center. Informed consent was obtained from each. The following protocol was used: day 1, history and physical exam, methacholine challenge; day 2, saline aerosol control challenge; day 3, low dose TDI challenge (10 ppb, 10 minutes); day 4, high dose TDI challenge (20 ppb, 20 minutes); and day 5, discharge. All medications not needed by the subjects were discontinued 48 hours prior to the TDI challenges. Inhaled isoetharine or metaproterenol was used if needed for control of respiratory symptoms. Theophylline and corticosteroids were not used on the bronchial challenge days unless needed to treat significant bronchospasm.

Pulmonary Function Tests

Pulmonary function tests were performed according to criteria established by the American Thoracic Society using a precalibrated Ohio Medical Company dry-rolling spirometer connected to a microprocessor. Measurement of FEV1, FVC, and flow rates were made in triplicate. The best value was chosen for analysis.

Inhalation Challenge to TDI

Inhalation challenge studies to TDI were performed using a specially designed inhalation facility for this purpose. The TDI vapors were generated by passing dry filtered air over the liquid surface of 99.6 percent 2,4-TDI. The TDI air stream leaving the generation system was diluted with another source of fresh filtered air at the chamber inlet. Different concentrations of TDI were generated by adjusting the various airflow rates. The air TDI-mixture passed into a 271 L inhalation chamber through which the patient breathed via a mouthpiece attached to the chamber. The concentration of TDI at a port next to the mouthpiece was continuously monitored by a rapid reading isocyanate recorder during and following TDI inhalation challenges. Periodic verification of TDI levels were made using the Marcali method. Serial pulmonary function tests were performed throughout day 2,3, and 4 of the study at time 10, 20, 30, 40, 60 minutes, hourly for six hours, and at 12 and 24 hours following the inhalation challenges. A positive challenge test was defined as a 20 percent fall in FEV1. No further testing was performed following a positive response to the low dose TDI challenge.

Bronchial Challenge to Detect Airways Hyperreactivity

In the majority of subjects, methacholine challenge tests were performed using a Collison nebulizer which delivered 11.94 μg methacholine per second (airflow rate 12.5 L/minute at 26 PSI; aerosol mass median aerodynamic diameter 1.10 μl with geometric standard deviation of 2.20 μ. The cumulative inspiratory time was measured using a Fairchild pressure sensor in combination with a Lafayette stop clock. Cumulative inspiratory dose of methacholine (in micrograms) delivered to the respiratory system was calculated from the cumulative inspiratory time and the known rate of methacholine delivery. The rate of breathing was controlled by coaching the patients to inspire for 5 to 6 seconds for each breath. The aerosol was inhaled via a disposable mouthpiece connected to a one-way Hans Rudolph valve.

Following baseline spirometry, the patient was given a 30-second isotonic saline challenge followed by repeat spirometry two minutes after challenge. Providing there is no reaction to saline, the first dose of methacholine is then given (usually 100 to 200 μg) followed by pulmonary function tests two minutes after exposure. A test is considered positive when there is a 20 percent or greater fall in FEV1s otherwise additional methacholine is administered until a total cumulative dose of 2,000 μg is given. Hie provocative dose corresponding to a 20 percent fall in FEV1 (PD,) is calculated by performing a linear regression of the log transformation of dose vs percentage fall in FEV1( Experience in our laboratory has shown that nearly all asthmatic patients respond to less than 2,000 μg methacholine using our generation system. Similar results have been reported by other investigators. In two subjects, a different method was employed. Five inhalations of increasing doses (2 mg/ml-25 mg/ ml) of methacholine were used until a 20 percent fall in FEV1 was reached.

A cold air challenge to assess the degree of nonspecific airway reactivity was performed in one subject according to a reported protocol. Briefly, a patient undergoes eucapnic hyperventilation with cold air (—40°C) for six minutes. A positive cold air challenge is defined as a 9 percent decrease in FEV1 when measured five and ten minutes postchallenge compared to a prechallenge FEVj measurement.

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Start Asthma Treatment With Ventolin Inhalers

Possible Causes for Differences

There are many factors which could explain the large differences in the views on chronic treatment between European specialists:

1. Uneven sampling of physicians for the survey and different response rates.

This factor cannot be ruled out, but it is rather unlikely to greatly influence the responses because patterns within countries are consistent and they are for seven countries at least, nearly identical to those of the 1983 pilot survey.

