PubMed Health⌕ Search

PubMed · 16607486

[Therapy-resistant asthma--a distinct phenotype?].

Abstract

While most patients respond well to conventional antiasthmatic therapy as outlined in current guidelines, a small percentage, however, have severe disease which is relatively or completely unresponsive to inhaled as well as oral medications. These patients who often have a long-standing "career" in asthma are frequently labeled steroid-resistant or difficult-to-control but this group of patients is not well defined. It is likely that a number of mechanisms contribute to therapy-resistant asthma such as socioeconomic status, mental disturbances but also characteristics of the individual subgroups within the syndrome of asthma such as aspirin-exacerbated airway disease or intrinsic asthma. A thorough and systematic approach is required in the work-up of these patients which sometimes involves repeated evaluations to determine that asthma and not other diseases such as chronic obstructive pulmonary disease (COPD), emphysema, gastroesophageal reflux, congestive heart failure and many others which can mimic asthma are present. Issues relating to compliance with prior or future therapies are warranted and doctor-patient communication should be checked. A meticulous search for possible triggers such as cigarette smoking, occupational allergens and comorbid conditions should be included in the work-up. High-dose combination therapy including frequent bursts or maintenance therapy with systemic corticosteroids is often necessary. Alternative therapies such as methotrexate and other immunosuppressants should be avoided based on current data but recent evidence from controlled studies suggests that anti-IgE or anti-tumor necrosis factor-(TNF-)alpha strategies might be of benefit in these patients. There is data that different phenotypes of therapy-resistant asthma might exist but little if any evidence to suggest a single phenotype of therapy-resistant asthma.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Christian Virchow. 2006-04-15. [Therapy-resistant asthma--a distinct phenotype?].. https://doi.org/10.1007/s00063-006-1038-4

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Rituximab for treatment of opsoclonus-myoclonus syndrome in neuroblastoma.

Opsoclonus-myoclonus syndrome (OMS) is a rare paraneoplastic syndrome that occurs in 2%-3% of patients with neuroblastoma. The cause of this syndrome is believed to be immune mediated, but the exact mechanism still remains unclear. There is an urgent need to improve our current strategies for treating patients with OMS, as many patients have significant long-term neurologic deficits and behavior disorders with current treatment approaches. Therapies that have shown to improve symptoms in these patients have ranged from ACTH and corticosteroids, to intravenous gammaglobulin and plasmapheresis. We report our experience with Rituximab in a patient with neuroblastoma and OMS.

Adrenal Cortex Hormones↗

Cyclosporine sparing with mycophenolate mofetil, daclizumab and corticosteroids in renal allograft recipients: the CAESAR Study.

Although the calcineurin inhibitors (CNI) cyclosporine (CsA) and tacrolimus are highly effective immunosuppressants, they are associated with serious side effects. There is great interest in immunosuppressive regimens that permit reduction or elimination of CNIs, while maintaining adequate immunosuppression and acceptable acute rejection rates. Patients (n = 536) receiving their first renal allograft were randomized to one of three immunosuppressant regimens: daclizumab, mycophenolate mofetil (MMF), corticosteroids (CS) and low-dose CsA (target trough levels of 50-100 ng/mL), weaned from month 4 and withdrawn by month 6; daclizumab, MMF, CS and low-dose CsA; or MMF, CS and standard-dose CsA. Mean GFR 12 months after transplantation (primary end point) was not statistically different in the CsA withdrawal and low-dose CsA groups (both 50.9 mL/min/1.73 m(2)) vs. the standard-dose CsA group (48.6 mL/min/1.73 m(2)). At 12 months, the incidence of biopsy-proven acute rejection was significantly higher in the CsA withdrawal group (38%) vs. the low- or standard-dose CsA groups (25.4% and 27.5%, respectively; p < 0.05). In summary, a regimen of continuous low-dose CsA with MMF, CS and daclizumab induction is a clinically safe and effective immunosuppressive regimen in renal transplant recipients.

Adrenal Cortex Hormones↗