Well for the last two months I have been suffering from Iritis, related to my HLA-B27 gene (AS).
I’ve had to attend the eye clinic at Burnley general hospital regularly, and have had steriod injections in the right eye. (OUCH)
I’m still taking dilatory drops and the steroid based Pred Forte eye drops.
There are two main types of iritis: acute and chronic. They differ in numerous ways. Acute iritis is a type of iritis that can heal independently within a few weeks. If treatment is provided, acute iritis improves quickly. Chronic iritis can exist for months or years before recovery occurs. Chronic iritis does not respond to treatment as well as acute iritis does. Chronic iritis is also accompanied by a higher risk of serious visual impairment.
* Ocular and periorbital pain
* Consensual photophobia (pain in affected eye when light is shone in unaffected eye)
* Blurred or cloudy vision
* Reddened eye, especially adjacent to the iris
* White blood cells (leukocytes) (seen as tiny white dots, clinically termed cells) and protein (resulting in a grey or near-white haze, clinically termed flare) leak into the anterior chamber.
* Synechia (adhesion of iris to lens or cornea)
* Motion sickness
Causes and Comorbidities
* Physical eye trauma
Inflammatory and Autoimmune Disorders:
* Ankylosing Spondylitis and other HLA-B27 related disorders
* Iridocyclitis, and other forms of uveal tract inflammation.
* Rheumatoid arthritis
* Behcet’s disease
* Crohn’s disease
* Graves disease
* Reactive arthritis
* Chronic psoriasis
* Psoriatic arthritis
* Ulcerative colitis
* corneal calcification
* posterior uveitis
* band keratopathy
* cystoid macular oedema.
Macular edema occurs when fluid and protein deposits collect on or under the macula of the eye, a yellow central area of the retina, causing it to thicken and swell. The swelling may distort a person’s central vision, as the macula is near the center of the retina at the back of the eyeball. This area holds tightly packed cones that provide sharp, clear central vision to enable a person to see form, color, and detail that is directly in the line of sight.
Macular edema is sometimes a complication appearing a few days or weeks after cataract surgery, but most such cases can be successfully treated with NSAID or cortisone eye drops.
Until recently there were no good treatments for macular edema caused by central retinal vein occlusion (CRVO). Laser photocoagulation has been used for macular edema caused by branch retinal vein occlusion (BRVO).
The macula is the part of the retina responsible for sharp vision due to its high density of cone photoreceptors. It is situated at the centre of the back of the retina (the posterior pole), lying about 3mm lateral to the optic disc. It has a central depression known as the fovea centralis. There are nothing but tightly packed cone photoreceptors in this area with no overlying blood vessels. This is where visual acuity is ultimately determined.
Macular oedema refers to the accumulation of fluid within the retina at the macular area (distinct from the condition where the fluid accumulates under the retina).This is frequently – but not always – cystoid in nature (cystoid macular oedema, CMO). There are many reasons why this can happen but most commonly, it is seen:
* Following intraocular surgery:1 where CMO occurs as a consequence of surgery, it is known as the Irvine-Gass syndrome. It is thought to occur as a result of release of inflammatory mediators within the eye and if it is prolonged or recurring, permanent damage can occur.
* In central (and occasionally) branch retinal vein occlusions:2 venous occlusion causes a rise in intra-venous and capillary pressure leading to stagnation of blood, hypoxia of the affected structures and damage to the capillary endothelial cells, so ending in extravasation of plasma constituents. In the case of branch retinal vein occlusion, macular oedema occurs when the temporal vein draining the macula is occluded.
* Other causes of CMO include inflammatory diseases (uveitis, birdshot chorioretinopathy, toxoplasmosis), various types of retinal vascular disease (idiopathic retinal telangiectasia, radiation retinopathy), retinal dystrophies (such as retinitis pigmentosa) and drug-induced (such as can occur with topical adrenaline 2%, particularly in patients without a lens).
When macular oedema occurs in the context of diabetic retinopathy, it is referred to as clinically significant macular oedema (CSMO). It occurs as a result of increased vascular permeability due to histological changes, so resulting in a compromise of the blood-retinal barrier and leakage of plasma constituents into the surrounding area. The oedema can be focal or diffuse – its nature will guide treatment.