2. Differences in the clinical features of asthma. Although there are no large scale comparative data, minor differences are quite likely. The prevalence of allergy may also be different, eg, in northern versus southern Europe, and this could affect the use of anti-allergic treatments. It is hard to believe that this could account for the differences in answers because divergent attitudes may be found between neighboring countries where asthma should have similar clinical features.

3. Differences in definition and diagnosis of asthma. No doubt this could be an important factor. What is called asthma in some countries may be called chronic (asthmatic) bronchitis in other countries and therefore may be treated somewhat differently. Furthermore, there may be a variable emphasis on allergic features of asthma. It is hard to believe this could account for all the differences. The asthma ventolin inhalers are the best ways of asthma treatment and arrest your attacks.

4. Differences in drug availability, dosage and promotion.

National health and drug registration policies could have serious effects on this factor and it surely influences responses. There are many examples of this within Europe, eg, oral ketotifen is hardly available in Scandinavia, metered-dose inhalers were until recently not reimbursed by Social Security in the Netherlands, and powdered inhalers and spacers are virtually not available in Belgium and several other countries.

5. Different impact of clinical pharmacology.

The standards and the impact of clinical pharmacology seem higher in Great Britain and Scandinavia. Chest physicians there could be expected to rely more heavily on high quality studies showing that apprehension towards instituting a properly dosed preventive therapy with inhaled broncho-dilators and steroids are unjustified.

6. Language of teaching and medical reading.

This may be the most important factor accounting for the differences within Europe. It is clear that French specialists have little contact with the English literature and vice versa: the largest differences were found between British and French specialists! Portuguese physicians are usually geared to French medicine and have indeed given comparable answers. In a similar survey conducted among 23 Tunisian chest specialists, their answers were also in the same line as those of their French colleagues. We are now also able to add some evidence from a survey among 325 Belgian general practitioners. Their answers, as well as those of 39 Belgian adult specialists, have been separated according to their language, and they were compared with those of Dutch and French specialists. Table 6 illustrates, for two important issues, the impact of the language factor in Belgium. Except for desensitization in children, all differences between both language groups of specialists and general practitioners are significant and their respective answers are much closer to those of their language colleagues of the neighboring countries. Language indeed seems the only factor which could explain such differences in a small country like Belgium.

Conclusions

The 1984 European Audit on Asthma Diagnosis and Treatment has confirmed that adult specialists (and probably all groups of physicians involved) on our continent have large and interesting differences in their views on how to treat the chronic stage of this disease. The main contrast is between Britain and Scandinavia favoring inhaled beta-agonists and corticosteroids and, on the other hand, France, Portugal and some other countries of central and southern Europe emphasizing the use of oral theophylline as well as desensitization for allergic asthma. The reliance on preventive inhaled therapy also leads to the use of high usual and maximal doses of metered-dose aerosols. All other countries take intermediate positions. An attempt to confirm these trends could be made by evaluating objective data on drug sales in all involved countries.

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Ventolin Inhaler - Inhaler for Treatment Asthma

All subjects studied had clinically stable mild asthma (Table 1). For the group, SRaw was 3.5±0.1 L-cm H2O/L*s-1 (mean±SE), and PC^His was 0.84±1.23 mg/ml. Prior to the day when the allergen was inhaled, the histamine dose-response curves obtained on separate days were quite similar (Fig 1). Bronchial challenge with physiologic saline solution did not affect either SRaw or histamine reactivity in any individual. The Δ log PC200 His before allergen for the group was —0.07±0.04.

On the day of ventolin inhalers of allergen, SRaw was similar to that measured inititally in all cases (Fig 1). Inhalation of bluegrass antigen produced an immediate asthmatic response in each subject. The mean fall in FEV1 for the group was 28 percent (the range was between 20 and 36 percent). Histamine challenges after the allergen were done when the FEVi and SRaw had returned to within 6 percent of the values before allergen; this took between 45 and 105 minutes in the subjects tested. Immediately following resolution of the immediate asthmatic response, the PC^His was lower in each individual (Fig 1). The mean PC200 His for the group at this time was 0.29 ± 1.42 mg/ml. The Δ log PC200 His immediately after the immediate asthmatic response for the group was 0.49±0.09, which was significantly different (p<0.01) from that determined prior to allergenic challenge (Fig 2). A late asthmatic response marked by bronchospasm occurred seven or more hours after the allergen in each individual and was severe enough to significantly affect peak expiratory flows.

