Uveitis and macular edema a complex relationship in economics

The population of interest was adults with non-infectious intermediate uveitis, posterior In relation to the interventions of interest, namely ADA and DEX, data .. However, specific clinical outcomes (e.g. visual acuity or macular oedema) were and makes it difficult to assess whether or not selective reporting occurred. Noninfectious uveitis results in vision loss and ocular complications without In other studies, macular edema has been estimated to be present in 85% of cases of .. or biologics for uveitis; however, those results are difficult to compare with those These ocular complications may add significantly to the overall economic . The exact pathology of macular edema is complicated and uncertain. . the management of uveitis complicated by macular edema as steroid-sparing agents to reduce . Additional data, Economic data, quality-of-life data Clinical heterogeneity was present between the studies in relation to dosage used.

Interventions showing promise in this disease include dexamethasone implants, immunomodulatory drugs and anti-vascular endothelial growth-factor agents. When macular edema has become refractory after multiple interventions, pars plana vitrectomy could be considered.

The disease pathophysiology is uncertain and the course of disease unpredictable. As there are no clear guidelines from the literature, interventions should be tailored to the individual patient. Macular edema most commonly occurs as a consequence of chronic intraocular inflammation. Optical coherence tomography OCT can further aid in diagnosis and provide quantitative measures of central macular thickness. Other causes of visual impairment in uveitis include glaucoma, optic nerve involvement, vitreous opacification from the inflammatory response, and cataract formation usually attributed to both the disease process and chronic steroid use.

The exact pathology of macular edema is complicated and uncertain. The autoimmune theory is acceptable in patients who have been identified as genetically susceptible to uveitis.

Inner and outer blood—retinal barrier breakdown in the central retina due to prolonged or severe inflammation leads to macular edema. The retinal vascular endothelium changes with activation of adhesion molecules and lymphocytes.

The fluid is predominantly located in the outer plexiform layer, as seen on OCT scanning. Development of an epiretinal membrane is also a consequence of chronic macular edema.

Thus it is important to treat macular edema early. Further chronic macular edema may become more difficult to treat. Refractory macular edema usually occurs in patients with chronic or recurrent uveitis. Epidemiology Most of the epidemiological data is related to developed countries. The estimated annual incidence of uveitis is 17—52 cases perUveitis is predominately a disease of adults between 20 and 60 years. The mechanism of action of steroids involves the inhibition of prostaglandin and leukotriene synthesis, as well as downregulation of cell adhesion and major histocompatibility molecules.

However, it is associated with systemic side effects. Long-term use of steroids can cause peptic ulceration, osteoporosis, and necrosis of the hip, weight gain, muscle weakness, hyperglycemia, and systemic hypertension, progression of glaucoma, and progression of cataracts. Less commonly, intravenous methyl prednisolone is used typically at much higher doses than that given orally, such as — mg doses repeated over 2—3 days.

Forms of periocular injections include subconjunctival, orbital floor, and sub-Tenon. A steroid-filled syringe is advanced with the bevel facing towards the globe, superotemporally along the curve of the globe. The needle is advanced until the hub touches the conjunctiva. The plunger is slightly withdrawn to rule out injecting steroids within a vessel. Conjunctiva along with Tenon is lifted approximately 10 mm away from the limbus using blunt serrated forceps.

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A gauge cannula is inserted and advanced 3 mm within the episcleral space. The cannula is advanced about 12—14 mm in the sub-Tenon space with the stylet withdrawn. The syringe is then loaded with the steroid and injected. It has been used to treat macular edema from a variety of other etiologies, including retinal vein occlusion, diabetic retinopathy, pseudophakic CME, and exudative macular degeneration. It is injected into the vitreous using an injector.

Dexamethasone is then released over 3—6 months. It can be inserted in the clinic, in contrast to nonbiodegradable implants, which require a surgical procedure in the operating theater. It is licensed in the US for posterior uveitis.

Cystoid Macular Edema

The implant itself is a 1. The implant is surgically placed into the vitreous cavity. Pharmacokinetic studies in rabbits have demonstrated the delivery of constant levels of the corticosteroid to the posterior pole. Although there is a reduction in systemic side effects, there are significant local side effects, including increased intraocular pressure requiring filtration surgery and cataract progression.

