Several clinical studies have demonstrated omalizumab effectiveness in patients with severe allergic asthma but the treatment period has always been relatively short (4-12 months). Only a few data is present for long-term omalizumab therapy. We aimed to assess the long-term clinical and functional effectiveness of omalizumab treatment in severe allergic asthmatic patients.

Methods: Medical records describing the patients' status starting before treatment and also having been registered at the end of 4th, 12th and 36th months from the commencement of treatment and at the last visit where the patient was evaluated were used for omalizumab effectiveness assessments. Twenty-six patients (female/male: 21/5) with severe allergic asthma, uncontrolled despite GINA 2006 Step 4 therapy, were included in the study. Effectiveness outcomes included spirometry measurements, level of asthma control measured by asthma control test (ACT), systemic glucocorticosteroid (sGCS) use, emergency room (ER) visits and hospitalizations for severe exacerbations. In addition, quality of life was assessed using the quality of life questionnaire AQLQ(S) before and 4 and 36 months after treatment.

Results: The mean age was 47.6±13.9 and duration of allergic asthma 22.7±10.1 years. Serum total IgE levels were 322.0±178.1 IU/mL. Mean duration of omalizumab treatment was 40.81±8.2 months. FEV1 improved significantly at all control points versus baseline (p<0.05). The level of asthma control as evaluated by ACT improved significantly after treatment (p<0.05). We determined significantly reduced numbers of exacerbation, emergency visits, hospitalizations, sGCS and SABA use by the end of 36 months (p<0.05). The proportion of patients with improvements larger than 1.5 points in AQLQ(S) total score was 80.7% at the 4th month and 96.1% at the 36th month of treatment.

Conclusions: This study showed that long-term therapy with omalizumab for up to 3 years was well tolerated with significant improvement both in symptoms and lung functions. Accordingly, long-term omalizumab treatment may be recommended for responders.

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Recent research suggests that asthma may originate through defects in the airways epithelium, acquired in utero, and an altered response to infections after birth. Here we examine whether asthma in adult life is associated with reduced body size at birth, and poor living conditions in childhood.

METHODS: We studied 658 people taking medication for asthma in a cohort of 13345 men and women born in Helsinki, Finland during 1934-44. Their body and placental size at birth, and their living conditions and growth in childhood, had beenrecorded.

RESULTS: The odds ratios for asthma was 0.93 (95% CI 0.89-0.97, p=0.001) per cm increase in birth length, and 0.92 (0.89-0.96, p<0.001) per cm increase in the length of placental surface. After allowing for size at birth, growth during childhood was unrelated to asthma. People who were born into families of low socio-economic status were at increased risk of later asthma.

CONCLUSIONS: Slow linear growth in utero, which could be a result of impaired placentation, increases the risk of later asthma. Slow linear growth may be associated with impaired development of the airways. Babies with impaired lung development born into families of low socio-economic status may be most vulnerable to the disease. This article is protected by copyright. All rights reserved.

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Chronic obstructive pulmonary disease (COPD) may cause some psychiatric disorders such as depression and anxiety, similar to other chronic diseases. Treatment adherence may be affected by worsening of cognitive functions.

We aimed to show whether the symptoms of anxiety and depression affect treatment adherence by patients.

Method Seventy-eight COPD patients were analysed at the first visit. The use of bronchodilator therapy was revised for standardization before they attended a second visit after six months. Hospital Anxiety and Depression Scale (HADS), Anxiety Sensitivity Index-3 (ASI-3) and SF-36 Questionnaire were carried out at that visit. 'National Guide of Turkish Thoracic Society for Asthma' was used for scoring method of use of the bronchodilator and evaluating treatment adherence (including maintenance therapy).

RESULTS: Sixty-two of 78 patients, 53 (85.5%) men and nine (14.5%) women with a mean age of 64.9 ± 9.9 joined the second visit. Thirty-three patients (53.2%) had a high-treatment adherence (HTA), whereas 29 (46.8%) had a low-treatment adherence (LTA). There were high scores of anxiety in 18 (29%) and depression in 11 (17.7%) patients. There was no statistical difference between the HTA and LTA groups in means of age, gender, educational level, presence of comorbidity, classification of COPD, high anxiety scores according to HADS and ASI-3 scores. Of the patients, 41.4% in the LTA group were still smoking, whereas it was only 12.1% in the HTA group (P = 0.009). The LTA group had higher depression scores (P = 0.004) than the HTA group. Dyspnea was found more frequent in LTA patients (P = 0.047); vitality score was also statistically low in this group (P = 0.01).

CONCLUSION: As a result, continuing smoking and the presence of depression symptoms may decrease adherence to treatment. Therefore, to increase the adherence to treatment and reduce symptoms such as dyspnea, it is important to treat any depressive symptoms that are present and to help patients cease smoking.

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The innate lymphoid cell (ILC) family has recently expanded with the discovery of type-2 innate lymphoid cells (ILC2). These cells arise from lymphoid progenitors in the bone marrow and, under the control of the transcriptional regulators RORα and Gata3, they mature to give rise to IL-5, IL-9 and IL-13 producing ILC2. These cells are critical components of the innate immune response to parasitic worm infections and have also been implicated in the pathogenesis of asthma and allergy.

Recent advances in our understanding of the molecular regulation of ILC2 development and function now present the opportunity to develop new genetic models to assess ILC2 immune function and to investigate possible therapeutic interventions.

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