Measurements of SRaw and PC^His performed seven or more days following inhalation of allergen were quite similar to those values determined before allergen in all cases (Fig 1). (Subjects 4, 5, and 6 were reassessed on the seventh day, subjects 1 and 7 on the ninth day, subject 3 on the 12th day, and subject 2 on the 14th day. The PC200 His for the group at this time was 0.84 ±1.23 mg/ml, and the Δ log PC200 His then was 0.02 ±0.03 (Fig 2). The most spread preparation for asthma is ventolin inhalers which may be ordered via http://buy-asthma-inhalers-online.com/.

Discussion

In this study, we found that bronchial reactivity to histamine was substantially increased immediately after resolution of the immediate asthmatic response in dual-responding bluegrass-allergic subjects. This increased reactivity occurred presumably at the peak of their recovery when their FEV1 had returned to baseline values. Seven or more days after allergen, reactivity in each subject had reverted to its initial level, suggesting that the early increase in airway responsiveness that we observed after antigen was a result of this exposure. The close similarity in histamine dose-response curves before and seven or more days after allergen may be ascribable to the mild and relatively stable asthmatic status of the subjects studied, and possibly to the testing technique we employed.

To our knowledge, airway reactivity status in man has not been previously examined immediately after resolution of antigen-induced immediate asthmatic responses. Past clinical studies have documented the increase in bronchial responsiveness that occurs six to eight hours after challenge and in relation to the late asthmatic response. Based upon these studies, it is thought that an allergen-induced increase in bronchial responsiveness is associated with the late response, but not with the immediate one. Furthermore, some investigators believe that the development of increased bronchial reactivity after allergen is causally related to the late asthmatic response. This response may require many hours to occur, as may the possibly analogous late allergic reaction that occurs in human skin.

There have been studies in animals which may pertain to our observations. In ovalbumin-sensitized guinea pigs, an enhancement in airway responsiveness to aerosol acetylcholine or histamine was found immediately following recovery from the initial broncho-spasm. In basenji-greyhound dogs sensitized to As-caris antigen, investigators have found muscarinic hyperreactivity 30 minutes after Ascaris antigen aerosol challenge. Furthermore, it has been shown that Ascaris-sensitive monkeys develop histamine hyperreactivity one hour after allergen-induced broncho-constriction. These data strongly suggest that mechanisms may develop soon after inhalation of antigen which potentiate airway reactivity. The factors at play, especially the possible mediators involved, have not been fully evaluated as yet in these experimental situations.

To date, the specific mediators linked with the immediate and late asthmatic responses in man have not been directly measured in vivo, although those associated with ragweed-induced rhinitis have been. Information derived from studies in vitro of allergen-sensitized human pulmonary tissue may provide insights. It is known that antigenic challenge of sensitized human bronchi results in the formation of a number of cyclooxygenase metabolites of arachidonic acid.- Furthermore, it appears that antigen-induced bronchospasm in vitro involves histamine and slow-reacting substance of anaphylaxis (SRS-A). SRS-A has been shown to consist of leukotrienes C4, D4, and E4, which are themselves potent bronchoconstrictors and which may also potentiate the responsiveness of airway muscle to other agonists such as histamine both in vivo15 and in vitro. Adams and colleagues have shown that lipoxygenase antagonists markedly inhibit the response of sensitized human airways to antigen. Although the release of SRS-A from airway tissue has not been directly measured by these investigators, their observations that indomethacin potentiated what they termed the “late phase” of antigen-induced bron-choconstriction is consistent with the possibility that SRS-A is generated upon exposure to antigen. This “late phase” reaction in vitro occurs within 20 minutes of exposure.

Linked with these observations, our findings lead us to the speculation that mediators may be elaborated in man during, or very soon after an allergen-induced immediate asthmatic response, that potentiate bronchial reactivity at that time. Whether these mediators and the early increase in airway reactivity that results are determinants o£ or share common characteristics with the late asthmatic response remains to be fully investigated.

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Allergy and Asthma Treated by Ventolin Inhaler

Asthma, particularly in the young, is a disease associated with an underlying atopic allergic hypersensitivity to one or more allergens. Atopic allergic sensitization is defined by production of IgE against environmental antigens such as proteins from house dust mites (HDMs), grass pollens, animal dander, insects, and foods. Allergic sensitization can lead to a variety of clinical manifestations including asthma, rhinitis, and atopic dermatitis. Allergic sensitization to common allergens can be detected in > 25% of the population of some industrialized nations,3 and the prevalence of allergic disease has increased markedly within the last 50 years. While atopy and the development of allergic diseases are associated with multiple susceptibility genes, it is clear that there has been no substantial change in the human genome in the last 50 years. It follows, therefore, that environmental factors contribute significantly to the recent increases in disease prevalence. Moreover, similar dramatic trends have been observed in autoimmune diseases such as type I diabetes and multiple sclerosis.4 Epidemiologic observations linking prevalence of allergic sensitization with birth order together with numerous subsequent studies investigating the influence of environmental stimuli on the allergic diathesis have lead to the development of the “hygiene hypothesis.” The central canon of the hypothesis is that reductions in exposure to infectious disease and microbial products (through the introduction of vaccines, antibiotics, and improved sanitation) in recent decades has resulted in deficient immune regulation resulting in hypersensitivity in both the T-helper type 1 (Th1) and T-helper type 2 (Th2) compartments.

In addition to the humoral IgE component, allergic immune responses are characterized by Th2 T cells specific for the allergen, and the production of Th2 cytokines (interleukin [IL]-4, IL-5, IL-9, IL-13, and others) and Th2-associated chemokines (thymus and activation-regulated chemokine [TARC], monocyte-derived chemokine [MDC]). IL-4 and IL-13 act as Ige heavy chain isotype switch factors leading to the production of IgE. IL-4, IL-5, and IL-9 enhance the survival of eosinophils and their progenitors and prime these cells for activation and chemotaxis. IL-9 is a growth factor for mast cells, and IL-13 has been associated with goblet-cell hyperplasia, mucus hypersecretion, and airway hyperresponsiveness (AHR). TARC and MDC recruit Th2 T cells to sites of allergic inflammation. Whether existing Th2 T cells are required to initiate IgE responses, or whether the presence of allergen-specific IgE is required to generate allergen-specific Th2 responses remain unresolved. The key element in asthma treatment is Ventolin for Asthma.

The acute or early phase of allergic inflammation is initiated when the allergen comes into contact with IgE-primed mast cells/basophils. Cross-linking of allergen-specific IgE on the surface of mast cells and basophils leads to the release of mediators including substantial quantities of Th2 cytokines. Mast cell/ basophil activation therefore may be sufficient to create the Th2 cytokine milieu that drives Th2 T-cell differentiation and expansion. Expression of IgE receptors on antigen presenting cells (eg, dendritic cells [DCs] and monocytes) allows these cells to capture allergen in a specific fashion through surface-bound IgE.6 The same is true of allergen-specific B cells that express specific membrane Ig. Facilitated antigen presentation of this kind promotes Th2 T-cell differentiation and activation and contributes to dysregulated immune responses to allergen. Thus, allergen-specific IgE amplifies allergen-specific Th2 responses and vice versa. Activation of mast cells/basophils results in the release of mediators such as histamine and leukotrienes that cause bronchoconstriction and airway narrowing through mechanisms that include elements of smooth-muscle constriction and edema.

The late phase of the allergic reaction is characterized by recruitment of activated CD4+ Th2 T cells and eosinophils to sites of allergen exposure. Release of Th2 cytokines (particularly IL-5) from T cells (and mast cells/basophils in the early phase response) leads to the mobilization of bone marrow eosinophils and their progenitors. Local eosinophil recruitment occurs under the influence of chemo-kines such as eotaxin released from structural cells at the site of allergen exposure. Eosinophils are believed to be important effector cells in the late asthmatic reaction (the late-phase allergic response in the airways of asthmatic individuals), causing epithelial cell damage through release of toxic granule proteins, bronchoconstriction through leukotri-ene production, and contributing to AHR.7 However, clinical studies’9 with neutralizing monoclonal antibodies to IL-5 showed no effect on airway function despite marked reduction in numbers of circulating eosinophils. Activation of allergen-specific Th2 T cells with synthetic peptides representing the immunodominant T-cell epitopes of an allergen can lead directly to symptoms of asthma and increased AHR in the absence of the mast cell/basophil component.”11 This relatively recent observation suggests that airway narrowing can occur through both early and late-phase allergic mechanisms, both of which are linked directly and indirectly to allergen-specific T cells and allergen-specific IgE.