Carbonic anhydrase catalyzes the hydration of carbon dioxide to bicarbonate, which dissociates to form hydrogen ions and bicarbonate. One subtype of carbonic anhydrase is isoenzyme IV, which is thought to be a membrane-bound fraction found in the apical region of the RPE cell. Inhibition of carbonic anhydrase reduces aqueous production and possibly fluid leaking from the RPE.

It is a potent inhibitor of the release of growth hormone and other hormones. Potential relationships between clinical grades of cells or flare and each of the 6 abnormalities or complications of uveitis were analyzed using the Mann-Whitney test.

The relationship between laser flare photometry values and visual acuity was analyzed with multiple linear regression. Results We evaluated patients with uveitis.

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There were 66 women and 45 men with a mean age of The characteristics of uveitis in these patients are summarized in Table 1 and Table 2. We did not find any significant relationships between laser flare photometry values and onset of disease, duration of disease, or anatomic classification. Measures of inflammation laser flare photometry value expressed as mean photon units per millisecond and as mean log of laser flare photometry value, clinical grade of flare, and clinical grade of cell in patients with and without abnormalities and complications associated with uveitis are listed in Table 3.

Cystoid Macular Edema - EyeWiki

The denominator used to calculate percentages varied for each abnormality or complication because the clinical record was incomplete for some patients; a patient was not included in a given analysis if there was no mention of either the presence or absence of the abnormality or complication being considered.

There were no significant differences in values between eyes that did and did not have the following abnormalities or complications: Logistic regression demonstrated that a 1-log unit fold increase in laser flare photometry value was associated with a 2. A 1-log unit increase in laser flare photometry value was associated with a 2. There were no other statistically significant associations between abnormalities or complications and clinical grades of either flare or cells.

As a secondary analysis, comparisons were repeated using data from the right eye of all patients with bilateral uveitis. Results were generally in close agreement with the primary analyses presented previously, which used data from the eye with the highest laser flare photometry value. This agreement indicates the robust nature of our results. The only discrepancies included the following: Linear regression was used to determine whether this correlation could be explained by complications of uveitis.

Comment We undertook this project as a pilot study to determine whether relationships exist between elevated laser flare photometry values and selected abnormalities and complications associated with uveitis.

The cross-sectional design allows rapid identification of such associations but does not confirm causal relationships. We purposefully studied a heterogeneous population of patients with a variety of disease categories and diagnoses. No relationship was found between laser flare photometry measurements and specific categories of disease or diagnoses. Thus, we found no evidence that the relationships between abnormalities or complications associated with uveitis and laser flare photometry values were indirect, attributable to higher rates of those abnormalities or complications with particular diseases that are characterized by high aqueous protein levels.

Future studies should control for potential confounding factors such as duration of disease. Although duration of disease most likely affects complication rates, we found no relationship between duration and laser flare photometry values.

Laser flare photometry has been used to characterize intraocular inflammatory reactions in a variety of disorders and clinical situations. Although we found the correlation between laser flare photometry values and clinical grades of flare to be statistically significant in this study, laser flare photometry values varied considerably for each clinical grade of flare. This fact may explain why relationships between clinical grades of flare and abnormalities or complications associated with uveitis have not been shown in this study or previous ones.

We found significantly higher laser flare photometry values in patients with posterior synechiae, cataracts or a history of cataract extraction, and macular edema. We also found an inverse relationship between laser flare photometry values and visual acuity that could not be explained on the basis of associations between laser flare photometry values and vision-limiting complications.

Similar relationships were not identified between clinical grades of cells and complications or visual acuity. The basis of the relationships between changes in aqueous humor protein composition or concentration as reflected by elevated laser flare photometry values and abnormalities or complications of uveitis is unknown, but it is possible that the proteins play a causal role. Breakdown of the blood-aqueous barrier in patients with uveitis is known to change the protein composition of the aqueous humor.

It is also possible that reactive chemokines, which probably represent a portion of aqueous humor proteins in the inflamed eye, play a role in the development of complications such as macular edema by altering vascular integrity or other cellular functions. Finally, the possibility remains that aqueous humor proteins do not cause damage but are merely markers linked to other disease processes that occur in an inflamed eye.

Possible relationships between aqueous humor protein levels and secondary cataracts are difficult to interpret. A significant relationship was identified when eyes with cataracts and those that had previously undergone cataract extraction were grouped together and compared with phakic eyes without cataracts.