Hi Glogs. I’m no expert, so maybe others have different experiences, but I’m familiar with steroid injections for acute asthma attacks and that slow release steroid injections are not the general course of treatment. One of our experts did write this article about corticosteroid injections and the fact that they can sting quite a bit: https:///living/steroid-injections-a-pain-in-the-butt/ . Hopefully others will have some input or ideas on better tolerating the oral steroids. The new specialist may also have have some alternative treatment recommendations. Please keep us posted on how things go. Best, Richard ( Team)
Family history is a risk factor for asthma, with many different genes being implicated.  If one identical twin is affected, the probability of the other having the disease is approximately 25%.  By the end of 2005, 25 genes had been associated with asthma in six or more separate populations, including GSTM1 , IL10 , CTLA-4 , SPINK5 , LTC4S , IL4R and ADAM33 , among others.  Many of these genes are related to the immune system or modulating inflammation. Even among this list of genes supported by highly replicated studies, results have not been consistent among all populations tested.  In 2006 over 100 genes were associated with asthma in one genetic association study alone;  more continue to be found. 
A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, . unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug.  Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE -mediated urticarial skin eruptions, angioedema , and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2) Comparatively mild to moderately severe T cell -mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rash , fixed drug eruptions , photosensitivity reactions , delayed urticaria , and contact dermatitis ; or 3) far more severe and potentially life-threatening t-cell-mediated delayed systemic reactions such as the DRESS syndrome , acute generalized exanthematous pustulosis , the Stevens–Johnson syndrome , and toxic epidermal necrolysis . Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1) exacerbations of asthmatic and rhinitis (see aspirin-induced asthma ) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema.