Those who have been keeping abreast of my recent original blog posts, will be aware that the beginning of 2019 has been decidedly mixed. Readers may also be aware that the Yuletide and New Year period were marred somewhat, by a flare of my own autoimmune disease. I carry Human Leukocyte Antigen B27 (which for the sake of brevity will henceforth be referred to as HLA-B27).
This antigen is not contagious but it is a genetic mutation that can remain inactive for many years. The genetic code that may trigger the development of HLA-B27 is found in only 8% of white Europeans and 4% of North Africans. It is even less common in those of Far Eastern origin. In northern Scandinavia almost one in five are HLA-B27 positive, yet only 1.8% of the Scandinavian population have ankylosing spondylitis; the most commonly associated autoimmune disease. Indeed, many people who carry HLA-B27 never develop any associated illness and why some do is not yet clearly understood.
HLA-B27 is associated with a range of autoimmune diseases including ankylosing spondylitis, psoriasis, inflammatory bowel disease and reactive arthritis. Other pathologies include psoriatic arthritis, ulcerative colitis associated spondyloarthritis and eye disorders such as acute anterior uveitis. Yet how this antigen is responsible for the development of these diseases remains a partial mystery and it does not appear to be the sole factor at play. Separate triggers in the form of another gene, an illness of some nature such as a viral infection or some environmental influence; may represent the mysterious factor X that in combination with HLA-B27 will activate manifestation of a disease.
My own particular autoimmune disease is anterior uveitis, which is an acute inflammation (not infection) of the uvea (usually the iris) and it can be agonisingly painful. It causes swelling which can potentially damage nerves, the eye becomes sore and sensitive to light (photophobia). Anterior uveitis is an ocular emergency, treatment must begin within a few hours of onset to prevent permanent damage and loss of vision. Treatment is however, relatively simple and usually requires a short course of anti-inflammatory eye drops in combination with a dilation fluid. The latter in relaxing muscles and relieving spasm, dilates the pupil. This can make the photophobia worse. Such is medicine.
On those occasions when a more active treatment is required, steroid injections directly into the eye are called for. I have had three of these most unpleasant treatments but they were necessary. I have been in danger of permanent vision loss on two occasions. I shall be eternally grateful to the doctors at my local ophthalmic unit for their interventions. They are my saviours.
All of this sounds terribly negative and by now the reader is no doubt wondering whether there has been a mistake in naming this piece 'Counting our Blessings?' Patience, there is more.
The majority of the time I am fit and well. Although I may suffer a flare once or twice a year, I generally recover quickly. I get fatigued as we all do but fatigue can be a precursor to a flare, a warning I should heed. Rarely unless the flare is severe, do I require time off work. I often have to wear sunglasses indoors and at work, I may be unable to read, enjoy the outdoors or use the computer. These are short term irritations.
I have my family, close friends who understand my condition and my employer is supportive, often putting me on unofficial light duties while I recover. I concentrate on hands on care delivery and paperwork, avoiding drug administration and long periods on the computers.
I may one day go blind but it is unlikely. I may one day develop glaucoma and although that is more likely, it is far from certain. Various investigations and blood screenings have cleared me of far more unpleasant autoimmune disorders. Nothing I have is terminal, I am not going to die. My autoimmune condition can be painful, it can be a bloody nuisance but it will never be a death sentence.