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Asthmatic Subjects Treated by Ventolin Inhalers

In this study, we found elevated MMP-9 activity and TIMP-1 expression in asthmatic patients who had a history of AMH that was confirmed at bronchoscopy or severe asthma, compared to healthy subjects and patients who had mild/moderate asthma. There were no differences in MMP-9/TIMP-1 ratios among groups. The clinical parameters of the AMH group were similar to those of the severe asthma group with the presence of frequent symptoms, comparable lung function, and high inhaled corticosteroid requirements. Thus, this subgroup of asthmatic patients that has evidence of AMH, with copious amounts of mucus present in the large airways seen bronchoscopically, may represent part of the spectrum of severe asthma.

Chronic mucus hypersecretion is a well-recognized pathology in patients who have COPD, in whom it has been found to be associated with exacerbations. In asthma patients, mucus hypersecretion is well-recognized as an important component of the pathogenesis of acute attacks, during which it is thought to cause further narrowing by causing physical obstruction of airways that are already inflamed and narrowed by bronchoconstriction. An increase in the number of goblet cells has also been found in postmortem studies of asthmatic subjects. Lange et al reported that AMH, defined by self-reported production of phlegm during at least 3 months per year for at least two consecutive years, was present in 63% of men and 54% of women who had asthma. More importantly, it has also been associated with a greater decline in lung function in asthmatic patients, regardless of smoking history and initial FEV1 values.

The association between mucus hypersecretion and faster decline in lung function in asthma suggests that there might be more airway inflammation and remodeling. Hence, there may also be greater MMP-9 activity given its association with eosinophilic and neutrophilic inflammation, and its potential role in tissue remodeling by degrading elastin, collagen, and proteoglycan. In two published studies of bronchial biopsies, immunohistochemical staining for MMP-9 was colocalized with neutro-phils and eosinophils, although there were no differences between asthmatic subjects, either treated with steroids or untreated, compared with healthy subjects. The activity of MMP-9 in the airway secretions of patients who have AMH has not been reported previously. The best opportunity to give up asthma is ventolin inhalers which may be bought using the link – buy-asthma-inhalers-online.

We defined mucus hypersecretion as the clear-cut presence of increased mucus in the airways causing airway obstruction, independently of asthma severity and of a history of chronic cough productive of phlegm. This was based on the “bronchitis index,” which was validated as a way of describing the severity of bronchitis seen during bronchoscopy. It is a four-component index that includes the presence of mucus in the airways, with airway occlusion being classified as the highest grade. Although we cannot be completely sure that mucous plugging was chronic, we think it is highly likely since we ensured that all patients were clinically stable (ie, they did not have symptoms of a recent respiratory tract infection), and seven of the eight patients reported having chronic cough and sputum production. If we had defined AMH by both history and bronchoscopic appearance, one patient would be reclassified as having mild/moderate asthma; however, this only increased the differences between the AMH and severe asthma groups, compared with the mild asthma group. We also found a high proportion of subjects who had severe asthma and also had a history of chronic productive cough but no mucous plugging seen at bronchoscopy. This may have been due to selection bias, with patients having chronic cough being more likely to respond to recruiting advertisements and more likely to agree to undergo bronchoscopy. These patients could have had intermittent mucous plugging.

The asthmatic subjects who had mucus hypersecretion had copious amount of sputum in the airways at bronchoscopy. Although it is not possible to determine how much this abnormal mucus secretion contributed to the spirometric abnormality, it was likely that it played a significant role not only by causing physical blockage, but also by increasing surface tension, thereby favoring airway closure during forced expiratory maneuvers. Furthermore, the presence of increased amounts of mucus in the bronchial tree may also impede the deposition of inhaled drugs to the inflamed airways, suggesting that better clearance of secretions might help to improve asthma treatment. AMH might represent a variation of the disease, and, although its causes are unclear, it might include the up-regulation of the T-helper type 2 cytokines interleukin (IL)-4, IL-5, IL-9, and IL-13, which have been implicated in increasing mucus secretion.

