Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Retrospective clinical trial evaluated efficacy and safety of phototherapeutic keratectomy (PTK) within 35 children (35 eyes) aged 8 to 18 years (mean 12.6 years). All children had a long time postoperative follow-up ranged from 2 to 5 years (mean 3.2 years). Indications for PTK in children were: recurrent corneal epithelial erosion syndrome, superficial scars after keratitis "e lagophthalmo", dry spots and mucous plaques after atopic- vernal eye disease, band keratopathy, anterior corneal dystrophies, corneal scars secondary to post-infectious keratitis (post-herpes simplex corneal scarring) and following trauma. The aim of treatment were to improve visual acuity and to reduce or eliminate subjective ocular discomfort-pain, lacrimation and photophobia. Fully informed parents consent was done at all cases. There was increased the best spectacle corrected visual acuity (BSCVA) in all Children, and episodes of ocular pain, lacrimation and photophobia diminished. The mean preoperative BSCVA 6/36 (ranged from 6/9 to 1/60) improved to mean value 6/12 (ranged from 6/6 to 6/60) as 2-5 years follow-up postoperatively. Seven children had 5 or more Snellen's lines gain of the BSCVA, ten children gained 4 lines, eight children gained 3 lines and five children gained 2 lines postoperatively in comparison to their preoperative values. At four cases were evaluated only 1 line gain of BSCVA, one eye unchanged, and no eye had BSCVA worsened after PTK. Phototherapeutic keratectomy in children seems to be an effective and safety procedure in the management of suitable anterior corneal disorders. Our clinical results suggest the most suitable diagnoses for treatment include recurrent corneal epithelial erosions, band keratopathy, dry spots, mucous plaques, anterior corneal dystrophies, and anterior post-keratitis and post-traumatic scars.
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PMID:[Phototherapeutic keratectomy in the treatment of corneal surface disorders in children]. 1204 43

Human keratoconus is a common corneal disease with non-inflammatory corneal ectasia, and a subset of this disease is heritable. In an effort to establish animal models for this disease, we discovered Japanese keratoconus (JKC) mice among Mishima molosinus (MSM) mice, an inbred strain of Japanese wild mice (Mus musculus molossinus). Typical phenotypic corneas of JKC mice are, like human keratoconus, conical in shape, although the corneas were often associated with a red punctum at the tip. In contrast to human keratoconus, histological examination revealed the inflammatory changes such as infiltration of capillaries and hematocytes in JKC mouse corneas. Although JKC mouse corneal change is probably secondary to keratitis and is a mouse-specific keratopathy, its pathogenesis may be relevant to that of human keratoconus. Linkage analysis mapped the responsible gene at the markers D13Mit21, D13Mit252, D13Mit279, and D13Mit39, which are located between 21.9 and 34.0 cm of the mouse Chr 13. Candidate genes in this region include genes for cathepsins, interleukin, and chemotaxin. Further study of JKC mice may shed light on pathogenesis of human keratoconus.
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PMID:Hereditary keratoconus-like keratopathy in Japanese wild mice mapped to mouse Chromosome 13. 1251 47

We report two cases of nontuberculous mycobacterial keratitis, occurring after corneal trauma with superficial foreign body and after perforating keratoplasty for alkali burn, respectively. Patients initially presented with indolent white corneal infiltrates, which did not respond to topical treatment. Both secondarily developed infectious crystalline keratopathy with unequal intensity. In the first case, the excised flap of lamellar keratectomy was cultured, allowing identification of Mycobacterium abscessus. Mycobacterium chelonae was isolated from a corneal biopsy in the second case. The clinical course showed poor response to antibiotic therapy consisting of ciprofloxacin and amikacin drops in conjunction with a new-generation oral macrolide. Corneal infection recurred after lamellar keratectomy in the first patient. Topical corticosteroid interruption burst corneal inflammation and induced stromal necrosis in the other patient. These intractable mycobacterial infections were finally controlled with penetrating keratoplasty. Our data suggest that a rapidly growing mycobacteria culture is required when clinical presentation consists of chronic bacterial keratitis or infectious crystalline keratopathy.
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PMID:[Nontuberculous mycobacterial keratitis: report of two cases causing infectious crystalline keratopathy]. 1266 May 93