The third group of patients prone to macular oedema are those suffering from certain forms of age related macular degeneration (ARMD): exudative (‘wet’) ARMD. This gives rise to formation of choroidal neovascular membranes which leak fluid and blood under the retina, so resulting in macular oedema.
Ankylosing spondylitis (AS, from Greek ankylos, bent; spondylos, vertebrae), previously known as Bekhterev’s disease, Bekhterev syndrome, and Marie-Strümpell disease, a form of Spondyloarthritis, is a chronic, inflammatory arthritis and autoimmune disease. It mainly affects joints in the spine and the sacroilium in the pelvis, and can cause eventual fusion of the spine.
It is a member of the group of the spondyloarthropathies with a strong genetic predisposition. Complete fusion results in a complete rigidity of the spine, a condition known as bamboo spine.
The typical patient is a young male, aged 20–40, when symptoms of the disease first appear, with chronic pain and stiffness in the lower part of the spine or sometimes the entire spine, often with pain referred to one or other buttock or the back of thigh from the sacroiliac joint.
Men are affected more than women by a ratio about of 3:1, with the disease usually taking a more painful course in men than women. In 40% of cases, ankylosing spondylitis is associated with an inflammation of the eye (iridocyclitis and uveitis), causing redness, eye pain, vision loss, floaters and photophobia. Another common symptom is generalized fatigue and sometimes nausea. Less commonly aortitis, apical lung fibrosis and ectasia of the sacral nerve root sheaths may occur.
When the condition presents before the age of 18, it is relatively likely to cause pain and swelling of large limb joints, particularly the knee. In pre-pubescent cases, pain and swelling may also manifest in the ankles and feet, where calcaneal spurs may also develop.
Pain is often severe at rest, but improves with physical activity. However, many experience inflammation and pain to varying degrees regardless of rest and movement.
Ankylosing spondylitis is one of a cluster of conditions known as seronegative spondyloarthropathies, in which the characteristic pathological lesion is an inflammation of the enthesis (the insertion of tensile connective tissue into bone).
Ankylosing spondylitis (AS) is a systemic rheumatic disease meaning it affects the entire body and is one of the seronegative spondyloarthropathies. Approximately 90% of AS patients express the HLA-B27 genotype, meaning that there is a strong genetic association. However, only 5% of individuals with the HLA-B27 genotype contract the disease.Tumor necrosis factor-alpha (TNF ?) and IL-1 are also implicated in ankylosing spondylitis. Autoantibodies specific for AS have not been identified. Anti-neutrophil cytoplasmic antibodies ANCA are associated with AS but don’t correlate with disease severity.
The association of AS with HLA-B27 suggests that the condition involves CD8 T cells, which interact with HLA-B. It is not proven that this interaction involves a self antigen and at least in the related Reiter’s syndrome (reactive arthritis), which follows infections, the antigens involved are likely to be derived from intracellular microorganisms. There is, however, a possibility that CD4 T cells are involved in an aberrant way, since HLA-B27 appears to have a number of unusual properties, including possibly an ability to interact with T cell receptors in association with CD4 (usually only T helper lymphocytes with CD8 reacts with HLAB antigen as it is a MHC class 1 antigen).
There has been a longstanding claim that AS arises from a cross-reaction between HLA-B27 and antigens of the Klebsiella bacterial strain (Tiwana et al. 2001). The problem with this idea is that no such cross reactivity with B27 has been found (i.e. although antibody responses to Klebsiella may be increased, there is no antibody response to B27, so there seems to be no cross reactivity.) Particular authorities argue that elimination of the prime nutrients of Klebsiella (starches) would decrease antigenemia and improve the musculoskeletal symptoms. However, as Khan (2002) argues, evidence for a correlation between Klebsiella and AS is circumstantial so far, and that the efficacy of low-starch diets has not yet been scientifically evaluated.Studies on low-starch diet and AS could be difficult to fund, while new biologics developed by the pharmaceutical industry may demonstrate efficacy, as well as financial benefit to the industry (whereas changing the diet would not).
Toivanen (1999) found no support for the role of Klebsiella in the etiology of primary AS.