Description, Causes and Risk Factors:
Chronic inflammation of the peripheral cornea that slowly progresses centrally with corneal thinning and sometimes perforation.
Mooren's ulcer, also referred to as Mooren ulcer, is a rare, painful, inflammatory condition affecting one or both eyes that results in the destruction of corneal tissue. The intensity of the disease can vary from mild damage to the edges of the cornea in one eye that responds quickly to therapy, to a blinding condition that results in severe damage to both eyes.
Although the cause is unknown, it has been suggested that there is a genetic as well as an environmental basis for the disease. The likely environmental factors include antecedent history of accidental trauma or surgery and exposure to viral and parasitic infections. However, an increase in the rate of hepatitis C infection has not been found in patients from India with Mooren's ulcer. An association with helminthiasis (intestinal worm infestation) has also been noted, but the disease can develop in the absence of helminthiasis. Even where helminthiasis is endemic, Mooren's ulcer is still rare. Human leukocyte antigens (HLAs) can confer susceptibility to several autoimmune disorders and in Asian and black African patients the presence of HLA-DR17 or DQ2 (histocompatibility antigens) may confer susceptibility to Mooren's ulcer. Researchers also reported increased expression of HLA DR in patients with the disease.
Researchers also demonstrated cellular and humoral immune responses to bovine corneal antigen in a patient with MU. Serum from this patient was used to purify a cornea-associated antigen (Co-Ag) from bovine corneal stromal extracts. The Co-Ag protein is found to contain 70 amino acids in a single chain and lacks cysteine, tryptophan, and methionine residues. These results have suggested that Co-Ag is a new member of the Ca2+ binding protein of the S-100 family of proteins and could provide an important framework to search for sequence similarity with microbial proteins as possible substrate for molecular mimicry and for identification of possible pathogenic epitopes in Co-Ag. Nevertheless, it is still unknown if cell-mediated and/or humoral immune mechanisms are involved directly in the pathogenesis of MU. It may be that they just accompany the corneal destruction that is caused by another mechanism.
Mooren's ulcer can range from mild cases affecting one eye that do not threaten vision to severe cases involving both eyes and threatening the vision. Because Mooren's ulcer is rare, detailed knowledge is not available which allows prediction of the severity of this disease in a particular patient. Some studies have tried to correlate gender, age, and race with outcomes, but there have been no large studies to confirm these reports.
The prevalence of Mooren's ulcer and the blindness caused by it worldwide is unknown. The disease is rare in the northern hemisphere but more common in southern and central Africa, China and the Indian subcontinent. It is more common in males (1.3:1) than females (1.6:1) and very rare in children.
Patients with Mooren ulcer typically present with redness, tearing, photophobia, but pain is the mostoutstanding feature. The pain often is incapacitating and may be out of proportion to theinflammation. There may be a decrease in visual acuity secondary to associated iritis, centralcorneal involvement, irregular astigmatism due to peripheral corneal thinning. The disease maybegin with several patchy, peripheral stromal infiltrates which coalesce, more often in the medialand lateral quadrants than in the superior and inferior ones.
Often, there is involvement of the limbus, in contrast to other forms of PUK (peripheral ulcerative keratitis), such as that seen inrheumatoid arthritis.The ulcerative process first spreads circumferentially and thencentrally to involve the entire cornea. The anterior one-third to one-half of the stroma is involved,characteristically with a steep, overhanging edge. The leading and central edge typically isundermined. This may not be easily apparent on slit-lamp examination, and probing of this edgemay reveal a surprising degree of stromal destruction. Healing and vascularization, over acourse of 4-18 months.
Portions of ulcer may be quiescent, while others are active. The end-stage result is typically ascarred, vascularized cornea that may be thinned to less than half of its original thickness. As theend stage of the process approaches, the patients may experience relief from the excruciatingpain that has been present throughout the course of the disease.
Complications from Mooren ulcer may include iritis, hypopyon, glaucoma, and cataract. Perforation mayoccur in 35 to 40% of cases, often associated with minor trauma to the weakened cornea.
Although the diagnosis may be difficult when a patient first presents with Mooren's ulceration, the clinical appearances are characteristic and should not be confused with other conditions which cause corneal ulceration. Based on the clinical presentation and the low-dose anterior segment fluorescein angiographic findings, there seem to be three distinct varieties of Mooren's ulceration: (1) Unilateral Mooren's ulceration (UM), characterized by an excessively painful progressive corneal ulceration in one eye in elderly patients, associated with non-perfusion of the superficial vascular plexus of the anterior segment. (2) Bilateral aggressive Mooren's ulceration (BAM), which occurs in young patients, progresses circumferentially and, only later, centrally in the cornea. Angiography shows vascular leakage and new vessel formation which extends into the base of the ulcer. (3) Bilateral indolent Mooren's ulceration (BIM), which usually occurs in middle-aged patients presenting with progressive peripheral corneal guttering in both eyes, with little inflammatory response. There is no change from the normal vascular architecture on angiography except an extension of new vessels into the ulcer. The management differs in each of these varieties.
There is no specific test at this time for Mooren's ulcer. Instead, testing attempts to rule out otherconditions that can cause similar eye problems such as rheumatoid arthritis (RA), systemic lupuserythematosus (SLE) or Wegener's granulomatosis. Blood tests and a chest X-ray may be ordered.Sometimes, corneal infections can mimic the findings of Mooren's ulcer and therefore testing thecornea for the presence of microorganisms (germs) may be performed. An ophthalmologistmakes the diagnosis of Mooren's ulcer once he is convinced that a patient's eye has changes thatare characteristic of Mooren's ulcer and that conditions which can mimic Mooren's ulcer havebeen excluded.
Currently, most ophthalmologists treat Mooren's ulcer with medications that suppress the immune system. In mild cases, this may be application of corticosteroid drops to the eye, but in more severe cases, corticosteroids may be administrated by mouth, or intravenously. If the ulceration is not controlled, stronger immunosuppressive medications such as cyclophosphamide may be required.
Surgery is sometimes performed on patients with Mooren's ulcer. A conjunctival resection may be helpful in reducing corneal inflammation and ulceration. Additionally, surgery may be required in patients who develop a perforation or hole in the cornea, to close the hole.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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