Objective: To define the best conditions for amniotic membrane preparation, storage and banking in its use for corneal reconstruction. Methods: Amniotic membrane pieces were prepared under sterile conditions from placentas selected on the basis of donor medical and social history, serology, microbiological tests and histology. The pieces were kept at -140 degrees C but before grafting they were thawed and stored at 4 degrees C in RPMI medium, to have a preparation usable within 72 h. This procedure was validated by testing its therapeutic effectiveness in 25 patients 13 of which had corneal ulcers of various origin, 3 had sequelae of herpes simplex keratitis, 3 band keratopathy and 6 corneal stem cell deficiency due to chemical or thermal burns. Results: The preparation showed appreciable anti-inflammatory and analgesic effects. In the absence of corneal stem cell deficiency a stable re-epithelialisation was achieved in 15 out of 19 patients. When the limbus was lesioned, the amniotic membrane decreased vascularization and increased the number of corneal epithelial cells only in 1 of the 6 patients. No adverse reactions attributable to the tissue were recorded. Conclusions: A ready-to-use amniotic membrane preparation stored at 4 degrees C after cryopreservation has been tested in corneal reconstruction. Like the amniotic membrane thawed immediately before grafting, this preparation displayed full therapeutic effect in epithelial defects with stromal ulceration but without severe limbal stem cell deficiency. In two years banking activity 463 pieces of the preparation were successfully distributed to 90 Italian hospitals.
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PMID:Further evaluation of amniotic membrane banking for transplantation in ocular surface diseases. 1525 13

This article discusses the diagnosis and medical treatment of stromal keratomalacia or "melting ulcers," stromal abscesses, eosinophilic keratitis (EK), and calcific band keratopathy. These are common and important inflammatory keratopathies of the equine corneal stroma. Keratomalacia and stromal abscesses are associated with infection, leukocytic invasion of the stroma, and loss of tissue and tear film proteinase homeostasis. Eosinophils infiltrate the stroma in response to unknown stimuli in EK. Calcium is deposited in the stroma and epithelium secondary to chronic equine recurrent uveitis in calcific band keratopathy. They are all associated with varying degrees of iridocyclitis.
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PMID:Inflammatory stromal keratopathies: medical management of stromal keratomalacia, stromal abscesses, eosinophilic keratitis, and band keratopathy in the horse. 1527 27

We describe pathological, ultrastructural, and spectrographic analyses of surgically resected cornea from a man with atypical corneal opacification, and discuss the corneal pathogenesis, and the utility of energy-dispersive X-ray microanalysis (EDXA). The histopathologic features of a case presenting with longstanding bilateral corneal clouding are reported, which was difficult to be diagnosed clinically as calcific band keratopathy. The patient underwent keratoplasty on his right eye. Paraffin sections of the host corneal button were subjected to hematoxylin and eosin (H&E). An adjacent section was studied by means of EDXA. Plastic sections were observed under a transmission electron microscope (TEM). H&E staining revealed flattened corneal epithelial cells and disappearing Bowman's membrane accompanied by numerous basophilic granular deposits within the underlying corneal stroma. EDXA demonstrated the elevated peaks of calcium and phosphorus within the area of granular deposits. TEM revealed electron dense material consistent with extracellular calcospherites. Given the patient's past medical and family history, and the serologic test results, the clinical presentation and histological findings were most consistent with calcific band keratopathy associated with preexisting minimal syphilitic keratitis. Extensive histologic studies including EDXA on resected corneal tissue can be helpful for the differential diagnosis and may elucidate the pathogenesis of corneal diseases.
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PMID:Application of energy-dispersive X-ray microanalysis on the diagnosis of atypical calcific band keratopathy. 1593

The cornea is naturally transparent. Anything that interferes with the cornea's stromal architecture, contributes to blood vessel migration, increases corneal pigmentation, or predisposes to corneal edema, disrupts the corneas transparency and indicates corneal disease. The color, location, and shape and pattern of a corneal lesion can help in determining the underlying cause for the disease. Corneal disease is typically divided into congenital or acquired disorders. Congenital disorders, such as corneal dermoids are rare in cats, whereas acquired corneal disease associated with nonulcerative or ulcerative keratitis is common. Primary ocular disease, such as tear film instability, adenexal disease (medial canthal entropion, lagophthalmus, eyelid agenesis), and herpes keratitis are associated with the majority of acquired corneal disease in cats. Proliferative/eosinophilic keratitis, acute bullous keratopathy, and Florida keratopathy are common feline nonulcerative disorders. Nonprogressive ulcerative disease in cats, such as chronic corneal epithelial defects and corneal sequestration are more common than progressive corneal ulcerations.
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PMID:Feline corneal disease. 1594 22