Our findings that MMP-9 activity and TIMP-1 expression are increased in the BALF of subjects who had severe asthma compared to healthy subjects and patients with mild/moderate asthma are in accordance with the findings of previous stud-ies.’’ Lemjabbar and colleagues found a 10-fold to 160-fold increase in MMP-9 activity in BALF in patients receiving mechanical ventilation for the treatment of acute severe asthma over that of nonasthmatic subjects. Mattos et al also demonstrated increased MMP-9 activity in the induced sputum of patients who had severe asthma compared with patients who had mild asthma and healthy subjects, although levels of MMP-9 in BALF was not different. Patients who had nocturnal asthma had a fourfold circadian increase in levels of MMP-9 in BALF compared with healthy subjects and asthmatic patients who did not have nocturnal asthma. Interestingly, the investigators observed that these differences in MMP-9 expression disappeared when MMP-9 activity was determined in the afternoon. This observation would indicate that the amount of MMP-9 found in the BALF of asthma patients correlates with the infiltration of inflammatory cells in the lung and therefore most probably is produced by such cell types rather than by resident lung cells.

In regard to the possible source of MMP-9 activity in the BALF of patients who have severe asthma or AMH, we found an increase in the percentage of neutrophils in these subjects, who also had high levels of MMP-9 activity despite receiving high doses of inhaled corticosteroids. This suggests that severe asthma is associated with a persistent airway neutrophilia that is poorly responsive to ventolin inhalers treatment. This then provides an ongoing source of MMP-9 and is consistent with previous findings of the poor response of MMP-9 activity to steroid treatment in patients with severe asthma. Neutrophils therefore could play a significant role in severe asthma and also in the inflammation associated with AMH. Thus, neutrophils might be important in asthmatic remodeling given the known presence of MMP-9 in neutrophils and our findings of an association between MMP-9 and the percentage of neutrophils. Interestingly, Corbel at al, in a murine model of asthma, also found that MMP-9 activity measured in BALF increased as the duration of repeated ovalbumin challenges progressed and that this was also correlated with the number of neutrophils in the BALF. This is analogous to chronic allergen exposure, which has also been shown to increase MMP-9 activity in the BALF of asthmatic subjects.

Our severity score was based on our national guidelines, which, like the Global Strategy for Asthma Management and Prevention guidelines, do not include the dose of inhaled steroids being administered. This explains why the doses of inhaled steroids were comparable between the different asthma groups, which perhaps suggests the limitations of such “clinical severity” scores such that they could be considered more appropriately to be measures of asthma control rather than severity.

As metalloproteinase inhibitors are now available for clinical trials in the treatment of diseases like osteoarthritis and rheumatoid arthritis, MMPs may be a target for novel therapy in asthma patients, Mechanical obstruction may play a role in AMH by decreasing mucociliary clearance, by trapping the inflammatory mediators with resulting persistent inflammation, and possibly by preventing the penetration of antiinflammatory medications.

We did not observe any differences among groups in our study in regard to the serum levels of MMP-9 or TIMP-1, suggesting that the increases in MMP-9 activity and TIMP-1 expression are restricted to the inflamed area of the lung. However, other groups have reported’ increased serum levels of MMP-9 in patients presenting with asthma exacerbations, although there are no published data of any increase in MMP-9 level in the blood of subjects who have severe but clinically stable asthma.

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Differential Flow Analysis of Exhaled Nitric Oxide in Patients With Asthma of Differing Severity: Introduction

Asthma is a complex, chronic inflammatory lung disease that is characterized by a specific pattern of airway inflammation airway smooth-muscle hypertrophy and hyperplasia and production of mucus.

The pathophysiology of asthma has traditionally been attributed to an inflammatory process that occurs predominantly in the large airways.

Pathology studies in patients who have died of asthma reveal extensive involvement of the peripheral airways with inflammatory and structural changes, with luminal occlusion with viscid mucus plugs. Transbronchial biopsies have confirmed peripheral airway involvement in severe asthma including the alveoli. On the basis of the physiologic and pathologic evidence, small or peripheral airways and lung parenchyma are clearly implicated in the pathogenesis of asthma, and this aspect seems to be an important feature of patients with asthma and has important implications for drug delivery.