Recurrent corneal erosions (RCE) are common. They are characterised by repeated episodes of pain, difficulty in opening the eyes, watering, and photophobia resulting from poor epithelial adhesion. In the majority of patients with RCE, trauma is the initiating factor. Epithelial, stromal, and endothelial corneal dystrophies have all been described in association with RCE. Other causes that may lead to RCE include chemical and thermal injuries, previous herpetic keratitis, meibomian gland dysfunction, ocular rosacea, diabetes mellitus, Salzmann's nodular degeneration, band keratopathy, previous bacterial ulceration, kerato-conjunctivitis sicca, and epidermolysis bullosa. The conditions that are associated with RCE can be either primary or secondary depending on whether the basement membrane complex abnormality is intrinsic or acquired. Primary types tend to be bilateral, symmetrical and develop in multiple corneal locations. The pathogenetic mechanism of this disorder is related to poor adhesion of the corneal epithelium to the underlying stroma. Excessive matrix metalloproteinase (MMP) activity may play a role in the pathogenesis. Although the majority of patients will respond to simple measures such as padding and antibiotic ointment, RCE resistant to simple measures require approaches that are more elaborate. The common goal of these approaches is to encourage proper formation of adhesion complexes between the epithelium and the stroma. The use of long-term contact lenses, autologous serum eye drops, botulinum toxin, induced ptosis, oral MMP inhibitors, diamond burr polishing of Bowman's membrane have been reported with varying degree of success in treating RCE. Anterior stromal puncture with insulin needles or Neodymium : aluminium-yttrium-garnet may enhance the epithelial adhesion to the basement membrane by scar formation and success rates of up to 80% have been reported in the treatment of recalcitrant RCE. Excimer laser photo-therapeutic keratectomy (PTK) is now a well-established treatment modality for RCE and is being used both safely and effectively. Partial ablation of Bowman's layer with PTK gives a smooth surface for the newly generating epithelium to migrate and form adhesion complexes. The pathogenesis, clinical features, and management options of this common disorder are discussed in this review article.
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PMID:Pathogenesis, clinical features and management of recurrent corneal erosions. 1757 Oct 89

We report a clear corneal wound infection occurring in a 74-year-old man caused by a member of the Mycobacterium chelonae-Mycobacterium abscessus complex, presenting as crystalline keratopathy with recurrent hypopyon. This led to perforation after phacoemulsification with posterior chamber intraocular lens implantation. Only after corneal biopsy of the incision was the causative organism isolated and found to be sensitive to clarithromycin and ciprofloxacin. Despite aggressive therapy, a full-thickness corneal perforation developed, requiring emergent cyanoacrylate glue to preserve ocular integrity. Both the difficulty and delays in obtaining a correct diagnosis led to severe ocular morbidity. Infectious lamellar keratitis limited to the clear cornea phacoemulsification incision is rare, but some unusual organisms such as atypical mycobacteria may be encountered.
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PMID:Mycobacterium chelonae-Mycobacterium abscessus complex clear corneal wound infection with recurrent hypopyon and perforation after phacoemulsification and intraocular lens implantation. 1610 23

Recent advances in corneal graft technology, including donor tissue retrieval, storage and surgical techniques, have greatly improved the clinical outcome of corneal grafts. Despite these advances, immune mediated corneal graft rejection remains the single most important cause of corneal graft failure. Several host factors have been identified as conferring a "high risk" status to the host. These include: more than two quadrant vascularisation, with associated lymphatics, which augment the afferent and efferent arc of the immune response; herpes simplex keratitis; uveitis; silicone oil keratopathy; previous failed (rejected) grafts; "hot eyes"; young recipient age; and multiple surgical procedures at the time of grafting. Large grafts, by virtue of being closer to the host limbus, with its complement of vessels and antigen-presenting Langerhans cells, also are more susceptible to rejection. The diagnosis of graft rejection is entirely clinical and in its early stages the clinical signs could be subtle. Graft rejection is largely mediated by the major histocompatibility antigens, minor antigens and perhaps blood group ABO antigens and some cornea-specific antigens. Just as rejection is mediated by active immune mediated events, the lack of rejection (tolerance) is also sustained by active immune regulatory mechanisms. The anterior chamber associated immune deviation (ACAID) and probably, conjunctiva associated lymphoid tissue (CALT) induced mucosal tolerance, besides others, play an important role. Although graft rejection can lead to graft failure, most rejections can be readily controlled if appropriate management is commenced at the proper time. Topical steroids are the mainstay of graft rejection management. In the high-risk situations however, systemic steroids, and other immunosuppressive drugs such as cyclosporin and tacrolimus (FK506) are of proven benefit, both for treatment and prevention of rejection.
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PMID:Corneal allograft rejection: risk factors, diagnosis, prevention, and treatment. 1613 Feb 77


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